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

We report on a 29-year-old patient who received high doses of prednisone and cyclosporine for the treatment of Still disease. She consulted about dorsolumbar pain leading to physical disability. She presented multiple vertebral fractures, decreased lumbar bone mineral density in the rank of osteoporosis, high bone turnover, and associated hypercalciuria. Cyclosporine and corticoids induced severe changes in bone and mineral metabolism. All patients in treatment with these drugs should undergo radiology, bone densitometry and biochemical determinations of mineral metabolism at the beginning of therapy. Treatment with high doses of intravenous pamidronate (225 mg in 3 months), calcitonin (200/400 IU daily), tiazide (25 mg/daily), and kinesiotherapy mitigated the pain quickly and she recovered motility. We discuss this approach of treating osteoporosis with corticoids and immunosuppressors according to the present knowledge of bone biology.
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PMID:[Vertebral osteoporosis induced by corticoids and cyclosporine ina a patient with Still disease]. 1147 83

Nephrotoxicity is the most common and clinically significant adverse effect of calcineurin inhibitors. Cyclosporine and tacrolimus nephrotoxicity is manifested by both acute azotemia and chronic progressive renal disease and tubular zdysfunction. An elevation in the plasma potassium concentration due to reduced efficiency of urinary potassium excretion is common in cyclosporine-treated patients; it may be severe and potentially life-threatening with concurrent administration of an angiotensin converting enzyme inhibitor, which diminishes aldosterone release. Tubular injury induced by cyclosporine can also impair acid excretion. This may be presented as a hyperchloremic metabolic acidosis associated with decreased aldosterone activity and suppression of ammonium excretion by hyperkalemia. Some patients treated with cyclosporine develop hypophosphatemia due to urinary phosphate wasting. Renal magnesium wasting is also common presumably due to drug effects on magnesium reabsorption. Hypomagnesemia has also been implicated as a contributor to the nephrotoxicity associated with cyclosporine. Both cyclosporine and tacrolimus are associated with hypercalciuria. Attention must be paid to drug dose, side effects, and drug interactions to minimize toxicity and maximize efficacy.
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PMID:Electrolyte and Acid-base disturbances induced by clacineurin inhibitors. 2445 11