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 Presentation
HIV-Associated Dyslipidemias
Roger J. Bedimo, MD, MS

Level: Advanced
23  

CME Post test  
  
   

You must answer at least 8 of 10 questions correctly (>80%) to receive a passing score and earn CME credit.


Case for Questions 1 to 5

A 35-year-old HIV and hepatitis C virus (HCV)-coinfected man presents for follow-up visit. He has no complaints except for some concerns about his appearance: He says that his limbs are getting thinner and his abdomen more protuberant. He reports excellent adherence to his antiretroviral regimen (zidovudine, lamivudine, and ritonavir-boosted lopinavir) without experiencing substantial adverse effects. His CD4+ cell count is 504/μL, and his plasma HIV RNA is below detectable levels. The patient was previously diagnosed with chronic kidney disease secondary to HIV-associated nephropathy. He reports smoking 20 cigarettes per day and is contemplating smoking cessation. His basic metabolic profile reveals elevated liver enzymes (not new): aspartate aminotransferase (AST) is 110 U/L, and alanine aminotransferase (ALT) is 94 U/L. His lipid profile follows:

  • total cholesterol (TC), 354 mg/dL

  • high-density lipoprotein cholesterol (HDL-C), 40 mg/dL

  • low-density lipoprotein cholesterol (LDL-C), 250 mg/dL

  • triglycerides, 320 mg/dL

 
 

1. Of the following conditions, which is not a likely risk factor for hypercholesterolemia for this patient?

 
a. Chronic kidney disease

b. Protease inhibitor (PI) use

c. A familial genetic disorder

d. Thymidine nucleoside analogue reverse transcriptase inhibitor (nRTI) use

e. HCV coinfection

 

2. Which statement is correct regarding this patient?

 
a. His dyslipidemia can be attributed to antiretroviral therapy use because the patient concomitantly developed morphologic changes consistent with lipodystrophy.

b. HIV-infected patients without hypercholesterolemia are not at increased risk of cardiovascular disease.

c. Dyslipidemias, lipoatrophy, and lipohypertrophy represent distinct metabolic toxicities of antiretroviral therapy and can occur independently of each other.

d. Thymidine nRTIs such as zidovudine are associated with a lower incidence of lipoatrophy than nonthymidine nRTIs.

 

3. Which intervention would be LEAST likely to succeed in lowering this patient’s total serum cholesterol to a range recommended in the National Cholesterol Education Program (NCEP) guidelines and reduce his cardiovascular risk?

 
a. Switching from zidovudine to tenofovir

b. Initiation of lipid-lowering therapy with pravastatin

c. Discontinuation of antiretroviral therapy

d. Switching from ritonavir-boosted lopinavir to nevirapine

 

4. Which statin is contraindicated in patients concomitantly taking HIV protease inhibitors (PIs)?

 
a. Pravastatin

b. Simvastatin

c. Rosuvastatin

d. Atorvastatin

 

5. Which of the following are potential complications of statin therapy in this patient?

 
a. Myalgia

b. Myositis

c. Elevation of liver enzymes

d. Rhabdomyositis

e. All of the above

 

6. The most common non-AIDS-related causes of morbidity and mortality among HIV-infected patients are chronic liver disease, metabolic complications including cardiovascular disease, and non–AIDS-defining malignancies.

 
a. True

b. False

 

7. Advanced HIV disease in the absence of combination antiretroviral therapy has been associated with hypertriglyceridemia and low levels of TC, LDL-C, and HDL-C.

 
a. True

b. False

 

8. Nonnucleoside analogue reverse transcriptase inhibitor (NNRTI) therapy can lead to marked decreases in HDL-C levels, greater with nevirapine than with efavirenz.

 
a. True

b. False

 

9. Lipid levels may decrease with substitution of an NNRTI for a PI, but increase with substitution of a nonthymidine nRTI for a thymidine nRTI.

 
a. True

b. False

 

10. When used in combination lipid lowering therapy, fenofibrate is more likely than gemfibrozil to increase simvastatin concentration to potentially toxic levels.

 
a. True

b. False