Possible Drug-Induced Severe Hypertriglyceridemia in a Patient Co-Infected with Human Immunodeficiency Virus and Hepatitis C Virus

Case Presentation

Austin J HIV/AIDS Res. 2016; 3(1): 1022.

Possible Drug-Induced Severe Hypertriglyceridemia in a Patient Co-Infected with Human Immunodeficiency Virus and Hepatitis C Virus

Riello III RJ¹ and Salvo MC²*

1Department of Pharmacy Services, Yale-New Haven Hospital, USA

²Department of Pharmacy Practice, University of Connecticut School of Pharmacy, USA

*Corresponding author: Salvo MC, Department of Pharmacy Practice, University of Connecticut School of Pharmacy, 69 North Eagleville Road Unit 3092, Storrs, CT 06269-3092, USA

Received: February 24, 2016; Accepted: March 03, 2016; Published: March 07, 2016


Lipid-related disturbances are commonly associated with Protease Inhibitor (PI) use; however, PI-sparing Human Immunodeficiency Virus (HIV) regimens are less frequently associated with increased lipids. A 53 year-old African American female, co-infected with Hepatitis C Virus (HCV) and HIV, maintained on a PI-sparing antiretroviral therapy, experienced a significant elevation in triglycerides following the initiation of HCV treatment with peginterferon Alfa-2a 180 mcg subcutaneously weekly, ribavirin 600 mg orally twice daily, and telaprevir 1125 mg orally three times daily. Two weeks after the start of treatment, a lipid panel was drawn with results: triglycerides (1678 mg/dL), high density lipoprotein-cholesterol (27 mg/dL), total cholesterol (257 mg/dL), and low density lipoprotein-cholesterol (not calculated). Fenofibrate 48mg orally daily was initiated 1 week later. After 7 weeks of fibrate therapy, the triglycerides remained elevated (1690 mg/dL). Marked triglyceride reduction (344 mg/dL) was achieved within 4 weeks of rosuvastatin 10 mg orally daily initiation.

Based on the Naranjo score of 4, it is possible that the patient’s hypertriglyceridemia was drug-induced by peginterferon Alfa-2a. Statin selection is an important component of dyslipidemia management in co-infected HIV and HCV patients with baseline lipid abnormalities.

Keywords: Hepatitis C virus; HIV; Peginterferon Alfa-2a; Severe hypertriglyceridemia


HIV: Human Immunodeficiency Virus; HCV: Hepatitis C Virus; PI: Protease Inhibitor; NNRTI: Non-Nucleoside Reverse Transcriptase Inhibitor; ART: Antiretroviral Therapy; CD4: Cluster of Differentiation 4; RNA: Ribonucleic Acid; IU: International Units; PO: By mouth; LDL-C: Low Density Lipoprotein-Cholesterol; HDL-C: High Density Lipoprotein-Cholesterol (HDL-C); CYP3A4: Cytochrome P450 3A4; AUC: Area Under The Curve; Cmin: Minimum Drug Concentration


Of the people living with human immunodeficiency virus (HIV) in the United States, 25% are co-infected with hepatitis C virus (HCV) [1]. Treatment options suppress HIV and clear HCV infection. However, antiviral medications are not free of adverse effects or potential drug interactions. For example, marked triglyceride elevations are a frequently reported adverse effect associated with protease inhibitor (PI) use for HIV management, but uncommon with PI-sparing regimens [2-6].

Documented cases of dyslipidemia in patients co-infected with HCV Genotype 1a and HIV, who are receiving a PI-sparing regimen, are rare; particularly, given that reports indicate HCV may promote favorable lipid profiles and reduce rates of dyslipidemia [7,8]. We report a case of severe hypertriglyceridemia in a co-infected HCV and HIV patient on a concomitant PI-sparing, non-nucleoside reverse transcriptase inhibitor (NNRTI) based antiretroviral therapy (ART) regimen and HCV treatment.

Case Presentation

A primary care provider requested a pharmacist consult for a hypertriglyceridemia therapy recommendation following 10 weeks of HCV treatment in a 53 year-old, 66 kg African American female. The patient’s medical history was significant for HCV Genotype 1a, diabetes mellitus type 2 (A1c of 5.8%, drawn 9 months prior to the start of HCV treatment), controlled hypertension, HIV (CD4 T cell count of 433 cells/uL and HIV RNA viral load of < 20 copies/mL, both drawn at the start of HCV treatment), and hypertriglyceridemia (triglycerides 430 mg/dL, drawn 9 months prior to the start of HCV treatment).There was no documentation of symptoms that may be associated with elevated triglycerides.

Table 1 contains the patient’s medications at the time of pharmacy consultation. To confirm adherence, the pharmacist called the patient’s community pharmacy to assess fill dates; compliance was deemed appropriate. No use of complementary and alternative medicine was noted, and the patient had no recorded drug allergies. Social history reported denial of current tobacco, alcohol, or illicit drug use, and the patient was employed as a residential assistant. Family history was not available. Adult vaccines, including influenza and Hepatitis A, were up-to-date.