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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary hyperparathyroidism resulted in calcium urolith formation and calcium nephropathy in 2 dogs. Uroliths composed of calcium phosphate were surgically removed from the bladder of one dog 3 months after surgical removal of a parathyroid adenoma. Five years later, hypercalcemia and urolithiasis had not recurred. In a second dog, calcium oxalate renal and bladder uroliths remained unchanged in size at 11 months after removal of a parathyroid adenoma. The possibility of primary hyperparathyroidism should be considered in any dog with calcium urolithiasis.
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PMID:Calcium urolithiasis in two dogs with parathyroid adenomas. 369 84

The use of C-terminal parathyroid (C-PTH) assays, performed at a commercial laboratory, was evaluated for one year at Charity Hospital, New Orleans. Of 72 patients, the most frequent diagnosis was primary hyperparathyroidism (1 degree HPT) (n = 17, 24 percent), followed by malignancy (n = 15, 21 percent), chronic renal disease (n = 10, 14 percent), and thiazide diuretics (n = 5, 7 percent). In the 1 degree HPT group, all were hypercalcemic (mean serum calcium, 11.6 ml per dL) and had elevated C-PTH. Patients with malignancy had higher mean serum calcium levels than patients with 1 degree HPT. Three patients with malignancy had elevated C-PTH; two had suspected coexisting 1 degree HPT and neoplasm; and one had suspected pseudohyperparathyroidism. Patients with chronic renal disease undergoing dialysis treatment had the highest C-PTH recorded (all had elevated C-PTH) but only 50 percent were hypocalcemic. Three of the five patients on thiazide diuretics had increased C-PTH, indicating that the withdrawal of this drug may unmask underlying hyperparathyroidism. Appropriate reasons for ordering C-PTH include evaluation of hypercalcemia (n = 32, 44 percent) or hypocalcemia (n = 12, 17 percent); indicated clinical reasons not included in the hyper- or hypocalcemic groups, including chronic renal disease in patients undergoing dialysis or transplant (n = 5, 7 percent); in suspected 1 degree HPT, (n = 5, 7 percent); and in patients with renal stones (n = 2, 3 percent) or on thiazide diuretics (n = 2, 3 percent). Based on laboratory and clinical criteria, C-PTH assay was appropriately used in 81 percent of the patients surveyed (58/72).
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PMID:Use of C-terminal parathyroid assays in a large metropolitan hospital. 397 May 18

Impairment of urine-concentrating ability is common in persons with chronic hypercalcemia. We assessed urine-concentrating ability in 40 patients with typical primary hyperparathyroidism and 10 patients with familial hypocalciuric hypercalcemia, a disorder resembling typical primary hyperparathyroidism but lacking some of its clinical complications. Urine-concentrating ability was determined during a dehydration test of 18-22 h. The two patient groups were comparable with respect to serum calcium concentration and creatinine clearance. In the group with familial hypocalciuric hypercalcemia, the duration of hypercalcemia was probably greater, because it commences during infancy; the urinary excretion rate for calcium was lower [6.6 +/- 5.4 (mean +/- 1 SD) vs. 14.8 +/- 7.5 meq/day; P less than 0.005]. Patients with familial hypocalciuric hypercalcemia showed higher maximal urinary osmolality (800 +/- 150 vs. 664 +/- 130 mosmol/kg; P less than 0.0005). Among the patients with typical primary hyperparathyroidism, there was a negative association between maximal urinary osmolality and urinary cAMP (r = -0.40; P less than 0.05), but there was no significant relation between maximal urinary osmolality and the urinary excretion rate for calcium. Among 18 patients retested within 1 month after surgical correction of typical primary hyperparathyroidism, urine-concentrating ability did not improve. In patients with typical primary hyperparathyroidism, impairment in urine-concentrating ability reflects features of the chronic disease state, as it is not rapidly reversible by correction of that state. However, in patients with familial hypocalciuric hypercalcemia, longstanding hypercalcemia is not associated with obvious impairment of urine-concentrating ability. Complete or partial freedom from impairment of urine-concentrating ability and from calcareous renal disease are expressions of the generally mild course in familial hypocalciuric hypercalcemia.
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PMID:Maximal urine-concentrating ability: familial hypocalciuric hypercalcemia versus typical primary hyperparathyroidism. 625 92

