IMMUNODEFICIENCY ASSOCIATED WITH ANOREXIA-NERVOSA IS SECONDARY AND IMPROVES AFTER REFEEDING

Several studies have addressed the question of starvation effects on i mmune function by means of changes in lymphocyte subsets, cytokine ind uction or lymphocyte activation. Anorexia nervosa (AN) patients are se verely malnourished and contradictory results have been obtained regar ding the accompanying immunodeficiency, including its assignation as a part of the primary nervous disorder. In the present work, an extensi ve immunological function examination was carried out on 40 AN patient s who were compared with a control group of 14 healthy girls. The AN p atients were also classified according to their nutritional status (by the Body Mass Index: BMI), this being critical for a better understan ding of these secondary immunodeficiency bases. Moreover, another immu ne system study was performed on five patients after refeeding. Lympho cyte subsets and function, cytokine induction and peripheral blood con centrations, and innate as well as humoral immunity were evaluated. De regulation in the cytokine network, owing to the interaction of the ce ntral nervous (CNS) and immune systems, seems to be the initial immune alteration in AN immunodeficiency but it has not been disproved that the immunodeficiency is a direct consequence of the original psychiatr ic perturbation. Spontaneous high levels of circulating interleukin-1 beta (IL-1 beta) and tumour necrosis factor-alpha (TNF-alpha) have bee n observed; this is probably one of the causes of the anomalies found in the T-cell subpopulations (mainly the naive CD4(+)CD45RA(+) reducti on and the cytotoxic CD8(+) increase) and T-cell activation status (ma inly the down-regulation of the CD2 and CD69 activation pathways). Thi s finally leads to an impairment, not only in T-cell function but also in T-cell to B-cell co-operation. The AN specificity of these results is confirmed by the fact that these immune alterations improve after refeeding and when nutritional status becomes less critical, which als o suggests that AN immunodeficiency is indeed secondary to malnutritio n.