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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe a case of pronounced symptomatic hypercalcemia as a consequence of thyrotoxicosis alone. Primary hyperparathyroidism and other secondary causes of hypercalcemia were excluded. Hypercalcemia completely abated after treatment of thyrotoxicosis. Notwithstanding that hypercalcemia is an unusual manifestation of hyperthyroidism, asymptomatic elevation of serum calcium concentration had been documented in up to one-fourth of patients with proved hyperthyroidism. The current case is unusual in that the patient demonstrated a significant degree of hypercalcemia secondary to hyperthyroidism alone, with a serum calcium level as high as 3.14 mmol/L. We further discuss the putative pathophysiology of this "thyroid bone disease," highlighting the repercussion on calcium and bone metabolism in hyperthyroidism.
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PMID:An unusual cause of hypercalcemia. 1525 27

Hypercalcaemia and hypertransaminasaemia are well recognized and not infrequent findings in hyperthyroidism in adults. Both conditions are seldom reported in children. Here we report the case of a 4-year-old girl with hyperthyroidism associated with hypercalcaemia and hypertransaminasaemia which were reversed after euthyroid state was achieved. We recommend that serum calcium and liver function should always be monitored in children with hyperthyroidism.
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PMID:Hypercalcaemia and hypertransaminasaemia in a child with hyperthyroidism. 1546 38

We describe the case of a 49-y-old female patient on long-term parenteral nutrition after abdominal surgery who failed to gain weight despite nutritional provision in excess of theoretical requirements. On investigation, she was found to have a negative nitrogen balance (-5.9 g) and to have a tri-iodothyronine thyrotoxicosis but without many of the typical clinical features of hyperthyroidism. The patient also had mild hypercalcemia and hyperphosphatemia, which resolved fully after mobilization and treatment of the thyrotoxicosis. A derangement of the liver function tests was observed, which worsened progressively during parenteral nutrition but resolved promptly at its discontinuation. This case illustrates the importance of carrying out appropriate investigations including all thyroid function tests on patients who fail to gain weight on nutritional support.
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PMID:Failure to gain weight on long-term parenteral nutrition attributed to tri-iodothyronine thyrotoxicosis. 1556 93

Hypercalcemia is a frequent finding in clinical practice. All possible causes must be considered in a patient with hypercalcemia. The association between both benign or malignant thyroid disease and primary hyperparathyroidism is well recognized. Up to 65% with primary hyperparathyroidism have associated thyroid abnormality. Hypercalcemia has also been associated with many malignant conditions. But, it is rarely seen in digestive tract cancer, such as carcinoma of gallbladder. Hypercalcemia syndrome is an absolutely rare entity. It is coexisting with hyperthyroidism, primary hyperparathyroidism and cancer of the gallbladder.
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PMID:Hypercalcemia syndrome. Coexisting hyperthyroidism, primary hyperparathyroidism and cancer of the gallbladder. 1604 66

In sarcoidosis, the thyroid and the kidneys are infrequently affected. Clinically recognizable thyroid involvement occurs in < 1% of sarcoidosis patients. Hyperthyroidism, myxodema, and thyroid occur with an equal frequency. It is important to distinguish sarcoidosis of the thyroid from other infections and disorders of the gland. Renal involvement may present as granulomatous infiltration of the renal parenchyma, glomerulonephritis, renal arteritis, and nephrocalcinosis or renal stones. The latter are due to abnormalities of calcium metabolism. Hypercalcemia occurs in about 10 to 13% of sarcoidosis patients; hypercalciuria is three times more frequent. Calcium abnormalities may precede, follow, or occur at any time during the course of sarcoidosis. An endogenous overproduction of 1,25-dihydroxyvitamin D [1,25-(OH (2))-D (3)] by granulomatous tissue and activated macrophages results in an increase of intestinal absorption of calcium. Corticosteriods, chloroquine, and hydroxychloroquine subdue 1,25-(OH (2))-D (3) production and correct hypercalcemia and hypercalciuria.
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PMID:Sarcoidosis of the thyroid and kidneys and calcium metabolism. 1608 53

