Immunodeficiency associated with anorexia nervosa is secondary and improves after refeeding.
Several studies have addressed the question of starvation effects on immune function by means of changes in lymphocyte subsets, cytokine induction or lymphocyte activation. Anorexia nervosa (AN) patients are severely malnourished and contradictory results have been obtained regarding the accompanying immunodeficiency, including its assignation as a part of the primary nervous disorder. In the present work, an extensive immunological function examination was carried out on 40 AN patients who were compared with a control group of 14 healthy girls. The AN patients were also classified according to their nutritional status (by the Body Mass Index: BMI), this being critical for a better understanding of these secondary immunodeficiency bases. Moreover, another immune system study was performed on five patients after refeeding. Lymphocyte subsets and function, cytokine induction and peripheral blood concentrations, and innate as well as humoral immunity were evaluated. Deregulation in the cytokine network, owing to the interaction of the central 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 psychiatric perturbation. Spontaneous high levels of circulating interleukin-1beta (IL-1beta) and tumour necrosis factor-alpha (TNF-alpha) have been observed; this is probably one of the causes of the anomalies found in the T-cell subpopulations (mainly the naive CD4+CD45RA+ reduction and the cytotoxic CD8+ increase) and T-cell activation status (mainly the down-regulation of the CD2 and CD69 activation pathways). This 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 also suggests that AN immunodeficiency is indeed secondary to malnutrition.
Allende
L M
LM
Department of Immunology, Hospital Universitario 12 de Octobre, Madrid, Spain.
Corell
A
A
Manzanares
J
J
Madruga
D
D
Marcos
A
A
Madroño
A
A
López-Goyanes
A
A
García-Pérez
M A
MA
Moreno
J M
JM
Rodrigo
M
M
Sanz
F
F
Arnaiz-Villena
A
A
D000293:Adolescent; D000856:Anorexia Nervosa / Q000276:immunology* / Q000628:therapy; D015992:Body Mass Index; D018801:CD2 Antigens; D017252:CD3 Complex; D016516:CD4-CD8 Ratio; D016022:Case-Control Studies; D005260:Female; D005502:Food; D006801:Humans; D007121:Immunocompetence; D007074:Immunoglobulin G / Q000097:blood; D007375:Interleukin-1 / Q000097:blood; D017493:Leukocyte Common Antigens; D008213:Lymphocyte Activation; D009748:Nutrition Disorders / Q000276:immunology*; D016176:T-Lymphocyte Subsets; D014409:Tumor Necrosis Factor-alpha
D018801:CD2 Antigens; D017252:CD3 Complex; D007074:Immunoglobulin G; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D017493:Leukocyte Common Antigens