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)

The dissemination and activity of systemic disease was evaluated retrospectively in 50 patients with neurosarcoidosis, 24 of whom presented with neurologic symptoms. During follow-up, five patients never developed detectable systemic disease. In 26 patients, sarcoidosis had previously been diagnosed, but in 11 (42%) of them the neurologic symptoms were initially not connected with this disease. During follow-up, extraneural features were those of sarcoidosis in general. However, 23 patients (46%) had normal chest X-ray on admission to neurologic examinations. Fourteen (35%) of 40 examined patients had ocular changes, 13 (33%) of 39 hypercalciuria and 13 (26%) of 50 skin manifestations. Serum angiotensin converting enzyme (ACE) was elevated in only 31% of the patients. Measureable amounts of ACE were recorded in the cerebrospinal fluid from 13 of 17 examined patients. During follow-up the activity of neurosarcoidosis seemed to be linked to the course of systemic disease in general.
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PMID:Systemic manifestations and enzyme studies in sarcoidosis with neurologic involvement. 299 9

1,25-Dihydroxyvitamin D (1,25-(OH)2D) plays a crucial role in the maintenance of blood calcium and phosphorus levels and in normal skeletal mineralization. The concentration of this metabolite in the blood is, by necessity, tightly regulated. The most important stimuli for renal 1,25-(OH)2D synthesis include parathyroid hormone (PTH), its second messenger cyclic adenosine monophosphate (cAMP) and phosphate deprivation. Hypocalcemia and calcitonin, initially thought to act via stimulation of PTH release, have now been shown to directly stimulate 1-hydroxylation. Estrogens also increase 1,25-(OH)2D production, probably by upregulating renal PTH receptors. Inhibitors of the renal 25-(OH)D 1 alpha-hydroxylase include 1,25-(OH)2D itself, hypercalcemia, and phosphate loading. The PTH-vitamin D axis as modulated by the serum ionized calcium level controls adaptation to alterations in dietary calcium and sodium intake and to changes in skeletal turnover based on the level of physical activity. Although normally the renal production of 1,25-(OH)2D is tightly regulated and changes little in response to vitamin D challenge, there are certain conditions in which 1,25-(OH)2D appears to be substrate-dependent. These include hypoparathyroidism, hyperparathyroidism, vitamin D deficiency, sarcoidosis and the anephric state, conditions in which PTH is not well-modulated by alterations in serum ionized calcium or in which extrarenal synthesis of 1,25-(OH)2D occurs. In several disorders, including absorptive hypercalciuria, pseudohypoparathyroidism, hypophosphatemic rickets, and tumoral calcinosis, the regulation of the renal 1 alpha-hydroxylase appears to be altered.
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PMID:Normal and abnormal regulation of 1,25-(OH)2D synthesis. 306 16

Altogether 190 sarcoidosis patients were investigated including cytology of bronchoalveolar rinses in 31 patients, lung scintigraphy with 67Ga in 48, determination of the blood angiotensin converting enzyme activity in 18, and daily calciuria in 100 patients; 50 patients had erythema nodosum which turned out to be one of the main clinical symptoms of sarcoidosis activity. Corticosteroid therapy in patients with erythema nodosum was performed only in the presence of pulmonary changes and/or changes of the other internal organs. Extrathoracic manifestations (liver, splenic, renal, cardiac, CNS lesions) observed in 34 patients, deteriorated prognosis. Prolonged corticosteroid therapy was necessitated in all the cases; 4 patients were operated upon (splenectomy, nephrectomy, implantation of an artificial pacemaker); 3 patients died suddenly or from uremia. Comparison of the results of instrumental and laboratory methods showed that an increase in the lymphocyte count in bronchoalveolar rinses (by greater than 28%), total T-lymphocytes and T-active cells, 67Ga accumulation in the lungs, raised blood angiotensin converting enzyme activity, and hypercalciuria over 300 mg/day could be used as criteria of alveolitis activity in sarcoidosis. Corticosteroid therapy should be performed in stage II patients with the above symptoms only.
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PMID:[Modern criteria of sarcoidosis activity and approaches to glucocorticoid therapy]. 322 37

