For human immunodeficiency virus (HIV)-infected patients, the 1990s were marked by the introduction of highly active antiretroviral therapy (HAART) representing a new perspective of life for these patients. The use of HAART was shown to effectively suppress the replication of HIV-1 and dramatically reduce mortality and morbidity, which led to a better and longer quality of life for HIV-1-infected patients. Apart from the substantial benefits that result from the use of various HAART regimens, laboratory and clinical experience has shown that HAART can induce severe and considerable adverse effects related to metabolic complications of lipid metabolism, characterized by signs of lipodystrophy, insulin resistance, central adiposity, dyslipidemia, increased risk of cardiovascular disease and even an increased risk of atherosclerosis. New drugs are being studied, new therapeutic strategies are being implemented, and the use of statins, fibrates, and inhibitors of intestinal cholesterol absorption have been effective alternatives. Changes in diet and lifestyle have also shown satisfactory results.

Iron is an essential metal for cell survival that is regulated by the peptide hormone hepcidin. However, its influence on certain diseases is directly related to iron metabolism or secondary to underlying diseases. Genetic alterations influence the serum hepcidin concentration, which can lead to an iron overload in tissues, as observed in haemochromatosis, in which serum hepcidin or defective hepcidin synthesis is observed. Another genetic imbalance of iron is iron-refractory anaemia, in which serum concentrations of hepcidin are increased, precluding the flow and efflux of extra- and intracellular iron. During the pathogenesis of certain diseases, the resulting oxidative stress, as well as the increase in inflammatory cytokines, influences the transcription of the HAMP gene to generate a secondary anaemia due to the increase in the serum concentration of hepcidin. To date, there is no available drug to inhibit or enhance hepcidin transcription, mostly due to the cytotoxicity described in the in vitro models. The proposed therapeutic targets are still in the early stages of clinical trials. Some candidates are promising, such as heparin derivatives and minihepcidins. This review describes the main pathways of systemic and genetic regulation of hepcidin, as well as its influence on the disorders related to iron metabolism.

The prevalence of infection by the hepatitis B (HBV) and C (HCV) viruses varies among geographical regions. We evaluated 263,795 blood donor samples collected from 1999-2001 in various cities in the state of Santa Catarina to determine the prevalence of HbsAg, anti-HBc and anti-HCV markers. The markers were analyzed by immunoenzymatic tests, as determined by the Ministry of Health, and the data were obtained from blood banks and from ANVISA (the Brazilian National Agency for Sanitary Vigilance). There was a significant reduction in the mean frequency of HbsAg and anti-HBc during the study period, from 0.98% to 0.64% and from 8.83% to 5.35%, respectively, though they varied considerably among the different regions. There was also a decrease in the mean frequency of anti-HCV, although it was not significant, decreasing from 0.38% to 0.34%. Even with this reduction, the frequency of these markers was still high compared with that found in other countries, indicating high rates of infection by hepatitis B and C viruses. This emphasizes the urgency of vaccination programs against HBV, especially in some regions of Santa Catarina state, in order to reduce the prevalence of this infection and consequently reduce the risk of transmission through sexual relations or from the donation of blood and/or hemocomponents.

These results suggest that abnormalities of antioxidant defence, mainly of SOD activity, are related to the progression of the HIV infection.

The first thrombocytopenia cases related to the human immunodeficiency virus (HIV) were described even before its isolation in 1983. Subsequently, multiple mechanisms have been proposed to elucidate the etiology of thrombocytopenia. In addition to other types of cytopenia affecting patients with HIV, thrombocytopenia is observed in about 10–50% HIV patients as one of the first clinical signs of infection. Thus, in this review we aim to summarize the mechanisms proposed for thrombocytopenia since the discovery of HIV, and especially the innovations in the field in recent years. Among the different mechanisms suggested for HIV-related thrombocytopenia, there is emphasis on the accelerated destruction of platelets (PLTs) due to the action of immune complexes, and the presence of anti-PLT and anti-HIV antibodies that cross-react with the PLT membrane. There are also secondary causes of thrombocytopenia, such as the effect of drugs and opportunistic diseases associated with HIV.