Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the United States.¹ In particular, NAFLD and the related inflammatory nonalcoholic steatohepatitis (NASH) often develop in individuals who are obese or who have prediabetes or type 2 diabetes, affecting up to 75% of patients with these conditions.²

In addition to NAFLD and NASH, other liver diseases associated with type 2 diabetes include cirrhosis, hepatocellular carcinoma, liver failure, and hepatitis.^1,3,4 Of patients with type 2 diabetes, more than 600,000 have cirrhosis; 4.4% of diabetes-related deaths have been attributed to cirrhosis.^4,5

NAFLD and NASH share a common pathophysiology in type 2 diabetes with respect to insulin resistance, which results in hyperlipidemias that enhance fatty deposits in the liver.^1,2 Hepatic fat accumulation is also associated with increasing measures of inflammation, including C-reactive protein.⁶

Resultant liver function test abnormalities and characteristic appearance on imaging studies (ultrasound, computed tomography [CT], or magnetic resonance imaging [MRI]) may be similar in NAFLD and NASH.^1-3 Liver biopsy therefore is necessary to distinguish NAFLD from NASH, with NASH showing characteristic inflammatory and fibrotic changes.^1,2 Evaluations of patients with minor liver test abnormalities reveal that up to 98% may have liver disease, most often fatty liver disease.⁷

Weight loss is a strategy for managing NAFLD and NASH, although large randomized controlled trials are lacking.^8-10 Several agents used for diabetes and dyslipidemias, including glucagon-like peptide-1 (GLP-1) mimetics, metformin, thiazolidinediones, and statins, have been studied as possible treatments for NAFLD and NASH.^8-13 Currently, these medications carry cautions or warnings about using them in patients with liver disease and are not indicated as treatments for NAFLD or NASH.

SUBJECTS AND METHODS

One hundred patients were randomly selected from a type 2 diabetes patient database at the Altru Health System (Grand Forks, ND) for cross-sectional analysis. Manual data extraction from “paper charts” was necessary in some cases, limiting the size of the study.

All subjects had a diagnosis of type 2 diabetes confirmed by American Diabetes Association criteria, were between the ages of 18 and 64 years, and had no known liver disease other than that associated with their diabetes. Other criteria included visiting a health care provider regarding diabetes management within the last year and having undergone laboratory blood testing of liver function within the last 5 years. The study population comprised an equal number of men and women.

We collected data about abnormal liver function from blood test results, including levels of aspartate transaminase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP); results of radiologic imaging of the liver (ultrasound, MRI, or CT) and liver biopsy; any interventions (medication changes, lifestyle management, or surgery); and referral to a specialist (gastroenterologist or surgeon).

DATA ANALYSIS

Of the 100 subjects, 40 had at least one abnormal serum liver function test (AST, ALT, or ALP), although we could find no record of tests for one of the 100 subjects. Of the 40 with abnormal test results, 17 (42.5%) were women and 23 (57.5%) were men. None of these patients had highly elevated levels of AST, ALT, or ALP.

Of the 40 patients with abnormal serum liver function tests, only 10 (25%) were specifically referred for imaging studies related to a possible diagnosis of fatty liver disease. Four of these 10 patients (1 woman and 3 men) had both ultrasound and CT imaging. Another 10 subjects (25%) had incidental findings of fatty liver disease on imaging performed for another presumed diagnosis or symptom, eg, abdominal pain. Overall, 11 (6 men, 5 women) of the 40 subjects (27.5%) with at least one abnormal liver function test received a diagnosis of fatty liver disease based on imaging findings. None of the subjects had a diagnosis of cirrhosis or other end-stage liver disease.

A medical intervention was offered to 4 of the 11 patients (2 women and 2 men) who received a diagnosis of fatty liver disease. Practitioners specifically referred one woman for medical weight loss management and another for weight loss surgery. One man was advised to stop taking metformin, and another was referred to a dietician for lifestyle weight loss management. No patient was referred to a gastroenterologist or any other specialist for further evaluation or biopsy.

DISCUSSION

Although a small sample size limits the strength of this pilot study, the finding that fatty liver disease is common in patients with type 2 diabetes in a rural community hospital population supports other published data. As only half of the subjects with abnormal liver function tests had imaging studies, it’s likely that some patients in the study group who did not undergo imaging also had NAFLD, NASH, or other liver disease, but it was not diagnosed.

While no specific screening guidelines for fatty liver disease in patients with type 2 diabetes have been issued, clinical interest in this area has been growing, and this study suggests some avenues for further exploration.³ In the institution where this study was conducted, it appears that liver function tests were most likely to be performed in conjunction with routine monitoring of the use of statins, metformin, or other medications or because of a symptom such as abdominal pain. Yet given the widespread availability and relatively low cost of such tests, periodic monitoring of serum liver function in patients with type 2 diabetes may be warranted.¹⁴

Patients found to have persistent or recurrent abnormal liver function tests could then be referred for further evaluation with ultrasound, CT, or MRI.¹⁴ Ultrasound has the benefit of lower cost and avoidance of intravenous contrast, which may be important for patients with renal dysfunction.¹⁴ Based on the results of these tests, appropriate medical interventions could then follow.

·Acknowledgements·

The author thanks Bonnie Lee and Diane Vold for their assistance in the design of this study and its preparation for publication. The author also thanks William Zaks, MD, PhD, and James Brosseau, MD, MPH, for their guidance and feedback.

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the United States.¹ In particular, NAFLD and the related inflammatory nonalcoholic steatohepatitis (NASH) often develop in individuals who are obese or who have prediabetes or type 2 diabetes, affecting up to 75% of patients with these conditions.²

In addition to NAFLD and NASH, other liver diseases associated with type 2 diabetes include cirrhosis, hepatocellular carcinoma, liver failure, and hepatitis.^1,3,4 Of patients with type 2 diabetes, more than 600,000 have cirrhosis; 4.4% of diabetes-related deaths have been attributed to cirrhosis.^4,5

NAFLD and NASH share a common pathophysiology in type 2 diabetes with respect to insulin resistance, which results in hyperlipidemias that enhance fatty deposits in the liver.^1,2 Hepatic fat accumulation is also associated with increasing measures of inflammation, including C-reactive protein.⁶

Resultant liver function test abnormalities and characteristic appearance on imaging studies (ultrasound, computed tomography [CT], or magnetic resonance imaging [MRI]) may be similar in NAFLD and NASH.^1-3 Liver biopsy therefore is necessary to distinguish NAFLD from NASH, with NASH showing characteristic inflammatory and fibrotic changes.^1,2 Evaluations of patients with minor liver test abnormalities reveal that up to 98% may have liver disease, most often fatty liver disease.⁷

Weight loss is a strategy for managing NAFLD and NASH, although large randomized controlled trials are lacking.^8-10 Several agents used for diabetes and dyslipidemias, including glucagon-like peptide-1 (GLP-1) mimetics, metformin, thiazolidinediones, and statins, have been studied as possible treatments for NAFLD and NASH.^8-13 Currently, these medications carry cautions or warnings about using them in patients with liver disease and are not indicated as treatments for NAFLD or NASH.

SUBJECTS AND METHODS

One hundred patients were randomly selected from a type 2 diabetes patient database at the Altru Health System (Grand Forks, ND) for cross-sectional analysis. Manual data extraction from “paper charts” was necessary in some cases, limiting the size of the study.

All subjects had a diagnosis of type 2 diabetes confirmed by American Diabetes Association criteria, were between the ages of 18 and 64 years, and had no known liver disease other than that associated with their diabetes. Other criteria included visiting a health care provider regarding diabetes management within the last year and having undergone laboratory blood testing of liver function within the last 5 years. The study population comprised an equal number of men and women.

We collected data about abnormal liver function from blood test results, including levels of aspartate transaminase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP); results of radiologic imaging of the liver (ultrasound, MRI, or CT) and liver biopsy; any interventions (medication changes, lifestyle management, or surgery); and referral to a specialist (gastroenterologist or surgeon).

DATA ANALYSIS

Of the 100 subjects, 40 had at least one abnormal serum liver function test (AST, ALT, or ALP), although we could find no record of tests for one of the 100 subjects. Of the 40 with abnormal test results, 17 (42.5%) were women and 23 (57.5%) were men. None of these patients had highly elevated levels of AST, ALT, or ALP.

Of the 40 patients with abnormal serum liver function tests, only 10 (25%) were specifically referred for imaging studies related to a possible diagnosis of fatty liver disease. Four of these 10 patients (1 woman and 3 men) had both ultrasound and CT imaging. Another 10 subjects (25%) had incidental findings of fatty liver disease on imaging performed for another presumed diagnosis or symptom, eg, abdominal pain. Overall, 11 (6 men, 5 women) of the 40 subjects (27.5%) with at least one abnormal liver function test received a diagnosis of fatty liver disease based on imaging findings. None of the subjects had a diagnosis of cirrhosis or other end-stage liver disease.

A medical intervention was offered to 4 of the 11 patients (2 women and 2 men) who received a diagnosis of fatty liver disease. Practitioners specifically referred one woman for medical weight loss management and another for weight loss surgery. One man was advised to stop taking metformin, and another was referred to a dietician for lifestyle weight loss management. No patient was referred to a gastroenterologist or any other specialist for further evaluation or biopsy.

DISCUSSION

Although a small sample size limits the strength of this pilot study, the finding that fatty liver disease is common in patients with type 2 diabetes in a rural community hospital population supports other published data. As only half of the subjects with abnormal liver function tests had imaging studies, it’s likely that some patients in the study group who did not undergo imaging also had NAFLD, NASH, or other liver disease, but it was not diagnosed.

While no specific screening guidelines for fatty liver disease in patients with type 2 diabetes have been issued, clinical interest in this area has been growing, and this study suggests some avenues for further exploration.³ In the institution where this study was conducted, it appears that liver function tests were most likely to be performed in conjunction with routine monitoring of the use of statins, metformin, or other medications or because of a symptom such as abdominal pain. Yet given the widespread availability and relatively low cost of such tests, periodic monitoring of serum liver function in patients with type 2 diabetes may be warranted.¹⁴

Patients found to have persistent or recurrent abnormal liver function tests could then be referred for further evaluation with ultrasound, CT, or MRI.¹⁴ Ultrasound has the benefit of lower cost and avoidance of intravenous contrast, which may be important for patients with renal dysfunction.¹⁴ Based on the results of these tests, appropriate medical interventions could then follow.

·Acknowledgements·

The author thanks Bonnie Lee and Diane Vold for their assistance in the design of this study and its preparation for publication. The author also thanks William Zaks, MD, PhD, and James Brosseau, MD, MPH, for their guidance and feedback.

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the United States.¹ In particular, NAFLD and the related inflammatory nonalcoholic steatohepatitis (NASH) often develop in individuals who are obese or who have prediabetes or type 2 diabetes, affecting up to 75% of patients with these conditions.²

In addition to NAFLD and NASH, other liver diseases associated with type 2 diabetes include cirrhosis, hepatocellular carcinoma, liver failure, and hepatitis.^1,3,4 Of patients with type 2 diabetes, more than 600,000 have cirrhosis; 4.4% of diabetes-related deaths have been attributed to cirrhosis.^4,5

NAFLD and NASH share a common pathophysiology in type 2 diabetes with respect to insulin resistance, which results in hyperlipidemias that enhance fatty deposits in the liver.^1,2 Hepatic fat accumulation is also associated with increasing measures of inflammation, including C-reactive protein.⁶

Resultant liver function test abnormalities and characteristic appearance on imaging studies (ultrasound, computed tomography [CT], or magnetic resonance imaging [MRI]) may be similar in NAFLD and NASH.^1-3 Liver biopsy therefore is necessary to distinguish NAFLD from NASH, with NASH showing characteristic inflammatory and fibrotic changes.^1,2 Evaluations of patients with minor liver test abnormalities reveal that up to 98% may have liver disease, most often fatty liver disease.⁷

Weight loss is a strategy for managing NAFLD and NASH, although large randomized controlled trials are lacking.^8-10 Several agents used for diabetes and dyslipidemias, including glucagon-like peptide-1 (GLP-1) mimetics, metformin, thiazolidinediones, and statins, have been studied as possible treatments for NAFLD and NASH.^8-13 Currently, these medications carry cautions or warnings about using them in patients with liver disease and are not indicated as treatments for NAFLD or NASH.

SUBJECTS AND METHODS

One hundred patients were randomly selected from a type 2 diabetes patient database at the Altru Health System (Grand Forks, ND) for cross-sectional analysis. Manual data extraction from “paper charts” was necessary in some cases, limiting the size of the study.

All subjects had a diagnosis of type 2 diabetes confirmed by American Diabetes Association criteria, were between the ages of 18 and 64 years, and had no known liver disease other than that associated with their diabetes. Other criteria included visiting a health care provider regarding diabetes management within the last year and having undergone laboratory blood testing of liver function within the last 5 years. The study population comprised an equal number of men and women.

We collected data about abnormal liver function from blood test results, including levels of aspartate transaminase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP); results of radiologic imaging of the liver (ultrasound, MRI, or CT) and liver biopsy; any interventions (medication changes, lifestyle management, or surgery); and referral to a specialist (gastroenterologist or surgeon).

DATA ANALYSIS

Of the 100 subjects, 40 had at least one abnormal serum liver function test (AST, ALT, or ALP), although we could find no record of tests for one of the 100 subjects. Of the 40 with abnormal test results, 17 (42.5%) were women and 23 (57.5%) were men. None of these patients had highly elevated levels of AST, ALT, or ALP.

Of the 40 patients with abnormal serum liver function tests, only 10 (25%) were specifically referred for imaging studies related to a possible diagnosis of fatty liver disease. Four of these 10 patients (1 woman and 3 men) had both ultrasound and CT imaging. Another 10 subjects (25%) had incidental findings of fatty liver disease on imaging performed for another presumed diagnosis or symptom, eg, abdominal pain. Overall, 11 (6 men, 5 women) of the 40 subjects (27.5%) with at least one abnormal liver function test received a diagnosis of fatty liver disease based on imaging findings. None of the subjects had a diagnosis of cirrhosis or other end-stage liver disease.

A medical intervention was offered to 4 of the 11 patients (2 women and 2 men) who received a diagnosis of fatty liver disease. Practitioners specifically referred one woman for medical weight loss management and another for weight loss surgery. One man was advised to stop taking metformin, and another was referred to a dietician for lifestyle weight loss management. No patient was referred to a gastroenterologist or any other specialist for further evaluation or biopsy.

DISCUSSION

Although a small sample size limits the strength of this pilot study, the finding that fatty liver disease is common in patients with type 2 diabetes in a rural community hospital population supports other published data. As only half of the subjects with abnormal liver function tests had imaging studies, it’s likely that some patients in the study group who did not undergo imaging also had NAFLD, NASH, or other liver disease, but it was not diagnosed.

While no specific screening guidelines for fatty liver disease in patients with type 2 diabetes have been issued, clinical interest in this area has been growing, and this study suggests some avenues for further exploration.³ In the institution where this study was conducted, it appears that liver function tests were most likely to be performed in conjunction with routine monitoring of the use of statins, metformin, or other medications or because of a symptom such as abdominal pain. Yet given the widespread availability and relatively low cost of such tests, periodic monitoring of serum liver function in patients with type 2 diabetes may be warranted.¹⁴

Patients found to have persistent or recurrent abnormal liver function tests could then be referred for further evaluation with ultrasound, CT, or MRI.¹⁴ Ultrasound has the benefit of lower cost and avoidance of intravenous contrast, which may be important for patients with renal dysfunction.¹⁴ Based on the results of these tests, appropriate medical interventions could then follow.

·Acknowledgements·

The author thanks Bonnie Lee and Diane Vold for their assistance in the design of this study and its preparation for publication. The author also thanks William Zaks, MD, PhD, and James Brosseau, MD, MPH, for their guidance and feedback.

In February, the Centers for Disease Control and Prevention (CDC) published the 2012 immunization schedules for infants and children, adolescents, and adults.^1,2 The schedules, which are available at http://www.cdc.gov/vaccines/recs/schedules/default.htm, are updated annually and incorporate additions and changes recommended by the Advisory Committee on Immunization Practices (ACIP) over the past year. While there were no major advances in new vaccines in 2011, there were a number of new indications for existing ones.