We determined the metabolic clearance and production rates of 1,25-dihydroxyvitamin D [1,25-(OH)2D] in 5 patients with sarcoidosis who had either hypercalciuria or hypercalcemia to examine whether abnormalities in the metabolism of this hormone existed. The mean MCR in the 5 patients with sarcoidosis [40 +/- 9 (+/- SD) mL/min] was similar to that in 13 normal subjects (37 +/- 6 mL/min) and that in 9 patients with absorptive hypercalciuria and renal stones (35 +/- 4 mL/min). However, the mean serum 1,25-(OH)2D concentration was significantly higher in the patients with sarcoidosis (211 +/- 60 pmol/L) than in either of the other 2 groups. The mean 1,25-(OH)2D production rate was markedly elevated in the patients with sarcoidosis (12.4 +/- 5.3 mumol/day), being more than 2-fold greater than the normal mean value (5.4 +/- 1.2 mumol/day). The highest production rates were found in patients with hypercalcemia, whereas subjects with hypercalciuria had production rates comparable to those in the patients with absorptive hypercalciuria. These data indicate that there is no impairment in the clearance of 1,25-(OH)2D in patients with sarcoidosis and that the elevated serum 1,25-(OH)2D levels are due to an increase in its production rate.
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PMID:Enhanced production rate of 1,25-dihydroxyvitamin D in sarcoidosis. 333 11

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 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

A case of chronic pulmonary sarcoidosis and hypercalciuria complicated by bilateral renal stones is reported. Urinary stones were pulverized by extracorporeal shockwave lithotripsy (ESWL) as the patient had declined any surgical procedure. The use of ESWL in conjunction with corticosteroids appears to be the treatment of choice in the management of renal stones secondary to abnormalities of calcium metabolism in sarcoidosis.
Sarcoidosis 1986 Mar
PMID:Hypercalciuria and renal stones in a sarcoidosis patient treated by extracorporeal shockwave lithotripsy. 357 18

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

A case of renal failure due to sarcoidosis with hypercalciuria and nephrocalcinosis is described. Prolonged treatment with inorganic absorbable phosphate significantly deteriorated the patient's renal function. After a sodium cellulose phosphate treatment, renal failure was completely reversed. We suggest that sodium cellulose phosphate is the treatment of choice in sarcoidotic renal failure induced by nephrocalcinosis.
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PMID:Sarcoid nephrocalcinotic renal failure reversed by sodium cellulose phosphate. 374 Jan 31

Although corticosteroids are effective in the treatment of hypercalciuria and hypercalcemia in chronic sarcoidosis, complications of their long-term use frequently limit therapy. We studied the efficacy of chloroquine in two patients with sarcoidosis who were unable to tolerate the dosage of corticosteroids required to control hypercalciuria and prevent the formation of renal stones. Over a three-year period, each patient received a 6-month and a 10-month course of oral chloroquine phosphate (500 mg per day) while continuing to receive corticosteroids at a fixed dose. Chloroquine therapy was associated with a significant reduction in levels of serum 1,25-dihydroxyvitamin D (1,25(OH)2D) and urinary calcium. We observed a direct correlation between serum 1,25-(OH)2D levels and 24-hour urinary calcium excretion, supporting the hypothesis that excessive serum 1,25-(OH)2D is responsible for the hypercalciuria in sarcoidosis. Serum levels of 25-hydroxyvitamin D (25-(OH)D) did not change with therapy, suggesting that chloroquine may act by inhibiting the conversion of 25-(OH)D to 1,25-(OH)2D. Current dosage guidelines and ophthalmologic-surveillance techniques, which allow chloroquine to be administered with little risk of retinopathy, should permit an expanded role for this agent in the treatment of the calcium abnormalities of sarcoidosis.
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PMID:The effects of chloroquine on serum 1,25-dihydroxyvitamin D and calcium metabolism in sarcoidosis. 375


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