We report a two-step immunochemical method for estimating serum intact PTH, as defined by immunochemical methods, and its validation by a newly developed osteosarcoma cell adenyl cyclase stimulation assay for PTH bioactivity. The first step involves extraction and concentration of serum PTH moieties with solid phase amino-terminal PTH antibodies; in the second step, the initial PTH immunoextract is analyzed with a sensitive midregion immunoassay. Intact PTH can thus be detected in virtually all normal subjects. Intact PTH levels in our group of primary hyperparathyroid persons average nearly 20 times higher than normal and do not overlap the normal range. Intact PTH is also elevated in chronic renal disease, but less dramatically than in primary hyperparathyroidism. Since total PTH immunoreactivity (intact plus fragments) is much higher in renal disease patients than in persons with primary hyperparathyroidism, serum intact PTH in renal disease apparently comprises a much smaller fraction of total circulating PTH immunoreactivity than in primary hyperparathyroidism. The finding that intact PTH accounts for a large portion of total circulating PTH immunoreactivity in primary hyperparathyroidism is contrary to published reports by us and others. Some of the possible reasons for the differences between our present results and previous reports are examined.
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PMID:Estimation of biologically active intact parathyroid hormone in normal and hyperparathyroid sera by sequential N-terminal immunoextraction and midregion radioimmunoassay. 631 57

Primary hyperparathyroidism was diagnosed in two German shepherd pups from a litter of four females. Clinical signs were apparent by two weeks of age and included stunted growth, muscular weakness, and polydipsia/polyuria. Radiography revealed diffuse reduction in bone density. Both pups had marked hypercalcemia, hypophosphatemia, increased plasma immunoreactive parathyroid hormone concentrations and increased fractional clearance of inorganic phosphate in the urine. Intravenous infusion of one affected pup with calcium gluconate failed to suppress the plasma concentration of immunoreactive parathyroid hormone, suggesting autonomous secretion of parathyroid hormone. Necropsy of the other pup at eight weeks of age revealed diffuse hyperplasia of parathyroid chief cells, nodular hyperplasia of thyroid C-cells, skeletal alterations consistent with fibrous osteodystrophy, hypercalcemic nephropathy, and extensive mineralization of the lungs and gastric mucosa. The dam and sire were half sibs. One male pup from a previous litter of six had developed similar clinical signs and radiographic lesions, suggesting autosomal recessive inheritance. This is the first report of hereditary primary hyperparathyroidism in domestic animals, a disease which may be analogous to hereditary neonatal primary hyperparathyroidism in children.
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PMID:Primary hyperparathyroidism in German shepherd dogs: a disorder of probable genetic origin. 646 98

Primary hyperparathyroidism and sarcoidosis were found in one patient with hypercalcemia and renal failure. Cervicotomy disclosed a parathyroid adenoma and renal biopsy demonstrated interstitial nephropathy. Association of sarcoidosis with hyperparathyroidism, if not fortuitous, has not yet been clearly established.
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PMID:[Hypercalcemic sarcoidosis and primary hyperparathyroidism disclosed by renal insufficiency]. 650 29

