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

In this study we examined the incidence of hypercalcaemia among patients with tuberculosis in Malaysia. Serum calcium concentration and other calcium metabolism parameters were studied in 43 newly diagnosed tuberculous patients from the Kuala Lumpur General Hospital and the National Tuberculosis Centre. Forty-four patients admitted to the medical wards of the General Hospital, Kuala Lumpur were recruited as controls. The incidence of hypercalcaemia was found to be only 1/43 (2.3%). There was no significant difference between the mean serum calcium and other calcium metabolism parameters between the patients and the controls. Despite earlier reported incidences of 30-50%, this study showed that hypercalcaemia in tuberculosis is uncommon in Malaysia.
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PMID:Low incidence of hypercalcaemia in tuberculosis in Malaysia. 825 12

In patients with granulomatous diseases, disturbances in calcium metabolism have been described. The aim of the study was to evaluate alterations in calcium metabolism in patients with tuberculosis. Forty patients with tuberculosis (TB) were studied in a baseline state (calcium intake 1000 mg/day). Fourteen of these patients were also studied after restrictive calcium diet (400 mg/calcium/day) and after a load of oral calcium of 1000 mg. In all the studies, calcium and phosphorus were measured in serum and urine, and parathyroid hormone (PTH) in plasma. In addition, serum 25OHD and 1,25(OH)2D (calcitriol) levels were measured in the baseline state and after the restrictive diet. In the baseline state, 25OHD levels were lower and urinary calcium higher in TB patients than in the control group. No patients had hypercalcemia, but hypercalciuria was present in 10 patients (25%). The patients with tuberculosis were divided according to the presence or absence of hypercalciuria. In both groups, the 25OHD levels were lower than in controls. Hypercalciuric patients had lower plasma parathyroid hormone levels and higher serum calcitriol levels than the control group and the TB patients without hypercalciuria. Urinary calcium excretion after a calcium load was higher in TB patients with hypercalciuria than in controls. A positive correlation was found between the calcitriol levels and postcalcium load urinary calcium excretion in patients with calcium hyperabsorption. These data indicate that absorptive hypercalciuria is frequently observed in patients with TB and is possible due to inappropriately high serum calcitriol levels.
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PMID:Evidence of absorptive hypercalciuria in tuberculosis patients. 829 51

Excessive vitamin D causes marked and prolonged hypercalcemia by accelerating intestinal calcium absorption and bone resorption. Vitamin D induced hypercalcemia includes the toxic ingestion of excessive amount of vitamin D preparations, granulomatous diseases and lymphoproliferative malignancies. In vitamin D toxicity, the clinical courses vary depending on the vitamin D preparation responsible for the hypercalcemia. Hypercalcemia state continues for several months when D2 or D3 are responsible for the toxicity whereas the hypercalcemia would subside in a week when 1 alpha(OH) D3 or 1,25 (OH)2D3 are responsible for the toxicity. Abnormal calcium metabolism can be treated by hydration and glucocorticoids. Hypercalcemia is associated with variety kinds of granulomatous diseases, including sarcoidosis and tuberculosis. The granulomatous tissue is believed to be the site of the ectopic production of 1,25(OH)2D3 in which the regulation of the synthesis is quite different from that in the normal kidney. Glucocorticoid markedly diminishes the synthesis. Hypercalcemia associated with elevated serum 1.25(OH)2D3 levels is also found in patients with lymphomas and some other malignancies. However, there still are not sufficient evidences to prove that the excessive amount of endogenous 1.25(OH)2D3 is the primary cause of the hypercalcemia.
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PMID:[Hypervitaminosis D]. 848 81

