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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Despite the increasing awareness of gastrinoma and its lethal peptic ulcer sequelae, the diagnosis is often initially missed or made as a terminal event. The authors screened all patients with peptic ulcer symptoms serious enough to warrant hospital admission or those associated with diarrhea, nephrolithiasis, hypercalcemia, or pituitary abnormality. In a one-year period (1979-1980) nine (of 14 suspected) new gastrinoma patients were identified using a sensitive and specific gastrin radioimmunoassay in combination with provocative tests including IV secretin, calcium, and food. Conventional upper GI series, CAT scan, arteriography, and endoscopy provided no additional information other than to confirm the presence of ulcer disease. Basal plasma gastrin levels were more than 200 pmol L-1 in only three of the nine (normal fasting plasma gastrin levels are less than 25 pmol L-1). Three patients presented with acute ulcer perforation, and the diagnosis of gastrinoma was suspected because of multiple ulcers and pancreatic masses. In three other patients, previous duodenal ulcer surgery had failed. One patient with dyspepsia, high basal plasma gastrin, negative secretin and calcium infusion studies, and a positive meal test was diagnosed as having G-cell hyperplasia; this was confirmed by biopsy and antral gastrin extraction. Antrectomy alone resulted in cure. In all patients tested, a positive calcium infusion or secretin bolus (greater than 100% rise over basal) strongly suggested the diagnosis of gastrinoma, which was confirmed at surgery. In the acute perforations, initial management with omental patch and cimetidine therapy allowed survival of two patients, while emergency total gastrectomy in the third resulted in death due to esophagojejunal leak. Elective patients were treated with cimetidine initially for at least two weeks before total gastrectomy. In this group there were no operative mortalities, and postoperative morbidity was minimal. This series illustrates three important points: (1) careful screening of an ulcer population using gastrin radioimmunoassay and provocative tests has enabled a high yield of gastrinomas while conventional investigations are of minimal values; (2) a high index of suspicion in appropriate cases is necessary; and (3) total gastrectomy performed under elective circumstances is safe and allows the patients to resume a normal and healthy life without the sequelae of aggressive peptic ulceration or daily drug administration.
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PMID:The early diagnosis of gastrinoma. 712 38

Sarcoidosis may involve the kidneys in several ways. Most commonly, aberrations of calcium metabolism, including hypercalcemia, hypercalciuria, and nephrocalcinosis, are responsible for the renal manifestations of sarcoidosis. Granulomatous infiltration of the renal interstitium may also produce severe derangements of renal function. Glomerulonephritis can occur with sarcoidosis, although the pathogenesis remains unclear. Besides renal insufficiency and frank renal failure, nephrotic syndrome, nephrolithiasis, hypertension, and a variety of tubular defects may complicate sarcoidosis. The sensitivity of "sarcoid nephropathy" to corticosteroids usually warrants therapeutic trial.
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PMID:Renal manifestations of sarcoidosis. 722 44

Between August 1975 and January 1981, 106 patients thought to have persistent or recurrent hyperparathyroidism underwent a total of 108 parathyroid re-explorations at the National Institutes of Health. These 106 patients had a total of 175 previous operations for hyperparathyroidism (156 cervical and 19 mediastinal). Nephrolithiasis (54% of patients) and bone disease (24% o patients) were the predominant symptoms. Arteriographic examination and selective venous sampling provided highly accurate localizing results in 33% of the patients, and were of some help in 64%. The final diagnoses after reoperation and re-evaluation were: single-gland disease in 58 patients, primary nonfamilial hyperplasia in 19 patients, familial hyperplasia in three patients, multiple endocrine neoplasia (MEN) Type I in ten patients, MEN Type II in two, parathyroid carcinoma in four patients, secondary hyperplasia in three patients, and familial hypocalciuric hypercalcemia (FHH) in two patients. The diagnosis was in doubt in five patients. In the 95 patients with unequivocal hyperparathyroidism, not due to parathyroid carcinoma, surgery eliminated hypercalcemia in 91 (96%). Two patients died after operation, one of disseminated candidiasis, and one patient, with an immunodeficiency, of sepsis. Five patients developed temporary, and one permanent, recurrent nerve damage; 41% of the patients were hypocalcemic, at the time of discharge from the hospital.
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PMID:Results of reoperation for persistent and recurrent hyperparathyroidism. 730 78

