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[Functional morphology of adenohypophysis, thymus, and adrenal cortex in sudden infant death syndrome].

Adrenal glands, hypophysis and thymus of infants (mean age-4 months), who died of SIDS (30 cases), AVRI (10 cases) and violence (4 cases) were studied by morphometrical methods. The following changes in SIDS (in comparison with AVRI and violent death) were observed: a decrease of hypothesis weight with decreased quantity and size of basophil cells; reduced adrenal weight with thinning of the cortex particularly in the fascicular zone; diminished volumes of the nuclei in the adrenocortical cells of the fascicular zone; thymomegaly with hyperplasia of the thymus cortex; increased number of correlation links between morphometric indices of hypophysis and adrenal cortex. These changes may be indicative of a subclinical hypophyseal-adrenal insufficiency in SIDS. Adrenal cortex hypofunction was indirectly confirmed by the presence of thymomegaly. Long-lasting glucocorticoid deficiency in secondary hypocorticoidism may cause sudden infant death following minor environmental causes.

Adrenal Cortex↗
PubMed1982

[Antibody to 1-24 ACTH and hypofunction of the adrenal cortex in a patient who was unilaterally adrenalectomized for Cushing's syndrome (author's transl)].

We report here on a patient who was unilaterally adrenalectomized for Cushing's syndrome, and who developed antibodies to 1-24 ACTH. A 49-year-old nurse had undergone right adrenalectomy for adrenal adenoma. After surgery, she was treated with 0.5 mg of 1-24 ACTH-Z together with glucocorticoid replacement therapy for 40 days. Thereafter she was given 0.25-0.5 mg of ACTH-Z every other day for 4 months. ACTH-Z was then stopped for a year but glucocorticoid therapy was continued. About one year prior to this admission, 1 mg of ACTH-Z was again initiated 1 to 2 times a week. Glucocorticoid therapy was not withdrawn during the four years after adrenalectomy. She was admitted for the purpose of withdrawal of glucocorticoids. Her serum was found to bind labeled ACTH. This labeled ACTH was competitively displaced from binding by unlabeled hormones. Finally, reaction with specific antihuman Ig demonstrated an antibody of the IgG class. The titer of the antibodies gradually decreased after the discontinuation of ACTH-Z, but it is still present in measurable quantity in her serum. The clinical significance of the circulating anti-ACTH antibody in her serum is discussed.

Adrenal Insufficiency↗