The Journal of Family Practice

CASE 1

Tyler M, age 40, otherwise healthy, and with a body mass index (BMI) of 30, presents to your office for his annual physical examination. He does not have a history of alcohol or tobacco use.

Mr. M’s obesity raises concern about metabolic syndrome, which warrants evaluation for hypertriglyceridemia (HTG). You offer him lipid testing to estimate his risk of atherosclerotic cardiovascular disease (ASCVD).

The only abnormal value on the lipid panel is a triglyceride (TG) level of 264 mg/dL (normal, < 175 mg/dL). Mr. M’s 10-yr ASCVD risk is determined to be < 5%.

What, if any, intervention would be triggered by the finding of moderate HTG?

© ALICIA BUELOW

CASE 2

Alicia F, age 30, with a BMI of 28 and ASCVD risk < 7.5%, comes to the clinic for evaluation of anxiety and insomnia. She reports eating a high-carbohydrate diet and drinking 3 to 5 alcoholic beverages nightly to help her sleep.

Ms. F’s daily alcohol use prompts evaluation for HTG. Results show a TG level of 1300 mg/dL and a high-density lipoprotein (HDL) level of 25 mg/dL (healthy HDL levels: adult females, ≥ 50 mg/dL; adult males, ≥ 40 mg/dL). Other test results are normal, except for elevated transaminase levels (just under twice normal).

What, if any, action would be prompted by the patient’s severe HTG and below-normal HDL level?

Continue to: How HTG is defined

 

 

How HTG is defined: Causes, cutoffs, signs

HTG is most commonly caused by obesity and a sedentary lifestyle; certain associated comorbid medical conditions can also be a precipitant (Table 1^1,2). Because the condition is a result of polygenic phenotypic expression, even a genetically low-risk patient can present with HTG when exposed to certain medical conditions and environmental causes.

Primary HTG (genetic or familial) is rare. Genetic testing may be considered for patients with TG > 1000 mg/dL (severely elevated TG = 500 to 1999 mg/dL, measured in fasting state*) or a family history of early ASCVD (TABLE 1^1,2).^2,3

Even a genetically low-risk patient can present with hypertriglyceridemia when exposed to certain medical conditions and environmental causes.

Typically, HTG is asymptomatic. Xanthelasmas, xanthomas, and lipemia retinalis are found in hereditary disorders of elevated TGs. Occasionally, HTG manifests as chylomicronemia syndrome, characterized by recurrent abdominal pain, nausea, vomiting, and, in severe HTG, pancreatitis.³

Fine points of TG measurement

Triglycerides are a component of a complete lipid profile, which also includes total cholesterol, calculated low-density lipoprotein (LDL-C), and HDL.⁴ As in both case vignettes, detection of HTG is often incidental, when a lipid profile is ordered to evaluate the risk of ASCVD. (Of note, for people older than 20 years, the US Preventive Services Task Force no longer addresses the question, “Which population should be screened for dyslipidemia?” Instead, current recommendations answer the question, “For which population should statin therapy be prescribed?”⁵)

Effect on ASCVD risk assessment. TG levels are known to vary, depending on fasting or nonfasting status, with lower levels reported when fasting. An elevated TG level can lead to inaccurate calculation of LDL when using the Friedewald formula⁶:

LDL = total cholesterol – (triglycerides/5) – HDL

Continue to: The purpose of testing...

The purpose of testing lipids in a fasting state (> 9 hours) is to minimize the effects of an elevated TG level on the calculated LDL. In severe HTG, beta-quantitation by ultracentrifugation and electrophoresis can be performed to determine the LDL level directly.

Advantage of nonfasting measurement. When LDL-C is not a concern, there is, in fact, value in measuring TGs in the nonfasting state. Why? Because a nonfasting TG level is a better indicator of a patient’s average TG status: Studies have found a higher ASCVD risk in the setting of an elevated postprandial TG level accompanied by a low HDL level.⁷

Studies have found a higher ASCVD risk in the setting of an elevated postprandial triglyceride level accompanied by a low HDL level.

The Copenhagen City Heart Study identified postprandial HTG as an independent risk factor for atherogenicity, even in the setting of a normal fasting TG level.⁸ American Association of Clinical Endocrinologists and American College of Endocrinology guidelines endorse testing the nonfasting TG level when the fasting TG level is elevated in a lipid profile; if the nonfasting TG level is > 500 mg/dL, evaluation for secondary causes is warranted^9,10 (Table 1^1,2).

In a practical sense, therefore, offering patients nonfasting lipid testing allows more people to obtain access to timely care.

Pancreatitis. Acute pancreatitis commonly prompts an evaluation for HTG. The risk of acute pancreatitis in the general population is 0.04%, but that risk increases to 8% to 31% for a person with HTG.¹¹ Incidence when the TG level is > 500 mg/dL is thought to be increased because chylomicrons, acting as a TG carrier in the bloodstream, are responsible for pancreatitis.³ Treating HTG can reduce both the risk and recurrence of pancreatitis^12,13; given that the postprandial TG level can change rapidly from severe to very severe (> 2000 mg/dL), multiple guidelines recommend pharmacotherapy to a TG goal of < 500-1000 mg/dL.^1,9,13,14

Continue to: An ASCVD risk-HTG connection?

An ASCVD risk–HTG connection? In the population already at higher risk of ASCVD (> 7.5%), HTG is recognized as a risk-enhancing factor because of its atherogenic potential (Table 2²); however, there is insufficient evidence that TGs have a role as an independent risk factor for ASCVD. In a population-based study of 58,000 people, 40 to 65 years of age, conducted at Copenhagen [Denmark] University Hospital, investigators found that those who did not meet criteria for statin treatment and who had a TG level > 264 mg/dL had a 10-year risk of a major adverse cardiovascular event similar to that of people who did meet criteria for statin therapy.¹⁵

The FIELD (Fenofibrate Intervention and Event Lowering in Diabetes) and AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides and Impact on Global Health Outcomes) studies, among others, have failed to show a significant reduction in coronary events by treating HTG.¹⁰

That said, it’s worth considering the findings of other trials:

• In the PROVE IT-TIMI 22 (Pravastatin or Atorvastatin Evaluation and Infection Therapy–Thrombolysis in Myocardial Infarction 22) trial, an overall 28% reduction in endpoint events (myocardial infarction, acute coronary syndrome) was seen with high-intensity statin therapy, compared to moderate-intensity therapy.¹⁰ However, there was a sizeable residual risk identified that was theorized by investigators to be associated with high non-HDL lipoproteins, including TGs.
• A 2016 study in Israel, in which 22 years of data on 15,355 patients with established ASCVD were studied, revealed that elevated TGs are associated with an increased long-term mortality risk that is independent of the HDL level.¹⁶
• A cross-sectional study, nested in the prospective Copenhagen City Heart Study, demonstrated that HTG is associated with an increase in ischemic stroke events.¹⁷

Treatment

Therapeutic lifestyle changes

Changes in lifestyle are the foundation of management of, and recommended first-line treatment for, all patients with HTG. Patients with a moderately elevated TG level (175-499 mg/dL, measured in a fasting or nonfasting state) can be treated with therapeutic lifestyle changes alone^1,2; a trial of 3 to 6 months (see specific interventions below) is recommended before considering adding medications.¹⁰

Weight loss. There is a strong association between BMI > 30 and HTG. Visceral adiposity is a much more significant risk than subcutaneous adipose tissue. Although weight loss to an ideal range is recommended, even a 10% to 15% reduction in an obese patient can reduce the TG level by 20%. A combination of moderate-intensity exercise and healthy eating habits appears to assist best with this intervention.¹⁸

Continue to: Exercise

Exercise. Thirty minutes a day of moderate-intensity exercise is associated with a significant drop in postprandial TG. This benefit can last as long as 3 days, suggesting a goal of at least 3 days a week of an active lifestyle. Such a program can include intermittent aerobics or mild resistance exercise.¹⁹

Healthy eating habits. The difference between a low-fat, high-carbohydrate diet and a high-fat, low-carbohydrate diet is less important than the overall benefit of weight loss from either of these diets. Complex carbohydrates are recommended over simple carbohydrates. A low-carbohydrate diet in a patient with diabetes has been demonstrated to improve the TG level, irrespective of weight change.²⁰

The risk of acute pancreatitis in the general population is 0.04%, but that risk increases to 8% to 31% for a person with hypertriglyceridemia

A Mediterranean diet can reduce the TG level by 10% to 15%, and is recommended over a low-fat diet.¹⁴ (This diet generally includes a high intake of extra virgin olive oil; leafy green vegetables, fruits, cereals, nuts, and legumes; moderate intake of fish and other meat, dairy products, and red wine; and low intake of eggs and sugars.) The American Heart Association recommends 2 servings of fatty fish a week for its omega-3 oil benefit of reducing ASCVD risk. Working with a registered dietician to assist with lipid lowering can produce better results than physician-only instruction on healthy eating.⁹

Alcohol consumption. Complete cessation or moderation of alcohol consumption (1 drink a day/women and 2 drinks a day/men*) is recommended to improve HTG. Among secondary factors, alcohol is commonly the cause of an unusually high elevation of the TG level.¹⁴

Smoking cessation. Smoking increases the postprandial TG level.¹⁰ Complete cessation for just 1 year can reduce a person’s ASCVD risk by approximately 50%. However, in a clinical trial,²² smoking cessation did not significantly decrease the TG level—possibly because of the counterbalancing effect of weight gain following cessation.

Continue to: Medical therapy

 

 

Medical therapy

In addition to lifestyle modification, medications are recommended to reduce atherogenic potential in patients with moderate or severe HTG and an ASCVD risk > 7.5% (Table 3^4,13,18,23 and Table 4^2,9). Before initiating medical therapy, we recommend that you engage in shared decision-making with patients to (1) delineate treatment goals and (2) describe the risks and benefits of medications for HTG.²

Statins. These agents are recommended first-line therapy for reducing ASCVD risk.² If the TG level remains elevated (> 500 mg/dL) after statin therapy is maximized, an additional agent can be added—ie, a fibrate or fish oil (see below).

