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LAWRENCE F. EICHENFIELD, MD; RICHARD B. JOHNSTON, JR, MD
Department of Pediatrics The Children's Hospital of Philadelphia 34th Street and Civic Center Boulevard Philadelphia, PA 19104

Am J Dis Child. 1989;143(12):1392.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

In Reply.—It appears that we do not disagree fundamentally with Drs Sigal and Snyder. Certainly, anorexia nervosa is not the same disease entity as malnutrition in Third-World countries. However, pairing them in the table as complement disorders, due primarily to decreased synthesis, is supported by the experimental evidence that is presently available. As we pointed out, circulating immune complexes and endotoxin in patients with malnutrition could deplete complement, but we believe that the weight of evidence at present favors decreased synthesis as the principal mechanism in both disorders. Although decreased levels of complement control proteins may lead to complement consumption in anorexia nervosa, the primary event is decreased production of these proteins. As we reported, complement abnormalities in both entities are rapidly corrected with appropriate feeding.^1,2 Perhaps this is the important point. . . . [Full Text PDF of this Article]

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