HIV-infection, HAART and hyperlipidaemia

History and admission findings: A 42-year-old man with long-standing HIV-infection (CDC C3) and multiple treatment failures was seen for follow-up 6 months after starting a new HAART (zidovudine, efavirenz, indinavir, ritonavir). The medical history is remarkable for a hypersensitivity reaction to abacavir, past smoking (10 pack years) and a family history of coronary heart disease of the patient's mother. Physical examination reaveled discrete signs of lipoatrophy of the face, arms and legs, but no lipoaccumulation (hip-waist ratio 0.94; body mass index 22kg/m(2)). Blood pressure measured 156/92 mmHg. Laboratory findings: A rise in CD4 cell count from 24/muL to 60/muL was noted. For the first time, the HIV viral load decreased to <50 copies/mL Concentrations of triglycerides and cholesterol were found to be increased to 26 mmol/L (2275mg/dL) and 15 mmol/L (580mg/dL), respectively, compared previously normal readings. Other parameters were in the normal range. Diagnosis and therapy: Continuation of HAART resulted in rising CD4 counts to>200/gL and HIV viral load suppression to<50 copies/mL. Neither dietary measures nor treatment with pravastatin significantly, changed the drug-induced mixed hyperlipidemia. Treatment with fenofibrate (200mg qd), however, was followed by a significant reduction of triglyceride and cholesterol concentrations to 12 mmol/L (1050mg/dL) and 10 mmol/L (387mg/dL). Addition of pravastatin did not result in further improvement. Arterial hypertension was diagnosed by ambulatory 24-h blood pressure monitoring (systolic 157+/-11 mmHg; diastolic 97+/-10 mmHg). Conclusion: HAART-induced mixed hyperlipidaemia is likely to increase the cardiovascular risk. According to first estimates, the 3-year risk of myocardial infarction amounts to 1.29 - 2.09% for our patient. The 3-year risk of HIV progression to AIDS or death is>30% if HAART is stopped or fails upon switching due to unkown archived drug resistence. Thus, despite unsatisfactory lipid profiles, a modification of HAART seems only acceptable, if new, equally potent, but less lipidaemic drug combinations are available.