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)

About 80 percent of sarcoidosis cases are benign and do not require treatment, but 20 percent will have chronic unremitting disease for which therapy is essential. It is important that the physician identify this group and begin therapy promptly. If the disease is active, treat. If it is inactive, do not treat. Activity depends upon three major tests: serum angiotensin converting enzyme, gallium 67 scan, and bronchoalveolar lavage. The other consideration is involvement of vital organ systems; ie, active ocular disease, progressive pulmonary involvement as evidenced by increasing symptoms, impaired and deteriorating pulmonary function, or radiographic changes; hypercalcemia or hypercalciuria; central nervous system involvement; disfiguring cutaneous lesions; and myocardial sarcoidosis. Following a therapeutic decision to treat, adrenocorticoids are the drugs of choice. Methylprednisolone, prednisone, and cortisol are listed in order of benefit. Alternate day and/or low-dose steroids are increasing in popularity. Chloroquine phosphate is beneficial for skin lesions, while oxyphenbutazone has been found to be at least as effective as prednisone. Immunosuppressives may be used also. Chlorambucil and azathioprine have shown variable results. Cyclosporine (Cyclosporin A) shows promise and is now undergoing therapeutic trials.
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PMID:When should sarcoidosis be treated? 378 58

Sarcoidosis is frequently attended by hypercalciuria and sometimes by hypercalcaemia. The type of hypercalciuria and its relationships with disease extension and activity have rarely been investigated. In order to clarify these issues we undertook an investigation by a calcium absorption test in 39 patients with untreated thoracic sarcoidosis, and tried to establish correlations with vitamin D3 metabolism and some features of the disease. We found three types of responses. Group I (n = 12) with a normal test had normal 1,25-(OH)2D3 and rare extrathoracic localisations. Group II (n = 14) with absorptive hypercalciuria had higher serum calcium; 1,25-(OH)2D3 (p less than 0.001) and the free 1,25-(OH)2D3 index (p less than 0.05) were raised. Sarcoidosis was more often inflammatory, developing and disseminated. Group III (n = 13) had resorptive hypercalciuria, and hypercalcaemia was frequent. 1,25-(OH)2D3 (p less than 0.01) and the free 1,25-(OH)2D3 index (p less than 0.05) were raised but to the same degree as in Group II. Sarcoidosis was more disseminated and developing than in Groups I and II. In the 39 patients, iPTH and nephrogenous cAMP were low. Post-calcium load urinary calcium/creatinine (Ca/Cr) and 1,25-(OH)2D3 were correlated (p less than 0.05). Extrathoracic extension was associated with higher fasting urinary Ca/Cr (p less than 0.001), and development with higher post-load urinary Ca/Cr (p less than 0.001). Thus, absorptive hypercalciuria is related to the development of sarcoidosis and can be explained by high free 1,25-(OH)2D3, while resorptive hypercalciuria seems to be linked with disease extension. In such a case, the mechanism of osteolysis is not solely accounted for by high 1,25(OH)2 vitamin D3 serum levels, and we postulate that some other factor is at work, related to the extent of the granulomatous process.
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PMID:Resorptive versus absorptive hypercalciuria in sarcoidosis: correlations with 25-hydroxy vitamin D3 and 1,25-dihydroxy vitamin D3 and parameters of disease activity. 383 15

We have studied a hypercalcemic patient with sarcoidosis and advanced renal failure. Bone biopsy and urinary cAMP excretion indicated suppression of parathyroid function. 1,25(OH)2D levels were moderately elevated and dropped to low normal levels during prednisolone treatment. Discontinuation of prednisolone treatment caused deterioration of renal function and hypercalcemia, 1,25(OH)2D serum levels being within the normal range. Our data demonstrate the rapid speed at which prednisolone causes a drop in serum 1,25(OH)2D level. Since hypercalcemia was observed both during periods of hypercalciuria and normal serum 1,25(OH)2D levels, increased sensitivity to active vitamin D seems likely. There was no significant correlation between 25(OH)D, 24,25(OH)2D or 25,26(OH)2D. Furthermore there was no correlation between any of these three metabolites and either 1,25(OH)2D or serum calcium.
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PMID:Rapid effect of prednisolone on serum 1,25-dihydroxycholecalciferol levels in hypercalcemic sarcoidosis. 384 60