In an effort to identify new trends in the presentation and treatment of primary hyperparathyroidism, 66 patients treated since 1975 were compared with 100 patients diagnosed and treated from 1948 to 1970. Despite widespread use of multichannel analyzers, the late patients had an insignificant increase in diagnosis while asymptomatic (18 percent versus 9 percent in the early group). Hypertension was the most common presenting complaint in patients seen since 1975, compared with renal disease in patients seen before 1970. Findings of diffuse hyperplasia were more common in the late patients (17 percent versus 3 percent in the early patients). There were no differences in rates of operative complications or persistent postoperative hypercalcemia. In the late series of patients persistent hypercalcemia after surgery for hyperplasia was due to inadequate resection of parathyroid tissue. In the adenoma patients, failure to locate the abnormal parathyroid gland was the cause of operative failure.
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PMID:Primary hyperparathyroidism in the seventies. A decade of change? 661 28

Forty-two patients with sarcoidosis were studied with special attention to renal disease and disturbance of calcium metabolism. Abnormal calcium metabolism was found in 19 patients and prednisone corrected hypercalcaemia in those affected within two weeks, except in one patient who had concomitant primary hyperparathyroidism. Renal failure was found in 19 patients, 15 of whom had hypercalcaemia. Prednisone had a beneficial effect on kidney function within four weeks in all patients except in one with co-existing glomerulonephritis. Arterial hypertension was found in six patients, proteinuria in six, and calcinosis in six. Among 14 patients who underwent renal biopsy, granulomas were found in five. In only one of these was granulomatosis extensive bringing out renal failure and death within two years after temporary remission with prednisone. Co-existent non-sarcoid diseases affecting the kidneys or calcium metabolism occurred in ten out of 23 patients with sarcoidosis and kidney disease/calcium abnormality. In most cases these conditions contributed more to the prognosis than did sarcoidosis. From the present series and review of the literature it appears that young males within the first two years of diagnosis are at the greatest risk of hypercalcaemia or kidney disease.
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PMID:Renal manifestations and abnormal calcium metabolism in sarcoidosis. 746 60

Twenty eight patients of sporadic primary hyperparathyroidism seen over a period of 10 years were studied. There were 18 females and 10 males with a mean age of 35.9 years. Bone involvement was the commonest clinical presentation (90%) followed by renal involvement (65%) and more than half the patients (54%) had involvement of both the skeletal and renal systems. The tumor was clinically palapable in six patients. Thalliumtechnetium subtraction scan had a sensitivity of 87% followed by computerised tomography (70%), and ultrasound (65%) in diagnosing parathyroid pathology. All the patients underwent surgical excision of the abnormal gland (S). Adenomas constituted the single largest group (90%). Histologically, only 32% of the patients had chief cell morphology. Clear cell (32%) mixed cell, and oxyphil cell (7.2%) types accounted for the remaining adenomas. Majority of the patients (82%) had symptomatic postoperative hypocalcemia requiring intravenous calcium with or without vitamin D supplementation. In contrast to western reports most of our patients were young, presented late with florid bone and renal disease and had large palpable tumors.
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PMID:Primary hyperparathyroidism--an Indian study. 792 52

We present two cases of hypercalcemic nephropathy associated with primary hyperparathyroidism. Case 1 is a 37-year-old man who had repeated bone fractures and recurrent ureteral stones, which led to the diagnosis of primary hyperparathyroidism. Case 2 is a 35-year-old man in whom parathyroid carcinoma was discovered because of secondary nephrogenic diabetes insipidus, resulting from severe hypercalcemia. Both patients developed mild renal dysfunction during the course of hyperparathyroidism. In the renal biopsy materials obtained from case 1, the renal interstitium showed chronic inflammatory changes. The tubules were partly damaged (focal necrosis). Deposition of calcium was sometimes noted within the mitochondria of the tubular epithelial cells. Some glomeruli showed glomerular sclerosis. In biopsy materials obtained from case 2 after resection of the carcinoma, similar histological features were observed, but tubular atrophy and necrosis were advanced. Polyuria and hypercalcemia were ameliorated after resection. These findings indicate that severe hypercalcemia might induce tubular dysfunction as well as organized changes.
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PMID:[Two cases of hypercalcemic nephropathy associated with primary hyperparathyroidism]. 826 8


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