Denise Napoli

NEW YORK - Clean, nonsterile gloves are just as effective in preventing infection in Mohs surgery as their more expensive sterile counterparts.

These findings from two studies add to a growing body of data that support the use of clean technique and could translate into significant cost savings for Mohs surgeons - up to several thousand dollars a year, by one estimate.

In the first study presented at the annual meeting of the American College of Mohs Surgery, researchers led by Dr. Heather D. Rogers of the University of Washington, Seattle, sought to evaluate the rate of surgical site infection (SSI) in Mohs surgery patients using clean surgical technique versus sterile technique for "all steps of MMS [Mohs micrographic surgery], including wound reconstruction, in the absence of prophylactic antibiotics."

The researchers evaluated 1,000 patients undergoing MMS using clean technique, which included the use of clean (vs. sterile) gloves, clean (vs. sterile) towels, and a "single pack" of sterile instruments for the entire wound reconstruction.

Infection was classified according to the Centers for Disease Control and Prevention parameters: A site was considered infected if it expressed purulent discharge, if it displayed edema or erythema, and if the patient complained of pain or tenderness at the site.

"There were 11 infections in 1,000 patients with 1,204 tumors," said Dr. Rogers, for an infection rate of 0.91%. Three of the infections were complications of hematomas.

"Our SSI rate of 0.91% is extremely low," she said, "underscoring the overall safety of MMS and its performance in the outpatient setting without the use of antibiotic prophylaxis or sterile technique."

The second study was presented by Dr. Yang Xia of the division of Mohs surgery at the Scripps Clinic, La Jolla, Calif. Dr. Xia conducted a prospective, subject-blinded pilot study of 60 patients at the clinic to assess the difference in infection rate between clean, nonsterile gloves and sterile gloves for the repair of surgical defects in MMS.

"Clean gloves were used for all patients in the tumor removal phase," said Dr. Xia.

After tumors were removed, patients were randomized to repair with either clean or sterile gloves. A total of 30 patients were enrolled in each arm. Sterile paper and trays were used during all repairs. The mean age of the clean group was 69 years (26 men); the mean age of the sterile group was 74 years (28 men). Patients were excluded from the study if they were taking antibiotics at the time of the procedure or if they had any serious comorbidities, such as HIV.

After surgery, patients were followed up for 5-21 days, and the wounds were assessed by a nurse or assistant who was not affiliated with the study.
In the clean group, there was one SSI, in a 67-year-old man who cultured positive for methicillin-susceptible Staphylococcus aureus (MSSA). He was prescribed cephalexin.

In the sterile group, there were two SSIs: one case of MSSA, which was treated with cephalexin and resolved, and one case of methicillin-resistant Staphylococcus aureus (MRSA), which resolved with administration of Septra (trimethoprim and sulfamethoxazole) twice a day for 14 days.

Given the equally low rates of infection in the two study arms, the potential cost-savings of switching from sterile to clean gloves for these procedures could be tremendous, Dr. Xia said. One online search put the cost of a box of 100 clean gloves at $4-$9, although Dr. Xia gave a figure of $4-$29 for a box of 150 gloves. In contrast, a box of 100 sterile surgical gloves costs $74-$250, according to Dr. Xia. (A separate online search found a box of 100 sterile gloves available for $45-$275.)

Depending on the annual volume of a surgeon's cases, switching from sterile to clean gloves could save $6,000 to $20,000 a year, Dr. Xia estimated.

Dr. Rogers and Dr. Xia said they had no disclosures to make in relation to their presentations.

NEW YORK - Clean, nonsterile gloves are just as effective in preventing infection in Mohs surgery as their more expensive sterile counterparts.

These findings from two studies add to a growing body of data that support the use of clean technique and could translate into significant cost savings for Mohs surgeons - up to several thousand dollars a year, by one estimate.

In the first study presented at the annual meeting of the American College of Mohs Surgery, researchers led by Dr. Heather D. Rogers of the University of Washington, Seattle, sought to evaluate the rate of surgical site infection (SSI) in Mohs surgery patients using clean surgical technique versus sterile technique for "all steps of MMS [Mohs micrographic surgery], including wound reconstruction, in the absence of prophylactic antibiotics."

The researchers evaluated 1,000 patients undergoing MMS using clean technique, which included the use of clean (vs. sterile) gloves, clean (vs. sterile) towels, and a "single pack" of sterile instruments for the entire wound reconstruction.

Infection was classified according to the Centers for Disease Control and Prevention parameters: A site was considered infected if it expressed purulent discharge, if it displayed edema or erythema, and if the patient complained of pain or tenderness at the site.

"There were 11 infections in 1,000 patients with 1,204 tumors," said Dr. Rogers, for an infection rate of 0.91%. Three of the infections were complications of hematomas.

"Our SSI rate of 0.91% is extremely low," she said, "underscoring the overall safety of MMS and its performance in the outpatient setting without the use of antibiotic prophylaxis or sterile technique."

The second study was presented by Dr. Yang Xia of the division of Mohs surgery at the Scripps Clinic, La Jolla, Calif. Dr. Xia conducted a prospective, subject-blinded pilot study of 60 patients at the clinic to assess the difference in infection rate between clean, nonsterile gloves and sterile gloves for the repair of surgical defects in MMS.

"Clean gloves were used for all patients in the tumor removal phase," said Dr. Xia.

After tumors were removed, patients were randomized to repair with either clean or sterile gloves. A total of 30 patients were enrolled in each arm. Sterile paper and trays were used during all repairs. The mean age of the clean group was 69 years (26 men); the mean age of the sterile group was 74 years (28 men). Patients were excluded from the study if they were taking antibiotics at the time of the procedure or if they had any serious comorbidities, such as HIV.

After surgery, patients were followed up for 5-21 days, and the wounds were assessed by a nurse or assistant who was not affiliated with the study.
In the clean group, there was one SSI, in a 67-year-old man who cultured positive for methicillin-susceptible Staphylococcus aureus (MSSA). He was prescribed cephalexin.

In the sterile group, there were two SSIs: one case of MSSA, which was treated with cephalexin and resolved, and one case of methicillin-resistant Staphylococcus aureus (MRSA), which resolved with administration of Septra (trimethoprim and sulfamethoxazole) twice a day for 14 days.

Given the equally low rates of infection in the two study arms, the potential cost-savings of switching from sterile to clean gloves for these procedures could be tremendous, Dr. Xia said. One online search put the cost of a box of 100 clean gloves at $4-$9, although Dr. Xia gave a figure of $4-$29 for a box of 150 gloves. In contrast, a box of 100 sterile surgical gloves costs $74-$250, according to Dr. Xia. (A separate online search found a box of 100 sterile gloves available for $45-$275.)

Depending on the annual volume of a surgeon's cases, switching from sterile to clean gloves could save $6,000 to $20,000 a year, Dr. Xia estimated.

Dr. Rogers and Dr. Xia said they had no disclosures to make in relation to their presentations.

NEW YORK - Clean, nonsterile gloves are just as effective in preventing infection in Mohs surgery as their more expensive sterile counterparts.

These findings from two studies add to a growing body of data that support the use of clean technique and could translate into significant cost savings for Mohs surgeons - up to several thousand dollars a year, by one estimate.

In the first study presented at the annual meeting of the American College of Mohs Surgery, researchers led by Dr. Heather D. Rogers of the University of Washington, Seattle, sought to evaluate the rate of surgical site infection (SSI) in Mohs surgery patients using clean surgical technique versus sterile technique for "all steps of MMS [Mohs micrographic surgery], including wound reconstruction, in the absence of prophylactic antibiotics."

The researchers evaluated 1,000 patients undergoing MMS using clean technique, which included the use of clean (vs. sterile) gloves, clean (vs. sterile) towels, and a "single pack" of sterile instruments for the entire wound reconstruction.

Infection was classified according to the Centers for Disease Control and Prevention parameters: A site was considered infected if it expressed purulent discharge, if it displayed edema or erythema, and if the patient complained of pain or tenderness at the site.

"There were 11 infections in 1,000 patients with 1,204 tumors," said Dr. Rogers, for an infection rate of 0.91%. Three of the infections were complications of hematomas.

"Our SSI rate of 0.91% is extremely low," she said, "underscoring the overall safety of MMS and its performance in the outpatient setting without the use of antibiotic prophylaxis or sterile technique."

The second study was presented by Dr. Yang Xia of the division of Mohs surgery at the Scripps Clinic, La Jolla, Calif. Dr. Xia conducted a prospective, subject-blinded pilot study of 60 patients at the clinic to assess the difference in infection rate between clean, nonsterile gloves and sterile gloves for the repair of surgical defects in MMS.

"Clean gloves were used for all patients in the tumor removal phase," said Dr. Xia.

After tumors were removed, patients were randomized to repair with either clean or sterile gloves. A total of 30 patients were enrolled in each arm. Sterile paper and trays were used during all repairs. The mean age of the clean group was 69 years (26 men); the mean age of the sterile group was 74 years (28 men). Patients were excluded from the study if they were taking antibiotics at the time of the procedure or if they had any serious comorbidities, such as HIV.

After surgery, patients were followed up for 5-21 days, and the wounds were assessed by a nurse or assistant who was not affiliated with the study.
In the clean group, there was one SSI, in a 67-year-old man who cultured positive for methicillin-susceptible Staphylococcus aureus (MSSA). He was prescribed cephalexin.

In the sterile group, there were two SSIs: one case of MSSA, which was treated with cephalexin and resolved, and one case of methicillin-resistant Staphylococcus aureus (MRSA), which resolved with administration of Septra (trimethoprim and sulfamethoxazole) twice a day for 14 days.

Given the equally low rates of infection in the two study arms, the potential cost-savings of switching from sterile to clean gloves for these procedures could be tremendous, Dr. Xia said. One online search put the cost of a box of 100 clean gloves at $4-$9, although Dr. Xia gave a figure of $4-$29 for a box of 150 gloves. In contrast, a box of 100 sterile surgical gloves costs $74-$250, according to Dr. Xia. (A separate online search found a box of 100 sterile gloves available for $45-$275.)

Depending on the annual volume of a surgeon's cases, switching from sterile to clean gloves could save $6,000 to $20,000 a year, Dr. Xia estimated.

Dr. Rogers and Dr. Xia said they had no disclosures to make in relation to their presentations.

Major Finding: Among patients taking proton pump inhibitors for at least 2 years, the risk of having a hip fracture was increased by 30%, but only when at least one other fracture risk factor (smoking, dementia, arthritis, visual impairment) was present. Among PPI users with none of these other risk factors, the odds ratio for fracture was 0.66.

Data Source: A nested case-control study using data from an integrated health services organization, including 33,752 cases and 130,471 controls.

Disclosures: Dr. Corley disclosed receiving research funding, unrelated to this study, from Wyeth Pharmaceuticals, which makes a proton pump inhibitor. The remaining authors disclose no conflicts of interest. The study was funded by Kaiser Permanente and a grant from the U.S. National Institutes of Health.

Hip fracture patients were 30% more likely to have a long-term history of proton pump inhibitor use, compared with controls, Dr. Douglas A. Corley and his colleagues reported.

Moreover, the association was found to be stronger with higher doses of PPIs, and the link diminished after PPI discontinuation, the researchers wrote.

“These findings do not recommend against acid suppression for persons with clear indications for treatment,” wrote Dr. Corley, a researcher with Kaiser Permanente Northern California (Gastroenterology July [doi: 10.1053/j.gastro.2010.03.055

Dr. Corley and his colleagues looked at 33,752 adult members of the Kaiser Permanente Northern California integrated health care delivery system who had an incident diagnosis of a hip fracture between January 1995 and September 2007. To be included in the study, patients had to have been in the Kaiser Permanente Northern California system for at least 2 years prior to their fracture. Patients who had a previous hip or femur fracture diagnosis were excluded.

Patients were roughly matched in a 4:1 ratio with demographically comparable controls, also from the Kaiser Permanente Northern California system. Controls had no history of hip fracture, and had also been in the Kaiser system for at least 2 years.

Patients were predominantly women (65.7%), 70 years of age or older (69.4%), and white (79.6%), according to the authors. Roughly 40% had received a prescription for a proton pump inhibitor while in the Kaiser Permanente Northern California system.

According to Dr. Corley, patients whose records indicated “long-term” use of PPIs (defined by the authors as greater than 2 years) had an odds ratio of having a fracture within the study period of 1.30, compared with nonusers (95% confidence interval, 1.21-1.39).