Fibrates. If a fibrate is used as an add-on to a statin, fenofibrate is preferred over gemfibrozil because it presents less risk of the severe myopathy that can develop when taken with a statin.¹³ Despite the effectiveness of fibrates in reducing the TG level, these drugs have not been shown to reduce overall mortality.²⁴ The evidence on improved cardiovascular outcomes is subgroup-specific (ie, prevention of a second myocardial infarction in the setting of optimal statin use and elevated non-HDL lipoproteins).¹² A study demonstrated that gemfibrozil reduced the incidence of transient ischemic attack and stroke in a subgroup of male US veterans who had coronary artery disease and a low HDL level.²⁵

Fish oil. The omega-3 ethyl esters eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), available as EPA alone or in combination with DHA, do not interact with statins and are tolerated well. They reduce hypertriglyceridemia by 20% to 50%.¹³

Eicosapentaenoic acid, EPA plus DHA, and icosapent ethyl, an ethyl ester product containing EPA without DHA, are approved by the US Food and Drug Administration for HTG > 500 mg/dL, at a dosage of 2000 mg twice daily. In the REDUCE-IT trial, adding icosapent ethyl, 2 g twice daily, to a statin in patients with HTG was associated with fewer ischemic events, compared to placebo.^23,26

Continue to: Fish oil formulations...

Fish oil formulations can inhibit platelet aggregation and increase bleeding time in otherwise healthy people; however, such episodes are minor and nonfatal. Patients on anticoagulation or an antiplatelet medication should be monitored periodically for bleeding events, although recommendations on how to monitor aren’t specified in a recent advisory by the American Heart Association.²³

There is a strong association between a BMI > 30 and hypertriglyceridemia.

DHA was thought to increase the LDL-C levels and, by doing so, potentially counterbalance benefit,^23,27 but most studies have failed to reproduce this effect.²⁸ Instead, studies have shown minimal elevation of LDL-C when DHA is used to treat HTG.^23,27

Niacin. At a dosage of 500-2000 mg/dL, niacin lowers the TG level by 10% to 30%. It also increases HDL by 10% to 40% and lowers LDL by 5% to 20%.¹³

Considerations in pancreatitis. For management of recurrent pancreatitis in patients with HTG, lifestyle modification remains the mainstay of treatment. When medication is considered for persistent severe HTG, fibrates have evidence of primary and secondary prevention of pancreatitis.¹¹ When a patient is intolerant of fibrates, consider a different option to reduce the TG level—eg, fish oil supplementation.

CASE 1

Recommendation for Mr. M: Therapeutic lifestyle changes to address moderate HTG.

Continue to: Because Mr. M's...

Because Mr. M’s 10-yr ASCVD risk is < 5%, statin therapy is not indicated for risk reduction. With a fasting TG value < 500 mg/dL, he is not considered at increased risk of pancreatitis.

CASE 2

Recommendations for Ms. F:

• Therapeutic lifestyle changes to address severe HTG. Ms. F agrees to wean off alcohol; add relaxation exercises before bedtime; do aerobic exercise 30 minutes a day, 3 times a week; decrease dietary carbohydrates daily by cutting portion size in half; and increase intake of fresh vegetables and lean protein.
• Treatment with fenofibrate to reduce the risk of pancreatitis. Ms. F begins a trial. Six months into treatment, she has reduced her BMI to 24 and the TG level has fallen to < 500 mg/dL. Ms. F also reports that she is sleeping well, believes that she is able to manage her infrequent anxiety, and is now in a routine that feels sustainable.

You congratulate Ms. F on her success and support her decision to undertake a trial of discontinuing fenofibrate, after shared decision-making about the risks and potential benefits of doing so.

Summing up: Management of HTG

Keep these treatment strategy highlights in mind:

• Lifestyle modification with a low-fat, low-carbohydrate diet, avoidance of alcohol, and moderate-intensity exercise is the mainstay of HTG management.
• The latest evidence supports that (1) HTG is a risk-enhancing factor for ­ASCVD and (2) statin therapy is recommended for patients who have HTG and an ASCVD risk > 7.5%.
• When the TG level remains elevated despite statin therapy and lifestyle changes, an omega-3 ethyl ester can be used as an adjunct for additional atherogenic risk reduction.
• For severe HTG, a regimen of therapeutic lifestyle changes plus a fibrate is recommended to reduce the risk and recurrence of pancreatitis.^1,24

* In comparison, a normal level of triglycerides is < 175 mg/dL; a moderately elevated level, measured in a fasting or nonfasting state, 175-499 mg/dL; and a very severely elevated level, ≥ 2000 mg/dL.²

CORRESPONDENCE
Ashwini Kamath Mulki, MD, Family Health Center, 1730 Chew Street, Allentown, PA 18104; [email protected].

CASE 1

Tyler M, age 40, otherwise healthy, and with a body mass index (BMI) of 30, presents to your office for his annual physical examination. He does not have a history of alcohol or tobacco use.

Mr. M’s obesity raises concern about metabolic syndrome, which warrants evaluation for hypertriglyceridemia (HTG). You offer him lipid testing to estimate his risk of atherosclerotic cardiovascular disease (ASCVD).

The only abnormal value on the lipid panel is a triglyceride (TG) level of 264 mg/dL (normal, < 175 mg/dL). Mr. M’s 10-yr ASCVD risk is determined to be < 5%.

What, if any, intervention would be triggered by the finding of moderate HTG?

© ALICIA BUELOW

CASE 2

Alicia F, age 30, with a BMI of 28 and ASCVD risk < 7.5%, comes to the clinic for evaluation of anxiety and insomnia. She reports eating a high-carbohydrate diet and drinking 3 to 5 alcoholic beverages nightly to help her sleep.

Ms. F’s daily alcohol use prompts evaluation for HTG. Results show a TG level of 1300 mg/dL and a high-density lipoprotein (HDL) level of 25 mg/dL (healthy HDL levels: adult females, ≥ 50 mg/dL; adult males, ≥ 40 mg/dL). Other test results are normal, except for elevated transaminase levels (just under twice normal).

What, if any, action would be prompted by the patient’s severe HTG and below-normal HDL level?

Continue to: How HTG is defined

 

 

How HTG is defined: Causes, cutoffs, signs

HTG is most commonly caused by obesity and a sedentary lifestyle; certain associated comorbid medical conditions can also be a precipitant (Table 1^1,2). Because the condition is a result of polygenic phenotypic expression, even a genetically low-risk patient can present with HTG when exposed to certain medical conditions and environmental causes.

Primary HTG (genetic or familial) is rare. Genetic testing may be considered for patients with TG > 1000 mg/dL (severely elevated TG = 500 to 1999 mg/dL, measured in fasting state*) or a family history of early ASCVD (TABLE 1^1,2).^2,3

Even a genetically low-risk patient can present with hypertriglyceridemia when exposed to certain medical conditions and environmental causes.

Typically, HTG is asymptomatic. Xanthelasmas, xanthomas, and lipemia retinalis are found in hereditary disorders of elevated TGs. Occasionally, HTG manifests as chylomicronemia syndrome, characterized by recurrent abdominal pain, nausea, vomiting, and, in severe HTG, pancreatitis.³

Fine points of TG measurement

Triglycerides are a component of a complete lipid profile, which also includes total cholesterol, calculated low-density lipoprotein (LDL-C), and HDL.⁴ As in both case vignettes, detection of HTG is often incidental, when a lipid profile is ordered to evaluate the risk of ASCVD. (Of note, for people older than 20 years, the US Preventive Services Task Force no longer addresses the question, “Which population should be screened for dyslipidemia?” Instead, current recommendations answer the question, “For which population should statin therapy be prescribed?”⁵)

Effect on ASCVD risk assessment. TG levels are known to vary, depending on fasting or nonfasting status, with lower levels reported when fasting. An elevated TG level can lead to inaccurate calculation of LDL when using the Friedewald formula⁶:

LDL = total cholesterol – (triglycerides/5) – HDL

Continue to: The purpose of testing...

The purpose of testing lipids in a fasting state (> 9 hours) is to minimize the effects of an elevated TG level on the calculated LDL. In severe HTG, beta-quantitation by ultracentrifugation and electrophoresis can be performed to determine the LDL level directly.

Advantage of nonfasting measurement. When LDL-C is not a concern, there is, in fact, value in measuring TGs in the nonfasting state. Why? Because a nonfasting TG level is a better indicator of a patient’s average TG status: Studies have found a higher ASCVD risk in the setting of an elevated postprandial TG level accompanied by a low HDL level.⁷

Studies have found a higher ASCVD risk in the setting of an elevated postprandial triglyceride level accompanied by a low HDL level.

The Copenhagen City Heart Study identified postprandial HTG as an independent risk factor for atherogenicity, even in the setting of a normal fasting TG level.⁸ American Association of Clinical Endocrinologists and American College of Endocrinology guidelines endorse testing the nonfasting TG level when the fasting TG level is elevated in a lipid profile; if the nonfasting TG level is > 500 mg/dL, evaluation for secondary causes is warranted^9,10 (Table 1^1,2).

In a practical sense, therefore, offering patients nonfasting lipid testing allows more people to obtain access to timely care.

Pancreatitis. Acute pancreatitis commonly prompts an evaluation for HTG. The risk of acute pancreatitis in the general population is 0.04%, but that risk increases to 8% to 31% for a person with HTG.¹¹ Incidence when the TG level is > 500 mg/dL is thought to be increased because chylomicrons, acting as a TG carrier in the bloodstream, are responsible for pancreatitis.³ Treating HTG can reduce both the risk and recurrence of pancreatitis^12,13; given that the postprandial TG level can change rapidly from severe to very severe (> 2000 mg/dL), multiple guidelines recommend pharmacotherapy to a TG goal of < 500-1000 mg/dL.^1,9,13,14

Continue to: An ASCVD risk-HTG connection?

