Metabolic Observations in a Case of Thyrotoxicosis With Hypercalcemia*

Kleeman, Charles R.; Tuttle, Stewart G.; Bassett, Samuel H.

doi:10.1210/jcem-18-5-477

Cited by 60 publications

(7 citation statements)

References 25 publications

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“…Elevation of the serum-calcium level in thyrotoxicosis, but without alteration in the serum phosphate or alkaline phosphatase, is recorded by many authors (Stanley and Fazekas, 1949;Rose and Boles, 1953 ;Pribek and Meade, 1957;Kleeman et al, 1958 ;Bortz et al, 1961). Laake (1955), Krane et al (1956), and Cook et al (1959) note alteration in the alkaline phosphatase alone, this only occurring during treatment in the patients described by the last-named authors.…”

Section: Results Of Biochemicalmentioning

confidence: 94%

Hypercalcaemia in Thyrotoxicosis

Guyer¹

1965

BMJ

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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.

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Section: Results Of Biochemicalmentioning

confidence: 94%

Hypercalcaemia in Thyrotoxicosis

Guyer¹

1965

BMJ

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“…Osteoporosis (Cook et al, 1959), and osteomalacia have also been described (Follis, 1953), although the more recent studies of Adams et al (1967) do not support the suggestion that osteomalacia is a feature of hyperthyroidism. Thyrotoxic bone disease is not seen more frequently because the underlying disorder in the majority of cases is corrected before the demineralization proceeds to a clinically demonstrable level (Kleeman, Tuttle & Bassett, 1958). Case 1 presumably had mild osteitis fibrosa as the phosphatase was raised before treatment and rose further after treatment, before eventually settling to normal, a phenomenon which has been noted previously by Dent & Harper (1958).…”

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confidence: 72%

Hypercalcaemia in thyrotoxicosis with and without hyperparathyroidism

Richards

1970

Postgraduate Medical Journal

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“…Decreased PTH concentration in hyperthyroid patients would account for the increase in tubular reabsorption of phosphorus and decreased calcium excretion (fractional tubular reabsorption of calcium [11].…”

Section: Discussionmentioning

confidence: 99%

Bone Mineral Density and Metabolic Indices in Hyperthyroidism

et al. 1991

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Hyperthyroidism can alter bone metabolism by increasing both bone resorption and formation. The increase in bone resorption predominates, leading to a decrease in bone mass. To assess the effect of hyperthyroidism on bone and mineral metabolism, we measured bone density using single photon absorptiometry in 30 untreated hyperthyroid patients. Patients were categorized into three groups based on sex and alkaline phosphatase levels: 44 sex-and agematched subjects were used as controls. Bone densities were significantly lower in all patient groups compared with controls. Alkaline phosphatase was found to be a useful marker for assessing severity of bone disease in hyperthyroid patients as there is significant correlation between the alkaline phosphastase level and degree of bone loss and decrease in bone density among patients with higher alkaline phosphatase value. Hyperthyroidism should be considered in the differential diagnosis of unexplained elevated alkaline phosphatase activity. Bone Mineral Density and Metabolic Indices in Hyperthyroidism. 1991; 11(5): 530-533 Thyroid disorders such as hyperthyroidism have profound effects on bone and mineral metabolism [1]. The skeletal changes in hyperthyroidism can be grouped into two main categories: first, localized changes in the fingers, consisting of periosteal hyperplasia leading to clubbing, a condition known as thyroid acropathy, which has been reported to occur in about 1% of the thyrotoxic patients; and second, a generalized loss of bone mass, taking the form of osteoporosis [2].There is a negative correlation between the duration of the disorder and the bone mass. Hyperthyroidism causes increased bone turnover leading to osteopenia and increased incidence of fracture [3].Both osteoblastic and osteoclastic activities are increased, with bone resorption exceeding bone formation.Bone biopsy usually shows decreased trabecular bone volume and increased cortical porosity [4]. Radiological signs of hyperthyroid bone disease vary between 3.5 and 50% [5], depending on the severity of the disease as well as on the observer, as it is a purely subjective assessment. Bone densitometry devices are used in assessing hyperthyroid bone disease and these often detect the skeletal complications that accompany hyperthyroidism, even when biochemical or radiological evidence of bone disease is absent [6].Single photon absorptiometry (SPA) is used to assess appendicular bones only, as tissue composition surrounding the bone mass has to be uniform and minimal. The method was based on the principle described by Cameron et al [7]. SPA was used in this study to examine the effect of hyperthyroidism on bone metabolism.

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Metabolic Observations in a Case of Thyrotoxicosis With Hypercalcemia*

Cited by 60 publications

References 25 publications

Hypercalcaemia in Thyrotoxicosis

Hypercalcaemia in Thyrotoxicosis

Hypercalcaemia in thyrotoxicosis with and without hyperparathyroidism

Bone Mineral Density and Metabolic Indices in Hyperthyroidism

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