However, all of the increased risk for fracture was present only in patients who had at least one other risk factor for fracture, such as smoking, dementia, arthritis, or visual impairment. Indeed, among patients with none of these risk factors, the odds ratio for fracture among PPI users was 0.66 (95% CI, 0.38-1.12).

The researchers also found a trend toward increased fracture risk among subjects taking higher daily doses of PPIs. For example, among patients taking an average of 0.01-0.74 pills/day, for a duration between 2 and 3.9 years, the OR for a fracture, compared with nonusers, was 1.23 (95% CI, 1.08-1.39); among users taking 0.75-1.49 pills/day, for the same duration of time, the OR was 1.43 (95% CI, 1.28-1.60), and for more than 1.49 pills/day the OR was 1.41 (95% CI, 1.21-1.64).

Despite the association with PPI dosage, there was no link between duration of PPI use and fracture risk.

The researchers also found that “the strength of the association between PPI use and hip fracture was greatest among current users and diminished after discontinuation of PPI use.” For example, while the OR for current users was 1.30 (95% CI, 1.21-1.41), it was 1.24 for patients whose most recent prescription was 1.0-1.9 years before the index date (95% CI, 0.90-1.72), and dropped to 1.09 for patients whose last PPI prescription was 2.0-2.9 years before the index date (95% CI, 0.64-1.85).

Dr. Corley proposed several mechanisms by which acid inhibition could influence fracture risk. For one, he said, acid inhibition could directly influence calcium absorption: he pointed to a small, randomized trial in which omeprazole decreased the absorption of radio-labeled calcium pills by 61%, compared with placebo (Am. J. Med. 2005;118:778-81).

“Second,” he wrote, “acid inhibition may induce hyperparathyroidism, which directly decreases bone mineral density, through hypergastrinemia, although this is controversial.”

Finally, he suggested that fracture risk may be mediated by interference by PPIs with bone remodeling. However, he added, “none of these mechanisms are proven.”

Fracture risk also was increased in patients using histamine₂-receptor antagonists, another class of drugs that inhibit acid secretion (OR, 1.18).

The authors concluded that acid inhibition might raise fracture risk in persons already at risk for osteoporosis, although confounding cannot be excluded.

Major Finding: Among patients taking proton pump inhibitors for at least 2 years, the risk of having a hip fracture was increased by 30%, but only when at least one other fracture risk factor (smoking, dementia, arthritis, visual impairment) was present. Among PPI users with none of these other risk factors, the odds ratio for fracture was 0.66.

Data Source: A nested case-control study using data from an integrated health services organization, including 33,752 cases and 130,471 controls.

Disclosures: Dr. Corley disclosed receiving research funding, unrelated to this study, from Wyeth Pharmaceuticals, which makes a proton pump inhibitor. The remaining authors disclose no conflicts of interest. The study was funded by Kaiser Permanente and a grant from the U.S. National Institutes of Health.

Hip fracture patients were 30% more likely to have a long-term history of proton pump inhibitor use, compared with controls, Dr. Douglas A. Corley and his colleagues reported.

Moreover, the association was found to be stronger with higher doses of PPIs, and the link diminished after PPI discontinuation, the researchers wrote.

“These findings do not recommend against acid suppression for persons with clear indications for treatment,” wrote Dr. Corley, a researcher with Kaiser Permanente Northern California (Gastroenterology July [doi: 10.1053/j.gastro.2010.03.055

Dr. Corley and his colleagues looked at 33,752 adult members of the Kaiser Permanente Northern California integrated health care delivery system who had an incident diagnosis of a hip fracture between January 1995 and September 2007. To be included in the study, patients had to have been in the Kaiser Permanente Northern California system for at least 2 years prior to their fracture. Patients who had a previous hip or femur fracture diagnosis were excluded.

Patients were roughly matched in a 4:1 ratio with demographically comparable controls, also from the Kaiser Permanente Northern California system. Controls had no history of hip fracture, and had also been in the Kaiser system for at least 2 years.

Patients were predominantly women (65.7%), 70 years of age or older (69.4%), and white (79.6%), according to the authors. Roughly 40% had received a prescription for a proton pump inhibitor while in the Kaiser Permanente Northern California system.

According to Dr. Corley, patients whose records indicated “long-term” use of PPIs (defined by the authors as greater than 2 years) had an odds ratio of having a fracture within the study period of 1.30, compared with nonusers (95% confidence interval, 1.21-1.39).

However, all of the increased risk for fracture was present only in patients who had at least one other risk factor for fracture, such as smoking, dementia, arthritis, or visual impairment. Indeed, among patients with none of these risk factors, the odds ratio for fracture among PPI users was 0.66 (95% CI, 0.38-1.12).

The researchers also found a trend toward increased fracture risk among subjects taking higher daily doses of PPIs. For example, among patients taking an average of 0.01-0.74 pills/day, for a duration between 2 and 3.9 years, the OR for a fracture, compared with nonusers, was 1.23 (95% CI, 1.08-1.39); among users taking 0.75-1.49 pills/day, for the same duration of time, the OR was 1.43 (95% CI, 1.28-1.60), and for more than 1.49 pills/day the OR was 1.41 (95% CI, 1.21-1.64).

Despite the association with PPI dosage, there was no link between duration of PPI use and fracture risk.

The researchers also found that “the strength of the association between PPI use and hip fracture was greatest among current users and diminished after discontinuation of PPI use.” For example, while the OR for current users was 1.30 (95% CI, 1.21-1.41), it was 1.24 for patients whose most recent prescription was 1.0-1.9 years before the index date (95% CI, 0.90-1.72), and dropped to 1.09 for patients whose last PPI prescription was 2.0-2.9 years before the index date (95% CI, 0.64-1.85).

Dr. Corley proposed several mechanisms by which acid inhibition could influence fracture risk. For one, he said, acid inhibition could directly influence calcium absorption: he pointed to a small, randomized trial in which omeprazole decreased the absorption of radio-labeled calcium pills by 61%, compared with placebo (Am. J. Med. 2005;118:778-81).

“Second,” he wrote, “acid inhibition may induce hyperparathyroidism, which directly decreases bone mineral density, through hypergastrinemia, although this is controversial.”

Finally, he suggested that fracture risk may be mediated by interference by PPIs with bone remodeling. However, he added, “none of these mechanisms are proven.”

Fracture risk also was increased in patients using histamine₂-receptor antagonists, another class of drugs that inhibit acid secretion (OR, 1.18).

The authors concluded that acid inhibition might raise fracture risk in persons already at risk for osteoporosis, although confounding cannot be excluded.

Major Finding: Among patients taking proton pump inhibitors for at least 2 years, the risk of having a hip fracture was increased by 30%, but only when at least one other fracture risk factor (smoking, dementia, arthritis, visual impairment) was present. Among PPI users with none of these other risk factors, the odds ratio for fracture was 0.66.

Data Source: A nested case-control study using data from an integrated health services organization, including 33,752 cases and 130,471 controls.

Disclosures: Dr. Corley disclosed receiving research funding, unrelated to this study, from Wyeth Pharmaceuticals, which makes a proton pump inhibitor. The remaining authors disclose no conflicts of interest. The study was funded by Kaiser Permanente and a grant from the U.S. National Institutes of Health.

Hip fracture patients were 30% more likely to have a long-term history of proton pump inhibitor use, compared with controls, Dr. Douglas A. Corley and his colleagues reported.

Moreover, the association was found to be stronger with higher doses of PPIs, and the link diminished after PPI discontinuation, the researchers wrote.

“These findings do not recommend against acid suppression for persons with clear indications for treatment,” wrote Dr. Corley, a researcher with Kaiser Permanente Northern California (Gastroenterology July [doi: 10.1053/j.gastro.2010.03.055

Dr. Corley and his colleagues looked at 33,752 adult members of the Kaiser Permanente Northern California integrated health care delivery system who had an incident diagnosis of a hip fracture between January 1995 and September 2007. To be included in the study, patients had to have been in the Kaiser Permanente Northern California system for at least 2 years prior to their fracture. Patients who had a previous hip or femur fracture diagnosis were excluded.

Patients were roughly matched in a 4:1 ratio with demographically comparable controls, also from the Kaiser Permanente Northern California system. Controls had no history of hip fracture, and had also been in the Kaiser system for at least 2 years.

Patients were predominantly women (65.7%), 70 years of age or older (69.4%), and white (79.6%), according to the authors. Roughly 40% had received a prescription for a proton pump inhibitor while in the Kaiser Permanente Northern California system.

According to Dr. Corley, patients whose records indicated “long-term” use of PPIs (defined by the authors as greater than 2 years) had an odds ratio of having a fracture within the study period of 1.30, compared with nonusers (95% confidence interval, 1.21-1.39).

However, all of the increased risk for fracture was present only in patients who had at least one other risk factor for fracture, such as smoking, dementia, arthritis, or visual impairment. Indeed, among patients with none of these risk factors, the odds ratio for fracture among PPI users was 0.66 (95% CI, 0.38-1.12).

The researchers also found a trend toward increased fracture risk among subjects taking higher daily doses of PPIs. For example, among patients taking an average of 0.01-0.74 pills/day, for a duration between 2 and 3.9 years, the OR for a fracture, compared with nonusers, was 1.23 (95% CI, 1.08-1.39); among users taking 0.75-1.49 pills/day, for the same duration of time, the OR was 1.43 (95% CI, 1.28-1.60), and for more than 1.49 pills/day the OR was 1.41 (95% CI, 1.21-1.64).

Despite the association with PPI dosage, there was no link between duration of PPI use and fracture risk.

The researchers also found that “the strength of the association between PPI use and hip fracture was greatest among current users and diminished after discontinuation of PPI use.” For example, while the OR for current users was 1.30 (95% CI, 1.21-1.41), it was 1.24 for patients whose most recent prescription was 1.0-1.9 years before the index date (95% CI, 0.90-1.72), and dropped to 1.09 for patients whose last PPI prescription was 2.0-2.9 years before the index date (95% CI, 0.64-1.85).

Dr. Corley proposed several mechanisms by which acid inhibition could influence fracture risk. For one, he said, acid inhibition could directly influence calcium absorption: he pointed to a small, randomized trial in which omeprazole decreased the absorption of radio-labeled calcium pills by 61%, compared with placebo (Am. J. Med. 2005;118:778-81).

“Second,” he wrote, “acid inhibition may induce hyperparathyroidism, which directly decreases bone mineral density, through hypergastrinemia, although this is controversial.”

Finally, he suggested that fracture risk may be mediated by interference by PPIs with bone remodeling. However, he added, “none of these mechanisms are proven.”

Fracture risk also was increased in patients using histamine₂-receptor antagonists, another class of drugs that inhibit acid secretion (OR, 1.18).

The authors concluded that acid inhibition might raise fracture risk in persons already at risk for osteoporosis, although confounding cannot be excluded.

Major Finding: Among patients taking proton pump inhibitors for at least 2 years, the risk of having a hip fracture was increased by 30%, but only when at least one other fracture risk factor (smoking, dementia, arthritis, visual impairment) was present. Among PPI users with none of these other risk factors, the odds ratio for fracture was 0.66.

Data Source: A nested case-control study using data from an integrated health services organization, including 33,752 cases and 130,471 controls, published in the July issue of the journal Gastroenterology.

Disclosures: Dr. Corley disclosed receiving research funding, unrelated to this study, from Wyeth Pharmaceuticals, which makes a proton pump inhibitor. The remaining authors disclose no conflicts of interest. The study was funded by Kaiser Permanente and a grant from the U.S. National Institutes of Health.

Hip fracture patients were 30% more likely to have a long-term history of proton pump inhibitor use, compared with controls, Dr. Douglas A. Corley and his colleagues reported.

Moreover, the association was found to be stronger with higher doses of PPIs, and the link diminished after PPI discontinuation, the researchers wrote.

“These findings do not recommend against acid suppression for persons with clear indications for treatment,” wrote Dr. Corley, a researcher with Kaiser Permanente Northern California (Gastroenterology July [doi: 10.1053/j.gastro.2010.03.055]). However, “they do advise appropriate vigilance in prescribing these medications to persons with defined indications and at the lowest effective dose.”

Dr. Corley and his colleagues looked at 33,752 adult members of the Kaiser Permanente Northern California integrated health care delivery system who had an incident diagnosis of a hip fracture between January 1995 and September 2007. To be included in the study, patients had to have been in the Kaiser Permanente Northern California system for at least 2 years prior to their fracture. Patients who had a previous hip or femur fracture diagnosis were excluded.