We report on a 33-year-old man with hypercalcemia and recurrent nephrolithiasis, who underwent the first neck exploration for primary hyperparathyroidism on September 27, 1973. No tumor was found and bilateral upper normal parathyroid glands were removed. However, hypercalcemia persisted postoperatively. Selective venous sampling for radioimmunoassay of parathyroid hormone 5 years later revealed a sharp unilateral gradient in the right vertebral vein. On November 2, 1978 the second neck exploration was performed and a right lower parathyroid adenoma was removed from the right lateral wall of the esophagus. Postoperatively, the serum calcium level decreased to 8.8 to 9.3 mg./dl. and convalescence was uneventful. In this case the pathway of parathyroid venous effluent might have been changed by the previous neck exploration and probably drained anomalously through the vertrbral vein. Selective venous sampling for radioimmunoassay of parathyroid hormone should include samplings from the vertebral veins as well as the thyroid veins, especially in cases with 1 or more previous neck explorations.
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PMID:Parathyroid adenoma found by vertebral vein sampling. 738 16

In a woman with bilateral recurrent calcium nephrolithiasis and hypercalciuria, hypercalcemia developed and she underwent parathyroid surgery, which led to excision of a histologically-confirmed adenoma. The patient became normocalcemic but remained hypercalciuric despite reduction of dietary calcium intake. Several calculi recurred in both kidneys. Four to six years after parathyroidectomy, hypercalcemia recurred and the patient underwent a new surgical exploration; a parathyroid gland with diffuse adenomatous aspects and another gland with pure hyperplasia were excised. Once again, after surgery the patient became normocalcemic but remained hypercalciuric. Evidence for a "renal calcium leak" hypercalciuria was obtained, and thiazide administration led to normalization of urinary calcium excretion. In calcium nephrolithiasis, persistent hypercalciuria may lead to recurrence of autonomous hyperparathyroidism.
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PMID:Recurrence of autonomous hyperparathyroidism in calcium nephrolithiasis. 742 48

We found primary hyperparathyroidism in 56 of 1,132 consecutive patients with nephrolithiasis. We describe 48 of these patients who have undergone curative parathyroidectomy. Thirty of the 48 patients had extremely mild hypercalcemia (serum calcium level, 10.15 to 10.95 mg/dL), often accompanied by very substantial hypercalciuria. Stone disease was of equal severity in these 30 patients and in the 18 with more pronounced hypercalcemia (serum calcium level above 11 mg/dL). In all 48 patients, recurrent stone formation was virtually abolished by parathyroidectomy.
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PMID:Hyperparathyroidism in nephrolithiasis. 743 44

Subcutaneous fat necrosis leading to hypercalcemia is rare but well documented in asphyxiated neonates. This paper presents two such neonates in whom sonography revealed the development of nephrocalcinosis and nephrolithiasis. The kidneys had initially been shown to be normal sonographically. In one infant, nephrocalcinosis developed as increasing echogenicity of the medullary pyramids. In the other, increased echogenicity of the renal cortex of uncertain cause developed together with nephrolithiasis. These sonographic appearances have not been described previously in this entity.
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PMID:Nephrocalcinosis and nephrolithiasis due to subcutaneous fat necrosis with hypercalcemia in two full-term asphyxiated neonates: sonographic findings. 759 62

