Differences in nocturnal basal and rhythmic prolactin secretion in untreated compared to treated HIV-infected men are associated with CD4+ T-lymphocytes.

The existence of decreased hypothalamic dopaminergic tone in HIV-infected men has been suggested. In a cross-sectional study, we determined 12 h nocturnal basal and pulsatile prolactin (PRL) release levels (by blood sampling every 10 min) and their correlation with CD4+ T cells in seven volunteer HIV-negative, healthy men (group 1), and 21 normoprolactinemic, euthyroid, HIV-infected men divided into 3 groups (each group = 7): (i) group 2, asymptomatic HIV-infected stage A1 men, untreated; (ii) group 3, AIDS stage C3 without active opportunistic infections, untreated; and (iii) group 4, previously stage C3 after at least 6 months of successful highly active antiretroviral therapy. Serum PRL was measured by radioimmunoanalysis and the results were analysed by waveform-independent deconvolution analysis. CD4+ T lymphocytes were measured by flow cytometry and viral load by a nucleic acid sequence-based amplification assay. No differences were detected in the first two groups. In the third group, however, 100% of prolactin secretion was found to be pulsatile with a shorter secretory burst duration (P = 0.04), and a greater circulating half-life and pulse amplitude (P < or = 0.04). Group 4 had the greatest basal prolactin secretion (P < or = 0.04), and a shorter secretory burst duration (P = 0.04 vs group 2), circulating half-life (P = 0.01 vs group 3) and intersecretory burst interval (P = 0.06 vs group 1). PRL approximate entropy was similar among all groups. Linear correlations existed between CD4+ T cell counts and PRL secretory burst half duration (r = 0.62, P = 0.002) and amplitude (r = -0.63, P = 0.001), and in circulating serum half-life (r = - 0.61, P = 0.002) in HIV-infected groups. Viral load showed no correlations. It is suggested that differential changes in nocturnal prolactin secretion among HIV-infected men occurred while maintaining the normal coordinate feedback and/or feedforward control within the lactotropic axis. These changes may represent an adaptative mechanism to sustain, by different means, the maximal physiologic PRL production to stimulate the highest cellular immune response and/or reconstitution in attempting to survive.

Aspectos inmunogenéticos de la tuberculosis pulmonar / Immunogenetic aspects of pulmonary tuberculosis

La tuberculosis tiene una elevada tasa de morbilidad y causa aproximadamente 3 millones de muertes cada año en todo el mundo. Los estudios de la infección por M. tuberculosis han revelado la presencia de factores ambientales y genéticos determinantes en la fisiopatogenia de la tuberculosis. Algunos genes como los del sistema HLA y el TNF-a localizados dentro del complejo principal de histocompatibilidad, entre otros, se han asociado con la susceptibilidad a la tuberculosis en distintos grupos étnicos. En la población mexicana se ha observado que la susceptibilidad a la tuberculosis pulmonar está determinada por los alelos HLA-DRB1*1501, HLA-DQA1*0101 y DQB1*0501. Por otro lado, los individuos con mutaciones en el gen del receptor 1 de IFN-g tienen defectos en el control de infecciones causadas por micobacterias. Hay otros genes que parecen estar involucrados en la susceptibilidad o resistencia a la tuberculosis, algunos de ellos son el receptor de la vitamina D, el gen NRAMP-1 o el gen de la proteína quimiotáctica de macrófagos (MCP-1), entre otros. El estudio de los marcadores genéticos polimórficos en la tuberculosis es importante para definir los mecanismos de susceptibilidad a la infección o a la progresión clínica de la enfermedad.