Patients were roughly matched in a 4:1 ratio with demographically comparable controls, also from the Kaiser Permanente Northern California system. Controls had no history of hip fracture, and had also been in the Kaiser system for at least 2 years.

Patients were predominantly women (65.7%), 70 years of age or older (69.4%), and white (79.6%), according to the authors. Roughly 40% had received a prescription for a proton pump inhibitor while in the Kaiser Permanente Northern California system.

According to Dr. Corley, patients whose records indicated “long-term” use of PPIs (defined by the authors as greater than 2 years) had an odds ratio of having a fracture within the study period of 1.30, compared with nonusers (95% confidence interval, 1.21-1.39).

However, all of the increased risk for fracture was present only in patients who had at least one other risk factor for fracture, such as smoking, dementia, arthritis, or visual impairment. Indeed, among patients with none of these risk factors, the odds ratio for fracture among PPI users was 0.66 (95% CI, 0.38-1.12).

The researchers also found a trend toward increased fracture risk among subjects taking higher daily doses of PPIs. For example, among patients taking an average of 0.01-0.74 pills/day, for a duration between 2 and 3.9 years, the OR for a fracture, compared with nonusers, was 1.23 (95% CI, 1.08-1.39); among users taking 0.75-1.49 pills/day, for the same duration of time, the OR was 1.43 (95% CI, 1.28-1.60), and for more than 1.49 pills/day the OR was 1.41 (95% CI, 1.21-1.64).

Despite the association with PPI dosage, there was no link between duration of PPI use and fracture risk.

The researchers also found that “the strength of the association between PPI use and hip fracture was greatest among current users and diminished after discontinuation of PPI use.” For example, while the OR for current users was 1.30 (95% CI, 1.21-1.41), it was 1.24 for patients whose most recent prescription was 1.0-1.9 years before the index date (95% CI, 0.90-1.72), and dropped to 1.09 for patients whose last PPI prescription was 2.0-2.9 years before the index date (95% CI, 0.64-1.85).

Dr. Corley proposed several mechanisms by which acid inhibition could influence fracture risk. For one, he said, acid inhibition could directly influence calcium absorption: He pointed to a small, randomized trial in which omeprazole decreased the absorption of radio-labeled calcium pills by 61%, compared with placebo (Am. J. Med. 2005;118:778-81). “Second,” he wrote, “acid inhibition may induce hyperparathyroidism, which directly decreases bone mineral density, through hypergastrinemia, although this is controversial.” Finally, he suggested that fracture risk may be mediated by interference by PPIs with bone remodeling. However, he added, “none of these mechanisms are proven.”

Major Finding: Among patients taking proton pump inhibitors for at least 2 years, the risk of having a hip fracture was increased by 30%, but only when at least one other fracture risk factor (smoking, dementia, arthritis, visual impairment) was present. Among PPI users with none of these other risk factors, the odds ratio for fracture was 0.66.

Data Source: A nested case-control study using data from an integrated health services organization, including 33,752 cases and 130,471 controls, published in the July issue of the journal Gastroenterology.

Disclosures: Dr. Corley disclosed receiving research funding, unrelated to this study, from Wyeth Pharmaceuticals, which makes a proton pump inhibitor. The remaining authors disclose no conflicts of interest. The study was funded by Kaiser Permanente and a grant from the U.S. National Institutes of Health.

Hip fracture patients were 30% more likely to have a long-term history of proton pump inhibitor use, compared with controls, Dr. Douglas A. Corley and his colleagues reported.

Moreover, the association was found to be stronger with higher doses of PPIs, and the link diminished after PPI discontinuation, the researchers wrote.

“These findings do not recommend against acid suppression for persons with clear indications for treatment,” wrote Dr. Corley, a researcher with Kaiser Permanente Northern California (Gastroenterology July [doi: 10.1053/j.gastro.2010.03.055]). However, “they do advise appropriate vigilance in prescribing these medications to persons with defined indications and at the lowest effective dose.”

Dr. Corley and his colleagues looked at 33,752 adult members of the Kaiser Permanente Northern California integrated health care delivery system who had an incident diagnosis of a hip fracture between January 1995 and September 2007. To be included in the study, patients had to have been in the Kaiser Permanente Northern California system for at least 2 years prior to their fracture. Patients who had a previous hip or femur fracture diagnosis were excluded.

Patients were roughly matched in a 4:1 ratio with demographically comparable controls, also from the Kaiser Permanente Northern California system. Controls had no history of hip fracture, and had also been in the Kaiser system for at least 2 years.

Patients were predominantly women (65.7%), 70 years of age or older (69.4%), and white (79.6%), according to the authors. Roughly 40% had received a prescription for a proton pump inhibitor while in the Kaiser Permanente Northern California system.

According to Dr. Corley, patients whose records indicated “long-term” use of PPIs (defined by the authors as greater than 2 years) had an odds ratio of having a fracture within the study period of 1.30, compared with nonusers (95% confidence interval, 1.21-1.39).

However, all of the increased risk for fracture was present only in patients who had at least one other risk factor for fracture, such as smoking, dementia, arthritis, or visual impairment. Indeed, among patients with none of these risk factors, the odds ratio for fracture among PPI users was 0.66 (95% CI, 0.38-1.12).

The researchers also found a trend toward increased fracture risk among subjects taking higher daily doses of PPIs. For example, among patients taking an average of 0.01-0.74 pills/day, for a duration between 2 and 3.9 years, the OR for a fracture, compared with nonusers, was 1.23 (95% CI, 1.08-1.39); among users taking 0.75-1.49 pills/day, for the same duration of time, the OR was 1.43 (95% CI, 1.28-1.60), and for more than 1.49 pills/day the OR was 1.41 (95% CI, 1.21-1.64).

Despite the association with PPI dosage, there was no link between duration of PPI use and fracture risk.

The researchers also found that “the strength of the association between PPI use and hip fracture was greatest among current users and diminished after discontinuation of PPI use.” For example, while the OR for current users was 1.30 (95% CI, 1.21-1.41), it was 1.24 for patients whose most recent prescription was 1.0-1.9 years before the index date (95% CI, 0.90-1.72), and dropped to 1.09 for patients whose last PPI prescription was 2.0-2.9 years before the index date (95% CI, 0.64-1.85).

Dr. Corley proposed several mechanisms by which acid inhibition could influence fracture risk. For one, he said, acid inhibition could directly influence calcium absorption: He pointed to a small, randomized trial in which omeprazole decreased the absorption of radio-labeled calcium pills by 61%, compared with placebo (Am. J. Med. 2005;118:778-81). “Second,” he wrote, “acid inhibition may induce hyperparathyroidism, which directly decreases bone mineral density, through hypergastrinemia, although this is controversial.” Finally, he suggested that fracture risk may be mediated by interference by PPIs with bone remodeling. However, he added, “none of these mechanisms are proven.”

Major Finding: Among patients taking proton pump inhibitors for at least 2 years, the risk of having a hip fracture was increased by 30%, but only when at least one other fracture risk factor (smoking, dementia, arthritis, visual impairment) was present. Among PPI users with none of these other risk factors, the odds ratio for fracture was 0.66.

Data Source: A nested case-control study using data from an integrated health services organization, including 33,752 cases and 130,471 controls, published in the July issue of the journal Gastroenterology.

Disclosures: Dr. Corley disclosed receiving research funding, unrelated to this study, from Wyeth Pharmaceuticals, which makes a proton pump inhibitor. The remaining authors disclose no conflicts of interest. The study was funded by Kaiser Permanente and a grant from the U.S. National Institutes of Health.

Hip fracture patients were 30% more likely to have a long-term history of proton pump inhibitor use, compared with controls, Dr. Douglas A. Corley and his colleagues reported.

Moreover, the association was found to be stronger with higher doses of PPIs, and the link diminished after PPI discontinuation, the researchers wrote.

“These findings do not recommend against acid suppression for persons with clear indications for treatment,” wrote Dr. Corley, a researcher with Kaiser Permanente Northern California (Gastroenterology July [doi: 10.1053/j.gastro.2010.03.055]). However, “they do advise appropriate vigilance in prescribing these medications to persons with defined indications and at the lowest effective dose.”

Dr. Corley and his colleagues looked at 33,752 adult members of the Kaiser Permanente Northern California integrated health care delivery system who had an incident diagnosis of a hip fracture between January 1995 and September 2007. To be included in the study, patients had to have been in the Kaiser Permanente Northern California system for at least 2 years prior to their fracture. Patients who had a previous hip or femur fracture diagnosis were excluded.

Patients were roughly matched in a 4:1 ratio with demographically comparable controls, also from the Kaiser Permanente Northern California system. Controls had no history of hip fracture, and had also been in the Kaiser system for at least 2 years.

Patients were predominantly women (65.7%), 70 years of age or older (69.4%), and white (79.6%), according to the authors. Roughly 40% had received a prescription for a proton pump inhibitor while in the Kaiser Permanente Northern California system.

According to Dr. Corley, patients whose records indicated “long-term” use of PPIs (defined by the authors as greater than 2 years) had an odds ratio of having a fracture within the study period of 1.30, compared with nonusers (95% confidence interval, 1.21-1.39).

However, all of the increased risk for fracture was present only in patients who had at least one other risk factor for fracture, such as smoking, dementia, arthritis, or visual impairment. Indeed, among patients with none of these risk factors, the odds ratio for fracture among PPI users was 0.66 (95% CI, 0.38-1.12).

The researchers also found a trend toward increased fracture risk among subjects taking higher daily doses of PPIs. For example, among patients taking an average of 0.01-0.74 pills/day, for a duration between 2 and 3.9 years, the OR for a fracture, compared with nonusers, was 1.23 (95% CI, 1.08-1.39); among users taking 0.75-1.49 pills/day, for the same duration of time, the OR was 1.43 (95% CI, 1.28-1.60), and for more than 1.49 pills/day the OR was 1.41 (95% CI, 1.21-1.64).

Despite the association with PPI dosage, there was no link between duration of PPI use and fracture risk.

The researchers also found that “the strength of the association between PPI use and hip fracture was greatest among current users and diminished after discontinuation of PPI use.” For example, while the OR for current users was 1.30 (95% CI, 1.21-1.41), it was 1.24 for patients whose most recent prescription was 1.0-1.9 years before the index date (95% CI, 0.90-1.72), and dropped to 1.09 for patients whose last PPI prescription was 2.0-2.9 years before the index date (95% CI, 0.64-1.85).

Dr. Corley proposed several mechanisms by which acid inhibition could influence fracture risk. For one, he said, acid inhibition could directly influence calcium absorption: He pointed to a small, randomized trial in which omeprazole decreased the absorption of radio-labeled calcium pills by 61%, compared with placebo (Am. J. Med. 2005;118:778-81). “Second,” he wrote, “acid inhibition may induce hyperparathyroidism, which directly decreases bone mineral density, through hypergastrinemia, although this is controversial.” Finally, he suggested that fracture risk may be mediated by interference by PPIs with bone remodeling. However, he added, “none of these mechanisms are proven.”

Major Finding: Patients with esophageal adenocarcinoma and esophagogastric junction adenocarcinoma were significantly less likely to have a history of H. pylori infection than population controls (odds ratios, 0.44 and 0.40, respectively).

Data Source: An Australian study of 269 patients with esophageal adenocarcinoma, 307 with esophagogastric junction adenocarcinoma, and 218 with esophageal squamous cell carcinoma, compared with 1,355 controls.

Disclosures: Dr. Whiteman and several of his colleagues disclosed receiving grants from the National Health and Medical Research Council of Australia. The study was supported by the Cancer Council Queensland and the National Health and Medical Research Council of Australia.

Patients with esophageal adenocarcinoma and esophagogastric junction adenocarcinoma were significantly less likely than population controls to have evidence of past Helicobacter pylori infection, Dr. David C. Whiteman and his colleagues reported.

The association persisted independently of known esophageal cancer risk factors, such as reflux and smoking, and also was independent of genetic factors, including polymorphisms in genes coding for interleukin-1B and tumor necrosis factor–alpha.

The findings add to a growing body of evidence suggesting that H. pylori might somehow be protective against esophageal cancers, even as it increases the risk of gastric cancer.

Dr. Whiteman, head of the Cancer Control Laboratory at the Queensland (Australia) Institute of Medical Research looked at 794 Australian patients aged 18-79 years with a primary invasive cancer of the esophagus or esophagogastric junction.

Overall, 269 patients had esophageal adenocarcinoma, 307 had esophagogastric junction adenocarcinoma, and 218 had esophageal squamous cell carcinoma.

