Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We measured the rate of oxalate flux across the red-cell membrane in the steady state in 114 patients with a history of calcium oxalate kidney stones and in 25 controls. Of the patients, 98 had recurrent, "idiopathic" kidney stones, 8 had primary hyperparathyroidism, 7 had renal or urinary tract malformations, and 1 had primary hyperoxaluria. Oxalate exchange was significantly higher in the 98 patients with idiopathic stone formation than in the controls (-1.10 +/- 0.95 [SD] X 10(-2) min-1 vs. -0.31 +/- 0.12 X 10(-2); P less than 0.001); it was above the upper limits of normal in 78 of these patients. All 8 patients with hyperparathyroidism and the patient with primary hyperoxaluria had values in the normal range; 2 of the patients with renal or urinary tract malformation had values at the upper normal limit. A study of five families indicated that the abnormality is an autosomal monogenic dominant trait with complete penetrance and variable expressivity. Oxalate-tolerance tests were carried out in five pairs of brothers. One brother in each pair had the abnormality in oxalate flux, and had a significantly higher percentage of oxalate excretion at two hours after oxalate loading (18.09 +/- 3.07 [SD] vs. 10.37 +/- 3.08 percent; t = 3.97; P less than 0.005) and four hours (14.87 +/- 2.91 vs. 9.89 +/- 2.93 percent; t = 2.70; P less than 0.05). Treatment with oral hydrochlorothiazide (50 mg per day) or amiloride (5 mg per day) or both restored normal or nearly normal red-cell oxalate exchange in all of 33 patients who initially had increased rates. We conclude that an inherited cellular defect in oxalate transport may be a factor in "primary" calcium oxalate stone formation and that this defect may be corrected with diuretics.
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PMID:An inheritable anomaly of red-cell oxalate transport in "primary" calcium nephrolithiasis correctable with diuretics. 394 45

In 65 jejunolleal (JI) bypasses done from 1973-1979, there were nine Scott and 56 Payne (with Y-shaped anastomosis). Preoperative excess body weight (EBW) translated to the 1983 Metropolitan Tables was 112 +/- 30%. Eight patients are lost to follow-up. We reversed seven patients for renal stones (12%) accompanied by a vertical banded gastroplasty (VBG) and one because she demanded a VBG. Five patients were reversed by surgeons elsewhere for minor problems (three with an accompanying gastric reduction operation), and all five regained and requested a JI bypass again, which we now refused to undertake. This leaves 44 JI bypass patients being followed: loss of EBW is 71 +/- 22% at 12-18 years. The eight reversed by us accompanied by a VBG regained some weight (loss of EBW from initial weight is 56 +/- 18%). Liver biopsies were done for 5 years in 31 patients, and showed improvement by 36 months. Patients took predigested collagen capsules plus high protein and multivitamins. Injections of B12 are indicated in 18 patients, given every 3 months. Liver dysfunction has not occurred in the long-term. Low serum carotene levels persist. Migratory arthraigias were controlled by oral metronidazole and did not occur after the fifth year. Oxalate crystals remain on urinalysis. Potassium and magnesium replacement is not required now, and a mean of 2.5 stools per day is not a problem, with infrequent diarrhea after greasy foods. Metronidazole is continued in 33 patients to prevent foul flatus. One patient developed a brain tumor, one myxedema, and one primary hyperparathyroidism, thought to be complications of the bypass until diagnosed. Most patients appear to be doing well.
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PMID:Long-term Outcome in a Series of Jejunoileal Bypass Patients. 1075 27