An ASCVD risk–HTG connection? In the population already at higher risk of ASCVD (> 7.5%), HTG is recognized as a risk-enhancing factor because of its atherogenic potential (Table 2²); however, there is insufficient evidence that TGs have a role as an independent risk factor for ASCVD. In a population-based study of 58,000 people, 40 to 65 years of age, conducted at Copenhagen [Denmark] University Hospital, investigators found that those who did not meet criteria for statin treatment and who had a TG level > 264 mg/dL had a 10-year risk of a major adverse cardiovascular event similar to that of people who did meet criteria for statin therapy.¹⁵

The FIELD (Fenofibrate Intervention and Event Lowering in Diabetes) and AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides and Impact on Global Health Outcomes) studies, among others, have failed to show a significant reduction in coronary events by treating HTG.¹⁰

That said, it’s worth considering the findings of other trials:

• In the PROVE IT-TIMI 22 (Pravastatin or Atorvastatin Evaluation and Infection Therapy–Thrombolysis in Myocardial Infarction 22) trial, an overall 28% reduction in endpoint events (myocardial infarction, acute coronary syndrome) was seen with high-intensity statin therapy, compared to moderate-intensity therapy.¹⁰ However, there was a sizeable residual risk identified that was theorized by investigators to be associated with high non-HDL lipoproteins, including TGs.
• A 2016 study in Israel, in which 22 years of data on 15,355 patients with established ASCVD were studied, revealed that elevated TGs are associated with an increased long-term mortality risk that is independent of the HDL level.¹⁶
• A cross-sectional study, nested in the prospective Copenhagen City Heart Study, demonstrated that HTG is associated with an increase in ischemic stroke events.¹⁷

Treatment

Therapeutic lifestyle changes

Changes in lifestyle are the foundation of management of, and recommended first-line treatment for, all patients with HTG. Patients with a moderately elevated TG level (175-499 mg/dL, measured in a fasting or nonfasting state) can be treated with therapeutic lifestyle changes alone^1,2; a trial of 3 to 6 months (see specific interventions below) is recommended before considering adding medications.¹⁰

Weight loss. There is a strong association between BMI > 30 and HTG. Visceral adiposity is a much more significant risk than subcutaneous adipose tissue. Although weight loss to an ideal range is recommended, even a 10% to 15% reduction in an obese patient can reduce the TG level by 20%. A combination of moderate-intensity exercise and healthy eating habits appears to assist best with this intervention.¹⁸

Continue to: Exercise

Exercise. Thirty minutes a day of moderate-intensity exercise is associated with a significant drop in postprandial TG. This benefit can last as long as 3 days, suggesting a goal of at least 3 days a week of an active lifestyle. Such a program can include intermittent aerobics or mild resistance exercise.¹⁹

Healthy eating habits. The difference between a low-fat, high-carbohydrate diet and a high-fat, low-carbohydrate diet is less important than the overall benefit of weight loss from either of these diets. Complex carbohydrates are recommended over simple carbohydrates. A low-carbohydrate diet in a patient with diabetes has been demonstrated to improve the TG level, irrespective of weight change.²⁰

The risk of acute pancreatitis in the general population is 0.04%, but that risk increases to 8% to 31% for a person with hypertriglyceridemia

A Mediterranean diet can reduce the TG level by 10% to 15%, and is recommended over a low-fat diet.¹⁴ (This diet generally includes a high intake of extra virgin olive oil; leafy green vegetables, fruits, cereals, nuts, and legumes; moderate intake of fish and other meat, dairy products, and red wine; and low intake of eggs and sugars.) The American Heart Association recommends 2 servings of fatty fish a week for its omega-3 oil benefit of reducing ASCVD risk. Working with a registered dietician to assist with lipid lowering can produce better results than physician-only instruction on healthy eating.⁹

Alcohol consumption. Complete cessation or moderation of alcohol consumption (1 drink a day/women and 2 drinks a day/men*) is recommended to improve HTG. Among secondary factors, alcohol is commonly the cause of an unusually high elevation of the TG level.¹⁴

Smoking cessation. Smoking increases the postprandial TG level.¹⁰ Complete cessation for just 1 year can reduce a person’s ASCVD risk by approximately 50%. However, in a clinical trial,²² smoking cessation did not significantly decrease the TG level—possibly because of the counterbalancing effect of weight gain following cessation.

Continue to: Medical therapy

 

 

Medical therapy

In addition to lifestyle modification, medications are recommended to reduce atherogenic potential in patients with moderate or severe HTG and an ASCVD risk > 7.5% (Table 3^4,13,18,23 and Table 4^2,9). Before initiating medical therapy, we recommend that you engage in shared decision-making with patients to (1) delineate treatment goals and (2) describe the risks and benefits of medications for HTG.²

Statins. These agents are recommended first-line therapy for reducing ASCVD risk.² If the TG level remains elevated (> 500 mg/dL) after statin therapy is maximized, an additional agent can be added—ie, a fibrate or fish oil (see below).

Fibrates. If a fibrate is used as an add-on to a statin, fenofibrate is preferred over gemfibrozil because it presents less risk of the severe myopathy that can develop when taken with a statin.¹³ Despite the effectiveness of fibrates in reducing the TG level, these drugs have not been shown to reduce overall mortality.²⁴ The evidence on improved cardiovascular outcomes is subgroup-specific (ie, prevention of a second myocardial infarction in the setting of optimal statin use and elevated non-HDL lipoproteins).¹² A study demonstrated that gemfibrozil reduced the incidence of transient ischemic attack and stroke in a subgroup of male US veterans who had coronary artery disease and a low HDL level.²⁵

Fish oil. The omega-3 ethyl esters eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), available as EPA alone or in combination with DHA, do not interact with statins and are tolerated well. They reduce hypertriglyceridemia by 20% to 50%.¹³

Eicosapentaenoic acid, EPA plus DHA, and icosapent ethyl, an ethyl ester product containing EPA without DHA, are approved by the US Food and Drug Administration for HTG > 500 mg/dL, at a dosage of 2000 mg twice daily. In the REDUCE-IT trial, adding icosapent ethyl, 2 g twice daily, to a statin in patients with HTG was associated with fewer ischemic events, compared to placebo.^23,26

Continue to: Fish oil formulations...

Fish oil formulations can inhibit platelet aggregation and increase bleeding time in otherwise healthy people; however, such episodes are minor and nonfatal. Patients on anticoagulation or an antiplatelet medication should be monitored periodically for bleeding events, although recommendations on how to monitor aren’t specified in a recent advisory by the American Heart Association.²³

There is a strong association between a BMI > 30 and hypertriglyceridemia.

DHA was thought to increase the LDL-C levels and, by doing so, potentially counterbalance benefit,^23,27 but most studies have failed to reproduce this effect.²⁸ Instead, studies have shown minimal elevation of LDL-C when DHA is used to treat HTG.^23,27

Niacin. At a dosage of 500-2000 mg/dL, niacin lowers the TG level by 10% to 30%. It also increases HDL by 10% to 40% and lowers LDL by 5% to 20%.¹³

Considerations in pancreatitis. For management of recurrent pancreatitis in patients with HTG, lifestyle modification remains the mainstay of treatment. When medication is considered for persistent severe HTG, fibrates have evidence of primary and secondary prevention of pancreatitis.¹¹ When a patient is intolerant of fibrates, consider a different option to reduce the TG level—eg, fish oil supplementation.

CASE 1

Recommendation for Mr. M: Therapeutic lifestyle changes to address moderate HTG.

Continue to: Because Mr. M's...

Because Mr. M’s 10-yr ASCVD risk is < 5%, statin therapy is not indicated for risk reduction. With a fasting TG value < 500 mg/dL, he is not considered at increased risk of pancreatitis.

CASE 2

Recommendations for Ms. F:

• Therapeutic lifestyle changes to address severe HTG. Ms. F agrees to wean off alcohol; add relaxation exercises before bedtime; do aerobic exercise 30 minutes a day, 3 times a week; decrease dietary carbohydrates daily by cutting portion size in half; and increase intake of fresh vegetables and lean protein.
• Treatment with fenofibrate to reduce the risk of pancreatitis. Ms. F begins a trial. Six months into treatment, she has reduced her BMI to 24 and the TG level has fallen to < 500 mg/dL. Ms. F also reports that she is sleeping well, believes that she is able to manage her infrequent anxiety, and is now in a routine that feels sustainable.

You congratulate Ms. F on her success and support her decision to undertake a trial of discontinuing fenofibrate, after shared decision-making about the risks and potential benefits of doing so.

Summing up: Management of HTG

Keep these treatment strategy highlights in mind:

• Lifestyle modification with a low-fat, low-carbohydrate diet, avoidance of alcohol, and moderate-intensity exercise is the mainstay of HTG management.
• The latest evidence supports that (1) HTG is a risk-enhancing factor for ­ASCVD and (2) statin therapy is recommended for patients who have HTG and an ASCVD risk > 7.5%.
• When the TG level remains elevated despite statin therapy and lifestyle changes, an omega-3 ethyl ester can be used as an adjunct for additional atherogenic risk reduction.
• For severe HTG, a regimen of therapeutic lifestyle changes plus a fibrate is recommended to reduce the risk and recurrence of pancreatitis.^1,24

* In comparison, a normal level of triglycerides is < 175 mg/dL; a moderately elevated level, measured in a fasting or nonfasting state, 175-499 mg/dL; and a very severely elevated level, ≥ 2000 mg/dL.²

CORRESPONDENCE
Ashwini Kamath Mulki, MD, Family Health Center, 1730 Chew Street, Allentown, PA 18104; [email protected].

CASE 1

Tyler M, age 40, otherwise healthy, and with a body mass index (BMI) of 30, presents to your office for his annual physical examination. He does not have a history of alcohol or tobacco use.

Mr. M’s obesity raises concern about metabolic syndrome, which warrants evaluation for hypertriglyceridemia (HTG). You offer him lipid testing to estimate his risk of atherosclerotic cardiovascular disease (ASCVD).

The only abnormal value on the lipid panel is a triglyceride (TG) level of 264 mg/dL (normal, < 175 mg/dL). Mr. M’s 10-yr ASCVD risk is determined to be < 5%.

What, if any, intervention would be triggered by the finding of moderate HTG?

© ALICIA BUELOW

CASE 2

Alicia F, age 30, with a BMI of 28 and ASCVD risk < 7.5%, comes to the clinic for evaluation of anxiety and insomnia. She reports eating a high-carbohydrate diet and drinking 3 to 5 alcoholic beverages nightly to help her sleep.

Ms. F’s daily alcohol use prompts evaluation for HTG. Results show a TG level of 1300 mg/dL and a high-density lipoprotein (HDL) level of 25 mg/dL (healthy HDL levels: adult females, ≥ 50 mg/dL; adult males, ≥ 40 mg/dL). Other test results are normal, except for elevated transaminase levels (just under twice normal).

What, if any, action would be prompted by the patient’s severe HTG and below-normal HDL level?

Continue to: How HTG is defined

 

 

How HTG is defined: Causes, cutoffs, signs

HTG is most commonly caused by obesity and a sedentary lifestyle; certain associated comorbid medical conditions can also be a precipitant (Table 1^1,2). Because the condition is a result of polygenic phenotypic expression, even a genetically low-risk patient can present with HTG when exposed to certain medical conditions and environmental causes.

Primary HTG (genetic or familial) is rare. Genetic testing may be considered for patients with TG > 1000 mg/dL (severely elevated TG = 500 to 1999 mg/dL, measured in fasting state*) or a family history of early ASCVD (TABLE 1^1,2).^2,3

Even a genetically low-risk patient can present with hypertriglyceridemia when exposed to certain medical conditions and environmental causes.

