TY  - JOUR
T1  - SElective hypopituitarism following tuberculous meningitis
AU  - Haslam RA, Winternitz WW, Howieson J
Y1  - 1969/12/01
N1  - 10.1001/archpedi.1969.02100040905017
JO  - American Journal of Diseases of Children
SP  - 903
EP  - 908
VL  - 118
IS  - 6
N2  - 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%.4If 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.5The following case demonstrates diabetes insipidus and deficiency of somatotropic (growth) hormone (STH) and of gonadotropins recognized ten years after recovery
SN  - 0002-922X
M3  - doi: 10.1001/archpedi.1969.02100040905017
UR  - http://dx.doi.org/10.1001/archpedi.1969.02100040905017
ER  -