Die Knochen der Basedow-Kranken

Askanazy, M.; E, Rutishauser

doi:10.1007/bf01891731

Cited by 49 publications

(3 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thyrotoxicosis is often associated with negative calcium balance, with increased urine calcium, increased sweat calcium, and increased fecal calcium (1). Thyrotoxic patients with negative calcium balance may have radiologic evidence of osteoporosis, and bone biopsy may show the histologic appearance of osteitis fibrosa, with marked osteoclast activity (3)(4)(5)(6)(7). Increased urine hydroxyproline in thyrotoxicosis supports the evidence that bone resorption is increased although some of the urinary hydroxyproline is also of skin origin (8).…”

Section: Introductionmentioning

confidence: 99%

Direct stimulation of bone resorption by thyroid hormones.

Mundy¹,

Shapiro²,

Bandelin³

et al. 1976

J. Clin. Invest.

349

127

View full text Add to dashboard Cite

A B S T R A C T Although hypercalcemia, osteoporosis, and increased bone turnover are associated with thyrotoxicosis, no direct effects of thyroid hormones on bone metabolism have been reported previously in organ culture. We have now demonstrated that prolonged treatment with thyroxine (T4) or triiodothyronine (T3) can directly increase bone resorption in cultured fetal rat long bones as measured by the release of previously incorporated 'Ca. T4 and T3 at 1 ;M to 10 nM increased 'Ca release by 10-60% of total bone 'Ca during 5 days of culture. The medium contained 4 mg/ml of bovine serum albumin to which 90% of T4 and T3 were bound, so that free concentrations were less than 0.1 uM. The response to T4 and T3 was inhibited by cortisol (1 AM) and calcitonin (100 mU/ml). Indomethacin did not inhibit T4 response suggesting that T4 stimulation of bone resorption was not mediated by increased prostaglandin synthesis by the cultured bone. Matrix resorption was demonstrated by a decrease in extracted dry weight and hydroxyproline concentration of treated bones and by histologic examination which also showed increased osteoclast activity. The effects of thyroid hormones were not only slower than those of other potent stimulators of osteoclastic bone resorption (parathyroid hormone, vitamin D metabolites, osteoclast activating factor, and prostaglandins), but the maximum response was not as great. We conclude that T4 and Ts can directly stimulate bone resorption in vitro at concentrations approaching those which occur in thyrotoxicosis. This effect may explain the disturbances of calcium metabolism seen in hyperthyroidism.

show abstract

Section: Introductionmentioning

confidence: 99%

Direct stimulation of bone resorption by thyroid hormones.

Mundy¹,

Shapiro²,

Bandelin³

et al. 1976

J. Clin. Invest.

349

127

View full text Add to dashboard Cite

show abstract

“…A loss of skeletal calcium due to a disturbance of the gastro-intestinal tract and kidney would be expected to cause osteomalacia with a lowered level of serum phosphorus. These pathologic and chemical changes have not been observed (3,(22)(23)(24).…”

Section: Serum Calcium and Phosphorus Levelsmentioning

confidence: 77%

“…The term thyrotoxic osteoporosis has been used to refer to the rare instances of extreme demineralization, particularly in cases in which there are such findings as spontaneous compression fractures of the spine (4-6). The extensive histologic studies of Follis (23) and of Askanazy and Rutihauser (24) have disclosed that the bone lesion is not one of osteoporosis but more closely resembles an osteitis fibrosa generalisata. These histologic observations have been confirmed by balance and radioisotope studies (25).…”

Section: Serum Calcium and Phosphorus Levelsmentioning

confidence: 98%

Metabolic Observations in a Case of Thyrotoxicosis With Hypercalcemia*

Kleeman¹,

Tuttle²,

Bassett³

1958

The Journal of Clinical Endocrinology & Metabolism

View full text Add to dashboard Cite

Hyperthyroidism characteristically causes excessive urinary and fecal excretion of calcium and, rarely, hypercalcemia. These abnormalities were studied in a 58-ycar-old thyrotoxic male. The investigation consisted of a 125-day balance study as the patient became euthyroid and a similar 50-day balance study during a recurrence of the thyrotoxicosis. The excessive urinary and fecal loss of calcium bore little relationship to the calcium or caloric content of the diet or to the level of nitrogen balance. A high phosphate diet ameliorated the metabolic abnormality and corrected the hypercalcemia. Successful treatment of the thyrotoxicosis produced similar changes in calcium metabolism. Hypercalcemia was not present during recurrence of the thyrotoxicosis.The metabolic observations in this case and those previously reported strongly suggest that the excessive urinary and fecal excretion of calcium in thyrotoxicosis is due to a direct effect of thyroid hormone on osseous metabolism. The hypercalcemia is probably secondary to a disorder in the homeostatic mechanism(s) regulating the content of ionized calcium in the extracellular fluid.