Human papillomavirus vaccine for males
Quadrivalent vaccine against human papillomavirus is now recommended for routine use for males ages 11 to 12 years to prevent genital warts and anal intraepithelial neoplasia.^3,4 Catch-up vaccination is also recommended for males ages 13 to 21 who have not received it. In addition, routine use is recommended for males ages 22 to 26 years who have sex with men or are HIV positive or immuno-compromised.

Tetanus toxoid, reduced strength diphtheria toxoid, and acellular pertussis (Tdap)
Indications for the routine use of Tdap were expanded to include children ages 7 to 10 years, pregnant women, and adults age 65 and older who have contact with infants.^5,6 Children ages 7 to 10 years who have not had the full series of DTaP should receive Td/Tdap according to the catch-up schedule,¹ with one of the doses being Tdap. Adults older than 65 who have never received Tdap and who have close contact with infants should receive one dose. No minimum interval is required between receipt of the Td and Tdap vaccines. Other older adults who ask for Tdap vaccination should receive it. Use of Tdap in those ages 7 to 10 years or 65 and older is off label.⁵

Pregnant women who have not received Tdap should receive 1 dose after week 20 of pregnancy, although receiving it earlier is not contraindicated if tetanus toxoid is needed for tetanus prevention following a wound.⁶

Hepatitis B virus (HBV) vaccine
Added to the list of high-risk adults who should receive HBV vaccine routinely are those ages 19 through 59 years with diabetes.⁷ Vaccinate as soon as possible after the diabetes diagnosis is confirmed. The decision as to whether to vaccinate patients ≥60 years with diabetes should be based on the likelihood that they will become infected. Considerations include the risks associated with an increased need for help with blood-glucose monitoring in long-term care facilities, the likelihood that the patient will experience chronic sequelae if infected, and the likelihood that the patient will mount a proper immune response to the vaccine.⁷ (The more frail patients are, the less likely they are to achieve adequate immunity.⁷)

Meningococcal conjugate vaccine, quadrivalent (MCV4)
An MCV4 vaccine (Menactra) has now been licensed for use in children as young as 9 months.⁸ At this time, however, neither Menactra nor its competitor, Menveo (licensed for use in those 2 years and older), is recommended for routine administration until the age of 11 to 12 years. Infants and children ages 9 through 23 months with complement deficiencies, or who will be traveling to countries with endemic high levels of meningococcus, should be vaccinated with 2 doses of Menactra 3 months apart, and with a booster dose after 3 years if risk persists. The recommendations regarding the use of MCV4 in those ≤2 years with high-risk conditions are listed in TABLE 1.

Another change regarding the use of MCV4 is a recommended booster dose for those age 16 and older who were first vaccinated at age 11 or 12 years.⁹ For those vaccinated at ages 13 to 15, a booster should be received at ages 16 to 18. No booster is needed if the first MCV4 dose is received at or after age 16. Recommendations for MCV4 use and booster doses for those 2 years and older are listed in TABLE 2.

TABLE 1
Recommended Menactra schedule for young children at high risk for invasive meningococcal disease⁸

TABLE 2
Recommended schedule for meningococcal conjugate vaccine in those ≥2 years, according to risk⁹

Herpes zoster vaccine
The herpes zoster vaccine was initially licensed for those 60 years and older. Last year the FDA approved lowering the age to 50 years and older. At this time, however, the ACIP continues to recommend that the vaccine be used routinely starting at age 60 years. The age was not lowered because of a concern about vaccine supply and the uncertainty about the possible need for a booster dose if administered at age 50.¹⁰

Influenza vaccine
As described in a previous Practice Alert,¹¹ a history of egg allergy is no longer a strict contraindication for receipt of the influenza vaccine. The other major adjustment is a simplified recommendation on how to determine the required number of doses for a child younger than 9 years. If the child received 1 or both doses of the 2010-2011 vaccine, give just a single dose of the 2011-2012 vaccine. If the history is uncertain, give 2 doses of the new vaccine at least 4 weeks apart.¹²

In February, the Centers for Disease Control and Prevention (CDC) published the 2012 immunization schedules for infants and children, adolescents, and adults.^1,2 The schedules, which are available at http://www.cdc.gov/vaccines/recs/schedules/default.htm, are updated annually and incorporate additions and changes recommended by the Advisory Committee on Immunization Practices (ACIP) over the past year. While there were no major advances in new vaccines in 2011, there were a number of new indications for existing ones.

Human papillomavirus vaccine for males
Quadrivalent vaccine against human papillomavirus is now recommended for routine use for males ages 11 to 12 years to prevent genital warts and anal intraepithelial neoplasia.^3,4 Catch-up vaccination is also recommended for males ages 13 to 21 who have not received it. In addition, routine use is recommended for males ages 22 to 26 years who have sex with men or are HIV positive or immuno-compromised.

Tetanus toxoid, reduced strength diphtheria toxoid, and acellular pertussis (Tdap)
Indications for the routine use of Tdap were expanded to include children ages 7 to 10 years, pregnant women, and adults age 65 and older who have contact with infants.^5,6 Children ages 7 to 10 years who have not had the full series of DTaP should receive Td/Tdap according to the catch-up schedule,¹ with one of the doses being Tdap. Adults older than 65 who have never received Tdap and who have close contact with infants should receive one dose. No minimum interval is required between receipt of the Td and Tdap vaccines. Other older adults who ask for Tdap vaccination should receive it. Use of Tdap in those ages 7 to 10 years or 65 and older is off label.⁵

Pregnant women who have not received Tdap should receive 1 dose after week 20 of pregnancy, although receiving it earlier is not contraindicated if tetanus toxoid is needed for tetanus prevention following a wound.⁶

Hepatitis B virus (HBV) vaccine
Added to the list of high-risk adults who should receive HBV vaccine routinely are those ages 19 through 59 years with diabetes.⁷ Vaccinate as soon as possible after the diabetes diagnosis is confirmed. The decision as to whether to vaccinate patients ≥60 years with diabetes should be based on the likelihood that they will become infected. Considerations include the risks associated with an increased need for help with blood-glucose monitoring in long-term care facilities, the likelihood that the patient will experience chronic sequelae if infected, and the likelihood that the patient will mount a proper immune response to the vaccine.⁷ (The more frail patients are, the less likely they are to achieve adequate immunity.⁷)

Meningococcal conjugate vaccine, quadrivalent (MCV4)
An MCV4 vaccine (Menactra) has now been licensed for use in children as young as 9 months.⁸ At this time, however, neither Menactra nor its competitor, Menveo (licensed for use in those 2 years and older), is recommended for routine administration until the age of 11 to 12 years. Infants and children ages 9 through 23 months with complement deficiencies, or who will be traveling to countries with endemic high levels of meningococcus, should be vaccinated with 2 doses of Menactra 3 months apart, and with a booster dose after 3 years if risk persists. The recommendations regarding the use of MCV4 in those ≤2 years with high-risk conditions are listed in TABLE 1.

Another change regarding the use of MCV4 is a recommended booster dose for those age 16 and older who were first vaccinated at age 11 or 12 years.⁹ For those vaccinated at ages 13 to 15, a booster should be received at ages 16 to 18. No booster is needed if the first MCV4 dose is received at or after age 16. Recommendations for MCV4 use and booster doses for those 2 years and older are listed in TABLE 2.

TABLE 1
Recommended Menactra schedule for young children at high risk for invasive meningococcal disease⁸

TABLE 2
Recommended schedule for meningococcal conjugate vaccine in those ≥2 years, according to risk⁹

Herpes zoster vaccine
The herpes zoster vaccine was initially licensed for those 60 years and older. Last year the FDA approved lowering the age to 50 years and older. At this time, however, the ACIP continues to recommend that the vaccine be used routinely starting at age 60 years. The age was not lowered because of a concern about vaccine supply and the uncertainty about the possible need for a booster dose if administered at age 50.¹⁰

Influenza vaccine
As described in a previous Practice Alert,¹¹ a history of egg allergy is no longer a strict contraindication for receipt of the influenza vaccine. The other major adjustment is a simplified recommendation on how to determine the required number of doses for a child younger than 9 years. If the child received 1 or both doses of the 2010-2011 vaccine, give just a single dose of the 2011-2012 vaccine. If the history is uncertain, give 2 doses of the new vaccine at least 4 weeks apart.¹²

In February, the Centers for Disease Control and Prevention (CDC) published the 2012 immunization schedules for infants and children, adolescents, and adults.^1,2 The schedules, which are available at http://www.cdc.gov/vaccines/recs/schedules/default.htm, are updated annually and incorporate additions and changes recommended by the Advisory Committee on Immunization Practices (ACIP) over the past year. While there were no major advances in new vaccines in 2011, there were a number of new indications for existing ones.

Human papillomavirus vaccine for males
Quadrivalent vaccine against human papillomavirus is now recommended for routine use for males ages 11 to 12 years to prevent genital warts and anal intraepithelial neoplasia.^3,4 Catch-up vaccination is also recommended for males ages 13 to 21 who have not received it. In addition, routine use is recommended for males ages 22 to 26 years who have sex with men or are HIV positive or immuno-compromised.

Tetanus toxoid, reduced strength diphtheria toxoid, and acellular pertussis (Tdap)
Indications for the routine use of Tdap were expanded to include children ages 7 to 10 years, pregnant women, and adults age 65 and older who have contact with infants.^5,6 Children ages 7 to 10 years who have not had the full series of DTaP should receive Td/Tdap according to the catch-up schedule,¹ with one of the doses being Tdap. Adults older than 65 who have never received Tdap and who have close contact with infants should receive one dose. No minimum interval is required between receipt of the Td and Tdap vaccines. Other older adults who ask for Tdap vaccination should receive it. Use of Tdap in those ages 7 to 10 years or 65 and older is off label.⁵

Pregnant women who have not received Tdap should receive 1 dose after week 20 of pregnancy, although receiving it earlier is not contraindicated if tetanus toxoid is needed for tetanus prevention following a wound.⁶

Hepatitis B virus (HBV) vaccine
Added to the list of high-risk adults who should receive HBV vaccine routinely are those ages 19 through 59 years with diabetes.⁷ Vaccinate as soon as possible after the diabetes diagnosis is confirmed. The decision as to whether to vaccinate patients ≥60 years with diabetes should be based on the likelihood that they will become infected. Considerations include the risks associated with an increased need for help with blood-glucose monitoring in long-term care facilities, the likelihood that the patient will experience chronic sequelae if infected, and the likelihood that the patient will mount a proper immune response to the vaccine.⁷ (The more frail patients are, the less likely they are to achieve adequate immunity.⁷)

Meningococcal conjugate vaccine, quadrivalent (MCV4)
An MCV4 vaccine (Menactra) has now been licensed for use in children as young as 9 months.⁸ At this time, however, neither Menactra nor its competitor, Menveo (licensed for use in those 2 years and older), is recommended for routine administration until the age of 11 to 12 years. Infants and children ages 9 through 23 months with complement deficiencies, or who will be traveling to countries with endemic high levels of meningococcus, should be vaccinated with 2 doses of Menactra 3 months apart, and with a booster dose after 3 years if risk persists. The recommendations regarding the use of MCV4 in those ≤2 years with high-risk conditions are listed in TABLE 1.

Another change regarding the use of MCV4 is a recommended booster dose for those age 16 and older who were first vaccinated at age 11 or 12 years.⁹ For those vaccinated at ages 13 to 15, a booster should be received at ages 16 to 18. No booster is needed if the first MCV4 dose is received at or after age 16. Recommendations for MCV4 use and booster doses for those 2 years and older are listed in TABLE 2.

TABLE 1
Recommended Menactra schedule for young children at high risk for invasive meningococcal disease⁸

TABLE 2
Recommended schedule for meningococcal conjugate vaccine in those ≥2 years, according to risk⁹

Herpes zoster vaccine
The herpes zoster vaccine was initially licensed for those 60 years and older. Last year the FDA approved lowering the age to 50 years and older. At this time, however, the ACIP continues to recommend that the vaccine be used routinely starting at age 60 years. The age was not lowered because of a concern about vaccine supply and the uncertainty about the possible need for a booster dose if administered at age 50.¹⁰

Influenza vaccine
As described in a previous Practice Alert,¹¹ a history of egg allergy is no longer a strict contraindication for receipt of the influenza vaccine. The other major adjustment is a simplified recommendation on how to determine the required number of doses for a child younger than 9 years. If the child received 1 or both doses of the 2010-2011 vaccine, give just a single dose of the 2011-2012 vaccine. If the history is uncertain, give 2 doses of the new vaccine at least 4 weeks apart.¹²

Discuss this article at www.facebook.com/CurrentPsychiatry

Dear Dr. Mossman:
A patient has invited me to “friend” her on Facebook. I’m uncomfortable with this request, but I don’t want her to feel rejected. How should I respond?—Submitted by “Dr. V”

Among the many cultural developments that characterize the Internet era, few have had the impact of the social networking Web site Facebook. Because of Facebook, “friend” has become a transitive verb, and “like,” “wall,” “poke,” and “post” have acquired meanings that reflect new modes of communication and interpersonal connection. As of early 2012, Facebook had >800 million users.¹ If you’re like most medical students, residents, and junior faculty members,² you have a Facebook page.

The ubiquity of Facebook has added new dimensions to defining, teaching, and modeling professionalism in medicine.^3,4 Facebook can be used to rapidly disseminate medical information through status updates and medical support groups.⁵ Professionals can create profiles, post their curricula vitae, and “like” professional journals—including Current Psychiatry.

But social media such as Facebook also present clinicians with new ethical and professional challenges.⁶ If you use Facebook personally or professionally, you need to decide how you will separate your personal and professional identities in a forum that rapidly distributes information across the Web for all to see. Sound, responsible decisions about your online profile can let you and your employing institutions prosper from the many benefits that accrue to savvy Facebook users—while avoiding potential embarrassments and liability.

Before you create a profile or “post” your next “status update” on your “wall,” you should:

• understand potential boundary violations
• know how to activate your security and privacy settings
• remember that you represent not only yourself but your profession.

Boundary crossings, violations

Feelings of online closeness and informality make receiving “friend” requests from patients far from uncommon.⁷ The Internet lets individuals quickly check out people and learn personal information (eg, where they live and what their homes cost) that was hard to discover 15 years ago. But the information on a person’s Facebook page usually is much more personal than what Internet searches reveal—and often much less dignified.

A quick Internet search of the phrase “professional boundaries” will show that concern about maintaining proper relationships between professionals and service recipients is not restricted to psychiatry. Yet the special, intensely personal nature of mental health care—especially psychotherapy—traditionally has made psychiatrists place special constraints on their relationships with patients.

Because psychiatrists recognize that even brief comments about ourselves can affect how patients feel, we refrain from forms of self-disclosure that non-psychiatric colleagues view as innocent.⁸ Psychiatrists also do not freely socialize with patients or provide care to persons we know well. We avoid blurring therapeutic and other types of relationships because such “boundary crossings” can cause problems and because “crossings” can be precursors to serious “boundary violations”—eg, sexual contact with patients.

Most doctors decline “friend” requests from patients because friending them could adversely affect the treatment relationship and could lead to new relationships that might interfere with patient care.⁹ The American Medical Association’s social media guidelines do not forbid friending patients, but physicians are advised to “consider separating personal and professional content online” and “maintain appropriate boundaries” with patients.¹⁰ The British Medical Association simply tells physicians to “politely refuse” patients’ friend requests.¹¹

Privacy problems

Psychiatrists who friend patients need to be aware of potential privacy breeches among Facebook users. Individuals whose presence among a psychiatrist’s friends becomes known (eg, via a wall post) are revealing their connection to the psychiatrist, and other friends may surmise that an individual is a patient.

Also, Facebook’s “find friends” feature ostensibly lets Facebook locate individuals who are common to pairs of people and who can then be suggested as potential friends to others, but “find friends” imports members’ entire e-mail address books. If doctors who are on Facebook have patients in their webmail address books and have allowed “find friends,” then Facebook will import e-mail addresses, potentially disclosing associations between patients and their doctors.¹²

Facebook has tools that let users block their profiles from public view, but these privacy settings can be difficult to access and understand. Although social networking among medical trainees and new graduates is common in the culture of emerging professionals, most Facebook users allow anyone to view their profile—the default privacy setting.^2,13 Even if you don’t friend patients, failing to privatize your account leaves your Facebook information readily available to the public, including your patients.

