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DOI 10.4158/ep.6.1.26

Медицинская библиотека · Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2000

Central diabetes insipidus due to herpes simplex in a patient immunosuppressed by Cushing's syndrome.

Torres A M, Kazee A M, Simon H, Knudson P E, Weinstock R S

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Аннотация

OBJECTIVE

To describe a patient immunocompromised by Cushing's syndrome in whom central diabetes insipidus developed as a complication of herpes simplex involvement of the hypothalamus.

METHODS

We present a case, including results of laboratory and histopathologic studies, in which herpes simplex was established as the causative agent for central diabetes insipidus.

RESULTS

A woman with ectopic corticotropin-dependent Cushing's syndrome, diabetes mellitus, carcinoid tumor, and a history of thyroid cancer had the precipitous onset of seizure and fever, and hypotonic polyuria and progressive hypernatremia developed. Central diabetes insipidus was diagnosed and successfully treated with desmopressin. Nevertheless, the patient's condition deteriorated and she died. Autopsy revealed herpes simplex encephalitis involving the magnicellular neurons of the hypothalamus.

CONCLUSION

Central diabetes insipidus caused by viral infections has been reported in immunosuppressed patients, such as those with acquired immunodeficiency syndrome (AIDS). To our knowledge, this is the first report of a herpes infection causing diabetes insipidus in a patient immunosuppressed by Cushing's syndrome. This case demonstrates that, in patients with Cushing's syndrome, diabetes insipidus may develop as a result of herpes simplex infection of the hypothalamus.

Для цитирования: Torres A M, Kazee A M, Simon H, Knudson P E, Weinstock R S. Central diabetes insipidus due to herpes simplex in a patient immunosuppressed by Cushing's syndrome.. Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists. 2000. DOI: 10.4158/ep.6.1.26.

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