Lipid disorders seen in human immunodeficiency virus (HIV) infected patients include: elevated concentration of triglycerides (TGs) and total cholesterol (TC), decreased high-density lipoprotein (HDL) and variable changes in low-density lipoprotein (LDL). The mechanism of lipid disturbances accompanying HIV infection is unexplained and probably multifactorial (1). While lipid profile abnormalities have been described before the HAART (Highly Active Antiretroviral Therapy) era, hyperlipidemia associated with antiretroviral (ARV) drugs use is now more common and more severe. Protease inhibitors (PIs) create the greatest risk of hypertriglyceridemia and hypercholesterolemia among the all classes of ARV drugs (2, 3).

In general, lipid disorders can be divided into primary and secondary defects of lipid metabolism. One of the most prominent secondary causes of hypertriglyceridemia is excessive alcohol use. The effects of alcohol on lipid metabolism are diverse and includes stimulation of TG synthesis, very low-density lipoprotein (VLDL) formation, and lipolysis in fatty tissue (4, 5).

Although hypertriglyceridemia is often asymptomatic, it is a risk factor for cardiovascular disease. Patients presenting with severe hypertriglyceridemia are at increased risk for acute pancreatitis (6, 7).

Here we present a case report of severe hypertriglyceridemia in HIV/HCV (hepatitis C virus) co-infected patient with a history of chronic alcohol abuse. Informed consent has been obtained from the patient.

A 36-years old Caucasian male identified 6 years earlier with HIV and HCV without any other health complaints and who declared good adherence to ARV treatment (saquinavir, ritonavir and abacavir/lamivudine) for the past 2 years, came to the clinic for a routine blood test. He was subsequently diagnosed to have dyslipidemia with severe hypertriglyceridemia (2417 mg/dL) based on current American Association of Clinical Endocrinologists’ (AACE) guidelines (8). The concentrations of TC, HDL and LDL were 537, 44 and 493 mg/dL, respectively. Laboratory tests also revealed elevated activities of alanine (ALT) and aspartate (AST) aminotransferases (80 U/L and 62 U/L respectively), gamma glutamyl transferase (GGT – 416 U/L) and increased mean corpuscular volume (MCV – 101fl). The most recent lymphocyte counts revealed: CD3+ – 1266 cells/μl, CD4+ – 563 cells/μl and CD8+ – 728 cells/μl. HIV-RNA was undetectable. Blood pressure was normal and patient body mass index was 24. It was further revealed that he had been smoking about 20 cigarettes a day and drinking a moderate amount of alcohol over the past weeks. Physical examination was unremarkable. The patient refused admission to the hospital. Fenofibrate was prescribed and he was advised to introduce low-fat diet as well as eliminate alcohol and cigarettes. In the subsequent months the patient remained asymptomatic, yet despite the hypolipidemic treatment, his serum was lipemic with lipid concentrations as follows: TG – 6011 and 8396 mg/dL, TC – 896 and 990 mg/dL. ARV treatment was modified and atazanavir was introduced instead of saquinavir. Four months later, the patient was admitted to the hospital. TG concentration at a day of admission was 7199 mg/dL and total cholesterol – 1018 mg/dL, GGT activity – 795 U/L, amylase activity and CRP concentration were in norm. Abdominal ultrasonography revealed hepatosteatosis, although no changes in the pancreas, gallbladder, bile ducts and other organs were found. Gastroscopy showed slight mucosal inflammation of the antrum. Fenofibrate treatment was maintained and during the subsequent weeks, TG concentration decreased to 475 mg/dL, TC to 320 mg/dL, GGT activity to 338 U/L. After leaving the hospital, the patient made monthly visits to the HIV outpatient center. During the past several months lipid levels and GGT activity were again found to increase. The patient admitted that he periodically consumed excessive amounts of alcohol during this time. He refused both hospital readmission and treatment for alcohol dependence. Successive laboratory test results showed simultaneous increases in the concentrations of TG and TC concentrations as well as GGT activity, a marker of toxic liver damage (fig. 1).