The authors present a case of disseminated tuberculosis in a patient under dialysis with endstage renal disease. Fever, nocturnal sweating, anorexia, asthenia, ascites, lymph node involvement and granulomatous involvement of the bone marrow were observed. In the twenty nine months of renal failure which preceded the beginning of the tuberculosis, serum calcium levels were normal or low-normal and there was a secondary hyperparathyroidism. During that period the patient was treated with calcium carbonate and calcitriol. At the onset of tuberculosis, serum calcium levels rose above normal. Treatment with calcium and calcitriol was withdrawn but hypercalcemia remained unchanged. Serum concentration of parathormone fell significantly. Antituberculosis drugs were started. The resolution of active tuberculosis was accompanied by normalization of serum calcium levels and by elevation above normal of serum concentration of parathormone.
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PMID:[Tuberculosis and hypercalcemia]. 900 10

Hypercalcemia has been known to be associated with tuberculosis. In some studies it has been reported to occur commonly. It seems that the studies in which tuberculosis was complicated by hypercalcemia were retrospective and therefore the other causes of hypercalcemia could not be excluded. We have a great deal of experience concerning tuberculosis and have not seen a patient with hypercalcemia due to tuberculosis itself. Therefore we aimed to investigate whether tuberculosis really cause hypercalcemia in a prospective study. We evaluated 104 patients with tuberculosis aged between 14-85 (mean +/- SD 38.5 +/- 15) years, 73 males and 31 females, and 50 age-matched healthy subjects aged between 19-70 (mean +/- SD 39 +/- 13) years, 33 males and 17 females. No significant differences between the patients and healthy subjects were detected in terms of 250HD3, calcium and phosphate levels. Albumin levels were significantly higher in the control group than in the tuberculous group (p < 0.02). No significant difference was found between the calcium levels measured before the therapy (2.4 +/- 0.1 nmol/L) and after the therapy (2.4 +/- 0.2). We think that patients with tuberculosis are not at risk for hypercalcemia either before or during treatment and the development of hypercalcemia as a result of tuberculosis is rather doubtful and needs to be clarified.
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PMID:Does tuberculosis really cause hypercalcemia? 900 99

The prevalence of hypercalcemia in patients with untreated tuberculosis (TB) varies widely between countries. Since the vitamin D status and calcium intake are important determinants of hypercalcemia in TB, these two factors were compared among four populations (U.K., Hong Kong, Malaysia, Thailand) with a low prevalence (<3%) and two populations (Sweden, Australia) with a high prevalence (>25%). In the three Asian countries, the circulating vitamin D levels are abundant, but the calcium intakes are low. Subjects from the U.K. have the lowest circulating vitamin D level of all, although their calcium intake is high. In Sweden and Australia, both the circulating vitamin D levels and calcium intakes are high. Since serum 1,25(OH)2D concentration will only be raised if its substance for extrarenal conversion, 25(OH)D, is plentiful and the effect of a given serum 1,25 (OH)2D concentration on serum calcium is determined by the calcium intake, it is postulated that the regional variation in the prevalence of hypercalcemia in TB may be due to differences in the circulating vitamin D levels and calcium intakes in these populations.
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PMID:Differences in vitamin D status and calcium intake: possible explanations for the regional variations in the prevalence of hypercalcemia in tuberculosis. 1082 87

This report describes a forty-seven-year-old female patient with a complex medical history. She was suffering from an unspecified interstitial lung disease, papillary thyroid carcinoma which had been treated, hypoparathyroidism after thyroidectomy for which she was receiving dihydrotachysterol and calcium, and atrial fibrillation and congestive heart failure as a result of mitral stenosis. Shortly after mitral valve replacement she developed a severe hypercalcemia (serum calcium 5.95 mmol/l) during a febrile illness. At that time anti-tuberculous agents were also being administered for presumed tuberculosis. The possible mechanisms for this severe elevation of the calcium level are discussed. Immobilization, while Paget's bone disease was present, and perhaps enhanced activation of dihydrotachysterol by rifampicin, could have led to increased calcium-release into the circulation. Continuous supplecation of calcium and vitamin D, provoked dehydration and the mechanism of the milk-alkali syndrome also contributed to this extremely high calcium level. It is concluded that hypoparathyroid patients being treated with vitamin D and calcium should be carefully monitored in the case of an intercurrent illness or a change in medication.
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PMID:Unaccountable severe hypercalcemia in a patient treated for hypoparathyroidism with dihydrotachysterol. 1004 91

