Panhypopituitarism after cured tuberculous meningitis.

Abstract

Though tuberculous granulomata of the pituitary or its stalk are often included in the lists of causes of hypopituitarism, most of the cases have in fact been diagnosed only at necropsy. Chronic clinical hypopituitarism due to proved tuberculosis has rarely been reported. CASE REPORTThe patient had developed tuberculosis of the lungs, spine, and meninges when she was aged 6. Streptomycin therapy was given for two years and she was discharged from hospital after a further tear. The menarche occurred at age 10; the periods lasted for only four cycles, though lower abdominal pain at monthly intervals continued for a further six months. Thereafter there was no cyclical pain or bleeding.At age 20 she was investigated elsewhere for amenorrhoea; she was short of stature (145 cm.) and no signs of active tuberculosis were obtained. A vaginal smear showed no evidence of oestrogenic activity. Curettage was attempted but no endometrium could be X-ray fihn of skull to show suprasellar calcification, presumably in the meninges.obtained from the small uterus. Cyclical oestrogen therapy was started and resulted in enlargement of the breasts and uterus and withdrawal bleedings. On discontinuing the therapy no spontaneous periods occurred.At age 27 she developed a sore throat, pyrexia, and hypotension (B.P. 90/60) and rapidly lapsed into a stuporous condition. No evidence of raised intracranial pressure was found. In view of the history and the finding of very scanty pubic and axillary hair she was treated with intramuscular hydrocortisone as well as ampicillin. A rapid recovery ensued and therapy was temporarily withheld while laboratory tests were performed.Investigations.-The plasma cortisol was 3.4 and 2.4 ,ug./100 ml. at 10 a.m. on two occasions. The urinary daily excretion of 17-hydroxycorticosteroids and 17-oxosteroids was 2.3 and 1.5 mg. respectively. On the day 3 g. of metyrapone was administered orally the 17-hydroxycorticosteroid excretion was 2.8 mg. and on the following day it was 2.0 mg. Injection of A.C.T.H. gel (20 units b.d. for three days) increased the 17-hydroxycorticosteroid excretion to 20.5 mg./24 hours. The serum protein-bound iodine was 2.9 ,ug./lO ml. and the serum thyroxine 4.3 pg./100 ml. The four-hour 182I uptake was 11.0%. This was increased to 29.2% after 10 units of thyroid stimulating hormone. The urinary excretion of gonadotrophins was less than 3 i.u./24 hours. The total urinary oestrogen excretion was 16 jug./24 hours. There was no polyuria and serum electrolytes were normal. X-ray examination of the skull showed suprasellar calcification (see Fig.).After treatment with cortisone and thyroxine the patient felt muchmore alert and active and less cold-sensitive. COMMENTThe laboratory investigations confirm the diagnosis of hypopituitarism. The lack of evidence suggestive of a spaceoccupying lesion and the presence of suprasellar calcification make it almost certain that the hypopituitarism followed the tuberculous meningitis.Tuberculosis has been reported to affect both the parenchyma of the ante...

Post-encephalitic hypothalamic-pituitary insufficiency

“…In most of the reports the endocrine deficiency has been caused by tuberculous menin¬ gitis and other causes seem to be extremely rare (Summers et al 1968;Haslam et al 1969;Sherman et al 1971;Udani et al 1971;Brooks et al 1973). There are, however, reports to show that other bacteria like group B ß-haemolytic streptococci, pneumococci and listeria may also cause hypothala¬ mic-pituitary dysfunction (Abramsky et al 1973;Fenton & Kleinman 1974;Pai et al 1976).…”

A case of pituitary apoplexy with spontaneous recovery.

“…Although it is well noticed that tuberculous meningitis may produce pituitary insufficiency (Summers et al, 1968;Haslam et al, 1969), it seemed unlikely that the acute meningitis itself caused the sudden development of pituitary failure in the present case. There are two factors to be responsible for the acute development of hypopituitarism with the apoplexy (Rovit et al, 1972).…”

Intra cranial complications of tuberculous otitis media

“…Pituitary and hypothalamus involvement due to ischemia may lead to obesity, diabetes insipidus or hypo gonadism. [ 41 42 43 ]…”