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

States of hypersecretion of PTH may occur primarily, or in response to other physiologic abnormalities. Primary hyperparathyroidism must be considered in the differential diagnosis of hypercalcemia, nephrolithiasis, metabolic bone disease, and pancreatitis and peptic-ulcer disease. The clinical manifestations of this disease have become more subtle with improved detection. The serum calcium level is almost always elevated, and when it it accompanied by relatively high serum PTH levels or increased urinary cAMP excretion, the diagnosis is usually secure. Findings of hypophosphatemia, decreased renal tubular reabsorption of phosphorus, hypercalciuria, and characteristic roentgenographic changes support the diagnosis of hyperparathyroidism, but are not prerequisites for that diagnosis. Most cases will come to operation, and experienced intraoperative assessment is necessary for the correct distinction between multiglandular disease and that involving only a single gland. We expect that a clearer understanding of the histopathologic features of these diseases, and improvement in the methods for measurement of PTH will be the main areas of advancement in the diagnosis of hyperparathyroidism in the next few years.
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PMID:Diagnosis of hyperparathyroidism. 19 30

Pancreatitis has been described previously following renal transplantation, but not in association with chronic renal failure. Analysis of 168 patients with renal transplants revealed five who developed pancreatitis, three of whom died. All five were on treatment with prednisone and azathioprine. Four patients were seen with definite attacks of pancreatitis and chronic, stable renal failure from a variety of causes. None had received immunosuppressive agents, prednisone nor thiazide diuretics, but two were on regular frusemide. One patient was on maintenance dialysis, which could not be related directly to the pancreatitis. In either group alcohol ingestion, cholethiathiasis, or hypercalcaemia was not a factor. This diagnosis of pancreatitis was established on clinical grounds and serum amylast levels of greater than 900 iu/1. Similar serum amylast elevation was not found ina random group of patients with chronic renal failure. Hyperlipidaemia was not present in any patient with pancreatitis. Although hypercalcaemia and primary hyperparathyroidism was not found in the transplant and non-transplant subjects, elevated serum parathormone levels have been described in uraemic patients with normocalcaemia. Hyperparathyroidism may be a factor in the development of pancreatitis in reanl failure. Pancreatitis carries a significant mortality risk in renal transplantation. The four non-transplanted patients have survived, despite recurrent attacks of pancreatitis.
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PMID:Pancreatitis and renal disease. 31 21

Pancreatitis is seldom seen as a severe complication of renal transplantation. In a review on 1321 renal transplants, 23 cases with 12 deaths are reported (Johnson and Nabseth, 1970). Single case reports may be added. In our departments pancreatitis has proved to be a fairly frequent complication. It developed in 10 (7 percent) of 147 patients with renal transplantation one week to seven and a half years after transplantation (patients with primary hyperparathyroidism excluded). Three of the eight acute cases had haemorrhagic pancreatitis, in two of them leading to death. Two patients had chronic calcifying pancreatitis. Pancreatitis was complicated in one case by abscess formation and in two by severe haemorrhage into a pseudo-cyst. In two patients the diagnosis was made at necropsy only and death was probably not related to the acute pancreatitis. The exact pathogenesis of pancreatitis after renal transplantation cannot be precisely assessed. Possible contributing factors are treatment with corticosteroids, azathioprin, and L-asparaginase, early hypercalcaemia after transplantation, surgery, infections of bacterial or viral origin, and unknown immunological processes.
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PMID:Pancreatitis after renal transplantation. 109 48