The 1,355 controls were randomly selected from the Australian Electoral Roll and were roughly matched to the patients by age, sex, and state of residence.

“Patients with [esophageal adenocarcinoma, or EAC] and [esophagogastric junction adenocarcinomas, or EGJAC] were significantly less likely than were controls to have antibodies to H. pylori,” wrote Dr. Whiteman (Gastroenterology July [doi: 10.1053/j.gastro.2010.04.009]).

Among the EAC patients, the odds ratio of being seropositive was 0.44 (95% confidence interval, 0.29-0.67) after researchers adjusted for age, sex, smoking history, education, and several other environmental factors.

In the EGJAC population, the OR was 0.40 (95% CI, 0.27-0.59).

There was no association between H. pylori and esophageal squamous cell carcinoma (OR 1.08, 95% CI 0.74-1.57), they reported.

Dr. Whiteman and his colleagues also looked to see whether esophageal cancer patients shared any common mutations in the genes coding for IL-1B and TNF-alpha.

“IL-1B is among the most potent inhibitors of gastric acid yet identified,” they wrote, and “a recent meta-analysis concluded that the TNF-A-308AA genotype is associated with a moderately increased risk of gastric cancer” (Br. J. Cancer 2008;98:1443-51).

However, the authors “found no evidence that the inverse associations between H. pylori infection and [esophageal adenocarcinomas or esophagogastric junction adenocarcinomas] were modified by the presence of polymorphisms at IL-1B-31, IL-1B-511, TNF-A 308, and TNF-A 238.”

Squamous cell carcinomas also had a null association with these genotypes, they reported.

Therefore, Dr. Whiteman and his colleagues asked, “Is the inverse relationship between H. pylori infection and EAC and EGJAC evidence of a biologically protective effect?” And if so, what is the mechanism?

“Several potential mechanisms have been proposed to explain the association, including hypoacidity subsequent to prolonged infection, dysregulation of host cytokine or immune responses, disturbances to microbial flora, and changes in the expression of locally acting hormones relating to obesity pathways (notably leptin and ghrelin),” wrote the authors.

“Each of these hypotheses is plausible, and all may indeed play a role,” they commented.

As for study limitations, the authors conceded that the overall prevalence of H. pylori antibodies (23% among controls) was much lower than in other populations, including in the United States.

However, the “50-60% risk reductions we observed for EAC were remarkably similar to those reported in other studies,” they wrote.

As to the possibility of misclassification of H. pylori exposure, Dr. Whiteman and his colleagues pointed out that for such an error to have occurred “would [have] required that patients with EAC and EGJAC, but not [esophageal squamous cell carcinomas], were incorrectly categorized, a highly improbable scenario.”

Major Finding: Patients with esophageal adenocarcinoma and esophagogastric junction adenocarcinoma were significantly less likely to have a history of H. pylori infection than population controls (odds ratios, 0.44 and 0.40, respectively).

Data Source: An Australian study of 269 patients with esophageal adenocarcinoma, 307 with esophagogastric junction adenocarcinoma, and 218 with esophageal squamous cell carcinoma, compared with 1,355 controls.

Disclosures: Dr. Whiteman and several of his colleagues disclosed receiving grants from the National Health and Medical Research Council of Australia. The study was supported by the Cancer Council Queensland and the National Health and Medical Research Council of Australia.

Patients with esophageal adenocarcinoma and esophagogastric junction adenocarcinoma were significantly less likely than population controls to have evidence of past Helicobacter pylori infection, Dr. David C. Whiteman and his colleagues reported.

The association persisted independently of known esophageal cancer risk factors, such as reflux and smoking, and also was independent of genetic factors, including polymorphisms in genes coding for interleukin-1B and tumor necrosis factor–alpha.

The findings add to a growing body of evidence suggesting that H. pylori might somehow be protective against esophageal cancers, even as it increases the risk of gastric cancer.

Dr. Whiteman, head of the Cancer Control Laboratory at the Queensland (Australia) Institute of Medical Research looked at 794 Australian patients aged 18-79 years with a primary invasive cancer of the esophagus or esophagogastric junction.

Overall, 269 patients had esophageal adenocarcinoma, 307 had esophagogastric junction adenocarcinoma, and 218 had esophageal squamous cell carcinoma.

The 1,355 controls were randomly selected from the Australian Electoral Roll and were roughly matched to the patients by age, sex, and state of residence.

“Patients with [esophageal adenocarcinoma, or EAC] and [esophagogastric junction adenocarcinomas, or EGJAC] were significantly less likely than were controls to have antibodies to H. pylori,” wrote Dr. Whiteman (Gastroenterology July [doi: 10.1053/j.gastro.2010.04.009]).

Among the EAC patients, the odds ratio of being seropositive was 0.44 (95% confidence interval, 0.29-0.67) after researchers adjusted for age, sex, smoking history, education, and several other environmental factors.

In the EGJAC population, the OR was 0.40 (95% CI, 0.27-0.59).

There was no association between H. pylori and esophageal squamous cell carcinoma (OR 1.08, 95% CI 0.74-1.57), they reported.

Dr. Whiteman and his colleagues also looked to see whether esophageal cancer patients shared any common mutations in the genes coding for IL-1B and TNF-alpha.

“IL-1B is among the most potent inhibitors of gastric acid yet identified,” they wrote, and “a recent meta-analysis concluded that the TNF-A-308AA genotype is associated with a moderately increased risk of gastric cancer” (Br. J. Cancer 2008;98:1443-51).

However, the authors “found no evidence that the inverse associations between H. pylori infection and [esophageal adenocarcinomas or esophagogastric junction adenocarcinomas] were modified by the presence of polymorphisms at IL-1B-31, IL-1B-511, TNF-A 308, and TNF-A 238.”

Squamous cell carcinomas also had a null association with these genotypes, they reported.

Therefore, Dr. Whiteman and his colleagues asked, “Is the inverse relationship between H. pylori infection and EAC and EGJAC evidence of a biologically protective effect?” And if so, what is the mechanism?

“Several potential mechanisms have been proposed to explain the association, including hypoacidity subsequent to prolonged infection, dysregulation of host cytokine or immune responses, disturbances to microbial flora, and changes in the expression of locally acting hormones relating to obesity pathways (notably leptin and ghrelin),” wrote the authors.

“Each of these hypotheses is plausible, and all may indeed play a role,” they commented.

As for study limitations, the authors conceded that the overall prevalence of H. pylori antibodies (23% among controls) was much lower than in other populations, including in the United States.

However, the “50-60% risk reductions we observed for EAC were remarkably similar to those reported in other studies,” they wrote.

As to the possibility of misclassification of H. pylori exposure, Dr. Whiteman and his colleagues pointed out that for such an error to have occurred “would [have] required that patients with EAC and EGJAC, but not [esophageal squamous cell carcinomas], were incorrectly categorized, a highly improbable scenario.”

Major Finding: Patients with esophageal adenocarcinoma and esophagogastric junction adenocarcinoma were significantly less likely to have a history of H. pylori infection than population controls (odds ratios, 0.44 and 0.40, respectively).

Data Source: An Australian study of 269 patients with esophageal adenocarcinoma, 307 with esophagogastric junction adenocarcinoma, and 218 with esophageal squamous cell carcinoma, compared with 1,355 controls.

Disclosures: Dr. Whiteman and several of his colleagues disclosed receiving grants from the National Health and Medical Research Council of Australia. The study was supported by the Cancer Council Queensland and the National Health and Medical Research Council of Australia.

Patients with esophageal adenocarcinoma and esophagogastric junction adenocarcinoma were significantly less likely than population controls to have evidence of past Helicobacter pylori infection, Dr. David C. Whiteman and his colleagues reported.

The association persisted independently of known esophageal cancer risk factors, such as reflux and smoking, and also was independent of genetic factors, including polymorphisms in genes coding for interleukin-1B and tumor necrosis factor–alpha.

The findings add to a growing body of evidence suggesting that H. pylori might somehow be protective against esophageal cancers, even as it increases the risk of gastric cancer.

Dr. Whiteman, head of the Cancer Control Laboratory at the Queensland (Australia) Institute of Medical Research looked at 794 Australian patients aged 18-79 years with a primary invasive cancer of the esophagus or esophagogastric junction.

Overall, 269 patients had esophageal adenocarcinoma, 307 had esophagogastric junction adenocarcinoma, and 218 had esophageal squamous cell carcinoma.

The 1,355 controls were randomly selected from the Australian Electoral Roll and were roughly matched to the patients by age, sex, and state of residence.

“Patients with [esophageal adenocarcinoma, or EAC] and [esophagogastric junction adenocarcinomas, or EGJAC] were significantly less likely than were controls to have antibodies to H. pylori,” wrote Dr. Whiteman (Gastroenterology July [doi: 10.1053/j.gastro.2010.04.009]).

Among the EAC patients, the odds ratio of being seropositive was 0.44 (95% confidence interval, 0.29-0.67) after researchers adjusted for age, sex, smoking history, education, and several other environmental factors.

In the EGJAC population, the OR was 0.40 (95% CI, 0.27-0.59).

There was no association between H. pylori and esophageal squamous cell carcinoma (OR 1.08, 95% CI 0.74-1.57), they reported.

Dr. Whiteman and his colleagues also looked to see whether esophageal cancer patients shared any common mutations in the genes coding for IL-1B and TNF-alpha.

“IL-1B is among the most potent inhibitors of gastric acid yet identified,” they wrote, and “a recent meta-analysis concluded that the TNF-A-308AA genotype is associated with a moderately increased risk of gastric cancer” (Br. J. Cancer 2008;98:1443-51).

However, the authors “found no evidence that the inverse associations between H. pylori infection and [esophageal adenocarcinomas or esophagogastric junction adenocarcinomas] were modified by the presence of polymorphisms at IL-1B-31, IL-1B-511, TNF-A 308, and TNF-A 238.”

Squamous cell carcinomas also had a null association with these genotypes, they reported.

Therefore, Dr. Whiteman and his colleagues asked, “Is the inverse relationship between H. pylori infection and EAC and EGJAC evidence of a biologically protective effect?” And if so, what is the mechanism?

“Several potential mechanisms have been proposed to explain the association, including hypoacidity subsequent to prolonged infection, dysregulation of host cytokine or immune responses, disturbances to microbial flora, and changes in the expression of locally acting hormones relating to obesity pathways (notably leptin and ghrelin),” wrote the authors.

“Each of these hypotheses is plausible, and all may indeed play a role,” they commented.

As for study limitations, the authors conceded that the overall prevalence of H. pylori antibodies (23% among controls) was much lower than in other populations, including in the United States.

However, the “50-60% risk reductions we observed for EAC were remarkably similar to those reported in other studies,” they wrote.

As to the possibility of misclassification of H. pylori exposure, Dr. Whiteman and his colleagues pointed out that for such an error to have occurred “would [have] required that patients with EAC and EGJAC, but not [esophageal squamous cell carcinomas], were incorrectly categorized, a highly improbable scenario.”

Patients who identified themselves as lactose intolerant recalled symptoms experienced at home as being much more severe than symptoms following a 50-gram lactose challenge, Dr. Francesc Casellas and colleagues reported.

In addition, more than half of these self-identified lactose intolerant individuals were not, in fact, lactase deficient, based on a hydrogen breath test conducted after the lactose challenge.

This means that “symptoms patients believe related to lactose are aggravated by the home environment or, more likely … are not due to lactose malabsorption but to other causes,” they wrote.

Dr. Casellas of the Digestive System Research Unit at the Hospital Universitari Vall d'Hebron in Barcelona looked at 353 white patients referred to their unit for evaluation of suspected lactose maldigestion. The cohort included 240 women, and the median age was 41 years (Clin. Gastroenterol. Hepatol. 2010 July [doi:10.1016/j.cgh.2010.03.027]).

Patients were asked to complete a questionnaire that assessed five symptoms common among lactose malabsorbers: diarrhea, abdominal cramping, vomiting, audible bowel sounds, and flatulence.

“Patients completed the validated questionnaire on lactose intolerance symptoms twice,” wrote Dr. Casellas and coauthors. The first time occurred before patients underwent a lactose hydrogen breath test: The questionnaire asked exclusively about symptoms occurring after “usual consumption of milk-based products at home,” or what the investigators referred to as “home symptoms.” The second time patients completed the questionnaire was following completion of the breath test; this time, they were asked to rate symptoms experienced in the laboratory after they ingested a 50-gram lactose test load.