Professionalism in cyberspace

Under some circumstances, medical advice given in casual, outside-the-office contexts can establish a doctor-patient relationship, with all its accompanying obligations and liability risks. This is true of Facebook communications. If you communicate medical information or advice to someone in a form specific enough to be relied upon, you may be establishing a doctor-patient relationship. If harm comes to a person who relied upon your information, a negligence lawsuit could result—even though you never saw or spoke to the “patient.”¹⁴

Medical training programs have found that medical students and residents have posted work-related comments on Facebook that directly referenced specific patient situations or other patient care matters. Such actions can breach the Health Insurance Portability and Accountability Act of 1996 and can jeopardize careers.¹⁵ Medical professionals also have posted uncouth, inappropriate, and embarrassing content—profanity, frankly discriminatory language, tales of intoxication, and sexually explicit information. In a recent survey of 78 medical schools, 60% responded that their students had posted unprofessional online content.¹⁶ In 45 cases, schools reported such incidents and responded to follow-up questions about disciplinary actions; 30 schools gave informal warnings, and 2 schools reported student dismissals.

Using Facebook

Should psychiatrists stay off Facebook? Of course not. Many prominent American psychiatrists are on Facebook because, like everyone else, they enjoy keeping in contact with friends and family.¹⁷ Thousands of professional groups (eg, the American Psychiatric Association) and physician practices have Facebook pages. Institutions, schools, and agencies use social media to promote their curricula, notify students and staff of course changes, or organize meetings. Professionals join groups or “like” groups associated with their specialty to affiliate with each other, and they use Facebook to promote their practices, disseminate information, and network with colleagues.

Psychiatrists need not shy away from establishing an account on Facebook,¹⁸ but they should do so with greater circumspection than most persons, including physicians in other specialties. Table 1 lists several examples of Facebook behavior that all physicians should avoid.^{2,13,16,19,20}

What about using Facebook to learn about your patients? Medical reports about checking Facebook to resolve emergencies have appeared,²⁰ and forensic psychiatrists can use Facebook and other Internet resources to learn about evaluees.²¹ But if doctors search for information about a patient’s out-of-office behavior or statements, it may be like “driving down a patient’s street to see what he or she is up to,” which, although legal, seems inappropriate in a professional relationship.²²

Recent experience suggests that medical schools and residencies should include “e-professionalism” in their curricula, emphasizing instruction and guidance on where personal and professional identities may intersect and where they should be kept separate. Table 2 lists several responses to the new challenges to medical professionalism posed by Facebook and other social media.^5,6

Table 1

Facebook errors: What to avoid

Table 2

Promoting e-professionalism

Responding to Dr. V

Psychiatrists should not “friend” patients. If you receive a “friend” request, you should proceed in 1 of the following ways:¹⁷

• Simply ignore the request. If your patient asks why you didn’t respond, explain that you use Facebook only for personal matters
• Ignore the request, and at the patient’s next appointment, mention the request and politely explain that you do not “friend” patients
• Ignore the request, but ask the patient about it at your next meeting. This is especially important for a patient whose treatment examines the doctor-patient relationship (eg, psychodynamic therapy), but may be valuable even in medication-focused care.

Related Resources

• Facebook. www.facebook.com.
• Foreman J. Think before you click. Boston Globe. April 12, 2010.

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Discuss this article at www.facebook.com/CurrentPsychiatry

Dear Dr. Mossman:
A patient has invited me to “friend” her on Facebook. I’m uncomfortable with this request, but I don’t want her to feel rejected. How should I respond?—Submitted by “Dr. V”

Among the many cultural developments that characterize the Internet era, few have had the impact of the social networking Web site Facebook. Because of Facebook, “friend” has become a transitive verb, and “like,” “wall,” “poke,” and “post” have acquired meanings that reflect new modes of communication and interpersonal connection. As of early 2012, Facebook had >800 million users.¹ If you’re like most medical students, residents, and junior faculty members,² you have a Facebook page.

The ubiquity of Facebook has added new dimensions to defining, teaching, and modeling professionalism in medicine.^3,4 Facebook can be used to rapidly disseminate medical information through status updates and medical support groups.⁵ Professionals can create profiles, post their curricula vitae, and “like” professional journals—including Current Psychiatry.

But social media such as Facebook also present clinicians with new ethical and professional challenges.⁶ If you use Facebook personally or professionally, you need to decide how you will separate your personal and professional identities in a forum that rapidly distributes information across the Web for all to see. Sound, responsible decisions about your online profile can let you and your employing institutions prosper from the many benefits that accrue to savvy Facebook users—while avoiding potential embarrassments and liability.

Before you create a profile or “post” your next “status update” on your “wall,” you should:

• understand potential boundary violations
• know how to activate your security and privacy settings
• remember that you represent not only yourself but your profession.

Boundary crossings, violations

Feelings of online closeness and informality make receiving “friend” requests from patients far from uncommon.⁷ The Internet lets individuals quickly check out people and learn personal information (eg, where they live and what their homes cost) that was hard to discover 15 years ago. But the information on a person’s Facebook page usually is much more personal than what Internet searches reveal—and often much less dignified.

A quick Internet search of the phrase “professional boundaries” will show that concern about maintaining proper relationships between professionals and service recipients is not restricted to psychiatry. Yet the special, intensely personal nature of mental health care—especially psychotherapy—traditionally has made psychiatrists place special constraints on their relationships with patients.

Because psychiatrists recognize that even brief comments about ourselves can affect how patients feel, we refrain from forms of self-disclosure that non-psychiatric colleagues view as innocent.⁸ Psychiatrists also do not freely socialize with patients or provide care to persons we know well. We avoid blurring therapeutic and other types of relationships because such “boundary crossings” can cause problems and because “crossings” can be precursors to serious “boundary violations”—eg, sexual contact with patients.

Most doctors decline “friend” requests from patients because friending them could adversely affect the treatment relationship and could lead to new relationships that might interfere with patient care.⁹ The American Medical Association’s social media guidelines do not forbid friending patients, but physicians are advised to “consider separating personal and professional content online” and “maintain appropriate boundaries” with patients.¹⁰ The British Medical Association simply tells physicians to “politely refuse” patients’ friend requests.¹¹

Privacy problems

Psychiatrists who friend patients need to be aware of potential privacy breeches among Facebook users. Individuals whose presence among a psychiatrist’s friends becomes known (eg, via a wall post) are revealing their connection to the psychiatrist, and other friends may surmise that an individual is a patient.

Also, Facebook’s “find friends” feature ostensibly lets Facebook locate individuals who are common to pairs of people and who can then be suggested as potential friends to others, but “find friends” imports members’ entire e-mail address books. If doctors who are on Facebook have patients in their webmail address books and have allowed “find friends,” then Facebook will import e-mail addresses, potentially disclosing associations between patients and their doctors.¹²

Facebook has tools that let users block their profiles from public view, but these privacy settings can be difficult to access and understand. Although social networking among medical trainees and new graduates is common in the culture of emerging professionals, most Facebook users allow anyone to view their profile—the default privacy setting.^2,13 Even if you don’t friend patients, failing to privatize your account leaves your Facebook information readily available to the public, including your patients.

Professionalism in cyberspace

Under some circumstances, medical advice given in casual, outside-the-office contexts can establish a doctor-patient relationship, with all its accompanying obligations and liability risks. This is true of Facebook communications. If you communicate medical information or advice to someone in a form specific enough to be relied upon, you may be establishing a doctor-patient relationship. If harm comes to a person who relied upon your information, a negligence lawsuit could result—even though you never saw or spoke to the “patient.”¹⁴

Medical training programs have found that medical students and residents have posted work-related comments on Facebook that directly referenced specific patient situations or other patient care matters. Such actions can breach the Health Insurance Portability and Accountability Act of 1996 and can jeopardize careers.¹⁵ Medical professionals also have posted uncouth, inappropriate, and embarrassing content—profanity, frankly discriminatory language, tales of intoxication, and sexually explicit information. In a recent survey of 78 medical schools, 60% responded that their students had posted unprofessional online content.¹⁶ In 45 cases, schools reported such incidents and responded to follow-up questions about disciplinary actions; 30 schools gave informal warnings, and 2 schools reported student dismissals.

Using Facebook

Should psychiatrists stay off Facebook? Of course not. Many prominent American psychiatrists are on Facebook because, like everyone else, they enjoy keeping in contact with friends and family.¹⁷ Thousands of professional groups (eg, the American Psychiatric Association) and physician practices have Facebook pages. Institutions, schools, and agencies use social media to promote their curricula, notify students and staff of course changes, or organize meetings. Professionals join groups or “like” groups associated with their specialty to affiliate with each other, and they use Facebook to promote their practices, disseminate information, and network with colleagues.

Psychiatrists need not shy away from establishing an account on Facebook,¹⁸ but they should do so with greater circumspection than most persons, including physicians in other specialties. Table 1 lists several examples of Facebook behavior that all physicians should avoid.^{2,13,16,19,20}

What about using Facebook to learn about your patients? Medical reports about checking Facebook to resolve emergencies have appeared,²⁰ and forensic psychiatrists can use Facebook and other Internet resources to learn about evaluees.²¹ But if doctors search for information about a patient’s out-of-office behavior or statements, it may be like “driving down a patient’s street to see what he or she is up to,” which, although legal, seems inappropriate in a professional relationship.²²

Recent experience suggests that medical schools and residencies should include “e-professionalism” in their curricula, emphasizing instruction and guidance on where personal and professional identities may intersect and where they should be kept separate. Table 2 lists several responses to the new challenges to medical professionalism posed by Facebook and other social media.^5,6

Table 1

Facebook errors: What to avoid

Table 2

Promoting e-professionalism

Responding to Dr. V

Psychiatrists should not “friend” patients. If you receive a “friend” request, you should proceed in 1 of the following ways:¹⁷

• Simply ignore the request. If your patient asks why you didn’t respond, explain that you use Facebook only for personal matters
• Ignore the request, and at the patient’s next appointment, mention the request and politely explain that you do not “friend” patients
• Ignore the request, but ask the patient about it at your next meeting. This is especially important for a patient whose treatment examines the doctor-patient relationship (eg, psychodynamic therapy), but may be valuable even in medication-focused care.

Related Resources

• Facebook. www.facebook.com.
• Foreman J. Think before you click. Boston Globe. April 12, 2010.

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Discuss this article at www.facebook.com/CurrentPsychiatry

Dear Dr. Mossman:
A patient has invited me to “friend” her on Facebook. I’m uncomfortable with this request, but I don’t want her to feel rejected. How should I respond?—Submitted by “Dr. V”

Among the many cultural developments that characterize the Internet era, few have had the impact of the social networking Web site Facebook. Because of Facebook, “friend” has become a transitive verb, and “like,” “wall,” “poke,” and “post” have acquired meanings that reflect new modes of communication and interpersonal connection. As of early 2012, Facebook had >800 million users.¹ If you’re like most medical students, residents, and junior faculty members,² you have a Facebook page.

The ubiquity of Facebook has added new dimensions to defining, teaching, and modeling professionalism in medicine.^3,4 Facebook can be used to rapidly disseminate medical information through status updates and medical support groups.⁵ Professionals can create profiles, post their curricula vitae, and “like” professional journals—including Current Psychiatry.

But social media such as Facebook also present clinicians with new ethical and professional challenges.⁶ If you use Facebook personally or professionally, you need to decide how you will separate your personal and professional identities in a forum that rapidly distributes information across the Web for all to see. Sound, responsible decisions about your online profile can let you and your employing institutions prosper from the many benefits that accrue to savvy Facebook users—while avoiding potential embarrassments and liability.

Before you create a profile or “post” your next “status update” on your “wall,” you should:

• understand potential boundary violations
• know how to activate your security and privacy settings
• remember that you represent not only yourself but your profession.

Boundary crossings, violations

Feelings of online closeness and informality make receiving “friend” requests from patients far from uncommon.⁷ The Internet lets individuals quickly check out people and learn personal information (eg, where they live and what their homes cost) that was hard to discover 15 years ago. But the information on a person’s Facebook page usually is much more personal than what Internet searches reveal—and often much less dignified.

A quick Internet search of the phrase “professional boundaries” will show that concern about maintaining proper relationships between professionals and service recipients is not restricted to psychiatry. Yet the special, intensely personal nature of mental health care—especially psychotherapy—traditionally has made psychiatrists place special constraints on their relationships with patients.

Because psychiatrists recognize that even brief comments about ourselves can affect how patients feel, we refrain from forms of self-disclosure that non-psychiatric colleagues view as innocent.⁸ Psychiatrists also do not freely socialize with patients or provide care to persons we know well. We avoid blurring therapeutic and other types of relationships because such “boundary crossings” can cause problems and because “crossings” can be precursors to serious “boundary violations”—eg, sexual contact with patients.

Most doctors decline “friend” requests from patients because friending them could adversely affect the treatment relationship and could lead to new relationships that might interfere with patient care.⁹ The American Medical Association’s social media guidelines do not forbid friending patients, but physicians are advised to “consider separating personal and professional content online” and “maintain appropriate boundaries” with patients.¹⁰ The British Medical Association simply tells physicians to “politely refuse” patients’ friend requests.¹¹

Privacy problems

Psychiatrists who friend patients need to be aware of potential privacy breeches among Facebook users. Individuals whose presence among a psychiatrist’s friends becomes known (eg, via a wall post) are revealing their connection to the psychiatrist, and other friends may surmise that an individual is a patient.

Also, Facebook’s “find friends” feature ostensibly lets Facebook locate individuals who are common to pairs of people and who can then be suggested as potential friends to others, but “find friends” imports members’ entire e-mail address books. If doctors who are on Facebook have patients in their webmail address books and have allowed “find friends,” then Facebook will import e-mail addresses, potentially disclosing associations between patients and their doctors.¹²

Facebook has tools that let users block their profiles from public view, but these privacy settings can be difficult to access and understand. Although social networking among medical trainees and new graduates is common in the culture of emerging professionals, most Facebook users allow anyone to view their profile—the default privacy setting.^2,13 Even if you don’t friend patients, failing to privatize your account leaves your Facebook information readily available to the public, including your patients.

Professionalism in cyberspace

Under some circumstances, medical advice given in casual, outside-the-office contexts can establish a doctor-patient relationship, with all its accompanying obligations and liability risks. This is true of Facebook communications. If you communicate medical information or advice to someone in a form specific enough to be relied upon, you may be establishing a doctor-patient relationship. If harm comes to a person who relied upon your information, a negligence lawsuit could result—even though you never saw or spoke to the “patient.”¹⁴

Medical training programs have found that medical students and residents have posted work-related comments on Facebook that directly referenced specific patient situations or other patient care matters. Such actions can breach the Health Insurance Portability and Accountability Act of 1996 and can jeopardize careers.¹⁵ Medical professionals also have posted uncouth, inappropriate, and embarrassing content—profanity, frankly discriminatory language, tales of intoxication, and sexually explicit information. In a recent survey of 78 medical schools, 60% responded that their students had posted unprofessional online content.¹⁶ In 45 cases, schools reported such incidents and responded to follow-up questions about disciplinary actions; 30 schools gave informal warnings, and 2 schools reported student dismissals.

Using Facebook

Should psychiatrists stay off Facebook? Of course not. Many prominent American psychiatrists are on Facebook because, like everyone else, they enjoy keeping in contact with friends and family.¹⁷ Thousands of professional groups (eg, the American Psychiatric Association) and physician practices have Facebook pages. Institutions, schools, and agencies use social media to promote their curricula, notify students and staff of course changes, or organize meetings. Professionals join groups or “like” groups associated with their specialty to affiliate with each other, and they use Facebook to promote their practices, disseminate information, and network with colleagues.

Psychiatrists need not shy away from establishing an account on Facebook,¹⁸ but they should do so with greater circumspection than most persons, including physicians in other specialties. Table 1 lists several examples of Facebook behavior that all physicians should avoid.^{2,13,16,19,20}

What about using Facebook to learn about your patients? Medical reports about checking Facebook to resolve emergencies have appeared,²⁰ and forensic psychiatrists can use Facebook and other Internet resources to learn about evaluees.²¹ But if doctors search for information about a patient’s out-of-office behavior or statements, it may be like “driving down a patient’s street to see what he or she is up to,” which, although legal, seems inappropriate in a professional relationship.²²

Recent experience suggests that medical schools and residencies should include “e-professionalism” in their curricula, emphasizing instruction and guidance on where personal and professional identities may intersect and where they should be kept separate. Table 2 lists several responses to the new challenges to medical professionalism posed by Facebook and other social media.^5,6

Table 1

Facebook errors: What to avoid

Table 2

Promoting e-professionalism

Responding to Dr. V

Psychiatrists should not “friend” patients. If you receive a “friend” request, you should proceed in 1 of the following ways:¹⁷

• Simply ignore the request. If your patient asks why you didn’t respond, explain that you use Facebook only for personal matters
• Ignore the request, and at the patient’s next appointment, mention the request and politely explain that you do not “friend” patients
• Ignore the request, but ask the patient about it at your next meeting. This is especially important for a patient whose treatment examines the doctor-patient relationship (eg, psychodynamic therapy), but may be valuable even in medication-focused care.