In 4 of our patients on chronic dialysis, we were intrigued by the association of hypercalcemia +/- hyperphosphatemia and normal intact PTH, with anicteric cholestasis without cytolysis. This picture occurred in 2 patients after they resumed dialysis because of a transplant rejection and in a third one after discontinuation of corticosteroids, prescribed for an idiopathic thrombocytopenia. No patient was under calcitriol, CaCO3 therapy, and their hypercalcemia persisted on a low calcium dialyzate (1.25 mmol/l). Obvious etiologies of hypercalcemia were not found: vitamin D or A intoxication, hyperparathyroidism, aluminum intoxication, hemopathy, HIV infection. The hypothesis of a granulomatous disease was made and a liver biopsy was performed showing granulomas with giant epitheloid cells. In one case foreign material (silicon ?) was present in the macrophages. Extensive investigations for sarcoidosis, tuberculosis and mycosis were negative. In 2 cases the so-called "dialysis" granulomatosis actually occurred in transplanted patients, suggesting the role of a transplantation related factor (toxic or virus). In the last case HCV seroconversion was present. In the 4 cases, corticotherapy led to the disappearance of hypercalcemia and to an increase of PTH. Our patients had the biological pattern of low bone turnover disease (hypercalcemia and normal intact PTH) and bone biopsy performed in 2 showed osteomalacia or ABD without aluminum. The association of this pattern with cholestasis should evoke liver granulomatosis, which should be confirmed by a liver biopsy and lead to a treatment by corticosteroids. The masking effect of previous corticoid therapy for transplantation should be pointed out. In 2 cases serial monitoring of plasma calcitriol showed a relation between decreasing high normal calcitriol with prednisone and normalization of calcemia, suggesting the role of inappropriate synthesis of calcitriol by the granuloma. In conclusion, liver granulomatosis should be looked for in dialysis patients on the association of unexplained hypercalcemia and normal PTH with anicteric cholestasis, and confirmed by a liver biopsy. Although still of unknown etiology, its evolution is favourable under corticotherapy.
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PMID:Liver granulomatosis is not an exceptional cause of hypercalcemia with hypoparathyroidism in dialysis patients. 1062 31

Hypercalcaemia is uncommon in HIV-infected patients and should suggest a different priority for differential diagnosis than would be considered in other settings. Although hypercalcaemia has long been associated with granulomatous diseases including tuberculosis, it has only recently been recognised that patients with illness due to Mycobacterium avium intracellulare (MAI) may develop it. We report a patient with AIDS in whom unexplained hypercalcaemia was the harbinger of clinically significant MAI infection. Patients with AIDS who develop hypercalcaemia should be closely evaluated for underlying MAI infection.
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PMID:Hypercalcaemia: a clue to Mycobacterium avium intracellulare infection in a patient with AIDS. 1066 39

Hypercalcemia occurs in most granulomatous disorders. High serum calcium levels are seen in about 10% of patients with sarcoidosis; hypercalciuria is about three times more frequent. Tuberculosis, fungal granulomas, berylliosis, and lymphomas are other conditions that are associated with disorders of calcium metabolism. These abnormalities of calcium metabolism are due to dysregulated production of 1,25-(OH2)D3 (calcitriol) by activated macrophages trapped in pulmonary alveoli and granulomatous inflammation. Undetected hypercalcemia and hypercalciuria can cause nephrocalcinosis, renal stones, and renal failure. Corticosteroids cause prompt reversal of the metabolic defect. Chloroquine, hydroxychloroquine, and ketoconazole are the drugs that should be used if the patient fails to respond or develops dangerous side effects to corticosteroid therapy.
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PMID:Hypercalcemia in granulomatous disorders: a clinical review. 1095 37


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