Typically, HTG is asymptomatic. Xanthelasmas, xanthomas, and lipemia retinalis are found in hereditary disorders of elevated TGs. Occasionally, HTG manifests as chylomicronemia syndrome, characterized by recurrent abdominal pain, nausea, vomiting, and, in severe HTG, pancreatitis.³

Fine points of TG measurement

Triglycerides are a component of a complete lipid profile, which also includes total cholesterol, calculated low-density lipoprotein (LDL-C), and HDL.⁴ As in both case vignettes, detection of HTG is often incidental, when a lipid profile is ordered to evaluate the risk of ASCVD. (Of note, for people older than 20 years, the US Preventive Services Task Force no longer addresses the question, “Which population should be screened for dyslipidemia?” Instead, current recommendations answer the question, “For which population should statin therapy be prescribed?”⁵)

Effect on ASCVD risk assessment. TG levels are known to vary, depending on fasting or nonfasting status, with lower levels reported when fasting. An elevated TG level can lead to inaccurate calculation of LDL when using the Friedewald formula⁶:

LDL = total cholesterol – (triglycerides/5) – HDL

Continue to: The purpose of testing...

The purpose of testing lipids in a fasting state (> 9 hours) is to minimize the effects of an elevated TG level on the calculated LDL. In severe HTG, beta-quantitation by ultracentrifugation and electrophoresis can be performed to determine the LDL level directly.

Advantage of nonfasting measurement. When LDL-C is not a concern, there is, in fact, value in measuring TGs in the nonfasting state. Why? Because a nonfasting TG level is a better indicator of a patient’s average TG status: Studies have found a higher ASCVD risk in the setting of an elevated postprandial TG level accompanied by a low HDL level.⁷

Studies have found a higher ASCVD risk in the setting of an elevated postprandial triglyceride level accompanied by a low HDL level.

The Copenhagen City Heart Study identified postprandial HTG as an independent risk factor for atherogenicity, even in the setting of a normal fasting TG level.⁸ American Association of Clinical Endocrinologists and American College of Endocrinology guidelines endorse testing the nonfasting TG level when the fasting TG level is elevated in a lipid profile; if the nonfasting TG level is > 500 mg/dL, evaluation for secondary causes is warranted^9,10 (Table 1^1,2).

In a practical sense, therefore, offering patients nonfasting lipid testing allows more people to obtain access to timely care.

Pancreatitis. Acute pancreatitis commonly prompts an evaluation for HTG. The risk of acute pancreatitis in the general population is 0.04%, but that risk increases to 8% to 31% for a person with HTG.¹¹ Incidence when the TG level is > 500 mg/dL is thought to be increased because chylomicrons, acting as a TG carrier in the bloodstream, are responsible for pancreatitis.³ Treating HTG can reduce both the risk and recurrence of pancreatitis^12,13; given that the postprandial TG level can change rapidly from severe to very severe (> 2000 mg/dL), multiple guidelines recommend pharmacotherapy to a TG goal of < 500-1000 mg/dL.^1,9,13,14

Continue to: An ASCVD risk-HTG connection?

An ASCVD risk–HTG connection? In the population already at higher risk of ASCVD (> 7.5%), HTG is recognized as a risk-enhancing factor because of its atherogenic potential (Table 2²); however, there is insufficient evidence that TGs have a role as an independent risk factor for ASCVD. In a population-based study of 58,000 people, 40 to 65 years of age, conducted at Copenhagen [Denmark] University Hospital, investigators found that those who did not meet criteria for statin treatment and who had a TG level > 264 mg/dL had a 10-year risk of a major adverse cardiovascular event similar to that of people who did meet criteria for statin therapy.¹⁵

The FIELD (Fenofibrate Intervention and Event Lowering in Diabetes) and AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides and Impact on Global Health Outcomes) studies, among others, have failed to show a significant reduction in coronary events by treating HTG.¹⁰

That said, it’s worth considering the findings of other trials:

• In the PROVE IT-TIMI 22 (Pravastatin or Atorvastatin Evaluation and Infection Therapy–Thrombolysis in Myocardial Infarction 22) trial, an overall 28% reduction in endpoint events (myocardial infarction, acute coronary syndrome) was seen with high-intensity statin therapy, compared to moderate-intensity therapy.¹⁰ However, there was a sizeable residual risk identified that was theorized by investigators to be associated with high non-HDL lipoproteins, including TGs.
• A 2016 study in Israel, in which 22 years of data on 15,355 patients with established ASCVD were studied, revealed that elevated TGs are associated with an increased long-term mortality risk that is independent of the HDL level.¹⁶
• A cross-sectional study, nested in the prospective Copenhagen City Heart Study, demonstrated that HTG is associated with an increase in ischemic stroke events.¹⁷

Treatment

Therapeutic lifestyle changes

Changes in lifestyle are the foundation of management of, and recommended first-line treatment for, all patients with HTG. Patients with a moderately elevated TG level (175-499 mg/dL, measured in a fasting or nonfasting state) can be treated with therapeutic lifestyle changes alone^1,2; a trial of 3 to 6 months (see specific interventions below) is recommended before considering adding medications.¹⁰

Weight loss. There is a strong association between BMI > 30 and HTG. Visceral adiposity is a much more significant risk than subcutaneous adipose tissue. Although weight loss to an ideal range is recommended, even a 10% to 15% reduction in an obese patient can reduce the TG level by 20%. A combination of moderate-intensity exercise and healthy eating habits appears to assist best with this intervention.¹⁸

Continue to: Exercise

Exercise. Thirty minutes a day of moderate-intensity exercise is associated with a significant drop in postprandial TG. This benefit can last as long as 3 days, suggesting a goal of at least 3 days a week of an active lifestyle. Such a program can include intermittent aerobics or mild resistance exercise.¹⁹

Healthy eating habits. The difference between a low-fat, high-carbohydrate diet and a high-fat, low-carbohydrate diet is less important than the overall benefit of weight loss from either of these diets. Complex carbohydrates are recommended over simple carbohydrates. A low-carbohydrate diet in a patient with diabetes has been demonstrated to improve the TG level, irrespective of weight change.²⁰

The risk of acute pancreatitis in the general population is 0.04%, but that risk increases to 8% to 31% for a person with hypertriglyceridemia

A Mediterranean diet can reduce the TG level by 10% to 15%, and is recommended over a low-fat diet.¹⁴ (This diet generally includes a high intake of extra virgin olive oil; leafy green vegetables, fruits, cereals, nuts, and legumes; moderate intake of fish and other meat, dairy products, and red wine; and low intake of eggs and sugars.) The American Heart Association recommends 2 servings of fatty fish a week for its omega-3 oil benefit of reducing ASCVD risk. Working with a registered dietician to assist with lipid lowering can produce better results than physician-only instruction on healthy eating.⁹

Alcohol consumption. Complete cessation or moderation of alcohol consumption (1 drink a day/women and 2 drinks a day/men*) is recommended to improve HTG. Among secondary factors, alcohol is commonly the cause of an unusually high elevation of the TG level.¹⁴

Smoking cessation. Smoking increases the postprandial TG level.¹⁰ Complete cessation for just 1 year can reduce a person’s ASCVD risk by approximately 50%. However, in a clinical trial,²² smoking cessation did not significantly decrease the TG level—possibly because of the counterbalancing effect of weight gain following cessation.

Continue to: Medical therapy

 

 

Medical therapy

In addition to lifestyle modification, medications are recommended to reduce atherogenic potential in patients with moderate or severe HTG and an ASCVD risk > 7.5% (Table 3^4,13,18,23 and Table 4^2,9). Before initiating medical therapy, we recommend that you engage in shared decision-making with patients to (1) delineate treatment goals and (2) describe the risks and benefits of medications for HTG.²

Statins. These agents are recommended first-line therapy for reducing ASCVD risk.² If the TG level remains elevated (> 500 mg/dL) after statin therapy is maximized, an additional agent can be added—ie, a fibrate or fish oil (see below).

Fibrates. If a fibrate is used as an add-on to a statin, fenofibrate is preferred over gemfibrozil because it presents less risk of the severe myopathy that can develop when taken with a statin.¹³ Despite the effectiveness of fibrates in reducing the TG level, these drugs have not been shown to reduce overall mortality.²⁴ The evidence on improved cardiovascular outcomes is subgroup-specific (ie, prevention of a second myocardial infarction in the setting of optimal statin use and elevated non-HDL lipoproteins).¹² A study demonstrated that gemfibrozil reduced the incidence of transient ischemic attack and stroke in a subgroup of male US veterans who had coronary artery disease and a low HDL level.²⁵

Fish oil. The omega-3 ethyl esters eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), available as EPA alone or in combination with DHA, do not interact with statins and are tolerated well. They reduce hypertriglyceridemia by 20% to 50%.¹³

Eicosapentaenoic acid, EPA plus DHA, and icosapent ethyl, an ethyl ester product containing EPA without DHA, are approved by the US Food and Drug Administration for HTG > 500 mg/dL, at a dosage of 2000 mg twice daily. In the REDUCE-IT trial, adding icosapent ethyl, 2 g twice daily, to a statin in patients with HTG was associated with fewer ischemic events, compared to placebo.^23,26

Continue to: Fish oil formulations...

Fish oil formulations can inhibit platelet aggregation and increase bleeding time in otherwise healthy people; however, such episodes are minor and nonfatal. Patients on anticoagulation or an antiplatelet medication should be monitored periodically for bleeding events, although recommendations on how to monitor aren’t specified in a recent advisory by the American Heart Association.²³

There is a strong association between a BMI > 30 and hypertriglyceridemia.

DHA was thought to increase the LDL-C levels and, by doing so, potentially counterbalance benefit,^23,27 but most studies have failed to reproduce this effect.²⁸ Instead, studies have shown minimal elevation of LDL-C when DHA is used to treat HTG.^23,27

Niacin. At a dosage of 500-2000 mg/dL, niacin lowers the TG level by 10% to 30%. It also increases HDL by 10% to 40% and lowers LDL by 5% to 20%.¹³

Considerations in pancreatitis. For management of recurrent pancreatitis in patients with HTG, lifestyle modification remains the mainstay of treatment. When medication is considered for persistent severe HTG, fibrates have evidence of primary and secondary prevention of pancreatitis.¹¹ When a patient is intolerant of fibrates, consider a different option to reduce the TG level—eg, fish oil supplementation.

CASE 1

Recommendation for Mr. M: Therapeutic lifestyle changes to address moderate HTG.

Continue to: Because Mr. M's...

Because Mr. M’s 10-yr ASCVD risk is < 5%, statin therapy is not indicated for risk reduction. With a fasting TG value < 500 mg/dL, he is not considered at increased risk of pancreatitis.

