With earlier initiation of highly active antiretroviral therapy (HAART) and increased longevity of HIV patients, practitioners are providing more comprehensive primary care. HIV increases the risk of heart disease, particularly at CD4 cell counts <500 cells/mm
14 as well as certain malignancies including cervical cancer, non-Hodgkin lymphoma, and anal cancer; however, since the advent of HAART, the majority of cancers affecting HIV patients are non-AIDS defining (i.e., lung and liver cancer, Hodgkin lymphoma).
9 Thus, it is imperative to address cardiovascular risk factors such as hyperlipidemia, diabetes, and tobacco abuse, and perform appropriate cancer screening.
HYPERLIPIDEMIA
HIV patients should have cholesterol goals guided by the National Cholesterol Education Program (see
Table 4-1).
10 Diet alone at 24 weeks can lower low density lipoprotein (LDL) by 5.5%. Advise patients to increase intake of whole grains, fruits, and vegetables and decrease saturated fats and refined sugars.
16 Baseline fasting lipids should be checked prior to initiating HAART and at 3 to 6 months after starting any new antiretroviral regimen.
7 One multicenter prospective study found increased rates of hyperlipidemia in HIV patients on protease inhibitor based regimens compared to patients not receiving protease inhibitors(11). Also, certain antiretrovirals are associated with hyperlipidemia including efavirenz, stavudine, ritonavir, and lopinavir/ritonavir (see
Table 4-2).
Check a fasting lipid profile and liver function tests (LFTs) prior to starting lipid therapy, and consider discontinuing therapy if patients have persistent transaminitis greater than three times the upper limit of normal, or creatine phosphokinase greater than five to ten times the upper limit of normal. Drug interactions with ritonavir and other protease inhibitors (PIs) are common as they are potent inhibitors of the cytochrome P450. Pravastatin and atorvastatin are first-line agents for patients with hyperlipidemia on PI-based regimens. Lovastatin and simvastatin are contraindicated for patients on PI regimens. Choose cholesterol drugs with respect to type of dyslipidemia. For example, in patients with isolated hypertriglyceridemia (>500), consider fibrates; for patients with isolated low high density lipoprotein (HDL), consider niacin; if LDL is above goal, triglycerides are 200 to 500 mg/dL, and non-HDL cholesterol is elevated, consider an HMG-CoA reductase inhibitor (statin).
7 Monitor LDL cholesterol levels 4 to 6 weeks after starting lipid therapy and monitor LFTs closely when initiating statins in patients who are concurrently receiving potentially hepatotoxic medications (i.e., ritonavir, saquinavir, amprenavir, efavirenz, and nevirapine).
If patients are at high cardiovascular risk (>20% risk of heart disease within 10 years using the Framingham score) and their lipids are not sufficiently controlled by medications, consider adjusting HAART to include more lipid friendly drugs.
7,10 Amprenavir and nelfinavir have intermediate effects, indinavir and saquinavir have little effect on lipids, and atazanavir has minimal effect.