Calcium is a major ion in human metabolism and its level is highly controlled. This regulation is performed via the Calcium Sensing Receptor, a discovery which ten years ago led to the explanation of a number of clinical disorders. The syndromes caused by CaSR abnormalities are characterized by hypercalcemia or hypocalcemia, associated with inappropriate calciuria. An underlying genetic or auto-immune cause may be demonstrated. High blood calcium levels linked to mutations of the CaSR gene lead to familial hypocalciuric hypercalcemia and the neonatal and non neonatal forms with severe hypercalcemic. Hypocalcemia determined by mutations in the CaSR gene include autosomal dominant hypocalcemia and its sporadic form. Another clinical presentation similar to Bartter syndrome has been reported. Auto-antibodies directed against CaSRs, seen in auto-immune diseases, can lead to similar clinical presentations. Finally, CaSR polymorphisms modulate the range of blood calcium levels. With diagnosis of these diseases deleterious therapeutics can be avoided. The discovery of this receptor has led to new therapeutic prospects such as calcimimetics for hyperthyroidism.
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PMID:[Calcium sensing receptor: physiology and pathology]. 1659 58

Primary hyperparathyroidism is the most frequent cause of hypercalcemia in ambulatory patients. Elevated serum parathyroid hormone in the presence of persistent hypercalcemia is the diagnostic sine qua non for primary hyperthyroidism. Since examination of serum calcium became a routine diagnostic test, most patients with primary hyperparathyroidism are asymptomatic at the time of diagnosis. Primary hyperparathyroidism in most of patients is caused by parathyroid adenoma, and parathyroid hyperplasia and cancer are rare causes of the disorder. Parathyroidectomy is the primary treatment of choice for primary hyperparathyroidism by any cause. Parathyroidectomy should be performed in most of patients with primary hyperparathyroidism, but asymptomatic or only mildly hypercalcemic patients are treated according to the guidelines for surgical treatment established by the NIH Consensus Development Conference in 2002. For patients with osteoporosis who are not indicated for or decline surgical procedures can be treated with bisphosphonates.
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PMID:[Primary hyperparathyroidism]. 1697 86

We report a case of theophylline-induced hypercalcemia. The patient, a 51 year old women, had been administered theophylline for about five years because of bronchial asthma. She was referred to us in March 2003 for the treatment of renal failure and hypercalcemia(15.2 mg/dL), which had been increasing since 2001. Clinical and laboratory findings were not consistent with any endocrinopathy. We suspected drug induced hypercalcemia. Three months after discontinuation of theophylline therapy, the hypercalcemia was completely cured. When admitted to our hospital, the patient was diagnosed as also having Hashimoto's disease. Hyperthyroidism might enhance the effect of theophylline on parathyroid hormone action. Therefore, theophylline induced hypercalcemia even though she was taking the therapeutic level. Moreover, her calcium excretion did not increase despite hypercalcemia. We concluded that her hypercalcemia was induced by theophylline and hyperthyroidism, and that hypocalciuria might have enhanced these conditions.
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PMID:[A case of theophylline induced hypercalcemia]. 1757 91

Systemic fungal infections are increasingly reported in immunocompromised patients with hematological malignancies, recipients of bone marrow and solid organ allografts, and patients with AIDS. Mycoses may infiltrate endocrine organs and adversely affect their function or produce metabolic complications, such as hypopituitarism, hyperthyroidism or hypothyroidism, pancreatitis, hypoadrenalism, hypogonadism, hypernatremia or hyponatremia, and hypercalcemia. Antifungal agents used for prophylaxis and/or treatment of mycoses also have adverse endocrine and metabolic effects, including hypoadrenalism, hypogonadism, hypoglycemia, dyslipidemia, hypernatremia, hypocalcemia, hyperphosphatemia, hyperkalemia or hypokalemia, and hypomagnesemia. Herein, we review how mycoses and conventional systemic antifungal treatment can affect the endocrine system and cause metabolic abnormalities. If clinicians are equipped with better knowledge of the endocrine and metabolic complications of fungal infections and antifungal therapy, they can more readily recognize them and favorably affect outcome.
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PMID:Endocrine and metabolic manifestations of invasive fungal infections and systemic antifungal treatment. 1877 5

The present study was aimed to evaluate the calcium bioavailability of pearl powder for humans. Both the nanonized pearl powder (NPP) and the micronized pearl powder (MPP) prepared by a dry grinder were tested. A group of healthy adults free from hyperthyroidism, hypercalcemia, and hypocalcemia were recruited as the subjects for oral administration with the pearl powder. The bioavailability was evaluated by the serum total calcium increment, the serum intact parathyroid hormone (iPTH) reduction, and the urine calcium/creatinine ratio increment in 6 h after administration. The results show better absorption and retention of calcium from NPP, as reflected with the shorter time elapsed before the maximum concentration of calcium appeared in the serum, higher iPTH reduction, more calcium absorption, and higher maximum calcium concentration (C(max)) in serum after ingestion, than that from MPP. We conclude that pearl powder is a beneficial source of calcium for adults and that nanonization improves its calcium bioavailability.
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PMID:Calcium bioavailability of nanonized pearl powder for adults. 1902 9


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