CASE 2

Recommendations for Ms. F:

• Therapeutic lifestyle changes to address severe HTG. Ms. F agrees to wean off alcohol; add relaxation exercises before bedtime; do aerobic exercise 30 minutes a day, 3 times a week; decrease dietary carbohydrates daily by cutting portion size in half; and increase intake of fresh vegetables and lean protein.
• Treatment with fenofibrate to reduce the risk of pancreatitis. Ms. F begins a trial. Six months into treatment, she has reduced her BMI to 24 and the TG level has fallen to < 500 mg/dL. Ms. F also reports that she is sleeping well, believes that she is able to manage her infrequent anxiety, and is now in a routine that feels sustainable.

You congratulate Ms. F on her success and support her decision to undertake a trial of discontinuing fenofibrate, after shared decision-making about the risks and potential benefits of doing so.

Summing up: Management of HTG

Keep these treatment strategy highlights in mind:

• Lifestyle modification with a low-fat, low-carbohydrate diet, avoidance of alcohol, and moderate-intensity exercise is the mainstay of HTG management.
• The latest evidence supports that (1) HTG is a risk-enhancing factor for ­ASCVD and (2) statin therapy is recommended for patients who have HTG and an ASCVD risk > 7.5%.
• When the TG level remains elevated despite statin therapy and lifestyle changes, an omega-3 ethyl ester can be used as an adjunct for additional atherogenic risk reduction.
• For severe HTG, a regimen of therapeutic lifestyle changes plus a fibrate is recommended to reduce the risk and recurrence of pancreatitis.^1,24

* In comparison, a normal level of triglycerides is < 175 mg/dL; a moderately elevated level, measured in a fasting or nonfasting state, 175-499 mg/dL; and a very severely elevated level, ≥ 2000 mg/dL.²

CORRESPONDENCE
Ashwini Kamath Mulki, MD, Family Health Center, 1730 Chew Street, Allentown, PA 18104; [email protected].

Based on the clinical appearance of hyperpigmented and hypopigmented scaly plaques in sun-exposed facial areas (with associated scarring and follicular plugging in affected lesions), the patient was given a diagnosis of discoid lupus erythematosus. The diagnosis was confirmed with a punch biopsy that showed characteristic interface dermatitis with superficial and deep perivascular and peri-adnexal lymphocytes. Direct immunofluorescence showed a band of C3 at the dermo-epidermal junction, consistent with various forms of cutaneous lupus.

A review of systems was negative for signs of systemic disease, including a lack of weakness, joint pain/swelling, fever, or known blood clots. An antinuclear antibody panel was also negative, largely excluding systemic disease.

Discoid lupus erythematosus is a form of cutaneous lupus. Patients often are genetically predisposed to autoimmune disease, and disease may be triggered by sun exposure. Up to 80% of patients develop lesions that are limited to the head and neck. Up to 25% of patients develop systemic lupus erythematosus that may occur months—or even decades—after the initial diagnosis. Lesions may lead to longstanding scars; this cannot always be prevented.

Two- to 3-week trials of topical potent or superpotent steroids applied to affected plaques may lead to clearance. Additionally, lesions may be treated with intralesional triamcinolone 3 mg/mL to 10 mg/mL and repeated every 3 to 4 weeks. Systemic therapies include hydroxychloroquine, chloroquine, retinoids, steroid sparing immunomodulators, and rarely prednisone.

This patient tolerated topical therapy well and though some scars remained, he was able to control flares with 2- to 3-week courses of clobetasol 0.05% twice daily. He is followed 2 to 3 times annually and has not developed signs or serologic findings of systemic disease over several years.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

Based on the clinical appearance of hyperpigmented and hypopigmented scaly plaques in sun-exposed facial areas (with associated scarring and follicular plugging in affected lesions), the patient was given a diagnosis of discoid lupus erythematosus. The diagnosis was confirmed with a punch biopsy that showed characteristic interface dermatitis with superficial and deep perivascular and peri-adnexal lymphocytes. Direct immunofluorescence showed a band of C3 at the dermo-epidermal junction, consistent with various forms of cutaneous lupus.

A review of systems was negative for signs of systemic disease, including a lack of weakness, joint pain/swelling, fever, or known blood clots. An antinuclear antibody panel was also negative, largely excluding systemic disease.

Discoid lupus erythematosus is a form of cutaneous lupus. Patients often are genetically predisposed to autoimmune disease, and disease may be triggered by sun exposure. Up to 80% of patients develop lesions that are limited to the head and neck. Up to 25% of patients develop systemic lupus erythematosus that may occur months—or even decades—after the initial diagnosis. Lesions may lead to longstanding scars; this cannot always be prevented.

Two- to 3-week trials of topical potent or superpotent steroids applied to affected plaques may lead to clearance. Additionally, lesions may be treated with intralesional triamcinolone 3 mg/mL to 10 mg/mL and repeated every 3 to 4 weeks. Systemic therapies include hydroxychloroquine, chloroquine, retinoids, steroid sparing immunomodulators, and rarely prednisone.

This patient tolerated topical therapy well and though some scars remained, he was able to control flares with 2- to 3-week courses of clobetasol 0.05% twice daily. He is followed 2 to 3 times annually and has not developed signs or serologic findings of systemic disease over several years.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

Based on the clinical appearance of hyperpigmented and hypopigmented scaly plaques in sun-exposed facial areas (with associated scarring and follicular plugging in affected lesions), the patient was given a diagnosis of discoid lupus erythematosus. The diagnosis was confirmed with a punch biopsy that showed characteristic interface dermatitis with superficial and deep perivascular and peri-adnexal lymphocytes. Direct immunofluorescence showed a band of C3 at the dermo-epidermal junction, consistent with various forms of cutaneous lupus.

A review of systems was negative for signs of systemic disease, including a lack of weakness, joint pain/swelling, fever, or known blood clots. An antinuclear antibody panel was also negative, largely excluding systemic disease.

Discoid lupus erythematosus is a form of cutaneous lupus. Patients often are genetically predisposed to autoimmune disease, and disease may be triggered by sun exposure. Up to 80% of patients develop lesions that are limited to the head and neck. Up to 25% of patients develop systemic lupus erythematosus that may occur months—or even decades—after the initial diagnosis. Lesions may lead to longstanding scars; this cannot always be prevented.

Two- to 3-week trials of topical potent or superpotent steroids applied to affected plaques may lead to clearance. Additionally, lesions may be treated with intralesional triamcinolone 3 mg/mL to 10 mg/mL and repeated every 3 to 4 weeks. Systemic therapies include hydroxychloroquine, chloroquine, retinoids, steroid sparing immunomodulators, and rarely prednisone.

This patient tolerated topical therapy well and though some scars remained, he was able to control flares with 2- to 3-week courses of clobetasol 0.05% twice daily. He is followed 2 to 3 times annually and has not developed signs or serologic findings of systemic disease over several years.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

The papules were clinically consistent with Kaposi sarcoma (KS) and confirmed with a biopsy from the buccal mucosa. The patient had not been given a diagnosis of human immunodeficiency virus (HIV) prior to this presentation. However, the physician confirmed the diagnosis with RNA titers. A CD4 count < 40 cells/mm³ (reference range, 500-1200 cells/mm³) pointed to her progression to AIDS. A chest X-ray revealed multiple nodules; a subsequent biopsy indicated that they were consistent with KS.

KS is a low-grade tumor of vascular origin associated with human herpesvirus-8 (HHV-8). It most often presents on the skin as flat to raised pink to deep purple lesions. It can manifest in the oral mucosa, viscera, and other organs, which can portend a worse prognosis because of the risks associated with bleeding and organ perforation.

There are 4 types of KS.

• Classic KS occurs most often in elderly men of Mediterranean descent.
• HIV-associated KS can occur at any time during HIV infection but is more common as CD4 counts fall. HIV-associated KS increased in frequency dramatically in the United States during the early years of the HIV pandemic prior to effective antiretroviral therapy (ART).
• Endemic KS occurs in equatorial Africa, where there is a natural increased transmission rate of HHV-8.
• Iatrogenic KS can occur following treatment with immunosuppressive therapies.

Our patient was admitted to the Infectious Disease Service and given ART. Chemotherapy was discussed (and sometimes is warranted in extensive visceral disease) but the patient and her specialists opted for ART alone. In addition to ART, she was started on daily trimethoprim-sulfamethoxazole for pneumocystis prophylaxis.

At 6 months’ follow-up with Infectious Disease, the patient’s oral lesions resolved, CD4 count increased above 200 cells/mm³, and HIV RNA titers fell.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

The papules were clinically consistent with Kaposi sarcoma (KS) and confirmed with a biopsy from the buccal mucosa. The patient had not been given a diagnosis of human immunodeficiency virus (HIV) prior to this presentation. However, the physician confirmed the diagnosis with RNA titers. A CD4 count < 40 cells/mm³ (reference range, 500-1200 cells/mm³) pointed to her progression to AIDS. A chest X-ray revealed multiple nodules; a subsequent biopsy indicated that they were consistent with KS.

KS is a low-grade tumor of vascular origin associated with human herpesvirus-8 (HHV-8). It most often presents on the skin as flat to raised pink to deep purple lesions. It can manifest in the oral mucosa, viscera, and other organs, which can portend a worse prognosis because of the risks associated with bleeding and organ perforation.

There are 4 types of KS.

• Classic KS occurs most often in elderly men of Mediterranean descent.
• HIV-associated KS can occur at any time during HIV infection but is more common as CD4 counts fall. HIV-associated KS increased in frequency dramatically in the United States during the early years of the HIV pandemic prior to effective antiretroviral therapy (ART).
• Endemic KS occurs in equatorial Africa, where there is a natural increased transmission rate of HHV-8.
• Iatrogenic KS can occur following treatment with immunosuppressive therapies.

Our patient was admitted to the Infectious Disease Service and given ART. Chemotherapy was discussed (and sometimes is warranted in extensive visceral disease) but the patient and her specialists opted for ART alone. In addition to ART, she was started on daily trimethoprim-sulfamethoxazole for pneumocystis prophylaxis.

At 6 months’ follow-up with Infectious Disease, the patient’s oral lesions resolved, CD4 count increased above 200 cells/mm³, and HIV RNA titers fell.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

The papules were clinically consistent with Kaposi sarcoma (KS) and confirmed with a biopsy from the buccal mucosa. The patient had not been given a diagnosis of human immunodeficiency virus (HIV) prior to this presentation. However, the physician confirmed the diagnosis with RNA titers. A CD4 count < 40 cells/mm³ (reference range, 500-1200 cells/mm³) pointed to her progression to AIDS. A chest X-ray revealed multiple nodules; a subsequent biopsy indicated that they were consistent with KS.

KS is a low-grade tumor of vascular origin associated with human herpesvirus-8 (HHV-8). It most often presents on the skin as flat to raised pink to deep purple lesions. It can manifest in the oral mucosa, viscera, and other organs, which can portend a worse prognosis because of the risks associated with bleeding and organ perforation.

