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December 1969

Selective Hypopituitarism Following Tuberculous Meningitis

Author Affiliations

Lexington, Ky
From the Department of Neurology, University of Kentucky Medical Center College of Medicine, Lexington, Ky. Dr. Howieson is now at the Yale University Medical School, New Haven, Conn.

Am J Dis Child. 1969;118(6):903-908. doi:10.1001/archpedi.1969.02100040905017

MENINGITIS REMAINS a most serious complication and the most common cause of death in childhood tuberculosis.1 Clinically significant sequelae of tuberculous meningitis (TBM) are frequent and include convulsions, paresis, optic atrophy, hydrocephalus, deafness, generalized organic brain damage leading to mental deficiency, and/or persistent psychiatric disturbances. Intracranial calcification following tuberculous meningitis was rare prior to the widespread use of isoniazid and streptomycin,2,3 but more recently the incidence of intracranial calcification has been reported as high as 77%.4

If the tuberculous lesions are strategically located in the hypothalamus, pituitary stalk, or the pituitary itself, various endocrine abnormalities can be expected. Endocrinopathies may become evident months or years after recovery from TBM, apparently because of progressive scarring of either the hypothalamus itself or of the adjacent basal cisterns.5

The following case demonstrates diabetes insipidus and deficiency of somatotropic (growth) hormone (STH) and of gonadotropins recognized ten years after recovery

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