Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Overproduction of the active metabolite of vitamin D 1,25-dihydroxyvitamin D (1,25(OH)2D) has been described in sarcoidosis and other granulomatous diseases. High circulating concentrations of 1,25(OH)2D lead to increased intestinal absorption of calcium, possibly to enhanced bone resorption, and may result in hypercalcaemia and/or hypercalciuria. Data obtained in vivo and in vitro demonstrated that the unregulated production of 1,25(OH)2D lies within the granulomatous tissue and is controlled by glucocorticoids. This abnormal production of 1,25(OH)2D seems to be a general phenomenon of granulomatous processes, which is not exceptional in sarcoidosis, but appears seldom in tuberculosis. These abnormalities, however, are not pathognomonic of granulomatous processes, since they have been described in other diseases such as lymphomas.
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PMID:Calcium and vitamin D metabolism in granulomatous diseases. 158 15

Hypercalcaemia and hypercalciuria were diagnosed in a 21-week-old boy with miliary tuberculosis. The tuberculosis was treated with isoniazid, rifampin and streptomycin. After 2 months, streptomycin was replaced by ethambutol. The hypercalcaemia was treated initially with prednisone, which decreased the serum 1.25 (OH)2 cholecalciferol level but the serum calcium level remained unaltered. After calcium and vitamin D restriction, the serum calcium level normalized within 1 day. The patient's tuberculosis was treated and he remains well.
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PMID:Hypercalcaemia in a child with miliary tuberculosis. 274 38

The "syndrome of inappropriate calcitriol secretion" may be observed in diseases with disseminated granulomas. The main examples are sarcoidosis and tuberculosis, but it can also be observed in fungal infections, in granulomas due to foreign bodies and in lymphomas. The syndrome is due to autonomous production of 1 alpha hydroxylase by granulomas. The insuing synthesis of calcitriol escapes normal regulation by serum calcium and phosphate levels. The syndrome includes hypercalcemia, hypercalciuria, high 1,25(OH)2D3 serum levels and reduced PTH secretion. It can supervene in anephric or hypoparathyroid patients. The notion that calcitriol may be secreted extrarenally is new. It could have important bearings on several issues in nephrology, immunology and oncology.
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PMID:[Inappropriate calcitriol secretion syndrome]. 295 94

A variety of abnormalities in calcium and vitamin D metabolism have been reported in patients with active tuberculosis (TB), including hypercalcaemia, hypercalciuria and increased sensitivity to vitamin D. In this article, the frequency and nature of these abnormalities and the importance of extrarenal 1,25(OH)2D production are discussed.
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PMID:Abnormal calcium and vitamin D metabolism in tuberculosis. 785 12

Antituberculous chemotherapy agents, particularly rifampicin and isoniazid, affect vitamin D metabolism and can create biochemical evidence of vitamin D deficiency. Vitamin D deficiency induces a state of resistance to parathyroid hormone. This study sought to explain the temporary resolution of hypercalcaemia and hypercalciuria, during antituberculous chemotherapy with rifampicin and isoniazid, in a subject with a surgically proven parathyroid adenoma and coincidental spinal tuberculosis. Serum ionized calcium, 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, plasma parathyroid hormone, and 24-hour urine excretions of calcium, inorganic phosphorus and hydroxyproline were sequentially measured over a 3-year interval that included 18 months of antituberculous chemotherapy. Initial serum ionized calcium was 1.52 mmol/l (normal 1.20-1.35 mmol/l), 24-hour urine calcium excretion was 9.40 mmol/day (normal 1.25 to 7.50 mmol/day) and plasma intact PTH was 9.2 pmol/l (normal 0.0-4.5 pmol/l). During antituberculous chemotherapy the serum ionized calcium and 24-hour urine calcium excretion were normal but the plasma PTH rose to higher levels. Following completion of the chemotherapy, hypercalcaemia and hypercalciuria returned with levels similar to those observed pretreatment. Serum 25-hydroxyvitamin D was low at 6.25 nmol/l (normal 20 to 90 nmol/l) during antituberculous chemotherapy, but was normal before and after. Serum 1,25-dihydroxyvitamin D was normal throughout the 3-year interval. We conclude that the antituberculous chemotherapy induced relative vitamin D deficiency and resistance to parathyroid hormone action, thereby masking the hyperparathyroidism and hypercalcaemia until the chemotherapy was completed.
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PMID:Primary hyperparathyroidism masked by antituberculous therapy-induced vitamin D deficiency. 764 6

