RESUMEN
Tuberculosis is the classic cause of "consumption," but the exact pathogenesis of such wasting is largely unknown. Animal studies in other conditions suggest that leptin may be a mediator between pro inflammatory cytokine activity and wasting. Because leptin is involved in weight regulation and cellular immunity, it may have a role in tuberculosis-associated wasting. Qims: 1] To estimate leptin concentration in a group of active pulmonary or extra pulmonary tuberculosis as compared to healthy control subjects. 2] To study the relationship between serum leptin, anorexia and wasting. 3] To study the correlation between serum leptin and proinflammatory cytokines [TNF-d, IL-1,IL-6] Patients and Non-diabetic Egyptian adults with pulmonary [n=26] and extrapulmonary tuberculosis [n=19] as well as 20 healthy controls were recruited into a case-control study. Body mass index [BMI], C- reactive protein, serum leptin, TNF-a, interleukin-1 and 6 were measured. According to the calculated BMI, eighteen patients were wasted [40%] and 27 [60%] were not wasted. Mean serum leptin was significantly lower in tuberculous patients than controls and in wasted than non-wasted patients. TNF-a, IL-l.IL-6 were significantly higher in patients than controls. Only IL-6 was significantly higher in wasted than non-wasted patients Serum leptin showed a significant positive correlation with BMI. While, IL-6 had a significant negative correlation with BMI Moreover, stepwise linear regression analyses showed that IL-6 was the only factor significantly contributing to loss of appetite [anorexia] in tuberculous patients. leptin does not appear to be part of the proinflammatory cytokine response in human tuberculosis. Changes in leptin are entirely appropriate for the changes in body mass index. Altered leptin activity cannot, therefore, be held responsible for the weight loss and anorexia so often associated with tuberculosis infection. Anorexia and wasting seem primarily determined by the level of inflammatory cytokine [IL-6]