Related Resources

• Facebook. www.facebook.com.
• Foreman J. Think before you click. Boston Globe. April 12, 2010.

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Discuss this article at www.facebook.com/CurrentPsychiatry

In 2011, a workgroup of experts from the Alzheimer’s Association and the National Institute on Aging published new criteria and guidelines for diagnosing Alzheimer’s disease (AD), the first new AD guidelines since 1984.^1-4 These criteria reflect data that suggest AD is not synonymous with dementia of the Alzheimer’s type (DAT) but is a disease that slowly develops over many years as a result of accumulated neuropathologic changes, with dementia representing only the final phase of the disease (Figure).^1-4

Figure: Cognitive decline in AD over time
AD: Alzheimer’s disease; MCI: mild cognitive impairment
Source: Adapted from reference 2

This article highlights the similarities and differences of the 1984 and 2011 AD diagnosis guidelines. We also discuss the new guidelines’ limitations and clinical implications.

The 1984 AD criteria

Both the 1984 AD criteria⁵ and DSM-IV-TR criteria⁶ rely on the concept that AD is a clinical diagnosis made after a patient develops dementia. That is, diagnosis rests on the physician’s clinical judgment about the etiology of the patient’s symptoms, taking into account reports from the patient, family, and friends, as well as results of neurocognitive testing and mental status evaluation. The 1984 criteria were developed with the expectation that if a patient who met clinical criteria for AD were to undergo an autopsy, he or she likely would have evidence of AD pathology as the underlying etiology. These criteria were developed before researchers discovered that in AD, pathologic changes occur over many years and clinical dementia is the end product of accumulated pathology. The 1984 criteria did not address important phases that precede clinical dementia—such as mild cognitive impairment (MCI). See the Table for a summary of the 1984 AD criteria.

Table

The 1984 NINCDS-ADRDA criteria for clinical diagnosis of AD

The 2011 AD criteria

The new AD criteria differ from the 1984 criteria in 2 major ways:

• expansion of AD into 3 phases, only 1 of which is characterized by dementia
• incorporation of biomarkers to provide information regarding pathophysiologic changes underlying the disease state (Table 1).^1-5

The 3 phases. The 2011 criteria expand the definition of AD to include an asymptomatic, preclinical phase; a symptomatic, pre-dementia phase; and a dementia phase. In the initial phase, neuronal toxins such as beta-amyloid (Aβ) plaques and elevated tau first become detectable. Patients in this phase are asymptomatic or have subtle symptoms. This phase should be viewed as part of a continuum and includes patients who may, for instance, develop Aβ plaques but do not progress to further neurodegeneration.² The diagnostic criteria of this phase are intended for research purposes only.^1,2

Patients in the symptomatic, pre-dementia phase—also known as the MCI phase—exhibit mild decline in memory, attention, and thinking. Although this decline is more than what is expected for the patient’s age and education, it does not compromise everyday activity and functioning.

A patient who develops cognitive or behavioral problems that interfere with his or her ability to function at work or in everyday activities has entered the dementia phase. Similar to the 1984 guidelines, the 2011 criteria classify patients into probable and possible AD dementia. All patients who would have satisfied criteria for probable AD under the 1984 guidelines will satisfy criteria for probable AD dementia under the 2011 criteria.⁴ The same is not true for possible AD dementia. The 2011 criteria include 2 other major categories for patients with AD dementia: probable and possible AD dementia with evidence of the AD pathophysiological process. These categories are intended for research purposes only, whereas the criteria for the MCI and dementia phases are intended to guide diagnosis in the clinical setting.

By incorporating phases of AD that precede dementia into the disease spectrum, the new guidelines are designed to move clinicians toward earlier diagnosis and treatment.^1-3 Similar to how early, pre-symptomatic detection and treatment of conditions such as diabetes and cancer can reduce mortality, improving diagnosis of AD in its early phases may allow clinicians to better test potential therapies and eventually use them to treat at-risk individuals.^2,3 Most pharmacotherapies for AD are FDA-approved only for patients diagnosed with clinical dementia. Furthermore, current pharmacotherapies do not alter the course of AD; they have a modest effect in slowing cognitive and functional decline.^7,8 If patients in the earlier phases of AD could be recruited for research studies, we may be able to develop new treatments to stop or reverse AD pathology and its clinical manifestations.

Biomarkers. The new criteria incorporate biomarkers to provide information about pathophysiologic changes underlying the disease process. These criteria define biomarkers as physiologic, biochemical, or anatomic parameters that can be measured in vivo and reflect specific features of disease-related pathophysiologic processes.¹ Presently, there are no cutoff values to demarcate “normal” levels from “abnormal,” and biomarkers are proposed primarily as research tools because they have not been studied adequately in community settings and laboratory techniques to measure biomarkers have not been standardized.^1-4,9

The 5 biomarkers incorporated into the new criteria are divided into 2 categories: biomarkers of Aβ accumulation and those of neuronal degeneration or injury (Table 2).^1-4 In the initial, preclinical phase, biomarkers are used to detect changes in the brain—such as amyloid accumulation and nerve cell degeneration—that may already be in process in an individual whose clinical symptoms are subtle or not yet evident.^1,2 In this phase, progressive evidence of biomarkers, such as both Aβ accumulation and neuronal injury rather than Aβ accumulation alone, may increase the probability that a patient will decline quickly into the MCI phase.² Biomarkers of neuronal degeneration or injury especially correlate with the likelihood that the disease will progress to clinical dementia.¹ Subtle cognitive symptoms in the preclinical phase also might predict rapid decline into MCI.²

In the MCI and dementia phases, biomarkers are used to determine the level of certainty that AD is responsible for the patient’s symptoms.^1,3,4 For example, a patient could meet criteria for a non-AD dementia such as dementia with Lewy bodies, but also meet pathologic criteria for AD on autopsy.³ The diagnostic category of possible AD dementia with evidence of the AD pathophysiologic process is intended for this type of scenario.⁴ For the MCI phase, the criteria propose levels of certainty that a patient’s MCI syndrome is caused by AD, ranging from MCI due to AD-high likelihood to MCI-unlikely due to AD.³

Research has demonstrated that a patient’s clinical picture doesn’t necessarily reflect the extent of the underlying pathology. For example, a patient could have extensive AD pathology, such as diffuse amyloid plaques, without any obvious clinical symptoms.³ Conversely, although both Aβ deposition and elevated tau are hallmarks of AD, variations in these proteins can be seen in neuropsychiatric disorders other than AD.¹⁰ That said, it appears that worsening of clinical symptoms often parallels worsening of neurodegenerative biomarkers.¹

Under the 2011 guidelines, biomarkers would not be used to diagnose or exclude AD or MCI, but instead would help improve diagnostic accuracy in individuals with cognitive decline.^1,3,4 In other words, AD remains a clinical diagnosis, but these biomarkers could raise or lower the positive predictive value of a clinician’s judgment about the etiology of a patient’s symptoms.

See the Box for a description of the potential risks and benefits of using the new diagnostic criteria.

Table 1

Comparing the 1984 and 2011 AD criteria

Table 2

5 biomarkers incorporated into the 2011 AD criteria

Box

Clinical applications

Although pharmacologic therapies for the early phases of AD are not yet available, research supports implementing nonpharmacologic modalities in older adults with MCI as well as those without any cognitive impairment (Table 3).^8,11 Growing evidence suggests physicians should encourage patients to lead an active and socially integrated lifestyle that includes leisure activities, cognitive stimulation, meditation, a balanced diet, and daily exercise.⁸ Practitioners should treat vascular risk factors in geriatric patients with and without cognitive impairment to optimize healthy brain aging and reduce the risk of cardiovascular disease and stroke.¹¹ By raising awareness of available treatments for early phases of AD, we may be able to reduce the anxiety and sense of helplessness or hopelessness that may accompany an AD diagnosis.

Depression and AD. Having depression nearly doubles one’s risk of developing AD later in life, and depression may exacerbate AD.¹² Although the precise mechanism linking depression to AD is unclear, depression seems to exert a toxic effect on the hippocampus.¹³ Treating depression may prevent or mitigate the rate of memory impairment and overall AD severity and improve a patient’s quality of life, overall health, and ability to function.

Almost one-third of family caregivers become depressed while helping a family member with DAT.¹⁴ Directing caregivers to peer support groups and providing them with tips on how to take care of themselves physically, emotionally, and psychologically can be extremely beneficial. Data suggest that improving the psychological and emotional well-being of caretakers may delay nursing home placement of patients with DAT.¹⁵ Delaying nursing home placement can substantially improve quality of life and reduce the financial strain on patients and caregivers.

Patients and families often turn to clinicians for advice on what problems they or their loved ones may encounter if they suffer from cognitive impairment. One benefit of the new guidelines is that they can help us become educated about the early phases of AD as well as the long and often difficult course of the disease. In turn, we can better educate our patients and their families about the disease.

As early screening of AD improves, patients in the early phases will have an opportunity to take part in clinical trials for potential pharmacologic treatments of the disease. Our role as clinicians will be to guide patients and their families to such trials and give them the opportunity to help change our understanding of and approach to treating AD. It is important to keep in mind that the new guidelines should not be considered final, but rather as a work in progress that periodically will be revised as AD research progresses.³

Table 3

Promoting healthy brain aging

Related Resources

• Alzheimer’s Association. www.alz.org.
• National Institute on Aging. Alzheimer’s disease education and referral center. www.nia.nih.gov/alzheimers.

Disclosures

Drs. Kimchi and Desai report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Grossberg is a consultant to Baxter, Forest Laboratories, Merck, Otsuka, and Novartis.

Discuss this article at www.facebook.com/CurrentPsychiatry

In 2011, a workgroup of experts from the Alzheimer’s Association and the National Institute on Aging published new criteria and guidelines for diagnosing Alzheimer’s disease (AD), the first new AD guidelines since 1984.^1-4 These criteria reflect data that suggest AD is not synonymous with dementia of the Alzheimer’s type (DAT) but is a disease that slowly develops over many years as a result of accumulated neuropathologic changes, with dementia representing only the final phase of the disease (Figure).^1-4

Figure: Cognitive decline in AD over time
AD: Alzheimer’s disease; MCI: mild cognitive impairment
Source: Adapted from reference 2

This article highlights the similarities and differences of the 1984 and 2011 AD diagnosis guidelines. We also discuss the new guidelines’ limitations and clinical implications.

The 1984 AD criteria

Both the 1984 AD criteria⁵ and DSM-IV-TR criteria⁶ rely on the concept that AD is a clinical diagnosis made after a patient develops dementia. That is, diagnosis rests on the physician’s clinical judgment about the etiology of the patient’s symptoms, taking into account reports from the patient, family, and friends, as well as results of neurocognitive testing and mental status evaluation. The 1984 criteria were developed with the expectation that if a patient who met clinical criteria for AD were to undergo an autopsy, he or she likely would have evidence of AD pathology as the underlying etiology. These criteria were developed before researchers discovered that in AD, pathologic changes occur over many years and clinical dementia is the end product of accumulated pathology. The 1984 criteria did not address important phases that precede clinical dementia—such as mild cognitive impairment (MCI). See the Table for a summary of the 1984 AD criteria.

Table

The 1984 NINCDS-ADRDA criteria for clinical diagnosis of AD

The 2011 AD criteria

The new AD criteria differ from the 1984 criteria in 2 major ways:

• expansion of AD into 3 phases, only 1 of which is characterized by dementia
• incorporation of biomarkers to provide information regarding pathophysiologic changes underlying the disease state (Table 1).^1-5

The 3 phases. The 2011 criteria expand the definition of AD to include an asymptomatic, preclinical phase; a symptomatic, pre-dementia phase; and a dementia phase. In the initial phase, neuronal toxins such as beta-amyloid (Aβ) plaques and elevated tau first become detectable. Patients in this phase are asymptomatic or have subtle symptoms. This phase should be viewed as part of a continuum and includes patients who may, for instance, develop Aβ plaques but do not progress to further neurodegeneration.² The diagnostic criteria of this phase are intended for research purposes only.^1,2

Patients in the symptomatic, pre-dementia phase—also known as the MCI phase—exhibit mild decline in memory, attention, and thinking. Although this decline is more than what is expected for the patient’s age and education, it does not compromise everyday activity and functioning.

A patient who develops cognitive or behavioral problems that interfere with his or her ability to function at work or in everyday activities has entered the dementia phase. Similar to the 1984 guidelines, the 2011 criteria classify patients into probable and possible AD dementia. All patients who would have satisfied criteria for probable AD under the 1984 guidelines will satisfy criteria for probable AD dementia under the 2011 criteria.⁴ The same is not true for possible AD dementia. The 2011 criteria include 2 other major categories for patients with AD dementia: probable and possible AD dementia with evidence of the AD pathophysiological process. These categories are intended for research purposes only, whereas the criteria for the MCI and dementia phases are intended to guide diagnosis in the clinical setting.

By incorporating phases of AD that precede dementia into the disease spectrum, the new guidelines are designed to move clinicians toward earlier diagnosis and treatment.^1-3 Similar to how early, pre-symptomatic detection and treatment of conditions such as diabetes and cancer can reduce mortality, improving diagnosis of AD in its early phases may allow clinicians to better test potential therapies and eventually use them to treat at-risk individuals.^2,3 Most pharmacotherapies for AD are FDA-approved only for patients diagnosed with clinical dementia. Furthermore, current pharmacotherapies do not alter the course of AD; they have a modest effect in slowing cognitive and functional decline.^7,8 If patients in the earlier phases of AD could be recruited for research studies, we may be able to develop new treatments to stop or reverse AD pathology and its clinical manifestations.

Biomarkers. The new criteria incorporate biomarkers to provide information about pathophysiologic changes underlying the disease process. These criteria define biomarkers as physiologic, biochemical, or anatomic parameters that can be measured in vivo and reflect specific features of disease-related pathophysiologic processes.¹ Presently, there are no cutoff values to demarcate “normal” levels from “abnormal,” and biomarkers are proposed primarily as research tools because they have not been studied adequately in community settings and laboratory techniques to measure biomarkers have not been standardized.^1-4,9

The 5 biomarkers incorporated into the new criteria are divided into 2 categories: biomarkers of Aβ accumulation and those of neuronal degeneration or injury (Table 2).^1-4 In the initial, preclinical phase, biomarkers are used to detect changes in the brain—such as amyloid accumulation and nerve cell degeneration—that may already be in process in an individual whose clinical symptoms are subtle or not yet evident.^1,2 In this phase, progressive evidence of biomarkers, such as both Aβ accumulation and neuronal injury rather than Aβ accumulation alone, may increase the probability that a patient will decline quickly into the MCI phase.² Biomarkers of neuronal degeneration or injury especially correlate with the likelihood that the disease will progress to clinical dementia.¹ Subtle cognitive symptoms in the preclinical phase also might predict rapid decline into MCI.²

In the MCI and dementia phases, biomarkers are used to determine the level of certainty that AD is responsible for the patient’s symptoms.^1,3,4 For example, a patient could meet criteria for a non-AD dementia such as dementia with Lewy bodies, but also meet pathologic criteria for AD on autopsy.³ The diagnostic category of possible AD dementia with evidence of the AD pathophysiologic process is intended for this type of scenario.⁴ For the MCI phase, the criteria propose levels of certainty that a patient’s MCI syndrome is caused by AD, ranging from MCI due to AD-high likelihood to MCI-unlikely due to AD.³

Research has demonstrated that a patient’s clinical picture doesn’t necessarily reflect the extent of the underlying pathology. For example, a patient could have extensive AD pathology, such as diffuse amyloid plaques, without any obvious clinical symptoms.³ Conversely, although both Aβ deposition and elevated tau are hallmarks of AD, variations in these proteins can be seen in neuropsychiatric disorders other than AD.¹⁰ That said, it appears that worsening of clinical symptoms often parallels worsening of neurodegenerative biomarkers.¹

Under the 2011 guidelines, biomarkers would not be used to diagnose or exclude AD or MCI, but instead would help improve diagnostic accuracy in individuals with cognitive decline.^1,3,4 In other words, AD remains a clinical diagnosis, but these biomarkers could raise or lower the positive predictive value of a clinician’s judgment about the etiology of a patient’s symptoms.