Hypercalcaemia can be caused by many disorders, but is most commonly due to primary hyperparathyroidism in outpatients, and to malignant disease in hospital inpatients. When mild (less than 3 mmol/L) it does not cause symptoms, but can have long term effects such as renal calculi. It is important that the aetiology of the hypercalcaemia be established, as it can reflect serious disease. In most patients the correct diagnosis can be suspected from clinical history and examination, and confirmed by laboratory tests and x-rays. The most difficult diagnostic problem is the patient with negative clinical findings, mild hypercalcaemia and mild renal impairment, when the parathyroid hormone level is normal or slightly elevated. When hypercalcaemia is severe (greater than 3.5 mmol/L), it can cause vomiting, polyuria, dehydration and renal impairment, and is then an important therapeutic problem. Therapy includes treatment of the cause, such as radiotherapy for malignant disease or surgery for primary hyperparathyroidism. In addition, it is usually necessary to treat the hypercalcaemia itself, and the initial step is always rehydration. If the plasma calcium concentration remains high, drug treatment must be added, the most effective and reliable agent being intravenous mithramycin. Aminohydroxypropylidene diphosphonate (APD), though less studied, may be equally useful in this situation. Glucocorticoids are not always effective, and phosphate may cause renal damage, particularly when given intravenously. For long term treatment of malignant hypercalcaemia, oral glucocorticoids and phosphate are often effective, and can be given in combination. When primary hyperparathyroidism cannot be corrected surgically, the hypercalcaemia (and hypercalciuria) are probably best treated with a low calcium diet and cellulose phosphate, a regimen also effective for the hypercalcaemia of sarcoidosis.
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PMID:Hypercalcaemia. What does it signify? 394 Aug 49

A case of sarcoidosis in a six months old male is reported. Clinical symptoms and biochemical and radiological data suggest involvement at least of three organs. Diagnosis was corroborated by pulmonary, hepatic an lymph node biopsy. Slight renal insufficiency appeared associated to hypercalcemia and hypercalciuria. Hyperaldosteronism also permits relationship with increased angiotensin-I-converting enzyme activity. Pulmonary lesions at this age, were note-worthy in this case. Finally, evolution was favorable with prednisone. Patient presents no symptoms during follow-up for four years.
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PMID:[Sarcoidosis in childhood. Presentation of a case in a very young child]. 406 74

Extensive experimental evidence has established a significant role of calciferol in the maintenance of normal calcium homeostasis. Present knowledge indicates that vitamin D(3) must first be converted to 25-OH-D(3) and then to 1,25(OH)(2)D(3), the most active known form of the steroid. Many of the factors regulating the rate of production of this last steroid from its precurser have been evaluated, and the concept that vitamin D functions as a steroid hormone seems to be well established. Deranged action of calciferol, caused by impaired metabolism of the steroid or through altered sensitivity of target tissues, may be involved in the pathophysiology of several disease states with abnormal calcium metabolism. It is noted that liver disease, osteomalacia due to anticonvulsant therapy, chronic renal failure, hypophosphatemic rickets, hypoparathyroidism, hyperparathyroidism, sarcoidosis and idiopathic hypercalciuria have possible relation to alterations in metabolism or action of vitamin D. The future clinical availability of 1,25(OH)(2)D(3) and other analogs of this steroid may offer potential therapeutic benefit in the treatment of certain of the disease entities discussed.
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PMID:Metabolism and action of the hormone vitamin D. Its relation to diseases of calcium homeostasis. 436 34

