In contrast, Julio Collazos, ., of Hospital de Galdakao in Vizcaya and colleagues reported in the April 12, 2002 issue of AIDS that in a study of nearly 200 clinically stable HIV-positive men (average CD4 cell count 451 cells/mm 3 ; 64% with undetectable viral load ), most subjects had testosterone levels within the normal range. Men receiving no anti-HIV therapy had the lowest testosterone, while those using a regimen combining three classes of antiretroviral drugs had the highest levels. Among the 15 men who had both pre- and post-treatment testosterone measurements, levels increased after starting HAART. But because testosterone levels normally begin to decline around age 40 (a phenomenon known as "andropause"), the beneficial effects of HAART on hypogonadism may be offset as treatment enables HIV-positive men to live to older ages.
In general, the burn wound or lungs are the most likely sites for an infection in the severely burned patient that subsequently develops MODS [ 1 ]. The release of endotoxins and/or exotoxins from an infective process initiates a cascade of inflammatory mediators that leads to organ damage and ultimately organ failure. Targeting the different cascade systems involved in the pathogenesis of burn-induced MODS is often not a feasible option [ 8 ]. Prevention of sepsis from burn wound infection is the most promising approach, as illustrated by the following examples:
Androgens are responsible for the growth spurt of adolescence and for the eventual termination of linear growth, which is brought about by fusion of the epiphyseal growth centers. In children, exogenous androgens accelerate linear growth rates but may cause a disproportionate advancement in bone maturation. Use over long periods may result in fusion of the epiphyseal growth centers and termination of growth process. Androgens have been reported to stimulate the production of red blood cells by enhancing the production of erythropoeitic stimulating factor. During exogenous administration of androgens,Â endogenous testosterone Â release is inhibited through feedback inhibition of pituitary luteinizing hormone (LH).