show abstract

Hypoparathyroidism and Recurrent Hyperthyroidism

Rothenberg¹,

Redleaf²

1959

Arch Intern Med

View full text Add to dashboard Cite

A 39-year-old white housewife was first seen on Feb. 19, 1958. She had had a subtotal thyroidectomy for a toxic nodular goiter in December, 1957. Following surgery, hypoparathyroidism and hypothyroidism developed. When we first saw the patient, she was taking 150,000 units of vitamin D, 8 gm. of calcium gluconate, and 2 grains (130 mg.) of thyroid extract per day.Initially, she complained only of aerai paresthesias and circumoral numbness. Physical ex¬ amination revealed a blood pressure of 130/80 and pulse of 80. There was a well-healed thyroidectomy scar. No thyroid tissue was palpable. Chvostek and Trousseau signs were easily elicited. White cell count, hemoglobin, urinalysis, blood urea nitrogen, serum albumin and globulin, and chest x-rays were all normal. A serum calcium was 8.2 mg. % ; serum phosphorus was 5.6 mg. %. A urinary Sulkowitch test gave a trace reaction.When seen on March 28, five weeks later, she had decreased her vitamin D to 50,000 units per day and had omitted calcium gluconate because of nausea and 4+ urinary Sulkowitch reactions. She had also noted recent weight loss and weakness. Her pulse was 120, and her palms were warm. Serum calcium was 9.1 mg. %, and phosphorus was 4.5 mg. %. The dose of thyroid was reduced to V/2 grains (97.5 mg.). Protein-bound-iodine determinations just before and one week after the reduction of thyroid medication were 9.5/ig. % and 6.5/ig. %, respectively.During the following month paresthesias re¬ curred and the patient resumed calcium gluconate and increased her vitamin D to 100,000 units per day. When seen on April 25, her pulse was 96. There was a questionable lid lag. Her palms were not sweaty. The Chvostek and Trousseau signs were easily elicited. Serum calcium was 8.2 mg. % and phosphorus 4.3 mg. % at this time. Thyroid medication was reduced to 1 grain (65 mg.) daily.Six weeks later, on June 6, a distinct nodule was palpable in the superior pole of the left lobe of the thyroid. The patient had noted this swelling herself since her last visit. Her pulse was 80. Her palms were cool. Serum calcium was 8.8 mg. % and phosphorus 4.1 mg. %.On July 18, she complained of palpitations, dyspnea on exertion, and increased thirst. Urinary Sulkowitch reactions had been 3+ and 4+. Her pulse was 94; her palms were warm, and the same thyroid nodule was palpable.A serum calcium determination was unsatisfac¬ tory at this time. Serum phosphorus was 4.5 mg. %, and protein-bound-iodine had risen to 11.5/tg. %. Vitamin D was decreased to 50,000 units daily. Thyroid extract was stopped.Two weeks later, on Aug. 1, the serum calcium was 10.0 mg. %, the highest value yet observed in this patient. Because the patient was still clinically hyperthyroid despite discontinuation of thyroid, methimazole, 40 mg. daily, was started.On Aug. 18, two and one-half weeks after beginning methimazole, the patient felt much bet¬ ter except for recurrence of paresthesias. Her pulse was 84. The palms were cool and dry, and

show abstract

Die Knochen der Basedow-Kranken

Cited by 49 publications

References 5 publications

Direct stimulation of bone resorption by thyroid hormones.

Direct stimulation of bone resorption by thyroid hormones.

Metabolic Observations in a Case of Thyrotoxicosis With Hypercalcemia*

Hypoparathyroidism and Recurrent Hyperthyroidism

Contact Info

Product

Resources

About