There are 4 types of KS.

• Classic KS occurs most often in elderly men of Mediterranean descent.
• HIV-associated KS can occur at any time during HIV infection but is more common as CD4 counts fall. HIV-associated KS increased in frequency dramatically in the United States during the early years of the HIV pandemic prior to effective antiretroviral therapy (ART).
• Endemic KS occurs in equatorial Africa, where there is a natural increased transmission rate of HHV-8.
• Iatrogenic KS can occur following treatment with immunosuppressive therapies.

Our patient was admitted to the Infectious Disease Service and given ART. Chemotherapy was discussed (and sometimes is warranted in extensive visceral disease) but the patient and her specialists opted for ART alone. In addition to ART, she was started on daily trimethoprim-sulfamethoxazole for pneumocystis prophylaxis.

At 6 months’ follow-up with Infectious Disease, the patient’s oral lesions resolved, CD4 count increased above 200 cells/mm³, and HIV RNA titers fell.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

This patient had prurigo nodularis (PN). The diagnosis usually is made clinically by the appearance of the lesions and the cycle of severe pruritus and scratching. In this case, the patient had acutely excoriated lesions in addition to more chronic lesions that had become hyperpigmented nodules. The distribution pattern on his back was typical and highlighted the clinical course of PN. There were no lesions present where the patient was unable to scratch; however, lesions were present where he could reach, hence the term Picker’s nodules. Often, these patients have a history of atopic dermatitis, and anxiety may play a role in patients nervously scratching the lesions.

Biopsy is indicated if there is suspicion of bullous pemphigoid or cutaneous T-cell lymphoma. Pathology of PN shows increased density of nerve fibers in the dermis along with an increased number of T cells, mast cells, and eosinophilic granulocytes. Most patients do not require biopsy unless the diagnosis is in doubt.

Treatment can be difficult due to the severe pruritis and subsequent scratching that appears to prolong the chronic cycle of inflammation. Daily use of nonsedating antihistamines (eg, loratadine, cetirizine) may help reduce pruritus and break the cycle. Sedating antihistamines (eg, diphenhydramine, hydroxyzine) can be used cautiously at bedtime; cotton gloves worn while sleeping may reduce nocturnal scratching and excoriations.

Topical steroids (eg, triamcinolone, betamethasone) can reduce the itching and local inflammation. Emollients can help with associated dyshidrosis and eczema, if present.

Second line therapies include topical calcineurin inhibitors (eg, tacrolimus, pimecrolimus), calcipotriene, and narrow beam UVB therapy.

This patient had done reasonably well with cetirizine and triamcinolone in the past, so treatment was restarted. He was counseled regarding the nature and chronicity of his PN and told that if he could achieve symptom control and stop scratching the lesions, his condition might resolve.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

This patient had prurigo nodularis (PN). The diagnosis usually is made clinically by the appearance of the lesions and the cycle of severe pruritus and scratching. In this case, the patient had acutely excoriated lesions in addition to more chronic lesions that had become hyperpigmented nodules. The distribution pattern on his back was typical and highlighted the clinical course of PN. There were no lesions present where the patient was unable to scratch; however, lesions were present where he could reach, hence the term Picker’s nodules. Often, these patients have a history of atopic dermatitis, and anxiety may play a role in patients nervously scratching the lesions.

Biopsy is indicated if there is suspicion of bullous pemphigoid or cutaneous T-cell lymphoma. Pathology of PN shows increased density of nerve fibers in the dermis along with an increased number of T cells, mast cells, and eosinophilic granulocytes. Most patients do not require biopsy unless the diagnosis is in doubt.

Treatment can be difficult due to the severe pruritis and subsequent scratching that appears to prolong the chronic cycle of inflammation. Daily use of nonsedating antihistamines (eg, loratadine, cetirizine) may help reduce pruritus and break the cycle. Sedating antihistamines (eg, diphenhydramine, hydroxyzine) can be used cautiously at bedtime; cotton gloves worn while sleeping may reduce nocturnal scratching and excoriations.

Topical steroids (eg, triamcinolone, betamethasone) can reduce the itching and local inflammation. Emollients can help with associated dyshidrosis and eczema, if present.

Second line therapies include topical calcineurin inhibitors (eg, tacrolimus, pimecrolimus), calcipotriene, and narrow beam UVB therapy.

This patient had done reasonably well with cetirizine and triamcinolone in the past, so treatment was restarted. He was counseled regarding the nature and chronicity of his PN and told that if he could achieve symptom control and stop scratching the lesions, his condition might resolve.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

This patient had prurigo nodularis (PN). The diagnosis usually is made clinically by the appearance of the lesions and the cycle of severe pruritus and scratching. In this case, the patient had acutely excoriated lesions in addition to more chronic lesions that had become hyperpigmented nodules. The distribution pattern on his back was typical and highlighted the clinical course of PN. There were no lesions present where the patient was unable to scratch; however, lesions were present where he could reach, hence the term Picker’s nodules. Often, these patients have a history of atopic dermatitis, and anxiety may play a role in patients nervously scratching the lesions.

Biopsy is indicated if there is suspicion of bullous pemphigoid or cutaneous T-cell lymphoma. Pathology of PN shows increased density of nerve fibers in the dermis along with an increased number of T cells, mast cells, and eosinophilic granulocytes. Most patients do not require biopsy unless the diagnosis is in doubt.

Treatment can be difficult due to the severe pruritis and subsequent scratching that appears to prolong the chronic cycle of inflammation. Daily use of nonsedating antihistamines (eg, loratadine, cetirizine) may help reduce pruritus and break the cycle. Sedating antihistamines (eg, diphenhydramine, hydroxyzine) can be used cautiously at bedtime; cotton gloves worn while sleeping may reduce nocturnal scratching and excoriations.

Topical steroids (eg, triamcinolone, betamethasone) can reduce the itching and local inflammation. Emollients can help with associated dyshidrosis and eczema, if present.

Second line therapies include topical calcineurin inhibitors (eg, tacrolimus, pimecrolimus), calcipotriene, and narrow beam UVB therapy.

This patient had done reasonably well with cetirizine and triamcinolone in the past, so treatment was restarted. He was counseled regarding the nature and chronicity of his PN and told that if he could achieve symptom control and stop scratching the lesions, his condition might resolve.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

Vidyard Video

This transcript has been edited for clarity.

Gary S. Ferenchick, MD, MS: I'm Gary Ferenchick with Hannah Ferenchick, who has agreed to join us to talk about the PPE and decontamination processes she's using. Why don't you introduce yourself?

Hannah R.B. Ferenchick, MD: I am Hannah Ferenchick. I'm an ER physician and medical intensivist. I split my time between the medical ICU and the emergency department at Detroit Medical Center.

PPE Routine at the Hospital

Dr Gary Ferenchick: You've developed your own PPE and decontamination routines. It's about protecting yourself at work but also about protecting your loved ones by not carrying the virus home. Could you walk us through it? I'll show it on the screen.

Dr Hannah Ferenchick: At work I wear scrubs, and I try to minimize any additional clothing. I don't wear a jacket over my scrubs, and I don't wear any T-shirts under my scrubs. If I'm going to be in a situation that might involve exposure to patient secretions or bodily fluids, then I also wear shoe covers.

Because so many of our patients are infected and we may be called upon at any time to do an aerosol-generating procedure, in the ED we have all taken to wearing N95 masks for our entire shift. I wear a fitted N95 mask. I cover that with a surgical mask.

We are anticipating N95 shortages because our use of the masks has increased exponentially. Every hospital has to think about how to protect their healthcare workers while conserving PPE. We cover the N95 mask with a surgical mask, so that if there is any soiling or droplets reaching the mask, we are able to change the surgical mask and continue to use the same N95.

In addition, eye protection is important. Generally throughout the shift I wear my own goggles. If I'm going to be involved in any procedure with the potential for aerosolization (intubation, performing CPR, bronchoscopy) then I wear a creation of my own, which is a welder's shield.

Many of our providers have chosen to use their own equipment, although we are still able to use hospital-provided equipment. There is probably no difference in effectiveness between these devices.

Cell Phones and Stethoscopes

I carry a personal cell phone at work (which I often use to look things up, use the calculator, and for other purposes), and I'm cognizant that when I touch it, I am potentially transmitting pathogens to my phone or its cover. So I've taken to keeping my phone in a plastic sandwich bag, which I disinfect a couple of times throughout the shift. The phone still works normally.

After my shift, in my "decontamination phase," I remove the phone from the plastic bag and disinfect the phone again.

I try to avoid bringing objects into the vicinity of the patient. That's different from my normal routine—I usually like to write down what the patient has told me—but unfortunately, carrying pen and paper or a clipboard into a patient's room is not feasible at this point. During this time, I've also avoided using my personal stethoscope.

There's also transmission risk associated with shared equipment. We share hospital-provided phones and they must be disinfected. We are each disinfecting our own workspaces: computer, keyboard, mouse, and countertop.

Obviously you are trying to minimize any contact with your mouth or face. You don't want to rub your eyes, touch your nose, or eat anything with your hands while you are at work. The assumption is that you are doing very frequent hand hygiene.

Decontamination Routine

One of our concerns as healthcare providers is the possibility that we could, either asymptomatically or through the objects that we use at work, be bringing the disease home. We want to protect the people who may be at higher risk just because they live with a healthcare provider. These are the decontamination practices I've developed for my own situation, taken from best practices and suggestions from others.

I remove my dirty scrubs and leave them at work, and I change into a clean pair of scrubs or clean clothes. I disinfect any inanimate objects that my hands may have touched during the shift using alcohol, sanitizer wipes, bleach wipes, or hospital-grade chemical wipes.

To keep those objects clean after disinfecting, I place them in clean plastic bags away from other objects (eg, a wallet or purse) that may not be easy to disinfect. Then I store those bags in the trunk of my car for my next shift, so I'm not taking them into my home.

I also change my shoes, leaving my work shoes in the trunk of my car, and wear another pair of shoes into the house.

When I get home, I basically do everything again. I disinfect my phone, I wash my hands, and I shower immediately. At that point, I consider myself sufficiently "disinfected."

Gary S. Ferenchick, MD, MS, is a family physician and professor in the Department of Medicine at Michigan State University in East Lansing, Michigan. His daughter, Hannah R.B. Ferenchick, MD, is an assistant professor in the Department of Emergency Medicine, Division of Pulmonary & Critical Care and Sleep Medicine at Wayne State University, Detroit, Michigan, and a medical intensivist and emergency medicine physician at Detroit Medical Center.