See the Box for a description of the potential risks and benefits of using the new diagnostic criteria.

Table 1

Comparing the 1984 and 2011 AD criteria

Table 2

5 biomarkers incorporated into the 2011 AD criteria

Box

Clinical applications

Although pharmacologic therapies for the early phases of AD are not yet available, research supports implementing nonpharmacologic modalities in older adults with MCI as well as those without any cognitive impairment (Table 3).^8,11 Growing evidence suggests physicians should encourage patients to lead an active and socially integrated lifestyle that includes leisure activities, cognitive stimulation, meditation, a balanced diet, and daily exercise.⁸ Practitioners should treat vascular risk factors in geriatric patients with and without cognitive impairment to optimize healthy brain aging and reduce the risk of cardiovascular disease and stroke.¹¹ By raising awareness of available treatments for early phases of AD, we may be able to reduce the anxiety and sense of helplessness or hopelessness that may accompany an AD diagnosis.

Depression and AD. Having depression nearly doubles one’s risk of developing AD later in life, and depression may exacerbate AD.¹² Although the precise mechanism linking depression to AD is unclear, depression seems to exert a toxic effect on the hippocampus.¹³ Treating depression may prevent or mitigate the rate of memory impairment and overall AD severity and improve a patient’s quality of life, overall health, and ability to function.

Almost one-third of family caregivers become depressed while helping a family member with DAT.¹⁴ Directing caregivers to peer support groups and providing them with tips on how to take care of themselves physically, emotionally, and psychologically can be extremely beneficial. Data suggest that improving the psychological and emotional well-being of caretakers may delay nursing home placement of patients with DAT.¹⁵ Delaying nursing home placement can substantially improve quality of life and reduce the financial strain on patients and caregivers.

Patients and families often turn to clinicians for advice on what problems they or their loved ones may encounter if they suffer from cognitive impairment. One benefit of the new guidelines is that they can help us become educated about the early phases of AD as well as the long and often difficult course of the disease. In turn, we can better educate our patients and their families about the disease.

As early screening of AD improves, patients in the early phases will have an opportunity to take part in clinical trials for potential pharmacologic treatments of the disease. Our role as clinicians will be to guide patients and their families to such trials and give them the opportunity to help change our understanding of and approach to treating AD. It is important to keep in mind that the new guidelines should not be considered final, but rather as a work in progress that periodically will be revised as AD research progresses.³

Table 3

Promoting healthy brain aging

Related Resources

• Alzheimer’s Association. www.alz.org.
• National Institute on Aging. Alzheimer’s disease education and referral center. www.nia.nih.gov/alzheimers.

Disclosures

Drs. Kimchi and Desai report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Grossberg is a consultant to Baxter, Forest Laboratories, Merck, Otsuka, and Novartis.

Discuss this article at www.facebook.com/CurrentPsychiatry

In 2011, a workgroup of experts from the Alzheimer’s Association and the National Institute on Aging published new criteria and guidelines for diagnosing Alzheimer’s disease (AD), the first new AD guidelines since 1984.^1-4 These criteria reflect data that suggest AD is not synonymous with dementia of the Alzheimer’s type (DAT) but is a disease that slowly develops over many years as a result of accumulated neuropathologic changes, with dementia representing only the final phase of the disease (Figure).^1-4

Figure: Cognitive decline in AD over time
AD: Alzheimer’s disease; MCI: mild cognitive impairment
Source: Adapted from reference 2

This article highlights the similarities and differences of the 1984 and 2011 AD diagnosis guidelines. We also discuss the new guidelines’ limitations and clinical implications.

The 1984 AD criteria

Both the 1984 AD criteria⁵ and DSM-IV-TR criteria⁶ rely on the concept that AD is a clinical diagnosis made after a patient develops dementia. That is, diagnosis rests on the physician’s clinical judgment about the etiology of the patient’s symptoms, taking into account reports from the patient, family, and friends, as well as results of neurocognitive testing and mental status evaluation. The 1984 criteria were developed with the expectation that if a patient who met clinical criteria for AD were to undergo an autopsy, he or she likely would have evidence of AD pathology as the underlying etiology. These criteria were developed before researchers discovered that in AD, pathologic changes occur over many years and clinical dementia is the end product of accumulated pathology. The 1984 criteria did not address important phases that precede clinical dementia—such as mild cognitive impairment (MCI). See the Table for a summary of the 1984 AD criteria.

Table

The 1984 NINCDS-ADRDA criteria for clinical diagnosis of AD

The 2011 AD criteria

The new AD criteria differ from the 1984 criteria in 2 major ways:

• expansion of AD into 3 phases, only 1 of which is characterized by dementia
• incorporation of biomarkers to provide information regarding pathophysiologic changes underlying the disease state (Table 1).^1-5

The 3 phases. The 2011 criteria expand the definition of AD to include an asymptomatic, preclinical phase; a symptomatic, pre-dementia phase; and a dementia phase. In the initial phase, neuronal toxins such as beta-amyloid (Aβ) plaques and elevated tau first become detectable. Patients in this phase are asymptomatic or have subtle symptoms. This phase should be viewed as part of a continuum and includes patients who may, for instance, develop Aβ plaques but do not progress to further neurodegeneration.² The diagnostic criteria of this phase are intended for research purposes only.^1,2

Patients in the symptomatic, pre-dementia phase—also known as the MCI phase—exhibit mild decline in memory, attention, and thinking. Although this decline is more than what is expected for the patient’s age and education, it does not compromise everyday activity and functioning.

A patient who develops cognitive or behavioral problems that interfere with his or her ability to function at work or in everyday activities has entered the dementia phase. Similar to the 1984 guidelines, the 2011 criteria classify patients into probable and possible AD dementia. All patients who would have satisfied criteria for probable AD under the 1984 guidelines will satisfy criteria for probable AD dementia under the 2011 criteria.⁴ The same is not true for possible AD dementia. The 2011 criteria include 2 other major categories for patients with AD dementia: probable and possible AD dementia with evidence of the AD pathophysiological process. These categories are intended for research purposes only, whereas the criteria for the MCI and dementia phases are intended to guide diagnosis in the clinical setting.

By incorporating phases of AD that precede dementia into the disease spectrum, the new guidelines are designed to move clinicians toward earlier diagnosis and treatment.^1-3 Similar to how early, pre-symptomatic detection and treatment of conditions such as diabetes and cancer can reduce mortality, improving diagnosis of AD in its early phases may allow clinicians to better test potential therapies and eventually use them to treat at-risk individuals.^2,3 Most pharmacotherapies for AD are FDA-approved only for patients diagnosed with clinical dementia. Furthermore, current pharmacotherapies do not alter the course of AD; they have a modest effect in slowing cognitive and functional decline.^7,8 If patients in the earlier phases of AD could be recruited for research studies, we may be able to develop new treatments to stop or reverse AD pathology and its clinical manifestations.

Biomarkers. The new criteria incorporate biomarkers to provide information about pathophysiologic changes underlying the disease process. These criteria define biomarkers as physiologic, biochemical, or anatomic parameters that can be measured in vivo and reflect specific features of disease-related pathophysiologic processes.¹ Presently, there are no cutoff values to demarcate “normal” levels from “abnormal,” and biomarkers are proposed primarily as research tools because they have not been studied adequately in community settings and laboratory techniques to measure biomarkers have not been standardized.^1-4,9

The 5 biomarkers incorporated into the new criteria are divided into 2 categories: biomarkers of Aβ accumulation and those of neuronal degeneration or injury (Table 2).^1-4 In the initial, preclinical phase, biomarkers are used to detect changes in the brain—such as amyloid accumulation and nerve cell degeneration—that may already be in process in an individual whose clinical symptoms are subtle or not yet evident.^1,2 In this phase, progressive evidence of biomarkers, such as both Aβ accumulation and neuronal injury rather than Aβ accumulation alone, may increase the probability that a patient will decline quickly into the MCI phase.² Biomarkers of neuronal degeneration or injury especially correlate with the likelihood that the disease will progress to clinical dementia.¹ Subtle cognitive symptoms in the preclinical phase also might predict rapid decline into MCI.²

In the MCI and dementia phases, biomarkers are used to determine the level of certainty that AD is responsible for the patient’s symptoms.^1,3,4 For example, a patient could meet criteria for a non-AD dementia such as dementia with Lewy bodies, but also meet pathologic criteria for AD on autopsy.³ The diagnostic category of possible AD dementia with evidence of the AD pathophysiologic process is intended for this type of scenario.⁴ For the MCI phase, the criteria propose levels of certainty that a patient’s MCI syndrome is caused by AD, ranging from MCI due to AD-high likelihood to MCI-unlikely due to AD.³

Research has demonstrated that a patient’s clinical picture doesn’t necessarily reflect the extent of the underlying pathology. For example, a patient could have extensive AD pathology, such as diffuse amyloid plaques, without any obvious clinical symptoms.³ Conversely, although both Aβ deposition and elevated tau are hallmarks of AD, variations in these proteins can be seen in neuropsychiatric disorders other than AD.¹⁰ That said, it appears that worsening of clinical symptoms often parallels worsening of neurodegenerative biomarkers.¹

Under the 2011 guidelines, biomarkers would not be used to diagnose or exclude AD or MCI, but instead would help improve diagnostic accuracy in individuals with cognitive decline.^1,3,4 In other words, AD remains a clinical diagnosis, but these biomarkers could raise or lower the positive predictive value of a clinician’s judgment about the etiology of a patient’s symptoms.

See the Box for a description of the potential risks and benefits of using the new diagnostic criteria.

Table 1

Comparing the 1984 and 2011 AD criteria

Table 2

5 biomarkers incorporated into the 2011 AD criteria

Box

Clinical applications

Although pharmacologic therapies for the early phases of AD are not yet available, research supports implementing nonpharmacologic modalities in older adults with MCI as well as those without any cognitive impairment (Table 3).^8,11 Growing evidence suggests physicians should encourage patients to lead an active and socially integrated lifestyle that includes leisure activities, cognitive stimulation, meditation, a balanced diet, and daily exercise.⁸ Practitioners should treat vascular risk factors in geriatric patients with and without cognitive impairment to optimize healthy brain aging and reduce the risk of cardiovascular disease and stroke.¹¹ By raising awareness of available treatments for early phases of AD, we may be able to reduce the anxiety and sense of helplessness or hopelessness that may accompany an AD diagnosis.

Depression and AD. Having depression nearly doubles one’s risk of developing AD later in life, and depression may exacerbate AD.¹² Although the precise mechanism linking depression to AD is unclear, depression seems to exert a toxic effect on the hippocampus.¹³ Treating depression may prevent or mitigate the rate of memory impairment and overall AD severity and improve a patient’s quality of life, overall health, and ability to function.

Almost one-third of family caregivers become depressed while helping a family member with DAT.¹⁴ Directing caregivers to peer support groups and providing them with tips on how to take care of themselves physically, emotionally, and psychologically can be extremely beneficial. Data suggest that improving the psychological and emotional well-being of caretakers may delay nursing home placement of patients with DAT.¹⁵ Delaying nursing home placement can substantially improve quality of life and reduce the financial strain on patients and caregivers.

Patients and families often turn to clinicians for advice on what problems they or their loved ones may encounter if they suffer from cognitive impairment. One benefit of the new guidelines is that they can help us become educated about the early phases of AD as well as the long and often difficult course of the disease. In turn, we can better educate our patients and their families about the disease.

As early screening of AD improves, patients in the early phases will have an opportunity to take part in clinical trials for potential pharmacologic treatments of the disease. Our role as clinicians will be to guide patients and their families to such trials and give them the opportunity to help change our understanding of and approach to treating AD. It is important to keep in mind that the new guidelines should not be considered final, but rather as a work in progress that periodically will be revised as AD research progresses.³

Table 3

Promoting healthy brain aging

Related Resources

• Alzheimer’s Association. www.alz.org.
• National Institute on Aging. Alzheimer’s disease education and referral center. www.nia.nih.gov/alzheimers.

Disclosures

Drs. Kimchi and Desai report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Grossberg is a consultant to Baxter, Forest Laboratories, Merck, Otsuka, and Novartis.

In one of our previous articles, we discussed a study of screening for prostate cancer.¹ Now we’re going to move up a bit, at least anatomically, and discuss a study of screening for lung cancer.² We have previously defined ourselves as curmudgeons and skeptics; to those self-descriptions we now add a new term, “chutzpahniks.” For those of you who may be unfamiliar with that Yiddish term, it means people who have chutzpah, which was defined by Leo Rosten³ as: “that quality enshrined in a man who, having killed his mother and father, throws himself on the mercy of the court because he is an orphan.” Our chutzpah stems from the fact that we are criticizing the results of a study that was published in the New England Journal of Medicine and highly praised in an editorial in that journal.⁴ If we had less chutzpah, we wouldn’t contemplate such a critique, but then again, if we had less chutzpah, we—a clinical psychologist and a nuclear physicist—wouldn’t be writing articles in a cancer journal. So, on to the study...

To read the full article, click on the PDF icon above.

In one of our previous articles, we discussed a study of screening for prostate cancer.¹ Now we’re going to move up a bit, at least anatomically, and discuss a study of screening for lung cancer.² We have previously defined ourselves as curmudgeons and skeptics; to those self-descriptions we now add a new term, “chutzpahniks.” For those of you who may be unfamiliar with that Yiddish term, it means people who have chutzpah, which was defined by Leo Rosten³ as: “that quality enshrined in a man who, having killed his mother and father, throws himself on the mercy of the court because he is an orphan.” Our chutzpah stems from the fact that we are criticizing the results of a study that was published in the New England Journal of Medicine and highly praised in an editorial in that journal.⁴ If we had less chutzpah, we wouldn’t contemplate such a critique, but then again, if we had less chutzpah, we—a clinical psychologist and a nuclear physicist—wouldn’t be writing articles in a cancer journal. So, on to the study...

To read the full article, click on the PDF icon above.

In one of our previous articles, we discussed a study of screening for prostate cancer.¹ Now we’re going to move up a bit, at least anatomically, and discuss a study of screening for lung cancer.² We have previously defined ourselves as curmudgeons and skeptics; to those self-descriptions we now add a new term, “chutzpahniks.” For those of you who may be unfamiliar with that Yiddish term, it means people who have chutzpah, which was defined by Leo Rosten³ as: “that quality enshrined in a man who, having killed his mother and father, throws himself on the mercy of the court because he is an orphan.” Our chutzpah stems from the fact that we are criticizing the results of a study that was published in the New England Journal of Medicine and highly praised in an editorial in that journal.⁴ If we had less chutzpah, we wouldn’t contemplate such a critique, but then again, if we had less chutzpah, we—a clinical psychologist and a nuclear physicist—wouldn’t be writing articles in a cancer journal. So, on to the study...

To read the full article, click on the PDF icon above.

Multiple myeloma (MM) is characterized by excess monoclonal plasma cells in the bone marrow (BM), in most cases associated with monoclonal protein in blood or urine. Nearly 50 years ago, the use of combined melphalan and prednisone was shown to extend median survival of patients with MM to 2-3 years. In an approach pioneered by Prof. Tim McElwain in the 1970s, high-dose melphalan followed by BM transplantation in the 1980s and peripheral blood stem cell rescue in the 1990s further increased median survival to 3-4 years. Since 1998, MM has represented a new paradigm in drug development due to the remarkable therapeutic efficacy of targeting tumor cells in their microenvironment^1,2—an approach perhaps best exemplified by the use of the proteasome inhibitor bortezomib and immunomodulatory drugs (IMiDs) thalidomide and lenalidomide to target the MM cell in the BM microenvironment. This approach has rapidly translated from bench to bedside, producing six new Food and Drug Administration (FDA)-approved treatments in the past 7 years and a doubling of patient survival from 3-4 to 7-8 years as a direct result.³ My colleagues and I have made contributions in the areas of identifying novel targets in the tumor and microenvironment, confirming the activity of inhibitors directed at these targets, and then leading clinical trials assessing the efficacy and safety of these agents...

*For a PDF of the full article, click on the link to the left of this introduction.

