Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary hyperparathyroidism has been increasingly diagnosed among whites since the advent of the biochemical autoanalyzer. However, the condition remains uncommon among Orientals. Our experience with 31 patients at the Queen Mary Hospital, University of Hong Kong, in the periods before and after we began to use the biochemical autoanalyzer was reviewed. The prevalence of primary hyperparathyroidism rose slightly from 3.1 to 3.7 per 100,000 hospital population. In both periods skeletal manifestation was the major clinical presentation, followed by hypercalcemic symptoms and urologic disease. Asymptomatic hypercalcemia occurred in three of 31 patients despite the use of the biochemical autoanalyzer. Preoperative localization was carried out in 27 patients and was helpful in nine (33.3%) of them. The surgeon explored all four parathyroids, removed the diseased gland(s), and examined a biopsy specimen of one normal-appearing gland. There were 27 adenomas, two carcinomas, one four-gland hyperplasia, and one sarcoidosis. Twenty-eight patients had transient hypocalcemia after parathyroidectomy and required calcium supplements for variable periods. Before and after we began to use the biochemical autoanalyzer, there was minimal change in the prevalence and clinical pattern of primary hyperparathyroidism seen in our hospital. In our experience, successful parathyroidectomy depends more on the surgeon's operative technique than on preoperative localization.
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PMID:Primary hyperparathyroidism: its clinical pattern and results of surgical treatment in Hong Kong Chinese. 336 91

We describe a patient who initially formed calcium-containing renal stones owing to gouty diathesis and hypocitraturia. On therapy with 300 mg. allopurinol and 60 mEq. potassium citrate daily serum uric acid decreased from 9.2 to 5.8 mg. per dl., urinary pH increased from less than 5.5 to 6.6 and urinary citrate increased from 223 to 1,005 mg. per day. Four months later while still on this medical regimen, the patient presented with hypercalcemia (13.4 mg. per dl.), high serum 1,25-dihydroxyvitamin D (65 pg. per ml.) and hypercalciuria (598 mg. per day), which subsequently were found to result from sarcoidosis. Prednisone therapy normalized the disturbances in calcium metabolism. During 33 months of combined treatment with 7.5 to 10 mg. prednisone a day, allopurinol and potassium citrate, the patient was free of stones and he had normal urinary calcium, pH and citrate. However, a calcium stone formed 1 month after discontinuation of prednisone therapy, although treatment with allopurinol and potassium citrate was continued. The patient had marked hypercalciuria of 447 to 465 mg. per day, despite normal urinary pH, citrate and uric acid. This case represents calcium stone formation in a patient with 2 separate etiologies for stone disease, that is gouty diathesis and sarcoidosis. Therapeutic regimens directed at the correction of both metabolic disturbances were required to control renal stone formation.
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PMID:Gouty diathesis and sarcoidosis in patient with recurrent calcium nephrolithiasis. 337 3

A 74-year-old woman was admitted with fever, muscle and joint pain and a mild hypercalcemia. Rather suddenly she turned unconscious and bilateral papilledema was found. A subsequent CT of the brain, however, did not disclose signs of space-occupying masses or increased intracranial pressure. She died two days later and at autopsy there were no signs of incarceration. Microscopic examination revealed non-caseating epithelioid granulomas throughout the meninges and brain consistent with sarcoidosis.
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PMID:Bilateral papilledema with normal CT-scan in neurosarcoidosis. 342 90

Of 123 patients with sarcoidosis observed from 1971 to 1986, 4 had histologically proven renal involvement. Hypercalcemia was present in all of these 4 patients, hypercreatinemia in 3 and urolithiasis in one. Histologically renal interstitial nephritis or fibrosis was found in all 4 cases, and 3 cases showed sarcoid-like renale granulomas. In addition, nephrocalcinosis or mesangioproliferative glomerulonephritis was present in one patient each. Corticosteroid therapy corrected hypercalcemia in 3 patients and improved renal function in the patient with glomerulonephritis and in the case with interstitial fibrosis. One patient died of granulomatous myocarditis, renal insufficiency having been unaffected by corticosteroids.
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PMID:[Sarcoidosis of the kidney]. 343 93

The history of illness of an eight-year-old boy is presented. Fifteen days old he had been hospitalized because of vomiting, diarrhoea and prolonged jaundice. Alpha 1-antitrypsin deficiency (genotype PiZZ) was diagnosed. At the age of nearly eight complaints started, such as headache, apathy, nausea and vomiting. Sarcoidosis was diagnosed on account of hypercalcemia (3.48-3.68 mmol/l), an elevated serum angiotensin converting enzyme (60 U/l), a positive Kveim test and the fact that other diseases could be excluded. The prognosis of a combination of a serious alpha 1-antitrypsin deficiency and sarcoidosis is discussed. This combination, as far as we have been able to trace, has not been described before.
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PMID:[A patient with type ZZ alpha 1-antitrypsin deficiency and hypercalcemia caused by sarcoidosis]. 349 14