Vidyard Video

This transcript has been edited for clarity.

Gary S. Ferenchick, MD, MS: I'm Gary Ferenchick with Hannah Ferenchick, who has agreed to join us to talk about the PPE and decontamination processes she's using. Why don't you introduce yourself?

Hannah R.B. Ferenchick, MD: I am Hannah Ferenchick. I'm an ER physician and medical intensivist. I split my time between the medical ICU and the emergency department at Detroit Medical Center.

PPE Routine at the Hospital

Dr Gary Ferenchick: You've developed your own PPE and decontamination routines. It's about protecting yourself at work but also about protecting your loved ones by not carrying the virus home. Could you walk us through it? I'll show it on the screen.

Dr Hannah Ferenchick: At work I wear scrubs, and I try to minimize any additional clothing. I don't wear a jacket over my scrubs, and I don't wear any T-shirts under my scrubs. If I'm going to be in a situation that might involve exposure to patient secretions or bodily fluids, then I also wear shoe covers.

Because so many of our patients are infected and we may be called upon at any time to do an aerosol-generating procedure, in the ED we have all taken to wearing N95 masks for our entire shift. I wear a fitted N95 mask. I cover that with a surgical mask.

We are anticipating N95 shortages because our use of the masks has increased exponentially. Every hospital has to think about how to protect their healthcare workers while conserving PPE. We cover the N95 mask with a surgical mask, so that if there is any soiling or droplets reaching the mask, we are able to change the surgical mask and continue to use the same N95.

In addition, eye protection is important. Generally throughout the shift I wear my own goggles. If I'm going to be involved in any procedure with the potential for aerosolization (intubation, performing CPR, bronchoscopy) then I wear a creation of my own, which is a welder's shield.

Many of our providers have chosen to use their own equipment, although we are still able to use hospital-provided equipment. There is probably no difference in effectiveness between these devices.

Cell Phones and Stethoscopes

I carry a personal cell phone at work (which I often use to look things up, use the calculator, and for other purposes), and I'm cognizant that when I touch it, I am potentially transmitting pathogens to my phone or its cover. So I've taken to keeping my phone in a plastic sandwich bag, which I disinfect a couple of times throughout the shift. The phone still works normally.

After my shift, in my "decontamination phase," I remove the phone from the plastic bag and disinfect the phone again.

I try to avoid bringing objects into the vicinity of the patient. That's different from my normal routine—I usually like to write down what the patient has told me—but unfortunately, carrying pen and paper or a clipboard into a patient's room is not feasible at this point. During this time, I've also avoided using my personal stethoscope.

There's also transmission risk associated with shared equipment. We share hospital-provided phones and they must be disinfected. We are each disinfecting our own workspaces: computer, keyboard, mouse, and countertop.

Obviously you are trying to minimize any contact with your mouth or face. You don't want to rub your eyes, touch your nose, or eat anything with your hands while you are at work. The assumption is that you are doing very frequent hand hygiene.

Decontamination Routine

One of our concerns as healthcare providers is the possibility that we could, either asymptomatically or through the objects that we use at work, be bringing the disease home. We want to protect the people who may be at higher risk just because they live with a healthcare provider. These are the decontamination practices I've developed for my own situation, taken from best practices and suggestions from others.

I remove my dirty scrubs and leave them at work, and I change into a clean pair of scrubs or clean clothes. I disinfect any inanimate objects that my hands may have touched during the shift using alcohol, sanitizer wipes, bleach wipes, or hospital-grade chemical wipes.

To keep those objects clean after disinfecting, I place them in clean plastic bags away from other objects (eg, a wallet or purse) that may not be easy to disinfect. Then I store those bags in the trunk of my car for my next shift, so I'm not taking them into my home.

I also change my shoes, leaving my work shoes in the trunk of my car, and wear another pair of shoes into the house.

When I get home, I basically do everything again. I disinfect my phone, I wash my hands, and I shower immediately. At that point, I consider myself sufficiently "disinfected."

Gary S. Ferenchick, MD, MS, is a family physician and professor in the Department of Medicine at Michigan State University in East Lansing, Michigan. His daughter, Hannah R.B. Ferenchick, MD, is an assistant professor in the Department of Emergency Medicine, Division of Pulmonary & Critical Care and Sleep Medicine at Wayne State University, Detroit, Michigan, and a medical intensivist and emergency medicine physician at Detroit Medical Center.

Vidyard Video

This transcript has been edited for clarity.

Gary S. Ferenchick, MD, MS: I'm Gary Ferenchick with Hannah Ferenchick, who has agreed to join us to talk about the PPE and decontamination processes she's using. Why don't you introduce yourself?

Hannah R.B. Ferenchick, MD: I am Hannah Ferenchick. I'm an ER physician and medical intensivist. I split my time between the medical ICU and the emergency department at Detroit Medical Center.

PPE Routine at the Hospital

Dr Gary Ferenchick: You've developed your own PPE and decontamination routines. It's about protecting yourself at work but also about protecting your loved ones by not carrying the virus home. Could you walk us through it? I'll show it on the screen.

Dr Hannah Ferenchick: At work I wear scrubs, and I try to minimize any additional clothing. I don't wear a jacket over my scrubs, and I don't wear any T-shirts under my scrubs. If I'm going to be in a situation that might involve exposure to patient secretions or bodily fluids, then I also wear shoe covers.

Because so many of our patients are infected and we may be called upon at any time to do an aerosol-generating procedure, in the ED we have all taken to wearing N95 masks for our entire shift. I wear a fitted N95 mask. I cover that with a surgical mask.

We are anticipating N95 shortages because our use of the masks has increased exponentially. Every hospital has to think about how to protect their healthcare workers while conserving PPE. We cover the N95 mask with a surgical mask, so that if there is any soiling or droplets reaching the mask, we are able to change the surgical mask and continue to use the same N95.

In addition, eye protection is important. Generally throughout the shift I wear my own goggles. If I'm going to be involved in any procedure with the potential for aerosolization (intubation, performing CPR, bronchoscopy) then I wear a creation of my own, which is a welder's shield.

Many of our providers have chosen to use their own equipment, although we are still able to use hospital-provided equipment. There is probably no difference in effectiveness between these devices.

Cell Phones and Stethoscopes

I carry a personal cell phone at work (which I often use to look things up, use the calculator, and for other purposes), and I'm cognizant that when I touch it, I am potentially transmitting pathogens to my phone or its cover. So I've taken to keeping my phone in a plastic sandwich bag, which I disinfect a couple of times throughout the shift. The phone still works normally.

After my shift, in my "decontamination phase," I remove the phone from the plastic bag and disinfect the phone again.

I try to avoid bringing objects into the vicinity of the patient. That's different from my normal routine—I usually like to write down what the patient has told me—but unfortunately, carrying pen and paper or a clipboard into a patient's room is not feasible at this point. During this time, I've also avoided using my personal stethoscope.

There's also transmission risk associated with shared equipment. We share hospital-provided phones and they must be disinfected. We are each disinfecting our own workspaces: computer, keyboard, mouse, and countertop.

Obviously you are trying to minimize any contact with your mouth or face. You don't want to rub your eyes, touch your nose, or eat anything with your hands while you are at work. The assumption is that you are doing very frequent hand hygiene.

Decontamination Routine

One of our concerns as healthcare providers is the possibility that we could, either asymptomatically or through the objects that we use at work, be bringing the disease home. We want to protect the people who may be at higher risk just because they live with a healthcare provider. These are the decontamination practices I've developed for my own situation, taken from best practices and suggestions from others.

I remove my dirty scrubs and leave them at work, and I change into a clean pair of scrubs or clean clothes. I disinfect any inanimate objects that my hands may have touched during the shift using alcohol, sanitizer wipes, bleach wipes, or hospital-grade chemical wipes.

To keep those objects clean after disinfecting, I place them in clean plastic bags away from other objects (eg, a wallet or purse) that may not be easy to disinfect. Then I store those bags in the trunk of my car for my next shift, so I'm not taking them into my home.

I also change my shoes, leaving my work shoes in the trunk of my car, and wear another pair of shoes into the house.

When I get home, I basically do everything again. I disinfect my phone, I wash my hands, and I shower immediately. At that point, I consider myself sufficiently "disinfected."

Gary S. Ferenchick, MD, MS, is a family physician and professor in the Department of Medicine at Michigan State University in East Lansing, Michigan. His daughter, Hannah R.B. Ferenchick, MD, is an assistant professor in the Department of Emergency Medicine, Division of Pulmonary & Critical Care and Sleep Medicine at Wayne State University, Detroit, Michigan, and a medical intensivist and emergency medicine physician at Detroit Medical Center.

References

1. Hepatitis C questions and answers for health professionals. Centers for Disease Control and Prevention Web site. www.cdc.gov/hepatitis/hcv/hcvfaq.htm#section1. Updated April 9, 2020. Accessed April 17, 2020.
2. Surveillance for Viral Hepatitis–United States, 2017. Centers for Disease Control and Prevention Web site. www.cdc.gov/hepatitis/statistics/2017surveillance/index.htm. Updated November 14, 2019. Accessed April 17, 2020.
3. Hepatitis C virus infection in adolescents and adults: screening. U.S. Preventive Services Task Force Web site. Published March 2, 2020. Accessed April 17, 2020.

References

1. Hepatitis C questions and answers for health professionals. Centers for Disease Control and Prevention Web site. www.cdc.gov/hepatitis/hcv/hcvfaq.htm#section1. Updated April 9, 2020. Accessed April 17, 2020.
2. Surveillance for Viral Hepatitis–United States, 2017. Centers for Disease Control and Prevention Web site. www.cdc.gov/hepatitis/statistics/2017surveillance/index.htm. Updated November 14, 2019. Accessed April 17, 2020.
3. Hepatitis C virus infection in adolescents and adults: screening. U.S. Preventive Services Task Force Web site. Published March 2, 2020. Accessed April 17, 2020.

References

1. Hepatitis C questions and answers for health professionals. Centers for Disease Control and Prevention Web site. www.cdc.gov/hepatitis/hcv/hcvfaq.htm#section1. Updated April 9, 2020. Accessed April 17, 2020.
2. Surveillance for Viral Hepatitis–United States, 2017. Centers for Disease Control and Prevention Web site. www.cdc.gov/hepatitis/statistics/2017surveillance/index.htm. Updated November 14, 2019. Accessed April 17, 2020.
3. Hepatitis C virus infection in adolescents and adults: screening. U.S. Preventive Services Task Force Web site. Published March 2, 2020. Accessed April 17, 2020.

Vidyard Video

This transcript has been edited for clarity.

