Thryoid problems causing religious mania-addition of T3 helps

[Guest guest]

Thought you might be inteested in this case study I just found in a

medical journal (1957). T3 had been discovered 5 years before in 1952.

Case History

A man aged 52 was given a therapeutic dose of '31I in

December, 1953, to ablate the thyroid gland. He had

suffered from severe angtna of effort for several years, wh.cn

was becoming progressively worse. He had been maintained

on carbimazole prior to ablation of the thyroid, and had

been greatly benefited by this treatment.

Following ablation of the thyroid he was kept on a

maintenance dose of 0.1 mg. of L-thyroxine daily, on which

dose he remained almost free of angina and was able to

resume light work. He obtained his supply of thyroxine

from hospital until September, 1954, at which time it was

arranged that he should obtain further supplies from h s

local chemist. At his next attendance, in February, 1955, it

was noted that his weight had increased by a stone (6.4 kg.),

but he was otherwise well. Five weeks later, in April, 1955.

he was seen at the request of his doctor, who reported that

he had developed religious mania. His wife confirmed that

he had taken his dose of thyroxine regularly and that he had

become mentally abnormal quite suddenly about a week

before.

On examination it was apparent that he was suffering from

a paranoid psychosis. He was not retarded, and maintained

a degree of animation which might have been considered incompatible

with a psychosis due to hypothyroidisrn. Knowing

his usual appearance, a slight alteration in his facial

expression and some puffiness of the lower lids was

noticeable. The skin of his forearms was dry and

scaly, but there were no other signs of hypothyroidism. It

was thought that the paranoia had been precipitated by

hypothyroidism, and a plasma cholesterol of 510 mg. per

100 ml. confirmed this opinion. It was difficult, however,

to understand why this should have occurred after he had

been maintained in a satisfactory state on a maintenance

dose of 0.1 mg. of thyroxine daily for over a year.

Before he could be admitted to hospital he became violent

and was admitted to an observation ward. He was transferred

to HammersrMith Hospital the following morning. On

admission he was given 10 pg. of L-triiodothyronine intravenously

followed by a maintenance dose of 0.1 mg. of Lcirculation with cutaneous

flushing was noted within two

hou.rs of giving triiodothyronine. T'riiodothyronine was

given by intravenous injection daily, the dose being increased

by 10 pg a day. By the fourth day he was receiving 40 Mg.,

which together with the daily dose of 0.1 mg. of thyroxine

constituted a full replacement dose of thyroid hormone.

He now showed some evidence of hyperthyroidism with a

marked increase in peripheral circulation and sweating of

the palms of the hands, but there was no tachycardia or

recurrence of angina. He was less co-operative and wished

to be discharged from hospital. The dose of triiodothyronine

was reduced. During the course of the next week noticeable

improvement occurred from day to day, and within three

weeks of admission his mental state was normal. His progress

is shown in the accompanying chart (Fig. 1). He has

remained well since and has shown no further tendency

to psychiatric disturbance.

It was later found that he was being supplied by his

chemist with 0.1 mg. of DL-thyroxine,* thus explaining the

development of hypothyroidism. Rapid correction of hypothyroidism

was desirable because of the onset of mania, but

a delicate balance had to be maintained to avoid any recurrence

of angina. Triiodothyronine was eminently suitable

in these rather unusual circumstances.

Taken from a British medical journal 1957