Any patient with severe hypopituitarism is liable to have episodes of a particular type of coma. She may recover from the first few attacks, but ultimately one of them proves fatal. A detailed description of this coma has already been given (Sheehan and Summers, 1949), and only the main aspects need be summarized here. To save space, the recent literature will not be analysed in the present paper.The coma does not usually develop until the hypopituitarism has been present for several years, though occasionally it has been reported as occurring within a few weeks after the destruction of the gland. In many cases it follows some minor infection, or attacks of vomiting and diarrhoea, or some surgical operation. The patient gradually becomes drowsy, and, within a day or so, stuporous. She then passes into deep coma, which is sometimes preceded by one or two convulsions. During the stage of coma she may lie in a rigid, curled-up position and resist interference, or she may be flaccid andunresponsive to stimruli. In many cases there is no pulse at the wrist, and the heart sounds are almost inaudible. The methods investigated in these patients were: (1) no therapy; (2) the administration of large doses of glucose, to treat any possible hypoglycaemia; (3) the administration of cortisone, with the object of correcting a possible acute deficiency of corticosteroid hormones; (4) the administration of sodium chloride and deoxycortone, in order to correct disturbances of electrolyte metabolism; and (5) direct treatment of the hypothermia. Cases Having No TherapyTwo of the patients who were not very deeply comatose were left without any specific therapy but under careful observation. With rest in a warmed bed they gradually recovered in the course of two to three days. The possibility that the warmth may have contributed to their recovery must be seriously considered in view of the results obtained by active treatment of hypothermia. GlucoseIn one patient, in whom a severe hypoglycaemic coma had been produced by insulin, the intravenous administration of 100 ml. of 25% glucose solution produced a dramatic and complete recovery within a few minutes. This is a special case, but the literature contains several reports of patients with hypopituitarism who spontaneously developed coma associated with severe hypoglycaemia, and whose coma responded equally rapidly to intravenous glucose.Four patients with spontaneous coma were given 1 to 2 litres of 10% glucose solution intravenously in the course of two hours. Two of these showed some improvement within a few minutes. Instead of lying flaccid they began to make spontaneous movements and resisted interference; when attempts were made to rouse them they became noisy but incoherent. With continued administration of glucose during the next two days both patients gradually returned to full consciousness. One of these patients had a blood sugar of 70 mg. per 100 ml. before the administration of the glucose; the blood sugar in the other patient is not known. In contrast to these benefici...

Four men and 4 women with active acromegaly were treated with bromocryptine for 4 to 5 weeks. Serum growth hormone levels response to a glucose load were measured before and in the last weed of treatment. In only 1 patient was the grwotoh hormone response rendered normal by the drug. This patient, but none of the others, also showed an improvement in glucose tolerance and a reductin of the raised serum insulin levels during the glucose load. In three of the 8 patients vomiting was troublesome side effect of treatment.

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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...