This article begins with a discussion on changes in the maternal calcium-parathyroid axis in response to pregnancy, followed by calcium disorders that can take place during pregnancy. Hypercalcemia and its subsequent disorders, including hyperparathyroidism, hypocalciuric hypercalcemia, and thyroid disease, are reviewed. Also, hypocalcemia and its subsequent disorders, including hypoparathyroidism, vitamin D deficiency, and hypomagnesemia, are addressed. Concluding the article are discussions on bone status and osteoporosis, calcium metabolism in pregnancy-induced hypertension and preeclampsia, and nephrolithiasis in pregnancy.
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PMID:Calcium disorders of pregnancy. 778 23

Due to unstable angina pectoris coronary arteriography was performed in a 57 year-old female, showing diffuse 3-vessel disease; aortocoronary bypass surgery was recommended. During routine pre-operative examination hypercalcemia, as well as an elevated value of parathormone were observed. Ultrasonography of the parathyroid glands showed two enlarged cranial glands. In a simultaneous surgical procedure 4 bypass grafts were performed and 4 hyperplastic parathyroid glands were removed, one of which was re-operated as an autotransplantation in the left musculus adductor magnus. Histological examination showed water clear cell hyperplasia of the parathyroid glands. Though the patient had suffered from stomach and duodenal ulcers and nephrolithiasis over several years, primary hyperparathyroidism was diagnosed only after angiographically proven coronary artery disease.
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PMID:[Coronary heart disease as the initial manifestation of primary hyperparathyroidism]. 797 64

Vitamin D and its metabolites are well-established regulators of bone mineral homeostasis. Their clearest role is in the prevention and treatment of rickets and osteomalacia, bone diseases characterized by inadequate bone formation, and mineralization. Much of the effectiveness of vitamin D and its active metabolite 1,25(OH)2D in treating such disorders rests with their ability to increase serum levels of calcium and phosphate principally by stimulating intestinal calcium and phosphate absorption. Osteoporosis is not a disease resulting from obvious deficiencies in vitamin D, calcium, and phosphate. More subtle deficiencies, however, may be found, especially among the elderly with decreased intake of dairy products, reduced sunlight exposure, and less efficient intestinal absorption of bone minerals. Such subtle deficiencies may account for the ability of vitamin D and calcium supplementation to have a beneficial effect on bone mineral density in this population. Estrogen administration to postmenopausal females raises 1,25(OH)2D levels, presumably through increased renal production, and this increase is associated with increased intestinal calcium transport. Serum measurements of the vitamin D metabolites in general, however, and 1,25(OH)2D in particular do not consistently show evidence of a decrease at the time of menopause. Although most studies show a fall in intestinal calcium transport with age, which can be reversed with 1,25(OH)2D or estrogen, even these observations have not been found consistently. Thus, some investigators have addressed the issue of tissue resistance to 1,25(OH)2D and have noted decreased VDR in the intestine and reduced 1,25(OH)2D accumulation by bone with age. Despite no obvious deficiency of vitamin D in most patients with osteoporosis, clinical trials with vitamin D or 1,25(OH)2D show promise. Vitamin D treatment will probably prove most efficacious in populations with marginal vitamin D intake and/or limited sunlight exposure; high doses would not be required, and the treatment would be safe. This would be a physiologic and not a pharmacologic use of vitamin D. The use of 1,25(OH)2D for treatment of osteoporosis in individuals with adequate nutrition and sunlight exposure may require somewhat higher than physiologic doses to be effective. Perhaps such doses are necessary to stimulate osteoblast activity and/or differentiation; by raising the serum calcium level, such doses of 1,25(OH)2D might block its otherwise stimulatory effect on osteoclast number and activity. Such doses run the risk of hypercalcemia and hypercalciuria, leading to nephrolithiasis and/or nephrocalcinosis. These undesirable side effects appear to be less common with the use of 1 alpha OHD compared with 1,25(OH)2D, but this may be because of the lower levels of calcium consumption in Japan where 1 alpha OHD is widely prescribed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of vitamin D, its metabolites, and analogs in the management of osteoporosis. 798 88


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