Sarcoidosis, a multisystem disease of unknown cause characterized by the formation of noncaseating granulomas, may involve any organ of the body, but the commonest sites of predilection are the lungs, lymph nodes, skin, and eyes. Sarcoidosis can be associated with polyclonal hyperglobulinemia, hypercalcemia, hypercalciuria, circulating immune complexes, cutaneous anergy, and in vitro depressed cell-mediated immunity. Recent studies of the cellular composition and cellular interactions of sarcoid-involved tissue have resulted in some insight into the pathophysiology of the disease. In early stages the predominance of activated T-helper cells in affected sites may account for many of the immunologic aberrations. The production of macrophage chemotactic substances by these cells may be the initial stimulus for the formation of the granuloma. The natural history of the disease is highly variable; the acute forms tend to resolve spontaneously, whereas the chronic forms rarely involute. Although multiple therapeutic modalities have been used and some have reportedly been effective, systemic corticosteroids remain the most effective available therapeutic agents.
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PMID:Sarcoidosis. An updated review. 637 53

A 22-year-old man with renal stones had persistent hypercalcemia with massive idiopathic hypercalciuria due to a primary renal tubular phosphorus leak. He did not have hyperparathyroidism or sarcoidosis but did have an elevated dihydroxycholecalciferol level, which contributed to his hypercalcemia.
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PMID:Hypercalcemia with elevated dihydroxycholecalciferol levels and hypercalciuria. A parathyroid concentration-independent mechanism. 669 52

According to the Subcommittee on Classification and Definition of Sarcoidosis, it is a multisystem granulomatous disorder of unknown etiology. It most commonly affects young adults and presents most frequently with bilateral hilar adenopathy, pulmonary infiltrates, and skin or eye lesions. The diagnosis is established when clinical findings and appropriate x-ray findings are supported by tissue biopsy specimens in which noncaseating epithelioid cell granulomas are found. Immunologic features of the disease include depression of delayed hypersensitivity reactions, suggestive of impaired cell mediated immunity, and increased or abnormal immunoglobulin levels. Hypercalciuria may occur, with or without hypercalcemia. The course and prognosis of the disease correlate with the mode of onset. An acute onset in the presence of erythema nodosum indicates a self-limited course with spontaneous resolution, whereas an insidious onset may be followed by a relentless course. Corticosteroids are useful when therapy is required, as well as to suppress inflammation and the occurrence of granulomatous changes.
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PMID:Sarcoidosis. 675 25

The state of vitamin D nutrition depends on synthesis in the skin under the influence of sunlight as well as on dietary intake. In European countries that do not fortify milk with vitamin D, reduced sun exposure is the major factor leading to a fall in body stores of vitamin D with age and to a high frequency of hypovitaminosis D in the elderly sick. In the US, because vitamin D is added to milk and the use of vitamin D supplements is more common, the dietary intake of vitamin D is relatively more important than in Europe, and the total vitamin D intake and body stores of vitamin D are generally higher. Nevertheless, body stores of vitamin D probably fall with age in the US as they do in Europe, and it is likely that some sick elderly persons in the US, especially among those confined to institutions, become vitamin D deficient. For several reasons, the vitamin D requirement increases with age, and a total supply of 15 to 20 micrograms/day (600 to 800 IU) from all sources is recommended. Special attention should be paid to persons most likely to need supplementation, such as the housebound, persons with malabsorption, and persons with interruption of the enterohepatic circulation. Osteomalacia, the bone disease produced by severe vitamin D deficiency, is less common in the US than in Europe, but subclinical vitamin D deficiency may contribute to the pathogenesis of hip fractures, both through increased liability to fall and through PTH-mediated bone loss. The extent to which vitamin D deficiency contributes to hip fractures in the US is unknown, and is an important area for future research. Excess intake of vitamin D or of its metabolites may result in hypercalcemia and extra-osseous calcification, particularly in arterial walls and in the kidney, leading to chronic renal failure. The dose of vitamin D that causes significant hypercalcemia is highly variable between individuals but is rarely less than 1000 micrograms/day. Smaller doses can cause hypercalciuria and nephrolithiasis and possibly impaired renal function. Vitamin D administration may raise plasma cholesterol but there is no convincing evidence that the risk of myocardial infarction is increased. The recommended total supply for the elderly of 20 micrograms/day is most unlikely to be harmful, except in patients with sarcoidosis or renal calculi.
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PMID:Vitamin D and bone health in the elderly. 676 68


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