Simultaneous hyperthyroidism and hyperparathyroidism

Frame, Boy; Durham, Robert H.

doi:10.1016/0002-9343(59)90199-8

Cited by 26 publications

(5 citation statements)

References 11 publications

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“…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. Cook et al also note that the plasma phosphate is normal or elevated, with which Puppel et al (1945) agree, andFrame andDurham (1959) suggest that a low serum phosphate accompanying hypercalcaemia in thyrotoxicosis suggests coincidental hyperparathyroidism.…”

Section: Results Of Biochemicalmentioning

confidence: 93%

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: 93%

Hypercalcaemia in Thyrotoxicosis

Guyer¹

1965

BMJ

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“…In most instances of clinical thyrotoxicosis, serum calcium levels remain within the usual range of normal. 46, 64 Rose and Boles 65 and others, 2,21,25,28,40,42,47,55,58,62,69,72 however, have reported hypercalcemia in thyrotoxicosis with disappearance during control of the hyperthyroidism. These rises were not associated with discernible changes in serum inorganic phosphorus and resemble those after various periods in our Na-DT 3-treated patients (who did not have hyperthyroidism).…”

Section: Discussionmentioning

confidence: 96%

“…Total protein 33 was increased by 0.5 and 0.6 gm% only at the end of 20 and 28 wk of therapy and was unchanged at the other 19 sampling points. Serum globulin74 was in-Dextrothyroxine effects 199 creased at16,20, 24,28,72, 88, and 104 wk and relatively stable at the end of the other 14 treatment intervals(Table Ill). The mean serum albumin levels 74 were slightly decreased only at 16 and 24 wk.…”

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confidence: 99%

Thyroid hormone‐like effects without thyrotoxicosis during one year's therapy with NA‐DT₃ for hypercholesterolemia

Danowski

Stephan

Nolan

et al. 1976

Clin Pharma and Therapeutics

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A thyroid hormone analogue, sodium dextro-triiodothyronine (NaDT3), at a dosage of 1 mg/day for 1 or 2 yr, decreased serum cholesterol levels about 30% in 26 hyperlipidemic adults. There were less sustained decreases in the serum phospholipids, and occasional lowering of the serum triglycerides, but no effects on body weight, blood pressure, or pulse rate. Changes recognized as variable concomitants of spontaneous or induced thyrotoxicosis, such as transient increases in fasting blood glucose, calcium, and globulin, persistent rises in alkaline phosphatase, and nonsustained decreases in hematocrit are consonant with the fact that Na-DT3 exerts about one tenth of the thyroid hormone activity of LT3. These changes, however, appear to represent actions of iodinated amino acids apart from those effects that result in clinical thyrotoxicosis.

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“…Hyperparathyroidism has been reported in association with various other endocrine disturbances including thyrotoxicosis (Frame and Durham, 1959), Cushing's syndrome (Raker, Henneman and Graf, 1962), acromegaly (Dent, 1962) and the Zollinger-Ellison syndrome (Summerskill et al, 1961). In addition, it is the principle endocrine disorder in the polyglandular syndrome (Ballard, Frame and Hartsock, 1964).…”

Section: Discussionmentioning

confidence: 99%

Diabetes mellitus and primary hyperparathyroidism

Walsh

Soler

Malins

1975

Postgraduate Medical Journal

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Summary Eight patients suffering from primary hyperparathyroidism and diabetes mellitus are reported. All of the patients are female. The clinical problems resulting from the co-existence of these two endocrine disorders and the similarity of their symptoms are discussed. The experience from a large diabetic clinic population suggests that the association of hyperparathyroidism with diabetes merits further investigation.

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Simultaneous hyperthyroidism and hyperparathyroidism

Cited by 26 publications

References 11 publications

Hypercalcaemia in Thyrotoxicosis

Hypercalcaemia in Thyrotoxicosis

Thyroid hormone‐like effects without thyrotoxicosis during one year's therapy with NA‐DT₃ for hypercholesterolemia

Diabetes mellitus and primary hyperparathyroidism

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Simultaneous hyperthyroidism and hyperparathyroidism

Cited by 26 publications

References 11 publications

Hypercalcaemia in Thyrotoxicosis

Hypercalcaemia in Thyrotoxicosis

Thyroid hormone‐like effects without thyrotoxicosis during one year's therapy with NA‐DT3 for hypercholesterolemia

Diabetes mellitus and primary hyperparathyroidism

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Product

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Thyroid hormone‐like effects without thyrotoxicosis during one year's therapy with NA‐DT₃ for hypercholesterolemia