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

The hypercalciuria evolution and other bone metabolism parameters were evaluated in patients with tuberculosis after treatment. Twenty-two patients with tuberculosis and 54 normal subjects were studied; they consumed an average diet (calcium intake 1000 mg/day). Ten of these patients and nine normal subjects were also studied after a low calcium diet (400 mg/calcium/day) and after a load of oral calcium of 1000 mg (calcium absorption test). The study with an average diet was performed after 1 week (basal) and 3, 6, and 12 months after the antituberculosis treatment was started; the calcium absorption test was carried out 2 weeks, 3 and 12 months after the treatment was started. On an average diet, patients with tuberculosis presented, at baseline state, lower calcidiol levels than normal controls. Serum calcitriol levels at baseline were higher than at 6 and 12 months. Serum parathyroid hormone (PTH) levels in patients with tuberculosis were lower than in normal controls at baseline, but these levels were similar to controls at 3, 6, and 12 months after treatment. During the calcium absorption test and under basal conditions, patients with tuberculosis showed lower serum PTH and calcidiol levels in all the dietetic situations than in normal controls. However, serum calcitriol levels were higher than in controls after the restrictive diet. After 3 months of treatment, urinary calcium excretion was normal in patients with tuberculosis during the average and low diets, but higher than in control group after calcium load. After 12 months of treatment, all the biochemical parameters of the patients with tuberculosis were similar to the control group under all the dietetic situations. These data indicate that antituberculous treatment, although it may contribute to the production of some alteration in the calcium and vitamin D metabolism, basically favors the correction of disturbances associated with tuberculosis.
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PMID:Remission of hypercalciuria in patients with tuberculosis after treatment. 866 78

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

The incidence of renal calculi has been evaluated to be 25% in urogenital tuberculosis patients. The stone could be caused due to the host, the pathogenic organism, or possibly by the treatment. Studies were carried out to find out the efficacy of vitamin E supplementation in reducing the risk of stone formation in renal tuberculosis patients. The study constituted four groups, Group I with 30 normal volunteers, the second group comprised of 36 renal tuberculosis patients (GuTb) a day before treatment. Third group comprised of 24 patients with regular anti tuberculosis drug regimen for sixty days. In the fourth group, 12 patients were treated with anti tuberculosis drug regimen along with supplementation of antioxidant vitamin E (200 mg/day) for sixty days. Hyperuricosuria and hypercalciuria were observed in group II and group III patients, along with increased excretion of oxalate and creatinine, accompanied by decreased excretion of inhibitors such as citrate and glycosaminoglycans (GAGs). Renal damage was evident with increased leakage of Lactate dehydrogenase (LDH), Alkaline phosphatase (ALP) and gamma-Glutamyl transferase (gamma-GT) in renal tuberculosis patients. From the results of the above study, it is obvious that increased urinary oxalate levels leads to cellular damage in GuTb patients, which is a prerequisite for crystal retention as revealed by the elevated urinary marker enzymes. Antioxidant therapy prevents membrane injury thereby reducing the risk of stone formation. Hence vitamin E supplementation has a salubrious effect in preventing stone forming tendency with routine anti tuberculosis drug regimen.
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PMID:Salubrious effect of vitamin E supplementation on renal stone forming risk factors in urogenital tuberculosis patients. 1528 96

Sarcoidosis is a multiorgan system disease that often presents insidiously. The diagnosis is often made fortuitously upon routine chest radiography or that done for other reasons. Blacks are more commonly affected than whites and age of onset is typically adolescents to young adults. Lung involvement is common and symptoms may include cough, dyspnea and chest pain. Extrapulmonary symptoms may include the skin, joint and eye findings. Bilateral hilar adenopathy is the classic finding on chest radiograph. Anemia or other cell line deficiencies, elevated liver enzymes, hypercalciuria, and EKG abnormalities may also be present. Angiotensin converting enzyme levels may be elevated but are not diagnostic. Histopathological confirmation of noncaseating granulomas is essential for diagnosis. It is generally performed through a biopsy of the most peripheral site possible, although transbronchial biopsy is commonly required. Finally, other possible etiologies must be evaluated and differentiated with a particular emphasis on tuberculosis due to the multiple overlapping symptoms and findings. Newer techniques such as proteomics and transcriptional gene signatures may contribute to the understanding of the pathophysiology of sarcoidosis, and may even serve as diagnostic tools in the future.
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PMID:Diagnostic criteria for sarcoidosis. 2442 72


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