Multiple myeloma (MM) is characterized by excess monoclonal plasma cells in the bone marrow (BM), in most cases associated with monoclonal protein in blood or urine. Nearly 50 years ago, the use of combined melphalan and prednisone was shown to extend median survival of patients with MM to 2-3 years. In an approach pioneered by Prof. Tim McElwain in the 1970s, high-dose melphalan followed by BM transplantation in the 1980s and peripheral blood stem cell rescue in the 1990s further increased median survival to 3-4 years. Since 1998, MM has represented a new paradigm in drug development due to the remarkable therapeutic efficacy of targeting tumor cells in their microenvironment^1,2—an approach perhaps best exemplified by the use of the proteasome inhibitor bortezomib and immunomodulatory drugs (IMiDs) thalidomide and lenalidomide to target the MM cell in the BM microenvironment. This approach has rapidly translated from bench to bedside, producing six new Food and Drug Administration (FDA)-approved treatments in the past 7 years and a doubling of patient survival from 3-4 to 7-8 years as a direct result.³ My colleagues and I have made contributions in the areas of identifying novel targets in the tumor and microenvironment, confirming the activity of inhibitors directed at these targets, and then leading clinical trials assessing the efficacy and safety of these agents...

*For a PDF of the full article, click on the link to the left of this introduction.

Multiple myeloma (MM) is characterized by excess monoclonal plasma cells in the bone marrow (BM), in most cases associated with monoclonal protein in blood or urine. Nearly 50 years ago, the use of combined melphalan and prednisone was shown to extend median survival of patients with MM to 2-3 years. In an approach pioneered by Prof. Tim McElwain in the 1970s, high-dose melphalan followed by BM transplantation in the 1980s and peripheral blood stem cell rescue in the 1990s further increased median survival to 3-4 years. Since 1998, MM has represented a new paradigm in drug development due to the remarkable therapeutic efficacy of targeting tumor cells in their microenvironment^1,2—an approach perhaps best exemplified by the use of the proteasome inhibitor bortezomib and immunomodulatory drugs (IMiDs) thalidomide and lenalidomide to target the MM cell in the BM microenvironment. This approach has rapidly translated from bench to bedside, producing six new Food and Drug Administration (FDA)-approved treatments in the past 7 years and a doubling of patient survival from 3-4 to 7-8 years as a direct result.³ My colleagues and I have made contributions in the areas of identifying novel targets in the tumor and microenvironment, confirming the activity of inhibitors directed at these targets, and then leading clinical trials assessing the efficacy and safety of these agents...

*For a PDF of the full article, click on the link to the left of this introduction.

Third-generation aromatase inhibitors (AIs) used in the treatment of hormone-responsive breast cancer are associated with arthralgia, which is the most common reason for treatment discontinuation. This review characterizes the observed arthralgia and describes its variable definitions in key clinical trials; its typical onset and duration; symptom management strategies; and symptom resolution. The symptomatic manifestations of AI-associated arthralgia are highly variable, with typical onset occurring 2-6 months after treatment initiation. Aromatase inhibitor-associated arthralgia is most often bilateral and symmetrical, involving hands and wrists. Other common locations include knees, hips, lower back, shoulders, and feet. To improve standardization of care as well as patient quality of life, we propose a diagnostic algorithm for the management of patients who receive AIs and who develop arthralgia or worsening symptoms from preexisting joint pain. We conclude that although arthralgia is often associated with AI therapy, prompt diagnosis and management of musculoskeletal symptoms may ensure continued AI treatment and improve quality of life...

*For a PDF of the full article, click on the link to the left of this introduction.

Third-generation aromatase inhibitors (AIs) used in the treatment of hormone-responsive breast cancer are associated with arthralgia, which is the most common reason for treatment discontinuation. This review characterizes the observed arthralgia and describes its variable definitions in key clinical trials; its typical onset and duration; symptom management strategies; and symptom resolution. The symptomatic manifestations of AI-associated arthralgia are highly variable, with typical onset occurring 2-6 months after treatment initiation. Aromatase inhibitor-associated arthralgia is most often bilateral and symmetrical, involving hands and wrists. Other common locations include knees, hips, lower back, shoulders, and feet. To improve standardization of care as well as patient quality of life, we propose a diagnostic algorithm for the management of patients who receive AIs and who develop arthralgia or worsening symptoms from preexisting joint pain. We conclude that although arthralgia is often associated with AI therapy, prompt diagnosis and management of musculoskeletal symptoms may ensure continued AI treatment and improve quality of life...

*For a PDF of the full article, click on the link to the left of this introduction.

Third-generation aromatase inhibitors (AIs) used in the treatment of hormone-responsive breast cancer are associated with arthralgia, which is the most common reason for treatment discontinuation. This review characterizes the observed arthralgia and describes its variable definitions in key clinical trials; its typical onset and duration; symptom management strategies; and symptom resolution. The symptomatic manifestations of AI-associated arthralgia are highly variable, with typical onset occurring 2-6 months after treatment initiation. Aromatase inhibitor-associated arthralgia is most often bilateral and symmetrical, involving hands and wrists. Other common locations include knees, hips, lower back, shoulders, and feet. To improve standardization of care as well as patient quality of life, we propose a diagnostic algorithm for the management of patients who receive AIs and who develop arthralgia or worsening symptoms from preexisting joint pain. We conclude that although arthralgia is often associated with AI therapy, prompt diagnosis and management of musculoskeletal symptoms may ensure continued AI treatment and improve quality of life...

*For a PDF of the full article, click on the link to the left of this introduction.

Less than 15% of healthcare professionals believe hospitals have closed the cultural and racial diversity gap in their leadership positions over the past five years, according to the results of a new survey (PDF).

Hospitalist leaders need to recognize the value of "cultural competence," particularly in an age when patients often tie their satisfaction to such questions as, "Does my doctor look like me?" and "Can I relate to my doctor?" according to James Gauss, senior vice president at executive search firm Witt/Kieffer, which penned the report.

Racial and ethnic disparity also will be important to address under provisions in the Affordable Care Act, which tie an economic impact to an organization's ability to deal with diverse populations of patients, says Gauss.

"We are now finally getting to a point where people might get paid correctly for dealing with these diversity issues because quality outcomes are going to be rewarded," he says.

Gauss says techniques that can help hospitals better balance the ethnic and racial makeup of their leadership include:

• implementing formal mentoring programs;

• understanding the patient and physician diversity of the geographic areas they serve; and

• establishing diversity recruiting goals.

For some groups, those goals might be as simple as recognizing that an organization is not doing enough. For others, the goals can be formal quotas.

"Some organizations set targets and they're very adamant about it," Gauss says. "But for some places, that may be two or three years down the road. … It depends on your starting point."

Less than 15% of healthcare professionals believe hospitals have closed the cultural and racial diversity gap in their leadership positions over the past five years, according to the results of a new survey (PDF).

Hospitalist leaders need to recognize the value of "cultural competence," particularly in an age when patients often tie their satisfaction to such questions as, "Does my doctor look like me?" and "Can I relate to my doctor?" according to James Gauss, senior vice president at executive search firm Witt/Kieffer, which penned the report.

Racial and ethnic disparity also will be important to address under provisions in the Affordable Care Act, which tie an economic impact to an organization's ability to deal with diverse populations of patients, says Gauss.

"We are now finally getting to a point where people might get paid correctly for dealing with these diversity issues because quality outcomes are going to be rewarded," he says.

Gauss says techniques that can help hospitals better balance the ethnic and racial makeup of their leadership include:

• implementing formal mentoring programs;

• understanding the patient and physician diversity of the geographic areas they serve; and

• establishing diversity recruiting goals.

For some groups, those goals might be as simple as recognizing that an organization is not doing enough. For others, the goals can be formal quotas.

"Some organizations set targets and they're very adamant about it," Gauss says. "But for some places, that may be two or three years down the road. … It depends on your starting point."

Less than 15% of healthcare professionals believe hospitals have closed the cultural and racial diversity gap in their leadership positions over the past five years, according to the results of a new survey (PDF).

Hospitalist leaders need to recognize the value of "cultural competence," particularly in an age when patients often tie their satisfaction to such questions as, "Does my doctor look like me?" and "Can I relate to my doctor?" according to James Gauss, senior vice president at executive search firm Witt/Kieffer, which penned the report.

Racial and ethnic disparity also will be important to address under provisions in the Affordable Care Act, which tie an economic impact to an organization's ability to deal with diverse populations of patients, says Gauss.

"We are now finally getting to a point where people might get paid correctly for dealing with these diversity issues because quality outcomes are going to be rewarded," he says.

Gauss says techniques that can help hospitals better balance the ethnic and racial makeup of their leadership include:

• implementing formal mentoring programs;

• understanding the patient and physician diversity of the geographic areas they serve; and

• establishing diversity recruiting goals.

For some groups, those goals might be as simple as recognizing that an organization is not doing enough. For others, the goals can be formal quotas.

"Some organizations set targets and they're very adamant about it," Gauss says. "But for some places, that may be two or three years down the road. … It depends on your starting point."

Clinical question: How does a brief period of CPR with early analysis of rhythm compare with the strategy of a longer period of CPR with delayed analysis of rhythm in patients with out-of-hospital cardiac arrest?

Background: Based on current guidelines, emergency medical service (EMS) personnel could provide two minutes of CPR before the first analysis of cardiac rhythm. However, there is a paucity of data on the outcomes of this strategy versus the short CPR and early rhythm analysis.

Study design: The EMS groups participating in the study were cluster-randomized to one strategy or the other.

Settings: The Resuscitation Outcome Consortium (ROC) is a clinical trial consortium comprising 10 U.S. and Canadian universities and their regional EMS systems. The trial was conducted at 150 of the 260 EMS agencies participating in the ROC.

Synopsis: This is a cluster-randomized trial involving adults with out-of-hospital cardiac arrest. Patients in the early-analysis group were assigned to receive 30 to 60 seconds of EMS-administered CPR, and those in the later-analysis group were assigned to receive 180 seconds of CPR, before the initial electrocardiographic analysis. The primary outcome was survival to hospital discharge with satisfactory functional status (a modified Rankin scale score of =3, on a scale of 0 to 6, with higher scores indicating greater disability).

The study included 9,933 patients, of whom 5,290 were assigned to early analysis of cardiac rhythm and 4,643 to later analysis. A total of 273 patients (5.9%) in the later-analysis group and 310 patients (5.9%) in the early-analysis group met the criteria for the primary outcome, with a cluster-adjusted difference of -0.2 percentage points (95% confidence interval, -1.1 to 0.7; P=0.59).

Analyses of the data with adjustment for confounding factors, as well as subgroup analyses, showed no survival benefit for either study group.

Bottom line: Among patients who had an out-of-hospital cardiac arrest, there is no difference in the outcomes with a brief period, as compared with a longer period, of EMS-administered CPR before the first analysis of cardiac rhythm.

Citation: Stiell IG, Nichol G, Leroux BG, et al. Early versus later rhythm analysis in patients with out-of-hospital cardiac arrest. N Engl J Med. 2011;365;787-797.

Check out more physician reviews of HM-relevant literature on our website.

Clinical question: How does a brief period of CPR with early analysis of rhythm compare with the strategy of a longer period of CPR with delayed analysis of rhythm in patients with out-of-hospital cardiac arrest?

Background: Based on current guidelines, emergency medical service (EMS) personnel could provide two minutes of CPR before the first analysis of cardiac rhythm. However, there is a paucity of data on the outcomes of this strategy versus the short CPR and early rhythm analysis.

Study design: The EMS groups participating in the study were cluster-randomized to one strategy or the other.

Settings: The Resuscitation Outcome Consortium (ROC) is a clinical trial consortium comprising 10 U.S. and Canadian universities and their regional EMS systems. The trial was conducted at 150 of the 260 EMS agencies participating in the ROC.

Synopsis: This is a cluster-randomized trial involving adults with out-of-hospital cardiac arrest. Patients in the early-analysis group were assigned to receive 30 to 60 seconds of EMS-administered CPR, and those in the later-analysis group were assigned to receive 180 seconds of CPR, before the initial electrocardiographic analysis. The primary outcome was survival to hospital discharge with satisfactory functional status (a modified Rankin scale score of =3, on a scale of 0 to 6, with higher scores indicating greater disability).

The study included 9,933 patients, of whom 5,290 were assigned to early analysis of cardiac rhythm and 4,643 to later analysis. A total of 273 patients (5.9%) in the later-analysis group and 310 patients (5.9%) in the early-analysis group met the criteria for the primary outcome, with a cluster-adjusted difference of -0.2 percentage points (95% confidence interval, -1.1 to 0.7; P=0.59).

Analyses of the data with adjustment for confounding factors, as well as subgroup analyses, showed no survival benefit for either study group.

Bottom line: Among patients who had an out-of-hospital cardiac arrest, there is no difference in the outcomes with a brief period, as compared with a longer period, of EMS-administered CPR before the first analysis of cardiac rhythm.

Citation: Stiell IG, Nichol G, Leroux BG, et al. Early versus later rhythm analysis in patients with out-of-hospital cardiac arrest. N Engl J Med. 2011;365;787-797.

Check out more physician reviews of HM-relevant literature on our website.

Clinical question: How does a brief period of CPR with early analysis of rhythm compare with the strategy of a longer period of CPR with delayed analysis of rhythm in patients with out-of-hospital cardiac arrest?

Background: Based on current guidelines, emergency medical service (EMS) personnel could provide two minutes of CPR before the first analysis of cardiac rhythm. However, there is a paucity of data on the outcomes of this strategy versus the short CPR and early rhythm analysis.

Study design: The EMS groups participating in the study were cluster-randomized to one strategy or the other.

Settings: The Resuscitation Outcome Consortium (ROC) is a clinical trial consortium comprising 10 U.S. and Canadian universities and their regional EMS systems. The trial was conducted at 150 of the 260 EMS agencies participating in the ROC.

Synopsis: This is a cluster-randomized trial involving adults with out-of-hospital cardiac arrest. Patients in the early-analysis group were assigned to receive 30 to 60 seconds of EMS-administered CPR, and those in the later-analysis group were assigned to receive 180 seconds of CPR, before the initial electrocardiographic analysis. The primary outcome was survival to hospital discharge with satisfactory functional status (a modified Rankin scale score of =3, on a scale of 0 to 6, with higher scores indicating greater disability).

The study included 9,933 patients, of whom 5,290 were assigned to early analysis of cardiac rhythm and 4,643 to later analysis. A total of 273 patients (5.9%) in the later-analysis group and 310 patients (5.9%) in the early-analysis group met the criteria for the primary outcome, with a cluster-adjusted difference of -0.2 percentage points (95% confidence interval, -1.1 to 0.7; P=0.59).

Analyses of the data with adjustment for confounding factors, as well as subgroup analyses, showed no survival benefit for either study group.

Bottom line: Among patients who had an out-of-hospital cardiac arrest, there is no difference in the outcomes with a brief period, as compared with a longer period, of EMS-administered CPR before the first analysis of cardiac rhythm.

Citation: Stiell IG, Nichol G, Leroux BG, et al. Early versus later rhythm analysis in patients with out-of-hospital cardiac arrest. N Engl J Med. 2011;365;787-797.

Check out more physician reviews of HM-relevant literature on our website.

click for large version

Roberta Gebhard, DO, thought that her 20 years of experience as a physician in the U.S., 10 of them as a hospitalist, would mean she would get paid more than a new graduate just out of residency would.

She was wrong.

Dr. Gebhard was working at a hospital run by the U.S. Department of Veterans Affairs when she learned that the less experienced doctor—a man—was making $10,000 more a year than she was.

“After that, the job was no longer interesting to me,” says Dr. Gebhard, who left the hospital over the pay discrepancy and now works as a hospitalist at WCA Hospital in Jamestown, N.Y. “Women think that things should be fair, so they assume that they are. I’m a good negotiator, and when that happened to me, I was like, ‘Wait a minute! I didn’t just take what they offered me.’ I pushed a few times and was basically told it was a government position, there was no wiggle room, and I couldn’t get more salary.

“It happens, and women need to know that it happens,” she says.

Earnings data and research show that the gender pay gap lingers. More problematic is pinpointing why the gap won’t close. Explanations range from ignorance of the issue and trading in compensation for other job benefits to women’s lack of negotiating skills to subtle gender discrimination.