Gary S. Ferenchick, MD, MS: I'm Gary Ferenchick with Hannah Ferenchick, who has agreed to join us to talk about what's going on in Detroit, and also about PPE and decontamination processes. Why don't you introduce yourself?

Hannah R.B. Ferenchick, MD: I am Hannah Ferenchick. I'm an ER physician and medical intensivist. I split my time between the medical ICU and the emergency department at Detroit Medical Center.

Dr Gary Ferenchick: We were talking earlier about some of the not-well-described clinical scenarios that patients with definitive COVID might present with. One of these was the idea of "silent hypoxemia." Could you describe that?

Dr Hannah Ferenchick: Silent hypoxemia is being described in many of these COVID patients. That means the patient is very hypoxemic—they may have an oxygen saturation of about 85% on room air, but clinically they look very comfortable—they are not dyspneic or tachypneic and may not even verbalize a significant sense of shortness of breath. It's not every patient, but it has been interesting to see patients sitting there looking fairly normal, with a resting oxygen saturation much lower than you would expect for someone who doesn't have underlying pulmonary disease or other symptoms.

Dr Gary Ferenchick: What abnormalities are you seeing on standard or not-so-standard lab tests?

Dr Hannah Ferenchick: Some of the characteristic lab findings we are seeing are lymphopenia and elevated inflammatory markers (eg, CRP). A couple of other atypical findings seem to be specific for COVID—elevated LDH, ferritin, CPK, and procalcitonin levels. Some of the hematologic markers that we look at—the coagulation profile studies—are also abnormal, showing thrombocytopenia and elevated D-dimer levels.

That constellation of symptoms represents more of a clinical picture. A lot of times we have only a very high clinical suspicion, because in many parts of the country it still takes days to get back a confirmatory PCR test.

Much like we do for the flu, the confirmatory test is a nasopharyngeal swab that is run for COVID/coronavirus PCR. Unfortunately the sensitivity of that test is not great. Some studies have quoted 75%-80%, so even a negative PCR does not necessarily rule out the disease, especially if you have a high clinical suspicion. A clinical suspicion is based on the typical symptoms. Many patients, although not all, will have symptoms of lower respiratory tract infection.

Dr Gary Ferenchick: So the right clinical scenario with the right hematologic/biochemical findings dramatically raises the chance that the patient has COVID?

Dr Hannah Ferenchick: Yes, and one thing that we have all been astonished by is how terrible some of these x-rays can look. There are a lot of typical findings on x-ray. Some describe them as looking like pulmonary edema, but the patient has no history of heart failure. Peripheral consolidation and ground-glass opacities are classically described. If you saw one of these x-rays from a patient with bacterial pneumonia, you would expect that patient to be very ill-appearing. Sometimes we get x-rays on patients who are sitting there, maybe mildly symptomatic on room air, and we are astonished by how terrible their x-rays look.

Unfortunately, imaging studies are something we haven't been able to rely on too much for diagnosis. Part of that is to maintain hospital safety, because to take a patient to CT scan, you have to consider the turnaround time for cleaning the CT scanner and the exposure of additional staff to a possibly infected patient. Some of those logistical considerations have limited the availability of radiography.

Gary S. Ferenchick, MD, MS, is a family physician and professor in the Department of Medicine at Michigan State University in East Lansing, Michigan. His daughter, Hannah R.B. Ferenchick, MD, is an assistant professor in the Department of Emergency Medicine, Division of Pulmonary & Critical Care and Sleep Medicine, at Wayne State University, Detroit, Michigan, and a medical intensivist and emergency medicine physician at Detroit Medical Center.

Vidyard Video

This transcript has been edited for clarity.

Gary S. Ferenchick, MD, MS: I'm Gary Ferenchick with Hannah Ferenchick, who has agreed to join us to talk about what's going on in Detroit, and also about PPE and decontamination processes. Why don't you introduce yourself?

Hannah R.B. Ferenchick, MD: I am Hannah Ferenchick. I'm an ER physician and medical intensivist. I split my time between the medical ICU and the emergency department at Detroit Medical Center.

Dr Gary Ferenchick: We were talking earlier about some of the not-well-described clinical scenarios that patients with definitive COVID might present with. One of these was the idea of "silent hypoxemia." Could you describe that?

Dr Hannah Ferenchick: Silent hypoxemia is being described in many of these COVID patients. That means the patient is very hypoxemic—they may have an oxygen saturation of about 85% on room air, but clinically they look very comfortable—they are not dyspneic or tachypneic and may not even verbalize a significant sense of shortness of breath. It's not every patient, but it has been interesting to see patients sitting there looking fairly normal, with a resting oxygen saturation much lower than you would expect for someone who doesn't have underlying pulmonary disease or other symptoms.

Dr Gary Ferenchick: What abnormalities are you seeing on standard or not-so-standard lab tests?

Dr Hannah Ferenchick: Some of the characteristic lab findings we are seeing are lymphopenia and elevated inflammatory markers (eg, CRP). A couple of other atypical findings seem to be specific for COVID—elevated LDH, ferritin, CPK, and procalcitonin levels. Some of the hematologic markers that we look at—the coagulation profile studies—are also abnormal, showing thrombocytopenia and elevated D-dimer levels.

That constellation of symptoms represents more of a clinical picture. A lot of times we have only a very high clinical suspicion, because in many parts of the country it still takes days to get back a confirmatory PCR test.

Much like we do for the flu, the confirmatory test is a nasopharyngeal swab that is run for COVID/coronavirus PCR. Unfortunately the sensitivity of that test is not great. Some studies have quoted 75%-80%, so even a negative PCR does not necessarily rule out the disease, especially if you have a high clinical suspicion. A clinical suspicion is based on the typical symptoms. Many patients, although not all, will have symptoms of lower respiratory tract infection.

Dr Gary Ferenchick: So the right clinical scenario with the right hematologic/biochemical findings dramatically raises the chance that the patient has COVID?

Dr Hannah Ferenchick: Yes, and one thing that we have all been astonished by is how terrible some of these x-rays can look. There are a lot of typical findings on x-ray. Some describe them as looking like pulmonary edema, but the patient has no history of heart failure. Peripheral consolidation and ground-glass opacities are classically described. If you saw one of these x-rays from a patient with bacterial pneumonia, you would expect that patient to be very ill-appearing. Sometimes we get x-rays on patients who are sitting there, maybe mildly symptomatic on room air, and we are astonished by how terrible their x-rays look.

Unfortunately, imaging studies are something we haven't been able to rely on too much for diagnosis. Part of that is to maintain hospital safety, because to take a patient to CT scan, you have to consider the turnaround time for cleaning the CT scanner and the exposure of additional staff to a possibly infected patient. Some of those logistical considerations have limited the availability of radiography.

Gary S. Ferenchick, MD, MS, is a family physician and professor in the Department of Medicine at Michigan State University in East Lansing, Michigan. His daughter, Hannah R.B. Ferenchick, MD, is an assistant professor in the Department of Emergency Medicine, Division of Pulmonary & Critical Care and Sleep Medicine, at Wayne State University, Detroit, Michigan, and a medical intensivist and emergency medicine physician at Detroit Medical Center.

Vidyard Video

This transcript has been edited for clarity.

Gary S. Ferenchick, MD, MS: I'm Gary Ferenchick with Hannah Ferenchick, who has agreed to join us to talk about what's going on in Detroit, and also about PPE and decontamination processes. Why don't you introduce yourself?

Hannah R.B. Ferenchick, MD: I am Hannah Ferenchick. I'm an ER physician and medical intensivist. I split my time between the medical ICU and the emergency department at Detroit Medical Center.

Dr Gary Ferenchick: We were talking earlier about some of the not-well-described clinical scenarios that patients with definitive COVID might present with. One of these was the idea of "silent hypoxemia." Could you describe that?

Dr Hannah Ferenchick: Silent hypoxemia is being described in many of these COVID patients. That means the patient is very hypoxemic—they may have an oxygen saturation of about 85% on room air, but clinically they look very comfortable—they are not dyspneic or tachypneic and may not even verbalize a significant sense of shortness of breath. It's not every patient, but it has been interesting to see patients sitting there looking fairly normal, with a resting oxygen saturation much lower than you would expect for someone who doesn't have underlying pulmonary disease or other symptoms.

Dr Gary Ferenchick: What abnormalities are you seeing on standard or not-so-standard lab tests?

Dr Hannah Ferenchick: Some of the characteristic lab findings we are seeing are lymphopenia and elevated inflammatory markers (eg, CRP). A couple of other atypical findings seem to be specific for COVID—elevated LDH, ferritin, CPK, and procalcitonin levels. Some of the hematologic markers that we look at—the coagulation profile studies—are also abnormal, showing thrombocytopenia and elevated D-dimer levels.

That constellation of symptoms represents more of a clinical picture. A lot of times we have only a very high clinical suspicion, because in many parts of the country it still takes days to get back a confirmatory PCR test.

Much like we do for the flu, the confirmatory test is a nasopharyngeal swab that is run for COVID/coronavirus PCR. Unfortunately the sensitivity of that test is not great. Some studies have quoted 75%-80%, so even a negative PCR does not necessarily rule out the disease, especially if you have a high clinical suspicion. A clinical suspicion is based on the typical symptoms. Many patients, although not all, will have symptoms of lower respiratory tract infection.

Dr Gary Ferenchick: So the right clinical scenario with the right hematologic/biochemical findings dramatically raises the chance that the patient has COVID?

Dr Hannah Ferenchick: Yes, and one thing that we have all been astonished by is how terrible some of these x-rays can look. There are a lot of typical findings on x-ray. Some describe them as looking like pulmonary edema, but the patient has no history of heart failure. Peripheral consolidation and ground-glass opacities are classically described. If you saw one of these x-rays from a patient with bacterial pneumonia, you would expect that patient to be very ill-appearing. Sometimes we get x-rays on patients who are sitting there, maybe mildly symptomatic on room air, and we are astonished by how terrible their x-rays look.

Unfortunately, imaging studies are something we haven't been able to rely on too much for diagnosis. Part of that is to maintain hospital safety, because to take a patient to CT scan, you have to consider the turnaround time for cleaning the CT scanner and the exposure of additional staff to a possibly infected patient. Some of those logistical considerations have limited the availability of radiography.

Gary S. Ferenchick, MD, MS, is a family physician and professor in the Department of Medicine at Michigan State University in East Lansing, Michigan. His daughter, Hannah R.B. Ferenchick, MD, is an assistant professor in the Department of Emergency Medicine, Division of Pulmonary & Critical Care and Sleep Medicine, at Wayne State University, Detroit, Michigan, and a medical intensivist and emergency medicine physician at Detroit Medical Center.