A 35-year-old white male with rheumatoid arthritis who had developed hypercalcemia, hypercalciuria, and nephrolithiasis was found to be abnormally sensitive to vitamin D as a result of lack of regulation of circulating 1,25-dihydroxyvitamin D (1,25-(OH)2D). An increase in daily intake of vitamin D from 10 micrograms (400 units) per day to 50 micrograms (2000 units) per day produced an abnormal elevation in serum 1,25-(OH)2D, hypercalcemia, and hypercalciuria which were corrected by prednisone. Serum 25-hydroxyvitamin D initially was abnormally low, and increased with vitamin D to values which were in the low normal range. There were significant positive correlations between serum 1,25-(OH)2D (p less than .05) and serum calcium and between serum 1,25-(OH)2D and urinary calcium (p less than .05). Serum immunoreactive parathyroid hormone, initially in the lower range of normal, decreased further during hypercalcemia. A radiograph of the chest, gallium scan, and serum angiotensin-converting enzyme activity were normal. No granulomas or evidence of lymphoma were found in biopsies of the liver and of several lymph nodes. It is concluded that the abnormal calcium metabolism in this patient resulted from increased circulating 1,25-(OH)2D and that the defect in vitamin D metabolism was not related to sarcoidosis, other granulomatous disease, Hodgkin's disease, or lymphoma. The relationship, if any, of the abnormal metabolism of vitamin D and calcium to rheumatoid arthritis remains to be established.
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PMID:Abnormal calcium metabolism caused by increased circulating 1,25-dihydroxyvitamin D in a patient with rheumatoid arthritis. 350 40

The sarcoidosis granuloma secretes 1-25 dihydroxyvitamin D (1-25(OH)2 D) at the origin of the hypercalcemia found in about 20 p. cent of sarcoidoses. Its mechanism was considered exclusively of a digestive nature, but the activity of osteoclastic stimulation of 1-25(OH)2 D must consider an associated bony origin. Nine patients with bouts of non-steroid sarcoidosis were studied by osseous histomorphometric analysis. In a patient with hypercalcemia and radiographic manifestations, a high degree of bone remodelling is demonstrated, with stimulation of osteoclastic and osteoblastic activity. In eight patients with normocalcemia, two subgroups are individualized: two patients present intramedullary sarcoidosis granulomas with increased contact resorption; six patients present a normal marrow: the total areas of resorption remain increased. It is concluded that the activity of osteoclastic resorption is increased in sarcoidosis, which may explain partially the hypercalcemia. The absence of titration of 1-25(OH)2 D in our study does not permit to precise the role of this enzyme in the genesis of hyperosteoclastosis, although this seems quite plausible.
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PMID:[The bone in non-corticoid-treated sarcoidosis. A histomorphometric study]. 356 82

Eight patients with sarcoidosis seen at the Royal Children's Hospital, Melbourne, during the past 10 years were reviewed. Five of the eight patients came from non-metropolitan areas. The major presenting symptoms were cough, fatigue and weight loss; peripheral lymphadenopathy and hepatomegaly were common. None of the patients had eye or central nervous system involvement. Seven patients had bilateral hilar adenopathy on chest radiograph and six had parenchymal lung changes. Angiotensin converting enzyme was measured in six patients and was elevated in all, while hypercalcaemia was present in three patients. Five patients had a tissue biopsy showing the characteristic non-caseating granulomas. Corticosteroid therapy was used for four patients and was given for hypercalcaemia in three patients and for severe restrictive lung disease in one patient.
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PMID:Sarcoidosis in children. 356 75

From October 1981 to the end of 1984, 13 patients with primary hyperparathyroidism (PHPT) and 17 with secondary hyperparathyroidism (SHPT) received fresh autografts of diseased parathyroid tissue into their subcutaneous abdominal adipose tissue. Because of previous surgery to treat hyperparathyroidism (HPT) (23%), concomitant thyroid surgery (26%), and a high proportion of multiglandular disease (73%), the patients were at high risk for HPT. During the follow-up period, hypercalcemia was diagnosed in five patients and successfully treated in four: by graft excision in two patients, by excision of a fourth gland from the neck in one patient, and with prednisolone in a patient with sarcoidosis. At follow-up (an average of 30 months after grafting), one patient had HPT and 29 others were euparathyroid. Parathyroid tissue can survive and function in adipose tissue, as was demonstrated by normocalcemia in 14 patients (whose only probable remaining parathyroid tissue had been transplanted into fat), by the demonstration that graft-dependent hypercalcemia could be eliminated by excision of the transplant, and by the demonstration of viable parathyroid tissue by microscopic examination of excised grafts. Autotransplantation of diseased parathyroid tissue into fat is simple and reliable. In cases of recurrent HPT, all or a portion of the graft can be removed while the patient is under local anaesthesia. If infiltrating growth occurs, broad excisions can be performed without sacrificing vital structures.
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PMID:Autotransplantation of diseased parathyroid glands into subcutaneous abdominal adipose tissue. 357 47

Calcium metabolism was evaluated in 39 patients with sarcoidosis. Hypercalcemia and/or hypercalciuria were found in 18 patients (46%) and serum 1,25-dihydroxyvitamin D was elevated in only 4 of 13 patients in whom this could be measured. By contrast, in patients with normal calcium metabolism serum 1,25-(OH)2D varied greatly, but the mean +/- SD value 156 +/- 70 pmol/l (n = 21) was also increased. This study provides further evidence for a kidney and parathyroid independent abnormal regulation of 1,25-(OH)2D in sarcoidosis. The results of follow-up (1-4 years) of untreated (n = 16) and treated (n = 15) patients support the suggestion that 1,25-(OH)2D may reflect the systemic granulomatous process (disease activity?). The mechanism for abnormal calcium metabolism remains very complex and may not result from increased serum levels of 1,25-(OH)2D alone. There was no correlation between serum 1,25-(OH)2D and either serum calcium or urinary calcium excretion. The sensitivity of target organs to 1,25-(OH)2D may be changed, whether or not resulting in abnormal calcium metabolism.
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PMID:Calcium metabolism in sarcoidosis. A follow-up study with respect to parathyroid hormone and vitamin D metabolites. 369 20


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