Only 164 out of the 353 patients (46%) were found to be true lactose malabsorbers following the hydrogen breath test. Among all 353 patients, at-home symptoms were ranked as being much worse than were symptoms following the lactose challenge, with the median score for home symptoms being 16 (range, 8-26) and the median score for symptoms in the laboratory being 8 (range, 2-18).

However, patients with true lactase deficiency according to the breath test reported more severe symptoms following the challenge than did patients with normal lactase levels: Malabsorbers reported a median of 15 for symptoms on the second, in-laboratory questionnaire (range, 7-25), compared with a median score of 4 on that survey among lactose absorbers (range, 0-11).

“These results suggest that, despite patient manifestations, symptoms experienced at home were unlikely to be directly related to lactose-containing foods,” especially among those patients without true lactase deficiency, the authors wrote. They speculated that the reported increased severity could be caused by the fact that “patients at home ingest lactose with other nutrients, such as fat, that could in themselves cause symptoms.”

In any case, “A record of symptoms does not suffice to establish lactose malabsorption,” they wrote. “Specific procedures such as the lactose breath test should be performed to confirm it.”

Disclosures: The study was supported in part by grants from the Generalitat de Catalunya and the Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas. The individual authors declared that they had no competing interests to disclose.

Patients who identified themselves as lactose intolerant recalled symptoms experienced at home as being much more severe than symptoms following a 50-gram lactose challenge, Dr. Francesc Casellas and colleagues reported.

In addition, more than half of these self-identified lactose intolerant individuals were not, in fact, lactase deficient, based on a hydrogen breath test conducted after the lactose challenge.

This means that “symptoms patients believe related to lactose are aggravated by the home environment or, more likely … are not due to lactose malabsorption but to other causes,” they wrote.

Dr. Casellas of the Digestive System Research Unit at the Hospital Universitari Vall d'Hebron in Barcelona looked at 353 white patients referred to their unit for evaluation of suspected lactose maldigestion. The cohort included 240 women, and the median age was 41 years (Clin. Gastroenterol. Hepatol. 2010 July [doi:10.1016/j.cgh.2010.03.027]).

Patients were asked to complete a questionnaire that assessed five symptoms common among lactose malabsorbers: diarrhea, abdominal cramping, vomiting, audible bowel sounds, and flatulence.

“Patients completed the validated questionnaire on lactose intolerance symptoms twice,” wrote Dr. Casellas and coauthors. The first time occurred before patients underwent a lactose hydrogen breath test: The questionnaire asked exclusively about symptoms occurring after “usual consumption of milk-based products at home,” or what the investigators referred to as “home symptoms.” The second time patients completed the questionnaire was following completion of the breath test; this time, they were asked to rate symptoms experienced in the laboratory after they ingested a 50-gram lactose test load.

Only 164 out of the 353 patients (46%) were found to be true lactose malabsorbers following the hydrogen breath test. Among all 353 patients, at-home symptoms were ranked as being much worse than were symptoms following the lactose challenge, with the median score for home symptoms being 16 (range, 8-26) and the median score for symptoms in the laboratory being 8 (range, 2-18).

However, patients with true lactase deficiency according to the breath test reported more severe symptoms following the challenge than did patients with normal lactase levels: Malabsorbers reported a median of 15 for symptoms on the second, in-laboratory questionnaire (range, 7-25), compared with a median score of 4 on that survey among lactose absorbers (range, 0-11).

“These results suggest that, despite patient manifestations, symptoms experienced at home were unlikely to be directly related to lactose-containing foods,” especially among those patients without true lactase deficiency, the authors wrote. They speculated that the reported increased severity could be caused by the fact that “patients at home ingest lactose with other nutrients, such as fat, that could in themselves cause symptoms.”

In any case, “A record of symptoms does not suffice to establish lactose malabsorption,” they wrote. “Specific procedures such as the lactose breath test should be performed to confirm it.”

Disclosures: The study was supported in part by grants from the Generalitat de Catalunya and the Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas. The individual authors declared that they had no competing interests to disclose.

Patients who identified themselves as lactose intolerant recalled symptoms experienced at home as being much more severe than symptoms following a 50-gram lactose challenge, Dr. Francesc Casellas and colleagues reported.

In addition, more than half of these self-identified lactose intolerant individuals were not, in fact, lactase deficient, based on a hydrogen breath test conducted after the lactose challenge.

This means that “symptoms patients believe related to lactose are aggravated by the home environment or, more likely … are not due to lactose malabsorption but to other causes,” they wrote.

Dr. Casellas of the Digestive System Research Unit at the Hospital Universitari Vall d'Hebron in Barcelona looked at 353 white patients referred to their unit for evaluation of suspected lactose maldigestion. The cohort included 240 women, and the median age was 41 years (Clin. Gastroenterol. Hepatol. 2010 July [doi:10.1016/j.cgh.2010.03.027]).

Patients were asked to complete a questionnaire that assessed five symptoms common among lactose malabsorbers: diarrhea, abdominal cramping, vomiting, audible bowel sounds, and flatulence.

“Patients completed the validated questionnaire on lactose intolerance symptoms twice,” wrote Dr. Casellas and coauthors. The first time occurred before patients underwent a lactose hydrogen breath test: The questionnaire asked exclusively about symptoms occurring after “usual consumption of milk-based products at home,” or what the investigators referred to as “home symptoms.” The second time patients completed the questionnaire was following completion of the breath test; this time, they were asked to rate symptoms experienced in the laboratory after they ingested a 50-gram lactose test load.

Only 164 out of the 353 patients (46%) were found to be true lactose malabsorbers following the hydrogen breath test. Among all 353 patients, at-home symptoms were ranked as being much worse than were symptoms following the lactose challenge, with the median score for home symptoms being 16 (range, 8-26) and the median score for symptoms in the laboratory being 8 (range, 2-18).

However, patients with true lactase deficiency according to the breath test reported more severe symptoms following the challenge than did patients with normal lactase levels: Malabsorbers reported a median of 15 for symptoms on the second, in-laboratory questionnaire (range, 7-25), compared with a median score of 4 on that survey among lactose absorbers (range, 0-11).

“These results suggest that, despite patient manifestations, symptoms experienced at home were unlikely to be directly related to lactose-containing foods,” especially among those patients without true lactase deficiency, the authors wrote. They speculated that the reported increased severity could be caused by the fact that “patients at home ingest lactose with other nutrients, such as fat, that could in themselves cause symptoms.”

In any case, “A record of symptoms does not suffice to establish lactose malabsorption,” they wrote. “Specific procedures such as the lactose breath test should be performed to confirm it.”

Disclosures: The study was supported in part by grants from the Generalitat de Catalunya and the Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas. The individual authors declared that they had no competing interests to disclose.

In a cohort of more than 5,000 patients with a total of 755 colorectal polyps, 100% of malignancies were associated with polyps greater than or equal to 10 mm, Dr. Perry J. Pickhardt and his colleagues reported.

Most of the polyps were smaller, however: “6-9 mm lesions represented as much as 61% of all … lesions,” the authors noted.

“These aggregate results suggest the potential for less aggressive management of some [computed tomographic colonography]–detected lesions,” especially those in the 6- to 9-mm range, wrote Dr. Pickhardt of the department of radiology at the University of Wisconsin-Madison.

They looked at 5,124 consecutive asymptomatic adults undergoing computed tomography colonography (CTC) between April 2004 and July 2008. Patients' mean age was 57 years, and 2,792 were women.

“Although individuals were not excluded for a positive family history of colorectal cancer, only 1.7% (89 adults) actually had a positive history according to [American Cancer Society] guidelines,” wrote Dr. Pickhardt (Clin. Gastroenterol. Hepatol. 2010 July [doi:10.1016/j.cgh.2010.03.007]).

Included in the analysis were all CTC-detected colorectal polyps greater than 6 mm that had corresponding endoscopic and/or surgical confirmation, wrote the authors, “including lesions not prospectively identified at CTC but found at subsequent colonoscopy.” Also “mucosal-based polyps that were confirmed at colonoscopy but were lost during retrieval, fulgurated, or otherwise ablated were also excluded.”

A total of 755 lesions greater than or equal to 6 mm were found in 479 patients. This included 464 lesions (61.5%) that were 6-9 mm, 216 lesions (28.6%) that were 10-19 mm, 33 lesions (4.4%) that measured 20-29 mm, and 42 (5.6%) that exceeded 30 mm.

According to Dr. Pickhardt, “In the small polyp group (6-9 mm), the rate of advanced adenomas was 3.9% (18 of 464).” Furthermore, only two polyps in this group were found to exhibit high-grade dysplasia, and none were classified as malignant.

That is in contrast to large polyps—those greater than 10 mm. Here, “the overall rate of advanced adenomas and malignancy was significantly higher compared to the smaller polyp group, at 61.9% (180/291) and 6.9% (20/291), respectively,” wrote the authors.

This included two malignant polyps in the 10- to 19-mm group (for a prevalence of 0.9% in this group, out of 216 total polyps), and two malignancies in the 20- to 29-mm group (for a prevalence of 6.1% in this group, out of 33 total polyps—a significantly higher proportion than the 0.9% prevalence in the 10- to 19-mm group, with P less than .001).

The remaining 16 malignancies were all found among the group of 42 polyps that measured greater than 30 mm, for a prevalence of 38.1%.

“For CTC-detected masses measuring 3 cm or greater, the risk of cancer clearly outweighs any procedural costs or risks related to its removal,” wrote the authors. However, “For CTC-detected colorectal lesions in the 1-2 cm and 2-3 cm size categories, the need for polypectomy referral has not been questioned in the past, although our findings show that the immediate benefit may not be as great as previously assumed.”

The authors conceded that the study was limited by the fact that the cohort included “average-risk screening subjects; higher rates of important histology would be expected amongst cohorts at increased risk for colorectal cancer.”

Disclosures: Dr. Pickhardt and one other author on this study disclosed that they are consultants for Viatronix Inc. and Medicsight PLC, medical and CT imaging companies, and are cofounders of VirtuoCTC LLC, which publishes guidance on CTC.

In a cohort of more than 5,000 patients with a total of 755 colorectal polyps, 100% of malignancies were associated with polyps greater than or equal to 10 mm, Dr. Perry J. Pickhardt and his colleagues reported.

Most of the polyps were smaller, however: “6-9 mm lesions represented as much as 61% of all … lesions,” the authors noted.

“These aggregate results suggest the potential for less aggressive management of some [computed tomographic colonography]–detected lesions,” especially those in the 6- to 9-mm range, wrote Dr. Pickhardt of the department of radiology at the University of Wisconsin-Madison.

They looked at 5,124 consecutive asymptomatic adults undergoing computed tomography colonography (CTC) between April 2004 and July 2008. Patients' mean age was 57 years, and 2,792 were women.

“Although individuals were not excluded for a positive family history of colorectal cancer, only 1.7% (89 adults) actually had a positive history according to [American Cancer Society] guidelines,” wrote Dr. Pickhardt (Clin. Gastroenterol. Hepatol. 2010 July [doi:10.1016/j.cgh.2010.03.007]).

Included in the analysis were all CTC-detected colorectal polyps greater than 6 mm that had corresponding endoscopic and/or surgical confirmation, wrote the authors, “including lesions not prospectively identified at CTC but found at subsequent colonoscopy.” Also “mucosal-based polyps that were confirmed at colonoscopy but were lost during retrieval, fulgurated, or otherwise ablated were also excluded.”

A total of 755 lesions greater than or equal to 6 mm were found in 479 patients. This included 464 lesions (61.5%) that were 6-9 mm, 216 lesions (28.6%) that were 10-19 mm, 33 lesions (4.4%) that measured 20-29 mm, and 42 (5.6%) that exceeded 30 mm.

According to Dr. Pickhardt, “In the small polyp group (6-9 mm), the rate of advanced adenomas was 3.9% (18 of 464).” Furthermore, only two polyps in this group were found to exhibit high-grade dysplasia, and none were classified as malignant.

That is in contrast to large polyps—those greater than 10 mm. Here, “the overall rate of advanced adenomas and malignancy was significantly higher compared to the smaller polyp group, at 61.9% (180/291) and 6.9% (20/291), respectively,” wrote the authors.

This included two malignant polyps in the 10- to 19-mm group (for a prevalence of 0.9% in this group, out of 216 total polyps), and two malignancies in the 20- to 29-mm group (for a prevalence of 6.1% in this group, out of 33 total polyps—a significantly higher proportion than the 0.9% prevalence in the 10- to 19-mm group, with P less than .001).

