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Among the adverse effects attributed to antiretroviral therapy, one of the most striking is probably the appearance of the lipodystrophy syndrome and its associated metabolic derangements, given its potential long-term effect as a cardiovascular risk factor. Since not all patients who receive antiretroviral drugs experience these adverse effects, a host genetic predisposition has been postulated. However, currently available data on this issue is inconclusive and preliminary. It has been consistently demonstrated that polymorphisms in the genes that encode for apolipoproteins A5, C3 and E, for the cholesterol ester transporter proteins (CETP), and in the ATP binding cassette type A1 (ABCA1) influence the development of dyslipidemia in patients treated with antiretroviral drugs, particularly if the therapeutic regimen includes protease inhibitors. Data on the effect of polymorphisms in the sterol regulatory ester binding protein type 1 (SREBP1) are inconsistent. The effect of mitochondrial DNA mutations on the risk of lipodystrophy has been assessed, with inconclusive data. No polymorphisms in the lamin A gene have been detected. Investigations have assessed the effect of diverse polymorphisms in the genes that encode for several proinflammatory cytokines such as tumour necrosis factor alpha (TNF-alpha), interleukin-1-beta (IL-1beta) and interleukin-6 (IL-6). The results show inconsistent data in the case of TNF-alpha, no association in the case of IL-6, and preliminary positive associations in IL-1beta. In contrast, polymorphisms in the genes encoding for stromal derived factor 1 (SDF-1) and for monocyte chemoattractant protein 1 (MCP-1) have been shown to influence the development of subclinical atherosclerosis in HIV-1-infected patients treated with antiretroviral drugs.

The degree of immune restoration in HIV-1-infected patients receiving the same antiretroviral regimen and achieving sustained virologic suppression is highly variable. Equally, not all persons receiving antiretroviral drugs experience adverse effects. Consequently, there seems to be wide interindividual variability in treatment response and toxicity due to antiretroviral therapy. Recent advances in pharmacogenetics and pharmacogenomics have identified several host genetic determinants that modulate treatment response and toxicity with these drugs. These findings contribute to the belief that personalized design of antiretroviral drug regimens, according to the host genetic background, may be feasible in the near future.

In order to determine the changes in the clinico-pathological pattern of admitted patients in an internal medicine department, 240 patients/year were compared during the years 1984 and 1989. A predominant proportion of males was registered (3:2); which did not vary by the year. An increased tendency of the median age (55.78 vs 58.48 years) was also established. The medium time of admission (8.98 vs 9.5 days) and mortality rate (6.3% vs 7.1%) did not change. A high rate (greater than 50%) of cardiovascular and respiratory disease was found on analyzing the cause of admission; in 1989 infection caused by HIV was detected and admissions to optimize the treatment of patients with diabetes mellitus were observed which did not exist in 1984. A slight but surprising decrease in admissions due to acute ischemic cardiopathy and significant decrease of admissions owing to respiratory disease were also noted. The majority of the patients admitted had a baseline disease (85% in 1984 and 87.1% in 1989). The knowledge of these data and their variations in every hospital department will, undoubtedly, assist in achieving a better use of technical and human health resources.