Hypercalcaemia in Thyrotoxicosis

Abstract

Hypercalcaemia is now well recognized as a complication of thyrotoxicosis. It is the purpose of this paper to record a case of severe thyrotoxicosis and biochemical changes suggesting hyperparathyroidism. The changes were corrected by treatment of the thyrotoxicosis. CASE REPORTA man aged 28 years was first seen on 17 March 1960, when he gave a history of having epigastric discomfort, vomiting, and eructation for four weeks. He had lost more than 20 lb. (9 kg.) in weight during the preceding few weeks, and he had noticed thirst and polyuria. A succussion splash was heard, and pyloric stenosis was considered as the likely diagnosis. After admission four days later slight ocular prominence was noted, but he had no goitre or tremor. His pulse rate was 100 per minute, and his blood-pressure was 120/60 mm. Hg. His serum sodium was 144 mEq/l., chlorides 100 mEq/l., potassium 4.5 mEq/l., alkali reserve 54 vol.%, blood urea 50 mg. %. The fasting gastric residue was 10 ml. on two occasions. A barium meal revealed some pylorospasm, but no organic lesion.There was no radiological evidence of osteoporosis. On three occasions his sleeping pulse rate was above 90 per minute and his basic metabolic rate was found to be +35%. Radioactive iodine studies revealed a 24-hour neck uptake of 77% of the dose, and potassium perchlorate 1,000 mg. daily was started. His symptoms continued, and altogether he lost 17 lb. (8 kg.) in weight during the first two weeks in hospital. His condition then deteriorated sharply: his vomiting increased, and he became dehydrated and developed signs suggesting an acute thyrotoxic myopathy. His blood urea was found to be 106 mg.%, serum sodium 178 mEq/l., chlorides 101 mEq/l. His serum calcium was found to be 13.5 mg.% (see Table). Intravenous therapy and oral Lugol's iodine were started, with immediate improvement in his condition. The initial alkaline phosphatase was 16 King-Armstrong units %, and the serum phosphate 2.6 mg.%, but the lowest serum phosphate reading obtained was 1.8 mg. %. The blood samples were obtained without fasting. The urinary calcium excretion was 440 mg. in 24 hours on unlimited diet at the height of the illness, but after three days during which calcium intake was restricted to 265 mg. calcium per day the daily urinary excretion dropped to 275 mg. Nine days after his sudden deterioration the tubular phosphate reabsorption was 81 % and the phosphate/ creatinine clearance (employing endogenous creatinine) was 0.19, both being normal. The phosphate-excretion index was also normal at +0.075. These tests performed after the vomiting had ceased suggested that the biochemical disturbance was due to the thyrotoxicosis, and in fact anti-thyroid treatment resulted in the biochemistry reverting to normal after 11 days. Treatment has ceased, and there has been no relapse two years after stopping treatment.

Hypercalcaemia in thyrotoxicosis with and without hyperparathyroidism

“…The first authentic report of thyrotoxic hypercalcaemia was by Wijnbladh (1937), and similar cases to to this present one have been reported (Stanley & Fazekas, 1949;Guyer, 1965;Harris-Jones, Nakadar & Wells, 1967). The height of plasma (or serum) calcium can be extremely variable, and bears no relation to the severity of the thyrotoxicosis (Bortz et al, 1961;Baxter & Bondy, 1966).…”

Hyperemesis gravidarum due to thyrotoxicosis

“…proportions (Skrabanek, 1976;Gordon et al, 1974;Rose and Boles, 1953;Twycross and Marks, 1969;Harper and Osborne Hughes, 1970;Guyer, 1965).…”