Because gender pay discrepancies persist and because theories abound as to the cause, the issue will be addressed during a “Women in Hospital Medicine” session at HM12 next month in San Diego, along with such topics as leadership challenges and work-life balance, says Patience Reich, MD, SFHM, a hospitalist and assistant professor of medicine at Wake Forest University School of Medicine in Winston-Salem, N.C.

“When we conceived the session, we were actually thinking about women in leadership, but decided to go for more general topics that affect women hospitalists, whether they are in leadership or not,” says Dr. Reich, a member of SHM’s Leadership Committee who helped coordinate the HM12 session.

According to the 2011 SHM-MGMA compensation and productivity survey, mean annual compensation for female hospitalists in family practice, internal medicine, and pediatrics is lower than that of their male counterparts. For example, female hospitalists in family practice, internal medicine, and pediatrics have mean annual compensations of $219,995, $215,012, and $170,535, respectively, or $4,448, $29,211, and $23,402 less than male counterparts in similar positions (see Figure 1). Such factors as practice location, practice ownership, and productivity have an effect on compensation and could be the reason behind the disparity, says Liz Boten, a spokeswoman for Englewood, Colo.-based Medical Group Management Association (MGMA).

But research that is controlled for numerous observable factors has shown that the gender earnings gap continues to exist among physicians.^1,2,3,4 Of particular note are two studies, including one focused on hospital medicine.

In 2004, a study authored by Timothy J. Hoff, PhD, an associate professor at State University of New York at Albany, controlled for a wide range of work and non-work variables, including clinical workload, compensation type, employer type, tenure, marital status, and tenure in hospital medicine.⁵ The data show that female hospitalists earned approximately $22,000 less per year than male hospitalists, despite similar work patterns. Additional study results showed that married female hospitalists with children worked just as much and carried as heavy a clinical workload as married male hospitalists who had children.

Last year, a study in Health Affairs generated considerable interest when it found that male physicians newly trained in New York state made on average $16,819 more than newly trained female physicians in 2008, compared with a $3,600 difference in 1999.⁶ The authors controlled for specialty type, hours worked, designation of hours, immigration status, age, and practice location. And by focusing on starting salaries, factors such as job tenure, institutional rank, and job productivity didn’t come into play, signifying that the experiences of married female and male hospitalists with children differed less than one might presume based upon perceptions that women with families sacrifice work commitments to take care of their spouses and children.

“It is studies like this that are going to be critically important for us to move forward,” says Janet Nagamine, RN, MD, SFHM, a hospitalist at Kaiser Permanente Medical Center in Santa Clara, Calif., and an SHM board member who is assisting with the “Women in Hospital Medicine” session at HM12. “As we talk about a pay gap, we need to be more evidence-based.”

Studies that show a gender earnings gap even among highly skilled professionals don’t surprise researchers. The U.S. Bureau of Labor Statistics collects earnings data on hundreds of occupations, including physicians, and men outearn women across the board, regardless of educational requirements, says Mary Gatta, PhD, past director of gender and workforce policy at the Center for Women and Work at Rutgers University in New Brunswick, N.J., and current senior research scholar at Wider Opportunities for Women, a Washington, D.C.-based organization that focuses on opportunity equality for women.

The Gap that Won’t Close

So why, in 2012, do gender-based pay discrepancies remain?

How much people earn typically is not public information, so women often don’t know they aren’t being paid equally and, therefore, don’t have information on which to act, Dr. Gatta says.

“My opinion on it is women don’t know about the pay gap,” says Dr. Gebhard, co-chair of the American Medical Women’s Association’s (AMWA) Gender Equity Task Force. She recalls a salary negotiation lecture she helped lead after which a woman finishing residency raised her hand to say she was joining a faculty where everyone was paid the same. “The entire room just groaned,” she says. “Clearly, women out there think everything is fair and people are paid the same. They don’t know they’re being paid less.”

In trying to explain the widening pay gap, authors of the 2011 Health Affairs study posited that the influx of women into the physician workforce is reshaping the practice and business of medicine.⁶

“The notion we suggest is that the increasing gender gap can be explained by new women physicians increasingly demanding non-pecuniary aspects of their jobs, and because of the greater aggregate presence of women in the physician labor market, being able to get it,” says lead author Anthony Lo Sasso, a professor and senior research scientist at the School of Public Health at the University of Illinois at Chicago. “Remember, cash wages are but one part of the compensation package in any job.”

click for large version

Hoff’s study also uncovered gender differences in employment preferences, with men attracted to HM for the compensation possibilities and women for the predictable hours and lifestyle flexibility. For this reason, Hoff suggested, hospitalist employers can use different recruiting pitches for women than men and, to the extent they hire female hospitalists, save money (see “Negotiating Strategies for Better Compensation,” below).

“The Hoff paper is a goldmine,” says Linda Brodsky, MD, a pediatric otolaryngologist in Buffalo, N.Y., who co-chairs AMWA’s Gender Equity Task Force and whose organization, Expediting the Inevitable, advocates for gender equity in healthcare. “How is it that when you have shift work, women are getting paid less per shift? Because Hoff tells you at the end, employers can get away with it. Even if they know they are underpaying women, they will take the chance because it’s so hard for anybody to take legal action.”

Women also find themselves in a double bind when it comes to negotiating higher compensation, says Barbara Gault, PhD, executive director of the Institute for Women’s Policy Research in Washington, D.C. Some suggest a pay gap exists because women are not negotiating for themselves, but research shows women tend to be perceived as less likable when they are more assertive about higher wages, she says.

Erin Stucky Fisher, MD, MHM, has seen this phenomena play out in her roles as medical director for quality at Rady Children’s Hospital in San Diego and associate program director for the University of California at San Diego Pediatric Residency Program.

“I do a lot of interviewing for the hospital, and it does seem, in general, that women are less likely to promote themselves than men in the same situation,” says Dr. Fisher, an SHM board member who is also assisting with the HM12 “Women in Hospital Medicine” session. “There are reasons behind it that might have to do with women not wanting to be perceived as self-serving or arrogant.”

I do a lot of interviewing for the hospital, and it does seem, in general, that women are less likely to promote themselves than men in the same situation. There are reasons behind it that might have to do with women not wanting to be perceived as self-serving or arrogant

—Erin Stucky Fisher, MD, FAAP, MHM, medical director for quality, Rady Children’s Hospital, associate program director, University of California at San Diego Pediatric Residency Program, SHM board member

Dr. Brodsky agrees with the perception issues facing physicians.

“Women are supposed to be grateful, accommodating, and get along, which are excellent qualities,” she says. “But when you’re expected to do that and you instead negotiate with any kind of spirit, it’s perceived as troublemaking, whereas in men, it’s perceived as strength.”

Subtle forms of gender discrimination continue to exist in workplaces, Dr. Gatta says. Beliefs remain that men have a family to support, so they should be paid more, and that women are in the workforce just for extra money, even though recent data show that women’s income is key to families’ well-being, she notes.

Common patterns of gender bias will be discussed at the HM12 session, says Dr. Reich, who was a victim of gender pay disparity when she worked a locum tenens job earlier in her career.

“There was no logical explanation. The men did less work by all measures, and the other woman and I didn’t have young children at home, so explanations of women trading in money for time with family didn’t apply,” she explains. “Why did they think I should be paid less? I didn’t understand, and I never got a logical reason.”

Potential Solutions

Shortly after arriving at Wake Forest in 2004, Dr. Reich had the opportunity to build the hospitalist program. A set of thorough, transparent criteria for determining compensation were established almost immediately to help prevent pay discrepancies.

“We tried to be as objective as we could, and we involved the group in talking about it because we felt it was important,” she says.

Any woman physician who is in the senior ranks must be obligated to start changing the culture and making sure the fairness issue gets raised and is an important part of their agenda. Enough women are now part of the physician population. They have to start saying, ‘We are a group to be reckoned with, and we are going to make changes.’

—Linda Brodsky, MD, pediatric otolaryngologist, Buffalo, N.Y., co-chair, AMWA Gender Equity Task Force

Organizations can conduct self-audits to assess whether men and women are being compensated equitably, then make adjustments when necessary, Dr. Gault says. Policies can be adopted to promote pay transparency and allow employees to discuss compensation and suggest ways it can be improved, she adds. In workplaces where compensation discussions are discouraged, women can try to informally speak with their male friends to gather information and determine if there’s a pay gap problem.

Equal pay laws, such as the Lily Ledbetter Fair Pay Act, exist at the federal level. But Dr. Gatta says work must be done on the enforcement end to make a real difference. Similarly, Dr. Brodsky describes the Equal Employment Opportunity Commission as a toothless oversight agency with limited power to investigate complaints and assess fines.

“It’s on women to go and be the whistleblower, the policeman, and pay for legal action. It’s impossible,” she says. “When you utter the words ‘gender discrimination,’ immediately, retaliation goes into high gear.”

While employers and enforcement agencies have a significant role in closing the pay gap, women themselves must collectively advocate for equal pay, Dr. Gault says.

“Any woman physician who is in the senior ranks must be obligated to start changing the culture and making sure the fairness issue gets raised and is an important part of their agenda,” Dr. Brodsky says. “Enough women are now part of the physician population. They have to start saying, ‘We are a group to be reckoned with, and we are going to make changes.’”

Lisa Ryan is a freelance writer based in New Jersey.

References

1. Wright AL, Schwindt LA, Bassford TL, et al. Gender differences in academic advancement: patterns, causes, and potential solutions in one US College of Medicine. Acad Med. 2003;78(5):500-508.
2. Ash AS, Carr PL, Goldstein R, et al. Compensation and advancement of women in academic medicine: is there equity? Ann Intern Med. 2004;141(3):205-212.
3. Ness RB, Ukoli F, Hunt S, et al. Salary equity among male and female internists in Pennsylvania. Ann Intern Med. 2000;133(2):104-110.
4. Weeks WB, Wallace TA, Wallace AE. How do race and sex affect the earnings of primary care physicians? Health Aff (Millwood). 2009;28(2):557-566.
5. Hoff TJ. Doing the same and earning less: male and female physicians in a new medical specialty. Inquiry. 2004;41:301-315.
6. Lo Sasso AT, Richards MR, Chou C, Gerber SE. The $16,819 pay gap for newly trained physicians: the unexplained trend of men earning more than women. Health Aff (Millwood). 2011;30:193-201.

click for large version

Roberta Gebhard, DO, thought that her 20 years of experience as a physician in the U.S., 10 of them as a hospitalist, would mean she would get paid more than a new graduate just out of residency would.

She was wrong.

Dr. Gebhard was working at a hospital run by the U.S. Department of Veterans Affairs when she learned that the less experienced doctor—a man—was making $10,000 more a year than she was.

“After that, the job was no longer interesting to me,” says Dr. Gebhard, who left the hospital over the pay discrepancy and now works as a hospitalist at WCA Hospital in Jamestown, N.Y. “Women think that things should be fair, so they assume that they are. I’m a good negotiator, and when that happened to me, I was like, ‘Wait a minute! I didn’t just take what they offered me.’ I pushed a few times and was basically told it was a government position, there was no wiggle room, and I couldn’t get more salary.

“It happens, and women need to know that it happens,” she says.

Earnings data and research show that the gender pay gap lingers. More problematic is pinpointing why the gap won’t close. Explanations range from ignorance of the issue and trading in compensation for other job benefits to women’s lack of negotiating skills to subtle gender discrimination.

Because gender pay discrepancies persist and because theories abound as to the cause, the issue will be addressed during a “Women in Hospital Medicine” session at HM12 next month in San Diego, along with such topics as leadership challenges and work-life balance, says Patience Reich, MD, SFHM, a hospitalist and assistant professor of medicine at Wake Forest University School of Medicine in Winston-Salem, N.C.

“When we conceived the session, we were actually thinking about women in leadership, but decided to go for more general topics that affect women hospitalists, whether they are in leadership or not,” says Dr. Reich, a member of SHM’s Leadership Committee who helped coordinate the HM12 session.

According to the 2011 SHM-MGMA compensation and productivity survey, mean annual compensation for female hospitalists in family practice, internal medicine, and pediatrics is lower than that of their male counterparts. For example, female hospitalists in family practice, internal medicine, and pediatrics have mean annual compensations of $219,995, $215,012, and $170,535, respectively, or $4,448, $29,211, and $23,402 less than male counterparts in similar positions (see Figure 1). Such factors as practice location, practice ownership, and productivity have an effect on compensation and could be the reason behind the disparity, says Liz Boten, a spokeswoman for Englewood, Colo.-based Medical Group Management Association (MGMA).

But research that is controlled for numerous observable factors has shown that the gender earnings gap continues to exist among physicians.^1,2,3,4 Of particular note are two studies, including one focused on hospital medicine.

In 2004, a study authored by Timothy J. Hoff, PhD, an associate professor at State University of New York at Albany, controlled for a wide range of work and non-work variables, including clinical workload, compensation type, employer type, tenure, marital status, and tenure in hospital medicine.⁵ The data show that female hospitalists earned approximately $22,000 less per year than male hospitalists, despite similar work patterns. Additional study results showed that married female hospitalists with children worked just as much and carried as heavy a clinical workload as married male hospitalists who had children.

Last year, a study in Health Affairs generated considerable interest when it found that male physicians newly trained in New York state made on average $16,819 more than newly trained female physicians in 2008, compared with a $3,600 difference in 1999.⁶ The authors controlled for specialty type, hours worked, designation of hours, immigration status, age, and practice location. And by focusing on starting salaries, factors such as job tenure, institutional rank, and job productivity didn’t come into play, signifying that the experiences of married female and male hospitalists with children differed less than one might presume based upon perceptions that women with families sacrifice work commitments to take care of their spouses and children.

“It is studies like this that are going to be critically important for us to move forward,” says Janet Nagamine, RN, MD, SFHM, a hospitalist at Kaiser Permanente Medical Center in Santa Clara, Calif., and an SHM board member who is assisting with the “Women in Hospital Medicine” session at HM12. “As we talk about a pay gap, we need to be more evidence-based.”

Studies that show a gender earnings gap even among highly skilled professionals don’t surprise researchers. The U.S. Bureau of Labor Statistics collects earnings data on hundreds of occupations, including physicians, and men outearn women across the board, regardless of educational requirements, says Mary Gatta, PhD, past director of gender and workforce policy at the Center for Women and Work at Rutgers University in New Brunswick, N.J., and current senior research scholar at Wider Opportunities for Women, a Washington, D.C.-based organization that focuses on opportunity equality for women.

The Gap that Won’t Close

So why, in 2012, do gender-based pay discrepancies remain?

How much people earn typically is not public information, so women often don’t know they aren’t being paid equally and, therefore, don’t have information on which to act, Dr. Gatta says.

“My opinion on it is women don’t know about the pay gap,” says Dr. Gebhard, co-chair of the American Medical Women’s Association’s (AMWA) Gender Equity Task Force. She recalls a salary negotiation lecture she helped lead after which a woman finishing residency raised her hand to say she was joining a faculty where everyone was paid the same. “The entire room just groaned,” she says. “Clearly, women out there think everything is fair and people are paid the same. They don’t know they’re being paid less.”

In trying to explain the widening pay gap, authors of the 2011 Health Affairs study posited that the influx of women into the physician workforce is reshaping the practice and business of medicine.⁶

“The notion we suggest is that the increasing gender gap can be explained by new women physicians increasingly demanding non-pecuniary aspects of their jobs, and because of the greater aggregate presence of women in the physician labor market, being able to get it,” says lead author Anthony Lo Sasso, a professor and senior research scientist at the School of Public Health at the University of Illinois at Chicago. “Remember, cash wages are but one part of the compensation package in any job.”

click for large version

Hoff’s study also uncovered gender differences in employment preferences, with men attracted to HM for the compensation possibilities and women for the predictable hours and lifestyle flexibility. For this reason, Hoff suggested, hospitalist employers can use different recruiting pitches for women than men and, to the extent they hire female hospitalists, save money (see “Negotiating Strategies for Better Compensation,” below).

“The Hoff paper is a goldmine,” says Linda Brodsky, MD, a pediatric otolaryngologist in Buffalo, N.Y., who co-chairs AMWA’s Gender Equity Task Force and whose organization, Expediting the Inevitable, advocates for gender equity in healthcare. “How is it that when you have shift work, women are getting paid less per shift? Because Hoff tells you at the end, employers can get away with it. Even if they know they are underpaying women, they will take the chance because it’s so hard for anybody to take legal action.”

