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Report of 10 Cases and Review of Literature

Toshihide Yamamoto, MD; Jiro Fukuyama, MD; Kyoichi Hasegawa, MD; Masahiko Sugiura, PhD

Arch Intern Med. 1992;152(8):1705-1712.

Abstract
The clinical and laboratory findings in 76 patients with isolated corticotropin deficiency (10 of our own and 66 from literature) were analyzed with the following observations. With the exceptions of hyperpigmentation and hyperkalemia, the similarity of symptoms and signs to those of Addison's disease and their reversibility by glucocorticoids indicate that most, but not all, manifestation of isolated corticotropin deficiency is caused by glucocorticoid deficiency. Isolated corticotropin deficiency seems to be of pituitary origin in most patients, as shown by lack of corticotropin response to insulin-induced hypoglycemia, vasopressin, or corticotropin-releasing factor. Secretion of other pituitary hormones is frequently abnormal, which is mostly attributable to glucocorticoid deficiency. Although the pathogenesis of isolated corticotropin deficiency is unknown in most patients, association with other autoimmune endocrinopathies, postpartum onset in women, or serum antipituitary antibodies suggests an autoimmune pathogenesis in some patients. In two of our 10 patients, cancer developed during glucocorticoid treatment. More observations of complications and long-term prognosis following glucocorticoid therapy are needed for optimal clinical decision making.

(Arch Intern Med. 1992;152:1705-1712)

Author Affiliations
From the Department of Medicine, Kishiwada Tokushukai Hospital, Osaka, Japan (Dr Yamamoto); Chigasaki (Japan) Tokushukai Hospital (Dr Fukuyama); Center for Adult Diseases, Osaka (Dr Hasegawa); and Biomedical Laboratories Inc, Kawagoe, Japan (Dr Sugiura).

Footnotes
Accepted for publication December 16, 1991.

Reprint requests to Department of Medicine, Kishiwada Tokushukai Hospital, 4-22-38 Isonokami-cho, Kishiwada, Osaka 596, Japan (Dr Yamamoto).

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