The remaining 16 malignancies were all found among the group of 42 polyps that measured greater than 30 mm, for a prevalence of 38.1%.

“For CTC-detected masses measuring 3 cm or greater, the risk of cancer clearly outweighs any procedural costs or risks related to its removal,” wrote the authors. However, “For CTC-detected colorectal lesions in the 1-2 cm and 2-3 cm size categories, the need for polypectomy referral has not been questioned in the past, although our findings show that the immediate benefit may not be as great as previously assumed.”

The authors conceded that the study was limited by the fact that the cohort included “average-risk screening subjects; higher rates of important histology would be expected amongst cohorts at increased risk for colorectal cancer.”

Disclosures: Dr. Pickhardt and one other author on this study disclosed that they are consultants for Viatronix Inc. and Medicsight PLC, medical and CT imaging companies, and are cofounders of VirtuoCTC LLC, which publishes guidance on CTC.

In a cohort of more than 5,000 patients with a total of 755 colorectal polyps, 100% of malignancies were associated with polyps greater than or equal to 10 mm, Dr. Perry J. Pickhardt and his colleagues reported.

Most of the polyps were smaller, however: “6-9 mm lesions represented as much as 61% of all … lesions,” the authors noted.

“These aggregate results suggest the potential for less aggressive management of some [computed tomographic colonography]–detected lesions,” especially those in the 6- to 9-mm range, wrote Dr. Pickhardt of the department of radiology at the University of Wisconsin-Madison.

They looked at 5,124 consecutive asymptomatic adults undergoing computed tomography colonography (CTC) between April 2004 and July 2008. Patients' mean age was 57 years, and 2,792 were women.

“Although individuals were not excluded for a positive family history of colorectal cancer, only 1.7% (89 adults) actually had a positive history according to [American Cancer Society] guidelines,” wrote Dr. Pickhardt (Clin. Gastroenterol. Hepatol. 2010 July [doi:10.1016/j.cgh.2010.03.007]).

Included in the analysis were all CTC-detected colorectal polyps greater than 6 mm that had corresponding endoscopic and/or surgical confirmation, wrote the authors, “including lesions not prospectively identified at CTC but found at subsequent colonoscopy.” Also “mucosal-based polyps that were confirmed at colonoscopy but were lost during retrieval, fulgurated, or otherwise ablated were also excluded.”

A total of 755 lesions greater than or equal to 6 mm were found in 479 patients. This included 464 lesions (61.5%) that were 6-9 mm, 216 lesions (28.6%) that were 10-19 mm, 33 lesions (4.4%) that measured 20-29 mm, and 42 (5.6%) that exceeded 30 mm.

According to Dr. Pickhardt, “In the small polyp group (6-9 mm), the rate of advanced adenomas was 3.9% (18 of 464).” Furthermore, only two polyps in this group were found to exhibit high-grade dysplasia, and none were classified as malignant.

That is in contrast to large polyps—those greater than 10 mm. Here, “the overall rate of advanced adenomas and malignancy was significantly higher compared to the smaller polyp group, at 61.9% (180/291) and 6.9% (20/291), respectively,” wrote the authors.

This included two malignant polyps in the 10- to 19-mm group (for a prevalence of 0.9% in this group, out of 216 total polyps), and two malignancies in the 20- to 29-mm group (for a prevalence of 6.1% in this group, out of 33 total polyps—a significantly higher proportion than the 0.9% prevalence in the 10- to 19-mm group, with P less than .001).

The remaining 16 malignancies were all found among the group of 42 polyps that measured greater than 30 mm, for a prevalence of 38.1%.

“For CTC-detected masses measuring 3 cm or greater, the risk of cancer clearly outweighs any procedural costs or risks related to its removal,” wrote the authors. However, “For CTC-detected colorectal lesions in the 1-2 cm and 2-3 cm size categories, the need for polypectomy referral has not been questioned in the past, although our findings show that the immediate benefit may not be as great as previously assumed.”

The authors conceded that the study was limited by the fact that the cohort included “average-risk screening subjects; higher rates of important histology would be expected amongst cohorts at increased risk for colorectal cancer.”

Disclosures: Dr. Pickhardt and one other author on this study disclosed that they are consultants for Viatronix Inc. and Medicsight PLC, medical and CT imaging companies, and are cofounders of VirtuoCTC LLC, which publishes guidance on CTC.

Major Finding: At least one novel influenza strain was discovered among swine tested during the height of the flu pandemic; neither antibodies from pandemic flu vaccine nor natural infection conferred protection against the novel strain in vitro.

Data Source: Study of 4,101 nasal and tracheal swabs gathered from swine from a Hong Kong slaughterhouse between June 2009 and February 2010.

Disclosures: None was reported.

Researchers are warning that the pandemic 2009 influenza (A)H1N1 strain has been quietly combining with other influenza strains among Hong Kong swine, and that further viral reassortment among global swine populations could once again cause a pandemic among humans, with unpredictable results.

“The 2009 pandemic, although mild and apparently contained at present, could undergo further reassortment in swine and gain virulence,” wrote Dr. Dhanasekaran Vijaykrishna and associates at the State Key Laboratory of Emerging Infectious Diseases at the University of Hong Kong.

The investigators called for “surveillance in swine [that] is greatly heightened, and that all eight gene segments are genetically characterized so that such reassortment events are rapidly identified.”

In their study, Dr. Vijaykrishna and colleagues looked at tracheal and nasal swab samples taken from swine at a Hong Kong slaughterhouse between June 11, 2009, and Feb. 4, 2010.

Samples were taken every 2 weeks on up to 252 swine per sampling occurrence, for a total of 4,101 samples of unique swine. Overall, H1N1 and H1N2 viruses were isolated from 32 samples (Science 2010;328:1529).

Pandemic flu viruses “isolated on the same sampling occasion were genetically identical, suggesting transmission of viruses occurred within swine herds,” Dr. Vijaykrishna and associates said.

However, “viruses from different sampling dates were genetically distinct from each other and also from [2009 H1N1]–like swine viruses isolated in other countries, indicating multiple independent introductions of these viruses from humans to swine,” the researchers said.

But the greatest concern comes from a January 2010 sampling where a novel reassortant was discovered; the new strain was named A/swine/Hong Kong/201/2010(H1N1).

Dr. Vijaykrishna and colleagues determined that this novel strain—whose hemagglutinin gene most closely resembled European avian-based influenzas, and whose neuraminidase gene was likely derived from the 2009 swine-derived H1N1 strain—could be particularly contagious.

“Neither [the 2009 H1N1] vaccine nor natural infection reliably elicits cross-protective antibody to A/swine/Hong Kong/201/2010,” the investigators wrote.

Further laboratory testing of the new strain revealed that while the virus was susceptible to oseltamivir, it was resistant to adamantanes such as amantadine or rimantadine.

“Experimentally infected swine developed mild illness and seroconverted,” according to the researchers. Additionally, they determined that viral shedding occurred among the infected swine for up to 13 days.

“Our results show that the introduction of [pandemic H1N1] virus to swine has provided it with opportunities for reassortment,” wrote Dr. Vijaykrishna and associates. This “reservoir of reassortment” could, if left unchecked, “produce novel viruses of potential threat to public health.”

Major Finding: At least one novel influenza strain was discovered among swine tested during the height of the flu pandemic; neither antibodies from pandemic flu vaccine nor natural infection conferred protection against the novel strain in vitro.

Data Source: Study of 4,101 nasal and tracheal swabs gathered from swine from a Hong Kong slaughterhouse between June 2009 and February 2010.

Disclosures: None was reported.

Researchers are warning that the pandemic 2009 influenza (A)H1N1 strain has been quietly combining with other influenza strains among Hong Kong swine, and that further viral reassortment among global swine populations could once again cause a pandemic among humans, with unpredictable results.

“The 2009 pandemic, although mild and apparently contained at present, could undergo further reassortment in swine and gain virulence,” wrote Dr. Dhanasekaran Vijaykrishna and associates at the State Key Laboratory of Emerging Infectious Diseases at the University of Hong Kong.

The investigators called for “surveillance in swine [that] is greatly heightened, and that all eight gene segments are genetically characterized so that such reassortment events are rapidly identified.”

In their study, Dr. Vijaykrishna and colleagues looked at tracheal and nasal swab samples taken from swine at a Hong Kong slaughterhouse between June 11, 2009, and Feb. 4, 2010.

Samples were taken every 2 weeks on up to 252 swine per sampling occurrence, for a total of 4,101 samples of unique swine. Overall, H1N1 and H1N2 viruses were isolated from 32 samples (Science 2010;328:1529).

Pandemic flu viruses “isolated on the same sampling occasion were genetically identical, suggesting transmission of viruses occurred within swine herds,” Dr. Vijaykrishna and associates said.

However, “viruses from different sampling dates were genetically distinct from each other and also from [2009 H1N1]–like swine viruses isolated in other countries, indicating multiple independent introductions of these viruses from humans to swine,” the researchers said.

But the greatest concern comes from a January 2010 sampling where a novel reassortant was discovered; the new strain was named A/swine/Hong Kong/201/2010(H1N1).

Dr. Vijaykrishna and colleagues determined that this novel strain—whose hemagglutinin gene most closely resembled European avian-based influenzas, and whose neuraminidase gene was likely derived from the 2009 swine-derived H1N1 strain—could be particularly contagious.

“Neither [the 2009 H1N1] vaccine nor natural infection reliably elicits cross-protective antibody to A/swine/Hong Kong/201/2010,” the investigators wrote.

Further laboratory testing of the new strain revealed that while the virus was susceptible to oseltamivir, it was resistant to adamantanes such as amantadine or rimantadine.

“Experimentally infected swine developed mild illness and seroconverted,” according to the researchers. Additionally, they determined that viral shedding occurred among the infected swine for up to 13 days.

“Our results show that the introduction of [pandemic H1N1] virus to swine has provided it with opportunities for reassortment,” wrote Dr. Vijaykrishna and associates. This “reservoir of reassortment” could, if left unchecked, “produce novel viruses of potential threat to public health.”

Major Finding: At least one novel influenza strain was discovered among swine tested during the height of the flu pandemic; neither antibodies from pandemic flu vaccine nor natural infection conferred protection against the novel strain in vitro.

Data Source: Study of 4,101 nasal and tracheal swabs gathered from swine from a Hong Kong slaughterhouse between June 2009 and February 2010.

Disclosures: None was reported.

Researchers are warning that the pandemic 2009 influenza (A)H1N1 strain has been quietly combining with other influenza strains among Hong Kong swine, and that further viral reassortment among global swine populations could once again cause a pandemic among humans, with unpredictable results.

“The 2009 pandemic, although mild and apparently contained at present, could undergo further reassortment in swine and gain virulence,” wrote Dr. Dhanasekaran Vijaykrishna and associates at the State Key Laboratory of Emerging Infectious Diseases at the University of Hong Kong.

The investigators called for “surveillance in swine [that] is greatly heightened, and that all eight gene segments are genetically characterized so that such reassortment events are rapidly identified.”

In their study, Dr. Vijaykrishna and colleagues looked at tracheal and nasal swab samples taken from swine at a Hong Kong slaughterhouse between June 11, 2009, and Feb. 4, 2010.

Samples were taken every 2 weeks on up to 252 swine per sampling occurrence, for a total of 4,101 samples of unique swine. Overall, H1N1 and H1N2 viruses were isolated from 32 samples (Science 2010;328:1529).

Pandemic flu viruses “isolated on the same sampling occasion were genetically identical, suggesting transmission of viruses occurred within swine herds,” Dr. Vijaykrishna and associates said.

However, “viruses from different sampling dates were genetically distinct from each other and also from [2009 H1N1]–like swine viruses isolated in other countries, indicating multiple independent introductions of these viruses from humans to swine,” the researchers said.

But the greatest concern comes from a January 2010 sampling where a novel reassortant was discovered; the new strain was named A/swine/Hong Kong/201/2010(H1N1).

Dr. Vijaykrishna and colleagues determined that this novel strain—whose hemagglutinin gene most closely resembled European avian-based influenzas, and whose neuraminidase gene was likely derived from the 2009 swine-derived H1N1 strain—could be particularly contagious.

“Neither [the 2009 H1N1] vaccine nor natural infection reliably elicits cross-protective antibody to A/swine/Hong Kong/201/2010,” the investigators wrote.

Further laboratory testing of the new strain revealed that while the virus was susceptible to oseltamivir, it was resistant to adamantanes such as amantadine or rimantadine.