Women also find themselves in a double bind when it comes to negotiating higher compensation, says Barbara Gault, PhD, executive director of the Institute for Women’s Policy Research in Washington, D.C. Some suggest a pay gap exists because women are not negotiating for themselves, but research shows women tend to be perceived as less likable when they are more assertive about higher wages, she says.

Erin Stucky Fisher, MD, MHM, has seen this phenomena play out in her roles as medical director for quality at Rady Children’s Hospital in San Diego and associate program director for the University of California at San Diego Pediatric Residency Program.

“I do a lot of interviewing for the hospital, and it does seem, in general, that women are less likely to promote themselves than men in the same situation,” says Dr. Fisher, an SHM board member who is also assisting with the HM12 “Women in Hospital Medicine” session. “There are reasons behind it that might have to do with women not wanting to be perceived as self-serving or arrogant.”

I do a lot of interviewing for the hospital, and it does seem, in general, that women are less likely to promote themselves than men in the same situation. There are reasons behind it that might have to do with women not wanting to be perceived as self-serving or arrogant

—Erin Stucky Fisher, MD, FAAP, MHM, medical director for quality, Rady Children’s Hospital, associate program director, University of California at San Diego Pediatric Residency Program, SHM board member

Dr. Brodsky agrees with the perception issues facing physicians.

“Women are supposed to be grateful, accommodating, and get along, which are excellent qualities,” she says. “But when you’re expected to do that and you instead negotiate with any kind of spirit, it’s perceived as troublemaking, whereas in men, it’s perceived as strength.”

Subtle forms of gender discrimination continue to exist in workplaces, Dr. Gatta says. Beliefs remain that men have a family to support, so they should be paid more, and that women are in the workforce just for extra money, even though recent data show that women’s income is key to families’ well-being, she notes.

Common patterns of gender bias will be discussed at the HM12 session, says Dr. Reich, who was a victim of gender pay disparity when she worked a locum tenens job earlier in her career.

“There was no logical explanation. The men did less work by all measures, and the other woman and I didn’t have young children at home, so explanations of women trading in money for time with family didn’t apply,” she explains. “Why did they think I should be paid less? I didn’t understand, and I never got a logical reason.”

Potential Solutions

Shortly after arriving at Wake Forest in 2004, Dr. Reich had the opportunity to build the hospitalist program. A set of thorough, transparent criteria for determining compensation were established almost immediately to help prevent pay discrepancies.

“We tried to be as objective as we could, and we involved the group in talking about it because we felt it was important,” she says.

Any woman physician who is in the senior ranks must be obligated to start changing the culture and making sure the fairness issue gets raised and is an important part of their agenda. Enough women are now part of the physician population. They have to start saying, ‘We are a group to be reckoned with, and we are going to make changes.’

—Linda Brodsky, MD, pediatric otolaryngologist, Buffalo, N.Y., co-chair, AMWA Gender Equity Task Force

Organizations can conduct self-audits to assess whether men and women are being compensated equitably, then make adjustments when necessary, Dr. Gault says. Policies can be adopted to promote pay transparency and allow employees to discuss compensation and suggest ways it can be improved, she adds. In workplaces where compensation discussions are discouraged, women can try to informally speak with their male friends to gather information and determine if there’s a pay gap problem.

Equal pay laws, such as the Lily Ledbetter Fair Pay Act, exist at the federal level. But Dr. Gatta says work must be done on the enforcement end to make a real difference. Similarly, Dr. Brodsky describes the Equal Employment Opportunity Commission as a toothless oversight agency with limited power to investigate complaints and assess fines.

“It’s on women to go and be the whistleblower, the policeman, and pay for legal action. It’s impossible,” she says. “When you utter the words ‘gender discrimination,’ immediately, retaliation goes into high gear.”

While employers and enforcement agencies have a significant role in closing the pay gap, women themselves must collectively advocate for equal pay, Dr. Gault says.

“Any woman physician who is in the senior ranks must be obligated to start changing the culture and making sure the fairness issue gets raised and is an important part of their agenda,” Dr. Brodsky says. “Enough women are now part of the physician population. They have to start saying, ‘We are a group to be reckoned with, and we are going to make changes.’”

Lisa Ryan is a freelance writer based in New Jersey.

References

1. Wright AL, Schwindt LA, Bassford TL, et al. Gender differences in academic advancement: patterns, causes, and potential solutions in one US College of Medicine. Acad Med. 2003;78(5):500-508.
2. Ash AS, Carr PL, Goldstein R, et al. Compensation and advancement of women in academic medicine: is there equity? Ann Intern Med. 2004;141(3):205-212.
3. Ness RB, Ukoli F, Hunt S, et al. Salary equity among male and female internists in Pennsylvania. Ann Intern Med. 2000;133(2):104-110.
4. Weeks WB, Wallace TA, Wallace AE. How do race and sex affect the earnings of primary care physicians? Health Aff (Millwood). 2009;28(2):557-566.
5. Hoff TJ. Doing the same and earning less: male and female physicians in a new medical specialty. Inquiry. 2004;41:301-315.
6. Lo Sasso AT, Richards MR, Chou C, Gerber SE. The $16,819 pay gap for newly trained physicians: the unexplained trend of men earning more than women. Health Aff (Millwood). 2011;30:193-201.

click for large version

Roberta Gebhard, DO, thought that her 20 years of experience as a physician in the U.S., 10 of them as a hospitalist, would mean she would get paid more than a new graduate just out of residency would.

She was wrong.

Dr. Gebhard was working at a hospital run by the U.S. Department of Veterans Affairs when she learned that the less experienced doctor—a man—was making $10,000 more a year than she was.

“After that, the job was no longer interesting to me,” says Dr. Gebhard, who left the hospital over the pay discrepancy and now works as a hospitalist at WCA Hospital in Jamestown, N.Y. “Women think that things should be fair, so they assume that they are. I’m a good negotiator, and when that happened to me, I was like, ‘Wait a minute! I didn’t just take what they offered me.’ I pushed a few times and was basically told it was a government position, there was no wiggle room, and I couldn’t get more salary.

“It happens, and women need to know that it happens,” she says.

Earnings data and research show that the gender pay gap lingers. More problematic is pinpointing why the gap won’t close. Explanations range from ignorance of the issue and trading in compensation for other job benefits to women’s lack of negotiating skills to subtle gender discrimination.

Because gender pay discrepancies persist and because theories abound as to the cause, the issue will be addressed during a “Women in Hospital Medicine” session at HM12 next month in San Diego, along with such topics as leadership challenges and work-life balance, says Patience Reich, MD, SFHM, a hospitalist and assistant professor of medicine at Wake Forest University School of Medicine in Winston-Salem, N.C.

“When we conceived the session, we were actually thinking about women in leadership, but decided to go for more general topics that affect women hospitalists, whether they are in leadership or not,” says Dr. Reich, a member of SHM’s Leadership Committee who helped coordinate the HM12 session.

According to the 2011 SHM-MGMA compensation and productivity survey, mean annual compensation for female hospitalists in family practice, internal medicine, and pediatrics is lower than that of their male counterparts. For example, female hospitalists in family practice, internal medicine, and pediatrics have mean annual compensations of $219,995, $215,012, and $170,535, respectively, or $4,448, $29,211, and $23,402 less than male counterparts in similar positions (see Figure 1). Such factors as practice location, practice ownership, and productivity have an effect on compensation and could be the reason behind the disparity, says Liz Boten, a spokeswoman for Englewood, Colo.-based Medical Group Management Association (MGMA).

But research that is controlled for numerous observable factors has shown that the gender earnings gap continues to exist among physicians.^1,2,3,4 Of particular note are two studies, including one focused on hospital medicine.

In 2004, a study authored by Timothy J. Hoff, PhD, an associate professor at State University of New York at Albany, controlled for a wide range of work and non-work variables, including clinical workload, compensation type, employer type, tenure, marital status, and tenure in hospital medicine.⁵ The data show that female hospitalists earned approximately $22,000 less per year than male hospitalists, despite similar work patterns. Additional study results showed that married female hospitalists with children worked just as much and carried as heavy a clinical workload as married male hospitalists who had children.

Last year, a study in Health Affairs generated considerable interest when it found that male physicians newly trained in New York state made on average $16,819 more than newly trained female physicians in 2008, compared with a $3,600 difference in 1999.⁶ The authors controlled for specialty type, hours worked, designation of hours, immigration status, age, and practice location. And by focusing on starting salaries, factors such as job tenure, institutional rank, and job productivity didn’t come into play, signifying that the experiences of married female and male hospitalists with children differed less than one might presume based upon perceptions that women with families sacrifice work commitments to take care of their spouses and children.

“It is studies like this that are going to be critically important for us to move forward,” says Janet Nagamine, RN, MD, SFHM, a hospitalist at Kaiser Permanente Medical Center in Santa Clara, Calif., and an SHM board member who is assisting with the “Women in Hospital Medicine” session at HM12. “As we talk about a pay gap, we need to be more evidence-based.”

Studies that show a gender earnings gap even among highly skilled professionals don’t surprise researchers. The U.S. Bureau of Labor Statistics collects earnings data on hundreds of occupations, including physicians, and men outearn women across the board, regardless of educational requirements, says Mary Gatta, PhD, past director of gender and workforce policy at the Center for Women and Work at Rutgers University in New Brunswick, N.J., and current senior research scholar at Wider Opportunities for Women, a Washington, D.C.-based organization that focuses on opportunity equality for women.

The Gap that Won’t Close

So why, in 2012, do gender-based pay discrepancies remain?

How much people earn typically is not public information, so women often don’t know they aren’t being paid equally and, therefore, don’t have information on which to act, Dr. Gatta says.

“My opinion on it is women don’t know about the pay gap,” says Dr. Gebhard, co-chair of the American Medical Women’s Association’s (AMWA) Gender Equity Task Force. She recalls a salary negotiation lecture she helped lead after which a woman finishing residency raised her hand to say she was joining a faculty where everyone was paid the same. “The entire room just groaned,” she says. “Clearly, women out there think everything is fair and people are paid the same. They don’t know they’re being paid less.”

In trying to explain the widening pay gap, authors of the 2011 Health Affairs study posited that the influx of women into the physician workforce is reshaping the practice and business of medicine.⁶

“The notion we suggest is that the increasing gender gap can be explained by new women physicians increasingly demanding non-pecuniary aspects of their jobs, and because of the greater aggregate presence of women in the physician labor market, being able to get it,” says lead author Anthony Lo Sasso, a professor and senior research scientist at the School of Public Health at the University of Illinois at Chicago. “Remember, cash wages are but one part of the compensation package in any job.”

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Hoff’s study also uncovered gender differences in employment preferences, with men attracted to HM for the compensation possibilities and women for the predictable hours and lifestyle flexibility. For this reason, Hoff suggested, hospitalist employers can use different recruiting pitches for women than men and, to the extent they hire female hospitalists, save money (see “Negotiating Strategies for Better Compensation,” below).

“The Hoff paper is a goldmine,” says Linda Brodsky, MD, a pediatric otolaryngologist in Buffalo, N.Y., who co-chairs AMWA’s Gender Equity Task Force and whose organization, Expediting the Inevitable, advocates for gender equity in healthcare. “How is it that when you have shift work, women are getting paid less per shift? Because Hoff tells you at the end, employers can get away with it. Even if they know they are underpaying women, they will take the chance because it’s so hard for anybody to take legal action.”

Women also find themselves in a double bind when it comes to negotiating higher compensation, says Barbara Gault, PhD, executive director of the Institute for Women’s Policy Research in Washington, D.C. Some suggest a pay gap exists because women are not negotiating for themselves, but research shows women tend to be perceived as less likable when they are more assertive about higher wages, she says.

Erin Stucky Fisher, MD, MHM, has seen this phenomena play out in her roles as medical director for quality at Rady Children’s Hospital in San Diego and associate program director for the University of California at San Diego Pediatric Residency Program.

“I do a lot of interviewing for the hospital, and it does seem, in general, that women are less likely to promote themselves than men in the same situation,” says Dr. Fisher, an SHM board member who is also assisting with the HM12 “Women in Hospital Medicine” session. “There are reasons behind it that might have to do with women not wanting to be perceived as self-serving or arrogant.”

I do a lot of interviewing for the hospital, and it does seem, in general, that women are less likely to promote themselves than men in the same situation. There are reasons behind it that might have to do with women not wanting to be perceived as self-serving or arrogant

—Erin Stucky Fisher, MD, FAAP, MHM, medical director for quality, Rady Children’s Hospital, associate program director, University of California at San Diego Pediatric Residency Program, SHM board member

Dr. Brodsky agrees with the perception issues facing physicians.

“Women are supposed to be grateful, accommodating, and get along, which are excellent qualities,” she says. “But when you’re expected to do that and you instead negotiate with any kind of spirit, it’s perceived as troublemaking, whereas in men, it’s perceived as strength.”

Subtle forms of gender discrimination continue to exist in workplaces, Dr. Gatta says. Beliefs remain that men have a family to support, so they should be paid more, and that women are in the workforce just for extra money, even though recent data show that women’s income is key to families’ well-being, she notes.

Common patterns of gender bias will be discussed at the HM12 session, says Dr. Reich, who was a victim of gender pay disparity when she worked a locum tenens job earlier in her career.

“There was no logical explanation. The men did less work by all measures, and the other woman and I didn’t have young children at home, so explanations of women trading in money for time with family didn’t apply,” she explains. “Why did they think I should be paid less? I didn’t understand, and I never got a logical reason.”

Potential Solutions

Shortly after arriving at Wake Forest in 2004, Dr. Reich had the opportunity to build the hospitalist program. A set of thorough, transparent criteria for determining compensation were established almost immediately to help prevent pay discrepancies.

“We tried to be as objective as we could, and we involved the group in talking about it because we felt it was important,” she says.

Any woman physician who is in the senior ranks must be obligated to start changing the culture and making sure the fairness issue gets raised and is an important part of their agenda. Enough women are now part of the physician population. They have to start saying, ‘We are a group to be reckoned with, and we are going to make changes.’

—Linda Brodsky, MD, pediatric otolaryngologist, Buffalo, N.Y., co-chair, AMWA Gender Equity Task Force

Organizations can conduct self-audits to assess whether men and women are being compensated equitably, then make adjustments when necessary, Dr. Gault says. Policies can be adopted to promote pay transparency and allow employees to discuss compensation and suggest ways it can be improved, she adds. In workplaces where compensation discussions are discouraged, women can try to informally speak with their male friends to gather information and determine if there’s a pay gap problem.

Equal pay laws, such as the Lily Ledbetter Fair Pay Act, exist at the federal level. But Dr. Gatta says work must be done on the enforcement end to make a real difference. Similarly, Dr. Brodsky describes the Equal Employment Opportunity Commission as a toothless oversight agency with limited power to investigate complaints and assess fines.

“It’s on women to go and be the whistleblower, the policeman, and pay for legal action. It’s impossible,” she says. “When you utter the words ‘gender discrimination,’ immediately, retaliation goes into high gear.”

While employers and enforcement agencies have a significant role in closing the pay gap, women themselves must collectively advocate for equal pay, Dr. Gault says.

“Any woman physician who is in the senior ranks must be obligated to start changing the culture and making sure the fairness issue gets raised and is an important part of their agenda,” Dr. Brodsky says. “Enough women are now part of the physician population. They have to start saying, ‘We are a group to be reckoned with, and we are going to make changes.’”

Lisa Ryan is a freelance writer based in New Jersey.

References

1. Wright AL, Schwindt LA, Bassford TL, et al. Gender differences in academic advancement: patterns, causes, and potential solutions in one US College of Medicine. Acad Med. 2003;78(5):500-508.
2. Ash AS, Carr PL, Goldstein R, et al. Compensation and advancement of women in academic medicine: is there equity? Ann Intern Med. 2004;141(3):205-212.
3. Ness RB, Ukoli F, Hunt S, et al. Salary equity among male and female internists in Pennsylvania. Ann Intern Med. 2000;133(2):104-110.
4. Weeks WB, Wallace TA, Wallace AE. How do race and sex affect the earnings of primary care physicians? Health Aff (Millwood). 2009;28(2):557-566.
5. Hoff TJ. Doing the same and earning less: male and female physicians in a new medical specialty. Inquiry. 2004;41:301-315.
6. Lo Sasso AT, Richards MR, Chou C, Gerber SE. The $16,819 pay gap for newly trained physicians: the unexplained trend of men earning more than women. Health Aff (Millwood). 2011;30:193-201.