“Experimentally infected swine developed mild illness and seroconverted,” according to the researchers. Additionally, they determined that viral shedding occurred among the infected swine for up to 13 days.

“Our results show that the introduction of [pandemic H1N1] virus to swine has provided it with opportunities for reassortment,” wrote Dr. Vijaykrishna and associates. This “reservoir of reassortment” could, if left unchecked, “produce novel viruses of potential threat to public health.”

Major Finding: Of 151,996 patients with a cutaneous melanoma diagnosis, 16,591 went on to have a second documented primary malignancy.

Data Source: A retrospective analysis of data from the SEER database for 1973-2003, encompassing over 1.3 million person-years of observation.

Disclosures: Dr. Spanogle reported having no relevant disclosures. His study has been accepted for publication in the Journal of the American Academy of Dermatology.

NEW YORK — The risk of developing a primary malignancy of the salivary gland, bone, prostate, and other areas is significantly—and in some cases dramatically—increased following a cutaneous melanoma diagnosis.

That's according to research by Dr. Joshua Spanogle, a resident in the department of dermatology at the Mayo Clinic in Rochester, Minn., presented during an abstract session at the meeting.

Dr. Spanogle performed an analysis of data from the Surveillance, Epidemiology, and End Results database (SEER) from 1973 to 2003, which included “over 1.3 million person-years of observation,” he said.

A total of 151,996 patients were found to have a cutaneous melanoma diagnosis during that period; 16,591 (11%) of these patients had a second documented primary malignancy sometime in the next 120 months. That observed rate was 32% higher than what would be expected among a healthy population in that time period, he said.

Further analysis of the results revealed that particular cancers carried a significantly higher risk than others.

The most striking result of the analysis, perhaps not surprisingly, was for a second primary cutaneous melanoma: There were 3,923 through 120 months of follow-up, for a standardized incidence ratio of 8.99.

“This is the 600-pound elephant in the room,” said Dr. Spanogle.

But other cancers had high standardized incidence ratios (SIRs) as well. Salivary gland malignancies following carcinoma had a SIR of 2.18 overall. Prostate cancer had a SIR of 1.13 following melanoma. Breast cancer showed a SIR of 1.07. And soft tissue cancers, including malignancies of the heart, had a SIR of 2.80.

On the other hand, “quite a few cancers had a decreased incidence following melanoma,” said Dr. Spanogle, including cancer of the liver (SIR 0.77), lungs (0.83), cervix (0.57), and pharynx (0.61).

The lower incidence of those kinds of cancer following melanoma could be because risk factors for melanoma are associated with higher socioeconomic status, like fair skin and intermittent high-intensity UV exposure (tanning), said Dr. Spanogle.

In contrast, risk factors for lung cancer and liver cancer are associated with comorbidities commonly found in lower socioeconomic patients, like smoking and hepatitis.

Moreover, according to Dr. Spanogle, the risks of secondary cancers of the prostate gland, bone, soft tissue, and salivary gland remained elevated throughout the study period, “implying no surveillance bias.”

Instead, he speculated that the link could be genetic, and said that future research into the possibility is warranted.

Major Finding: Of 151,996 patients with a cutaneous melanoma diagnosis, 16,591 went on to have a second documented primary malignancy.

Data Source: A retrospective analysis of data from the SEER database for 1973-2003, encompassing over 1.3 million person-years of observation.

Disclosures: Dr. Spanogle reported having no relevant disclosures. His study has been accepted for publication in the Journal of the American Academy of Dermatology.

NEW YORK — The risk of developing a primary malignancy of the salivary gland, bone, prostate, and other areas is significantly—and in some cases dramatically—increased following a cutaneous melanoma diagnosis.

That's according to research by Dr. Joshua Spanogle, a resident in the department of dermatology at the Mayo Clinic in Rochester, Minn., presented during an abstract session at the meeting.

Dr. Spanogle performed an analysis of data from the Surveillance, Epidemiology, and End Results database (SEER) from 1973 to 2003, which included “over 1.3 million person-years of observation,” he said.

A total of 151,996 patients were found to have a cutaneous melanoma diagnosis during that period; 16,591 (11%) of these patients had a second documented primary malignancy sometime in the next 120 months. That observed rate was 32% higher than what would be expected among a healthy population in that time period, he said.

Further analysis of the results revealed that particular cancers carried a significantly higher risk than others.

The most striking result of the analysis, perhaps not surprisingly, was for a second primary cutaneous melanoma: There were 3,923 through 120 months of follow-up, for a standardized incidence ratio of 8.99.

“This is the 600-pound elephant in the room,” said Dr. Spanogle.

But other cancers had high standardized incidence ratios (SIRs) as well. Salivary gland malignancies following carcinoma had a SIR of 2.18 overall. Prostate cancer had a SIR of 1.13 following melanoma. Breast cancer showed a SIR of 1.07. And soft tissue cancers, including malignancies of the heart, had a SIR of 2.80.

On the other hand, “quite a few cancers had a decreased incidence following melanoma,” said Dr. Spanogle, including cancer of the liver (SIR 0.77), lungs (0.83), cervix (0.57), and pharynx (0.61).

The lower incidence of those kinds of cancer following melanoma could be because risk factors for melanoma are associated with higher socioeconomic status, like fair skin and intermittent high-intensity UV exposure (tanning), said Dr. Spanogle.

In contrast, risk factors for lung cancer and liver cancer are associated with comorbidities commonly found in lower socioeconomic patients, like smoking and hepatitis.

Moreover, according to Dr. Spanogle, the risks of secondary cancers of the prostate gland, bone, soft tissue, and salivary gland remained elevated throughout the study period, “implying no surveillance bias.”

Instead, he speculated that the link could be genetic, and said that future research into the possibility is warranted.

Major Finding: Of 151,996 patients with a cutaneous melanoma diagnosis, 16,591 went on to have a second documented primary malignancy.

Data Source: A retrospective analysis of data from the SEER database for 1973-2003, encompassing over 1.3 million person-years of observation.

Disclosures: Dr. Spanogle reported having no relevant disclosures. His study has been accepted for publication in the Journal of the American Academy of Dermatology.

NEW YORK — The risk of developing a primary malignancy of the salivary gland, bone, prostate, and other areas is significantly—and in some cases dramatically—increased following a cutaneous melanoma diagnosis.

That's according to research by Dr. Joshua Spanogle, a resident in the department of dermatology at the Mayo Clinic in Rochester, Minn., presented during an abstract session at the meeting.

Dr. Spanogle performed an analysis of data from the Surveillance, Epidemiology, and End Results database (SEER) from 1973 to 2003, which included “over 1.3 million person-years of observation,” he said.

A total of 151,996 patients were found to have a cutaneous melanoma diagnosis during that period; 16,591 (11%) of these patients had a second documented primary malignancy sometime in the next 120 months. That observed rate was 32% higher than what would be expected among a healthy population in that time period, he said.

Further analysis of the results revealed that particular cancers carried a significantly higher risk than others.

The most striking result of the analysis, perhaps not surprisingly, was for a second primary cutaneous melanoma: There were 3,923 through 120 months of follow-up, for a standardized incidence ratio of 8.99.

“This is the 600-pound elephant in the room,” said Dr. Spanogle.

But other cancers had high standardized incidence ratios (SIRs) as well. Salivary gland malignancies following carcinoma had a SIR of 2.18 overall. Prostate cancer had a SIR of 1.13 following melanoma. Breast cancer showed a SIR of 1.07. And soft tissue cancers, including malignancies of the heart, had a SIR of 2.80.

On the other hand, “quite a few cancers had a decreased incidence following melanoma,” said Dr. Spanogle, including cancer of the liver (SIR 0.77), lungs (0.83), cervix (0.57), and pharynx (0.61).

The lower incidence of those kinds of cancer following melanoma could be because risk factors for melanoma are associated with higher socioeconomic status, like fair skin and intermittent high-intensity UV exposure (tanning), said Dr. Spanogle.

In contrast, risk factors for lung cancer and liver cancer are associated with comorbidities commonly found in lower socioeconomic patients, like smoking and hepatitis.

Moreover, according to Dr. Spanogle, the risks of secondary cancers of the prostate gland, bone, soft tissue, and salivary gland remained elevated throughout the study period, “implying no surveillance bias.”

Instead, he speculated that the link could be genetic, and said that future research into the possibility is warranted.

NEW YORK — Roughly 30% of Moh's surgeons currently employ physician assistants in their practice for presurgical consults, postoperative assessments, intraoperative suturing, and more.

The data, from a small survey presented at the meeting, are among the first to assess the use of physician assistants (PAs) among Mohs surgeons.

"The inherent tie between pathology and surgery in the Mohs specialty makes it very important that the PA act as an appendage of the Mohs surgeon," said Mr. Mark Hyde, a PA-C in the cutaneous oncology department at the Huntsman Cancer Institute at the University of Utah, Salt Lake City.

However, "with the employment of PAs in Mohs surgery, [physicians] can spend more face-to-face time with patients," he said at the annual meeting of the American College of Mohs Surgery.

Mr. Hyde mailed surveys to 576 members of the American College of Mohs Surgery in January 2009, asking whether the physician used a PA and if so, to do what. About a quarter of the physicians replied (143), and of those, 43 (30%) reported using a PA.

Mr. Hyde conceded that the response rate was low, but "because the data are not found anywhere else, we still felt this was important," he said.

Overall, 15 of 43 Moh's surgeons using PAs reported the PA at their practice performed preoperative consults. A total of 25 of the 43 surgeons, meanwhile, responded that their PA conducted postoperative follow-up.

Intraoperatively, 18 of 43 surgeons reported that PAs at their practice were participating in some aspect of repairs. These included primary repair design (8 of 43), dermal sutures on the primary tissue repair (12 of 43), epidermal sutures on the primary repair (18 of 43), dermal and epidermal sutures on the adjacent tissue transfer (8 and 14 of 43, respectively), and suturing of the skin graft (dermal, 10 of 43; epidermal, 16 of 43).

One surgeon reported that the PA at his facility excised Mohs sections, and another reported that their PA inked excised tissue.

No surgeons reported letting their PAs map Mohs sections, nor did any report letting PAs interpret pathology reports.

"There are some tasks that are rarely assigned to PAs in Mohs micrographic surgery--excision of the stages, mapping tissues, inking and grossing tissue, and interpreting pathology," said Mr. Hyde. However, "in our experience, PAs can ink and gross tissue, and increase efficiency by doing so."

He also pointed to an area in which PAs were especially useful to the physicians surveyed--seeing general dermatology patients. A total of 35 out of 43 surgeons, or more than 80%, reported using their PAs in this way.

In fact, he said, in the program at the University of Utah, PAs "act as a source of referrals for the Mohs surgeon."

Despite the use of the PAs in these practices, Mr. Hyde said there was no evidence to suggest that surgeons using PAs remove more tumors per week, or see more patients.

Nevertheless, as the use of PAs increases among Mohs surgeons, the need to identify which tasks PAs routinely perform is crucial to "allow PA programs and PA education providers to focus their training."

The survey was funded by the Society of Dermatology Physician Assistants with an unrestricted research grant. Mr. Hyde is on the board of the society.

NEW YORK — Roughly 30% of Moh's surgeons currently employ physician assistants in their practice for presurgical consults, postoperative assessments, intraoperative suturing, and more.

The data, from a small survey presented at the meeting, are among the first to assess the use of physician assistants (PAs) among Mohs surgeons.

"The inherent tie between pathology and surgery in the Mohs specialty makes it very important that the PA act as an appendage of the Mohs surgeon," said Mr. Mark Hyde, a PA-C in the cutaneous oncology department at the Huntsman Cancer Institute at the University of Utah, Salt Lake City.

However, "with the employment of PAs in Mohs surgery, [physicians] can spend more face-to-face time with patients," he said at the annual meeting of the American College of Mohs Surgery.

Mr. Hyde mailed surveys to 576 members of the American College of Mohs Surgery in January 2009, asking whether the physician used a PA and if so, to do what. About a quarter of the physicians replied (143), and of those, 43 (30%) reported using a PA.

Mr. Hyde conceded that the response rate was low, but "because the data are not found anywhere else, we still felt this was important," he said.

Overall, 15 of 43 Moh's surgeons using PAs reported the PA at their practice performed preoperative consults. A total of 25 of the 43 surgeons, meanwhile, responded that their PA conducted postoperative follow-up.

Intraoperatively, 18 of 43 surgeons reported that PAs at their practice were participating in some aspect of repairs. These included primary repair design (8 of 43), dermal sutures on the primary tissue repair (12 of 43), epidermal sutures on the primary repair (18 of 43), dermal and epidermal sutures on the adjacent tissue transfer (8 and 14 of 43, respectively), and suturing of the skin graft (dermal, 10 of 43; epidermal, 16 of 43).

One surgeon reported that the PA at his facility excised Mohs sections, and another reported that their PA inked excised tissue.

No surgeons reported letting their PAs map Mohs sections, nor did any report letting PAs interpret pathology reports.

"There are some tasks that are rarely assigned to PAs in Mohs micrographic surgery--excision of the stages, mapping tissues, inking and grossing tissue, and interpreting pathology," said Mr. Hyde. However, "in our experience, PAs can ink and gross tissue, and increase efficiency by doing so."

He also pointed to an area in which PAs were especially useful to the physicians surveyed--seeing general dermatology patients. A total of 35 out of 43 surgeons, or more than 80%, reported using their PAs in this way.

In fact, he said, in the program at the University of Utah, PAs "act as a source of referrals for the Mohs surgeon."

Despite the use of the PAs in these practices, Mr. Hyde said there was no evidence to suggest that surgeons using PAs remove more tumors per week, or see more patients.

Nevertheless, as the use of PAs increases among Mohs surgeons, the need to identify which tasks PAs routinely perform is crucial to "allow PA programs and PA education providers to focus their training."

The survey was funded by the Society of Dermatology Physician Assistants with an unrestricted research grant. Mr. Hyde is on the board of the society.

NEW YORK — Roughly 30% of Moh's surgeons currently employ physician assistants in their practice for presurgical consults, postoperative assessments, intraoperative suturing, and more.

The data, from a small survey presented at the meeting, are among the first to assess the use of physician assistants (PAs) among Mohs surgeons.

"The inherent tie between pathology and surgery in the Mohs specialty makes it very important that the PA act as an appendage of the Mohs surgeon," said Mr. Mark Hyde, a PA-C in the cutaneous oncology department at the Huntsman Cancer Institute at the University of Utah, Salt Lake City.

However, "with the employment of PAs in Mohs surgery, [physicians] can spend more face-to-face time with patients," he said at the annual meeting of the American College of Mohs Surgery.

Mr. Hyde mailed surveys to 576 members of the American College of Mohs Surgery in January 2009, asking whether the physician used a PA and if so, to do what. About a quarter of the physicians replied (143), and of those, 43 (30%) reported using a PA.

Mr. Hyde conceded that the response rate was low, but "because the data are not found anywhere else, we still felt this was important," he said.

Overall, 15 of 43 Moh's surgeons using PAs reported the PA at their practice performed preoperative consults. A total of 25 of the 43 surgeons, meanwhile, responded that their PA conducted postoperative follow-up.

Intraoperatively, 18 of 43 surgeons reported that PAs at their practice were participating in some aspect of repairs. These included primary repair design (8 of 43), dermal sutures on the primary tissue repair (12 of 43), epidermal sutures on the primary repair (18 of 43), dermal and epidermal sutures on the adjacent tissue transfer (8 and 14 of 43, respectively), and suturing of the skin graft (dermal, 10 of 43; epidermal, 16 of 43).

One surgeon reported that the PA at his facility excised Mohs sections, and another reported that their PA inked excised tissue.

No surgeons reported letting their PAs map Mohs sections, nor did any report letting PAs interpret pathology reports.

"There are some tasks that are rarely assigned to PAs in Mohs micrographic surgery--excision of the stages, mapping tissues, inking and grossing tissue, and interpreting pathology," said Mr. Hyde. However, "in our experience, PAs can ink and gross tissue, and increase efficiency by doing so."

He also pointed to an area in which PAs were especially useful to the physicians surveyed--seeing general dermatology patients. A total of 35 out of 43 surgeons, or more than 80%, reported using their PAs in this way.

In fact, he said, in the program at the University of Utah, PAs "act as a source of referrals for the Mohs surgeon."

Despite the use of the PAs in these practices, Mr. Hyde said there was no evidence to suggest that surgeons using PAs remove more tumors per week, or see more patients.

Nevertheless, as the use of PAs increases among Mohs surgeons, the need to identify which tasks PAs routinely perform is crucial to "allow PA programs and PA education providers to focus their training."

The survey was funded by the Society of Dermatology Physician Assistants with an unrestricted research grant. Mr. Hyde is on the board of the society.

NEW YORK — Use of positron emission tomography/computed tomography to assess lymph node involvement in Merkel cell carcinoma gives the best sensitivity and equal specificity, compared with more traditional imaging modalities.

"CT or MRI have been the imaging modalities of choice when staging patients with Merkel cell carcinoma," Dr. Michael B. Colgan said at the annual meeting of the American College of Mohs Surgery "We also know these techniques have shortcomings."

However, "We know from our colleagues in oncology … that PET/CT has become their go-to for staging and oftentimes restaging of disease."

Dr. Colgan, of the dermatology department at the Mayo Clinic in Rochester, Minn., looked at patients from three centers diagnosed with primary Merkel cell carcinoma between 1986 and 2008.

All patients had, as part of their cancer staging, a documented imaging study of their regional lymph node basin. Overall, 75 patients underwent a CT scan for this purpose; 34 had a PET/CT scan; and 10 patients had an MRI.

According to Dr. Colgan, the MRI results, when compared to the preferred method of histopathologic confirmation, were "dismal." The sensitivity in these cases was 0%; the specificity was 86%, the positive predictive value 0%, and the negative predictive value 67% in "detecting nodal basin involvement."

The CT scan results were slightly better - 54% sensitivity, said Dr. Colgan. "But if my radiologist tells me the CT is negative, 3 out of 10 times it's probably not the case," he said, for a negative predictive value of 70%. The specificity was 95%, and the positive predictive value was 90%.

The PET/CT results, on the other hand, offered a sensitivity of 77% - significantly higher than the other two modalities - a specificity of 95%, a positive predictive value of 91%, and a negative predictive value of 87% in detecting regional lymph node involvement.

"PET/CT can affect the stage and ultimately the clinical plan for these patients," he said.

He added that in three cases of PET/CT false negatives, there was either single node involvement or a small micrometastasis that went undetected.

"The big question when we're dealing with Merkel cell carcinoma is, if PET/CT still misses micromets [microscopic metastases], how are these scans best utilized?" asked Dr. Colgan. "That's a debate we need to have."

He pointed to some limitation of the study, including its retrospective design and the possibility of sampling bias, given that "all these patients went to get scanned."

A prospective study, of the "same patient, same node, at the same point in time" is needed.

Nevertheless, he said, especially compared with MRI, "If you were going to look at these two imaging modalities side by side, my choice is the PET/CT."
In an interview following the meeting, Dr. Colgan was asked whether PET/CT scans ought to be the standard for detecting lymph node involvement in other cancers, too.

"I would hesitate to extrapolate these results to other tumors, as each tumor has a unique metabolic signature and route of metastasis," he said.

"It is a remarkable imaging technique, but the studies need to be done."

Dr. Colgan stated that he had no conflicts of interest to disclose in relation to this study.

NEW YORK — Use of positron emission tomography/computed tomography to assess lymph node involvement in Merkel cell carcinoma gives the best sensitivity and equal specificity, compared with more traditional imaging modalities.

"CT or MRI have been the imaging modalities of choice when staging patients with Merkel cell carcinoma," Dr. Michael B. Colgan said at the annual meeting of the American College of Mohs Surgery "We also know these techniques have shortcomings."

However, "We know from our colleagues in oncology … that PET/CT has become their go-to for staging and oftentimes restaging of disease."

Dr. Colgan, of the dermatology department at the Mayo Clinic in Rochester, Minn., looked at patients from three centers diagnosed with primary Merkel cell carcinoma between 1986 and 2008.

All patients had, as part of their cancer staging, a documented imaging study of their regional lymph node basin. Overall, 75 patients underwent a CT scan for this purpose; 34 had a PET/CT scan; and 10 patients had an MRI.

According to Dr. Colgan, the MRI results, when compared to the preferred method of histopathologic confirmation, were "dismal." The sensitivity in these cases was 0%; the specificity was 86%, the positive predictive value 0%, and the negative predictive value 67% in "detecting nodal basin involvement."

The CT scan results were slightly better - 54% sensitivity, said Dr. Colgan. "But if my radiologist tells me the CT is negative, 3 out of 10 times it's probably not the case," he said, for a negative predictive value of 70%. The specificity was 95%, and the positive predictive value was 90%.

The PET/CT results, on the other hand, offered a sensitivity of 77% - significantly higher than the other two modalities - a specificity of 95%, a positive predictive value of 91%, and a negative predictive value of 87% in detecting regional lymph node involvement.

"PET/CT can affect the stage and ultimately the clinical plan for these patients," he said.

He added that in three cases of PET/CT false negatives, there was either single node involvement or a small micrometastasis that went undetected.

"The big question when we're dealing with Merkel cell carcinoma is, if PET/CT still misses micromets [microscopic metastases], how are these scans best utilized?" asked Dr. Colgan. "That's a debate we need to have."

He pointed to some limitation of the study, including its retrospective design and the possibility of sampling bias, given that "all these patients went to get scanned."

A prospective study, of the "same patient, same node, at the same point in time" is needed.

Nevertheless, he said, especially compared with MRI, "If you were going to look at these two imaging modalities side by side, my choice is the PET/CT."
In an interview following the meeting, Dr. Colgan was asked whether PET/CT scans ought to be the standard for detecting lymph node involvement in other cancers, too.

"I would hesitate to extrapolate these results to other tumors, as each tumor has a unique metabolic signature and route of metastasis," he said.

"It is a remarkable imaging technique, but the studies need to be done."

Dr. Colgan stated that he had no conflicts of interest to disclose in relation to this study.

NEW YORK — Use of positron emission tomography/computed tomography to assess lymph node involvement in Merkel cell carcinoma gives the best sensitivity and equal specificity, compared with more traditional imaging modalities.

"CT or MRI have been the imaging modalities of choice when staging patients with Merkel cell carcinoma," Dr. Michael B. Colgan said at the annual meeting of the American College of Mohs Surgery "We also know these techniques have shortcomings."

However, "We know from our colleagues in oncology … that PET/CT has become their go-to for staging and oftentimes restaging of disease."

Dr. Colgan, of the dermatology department at the Mayo Clinic in Rochester, Minn., looked at patients from three centers diagnosed with primary Merkel cell carcinoma between 1986 and 2008.

All patients had, as part of their cancer staging, a documented imaging study of their regional lymph node basin. Overall, 75 patients underwent a CT scan for this purpose; 34 had a PET/CT scan; and 10 patients had an MRI.

According to Dr. Colgan, the MRI results, when compared to the preferred method of histopathologic confirmation, were "dismal." The sensitivity in these cases was 0%; the specificity was 86%, the positive predictive value 0%, and the negative predictive value 67% in "detecting nodal basin involvement."

The CT scan results were slightly better - 54% sensitivity, said Dr. Colgan. "But if my radiologist tells me the CT is negative, 3 out of 10 times it's probably not the case," he said, for a negative predictive value of 70%. The specificity was 95%, and the positive predictive value was 90%.

The PET/CT results, on the other hand, offered a sensitivity of 77% - significantly higher than the other two modalities - a specificity of 95%, a positive predictive value of 91%, and a negative predictive value of 87% in detecting regional lymph node involvement.

"PET/CT can affect the stage and ultimately the clinical plan for these patients," he said.

He added that in three cases of PET/CT false negatives, there was either single node involvement or a small micrometastasis that went undetected.

"The big question when we're dealing with Merkel cell carcinoma is, if PET/CT still misses micromets [microscopic metastases], how are these scans best utilized?" asked Dr. Colgan. "That's a debate we need to have."

He pointed to some limitation of the study, including its retrospective design and the possibility of sampling bias, given that "all these patients went to get scanned."

A prospective study, of the "same patient, same node, at the same point in time" is needed.

Nevertheless, he said, especially compared with MRI, "If you were going to look at these two imaging modalities side by side, my choice is the PET/CT."
In an interview following the meeting, Dr. Colgan was asked whether PET/CT scans ought to be the standard for detecting lymph node involvement in other cancers, too.

"I would hesitate to extrapolate these results to other tumors, as each tumor has a unique metabolic signature and route of metastasis," he said.

"It is a remarkable imaging technique, but the studies need to be done."

Dr. Colgan stated that he had no conflicts of interest to disclose in relation to this study.