The only causal treatment of primary hyperparathyroidism (PHPT) is parathyroidectomy. There are indications in the literature that despite operation expectation of life is shortened because of an increased frequency of cardiovascular and malignant diseases leading to the recommendation for early surgery even in uncomplicated PHPT. It is easier to convince an asymptomatic patient of an operation when he is informed about complications and consequences of an expectative attitude. Therefore, we reviewed our 71 patients operated upon during a 4-year-interval, 58 of whom were followed-up. During 82 operations 115 pathologically altered parathyroid glands were removed. Two persistent paralyses of the recurrent nerve occurred, however, without alteration of the voice. Follow-up of 82% of patients revealed 2 cases of recurrent nephrolithiasis (1 hypercalcaemia, 1 normocalcaemia). Three (5%) true recurrences were found, but neither a pancreatitis nor a peptic ulcer was noted during long-term follow-up. None of the 137 patients operated for a bleeding or perforated peptic ulcer during the last 10 years and 1 of 55 patients with acute pancreatitis during the past 8 years suffered from a PH-PT. However, morbidity and mortality of these two conditions was high. Although correlation to PHPT was low we recommend early operation of PHPT because of the low morbidity rate, zero lethality and reduced expectation of life.
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PMID:[Preventive or therapeutic parathyroidectomy in primary hyperparathyroidism]. 140 51

We describe an adult patient who developed persistent hypercalcemia while bedridden for more than three months with pancreatitis and sepsis. On the basis of hypercalciuria, suppressed serum intact PTH, suppressed serum 1,25-dihydroxy vitamin D3 and no clinical evidence of malignancy, the diagnosis of immobilization hypercalcemia was established His hypercalcemia improved during treatment with saline, calcitonin and/or etidronate. With active mobilization and weight-bearing exercises, serum calcium finally normalized. We discuss clinical and laboratory features as well as current modalities of treatment of this rare form of hypercalcemia in adults.
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PMID:Immobilization hypercalcemia in an adult patient with pancreatitis and sepsis: case report. 148 89

In pregnant women with symptomatic hyperparathyroidism, parathyroidectomy should be undertaken during the second trimester. We feel that the woman who is initially diagnosed well into the third trimester should be treated medically unless the hypercalcemia worsens or other complications occur. Since the treatment of asymptomatic hyperparathyroidism itself is controversial, it is even more difficult to define the treatment plan for an asymptomatic pregnant patient who has primary hyperparathyroidism. However, a recent consensus panel recommended that young patients with asymptomatic hyperparathyroidism be treated surgically. Accordingly, we believe that the asymptomatic pregnant patient should also be treated surgically, preferably in the second trimester. Whether a patient is treated medically or surgically in these situations, the pregnancy should be considered high-risk. The neonate should be monitored carefully for signs of hypocalcemia or impending tetany. If the mother is treated medically to term (or if spontaneous or elective abortion occurs), the mother should be monitored for hyperparathyroid crisis postpartum. Sudden worsening of hypercalcemia can result from the loss of the placenta (active placental calcium transport may be somewhat protective) and dehydration. Finally, every effort should be made to make the definitive diagnosis early in pregnancy in order to initiate optimal management. The diagnosis should be suspected during pregnancy if the following conditions exist: appropriate clinical signs or symptoms (especially nephrolithiasis or pancreatitis), hyperemesis beyond the first trimester, history of recurrent spontaneous abortions/stillbirths or neonatal deaths, neonatal hypocalcemia or tetany, or a total serum calcium concentration greater than 10.1 mg/dL (2.52 mmol/L) or 8.8 mg/dL (2.2 mmol/L) during the second or third trimester, respectively.
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PMID:Hyperparathyroidism and pregnancy: case report and review. 150 54

The low-pressure duct perfusion model reliably produces acute pancreatitis in cats. The main pancreatic duct is made permeable in one of several ways: the perfusion of glycodeoxycholic acid along the main pancreatic duct, the administration of intragastric ethanol, the stimulation of pancreatic secretion into an obstructed duct, or the creation of acute hypercalcemia. Active pancreatic enzymes are then perfused through the main pancreatic duct via a catheter inserted into the duct in the tail of the gland, and acute edematous pancreatitis results. Simultaneous infusion of 16,16-dimethylprostaglandin E2 converts acute edematous into acute hemorrhagic pancreatitis. Histologically, the characteristic changes of human acute pancreatitis are manifest 24 h later: necrosis, polymorphonuclear leukocyte infiltrate, hemorrhage and edema.
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PMID:The low-pressure duct perfusion model of acute pancreatitis. 160 Oct 24

In 1957, Cope and his associates first noted 2 cases of pancreatitis associated with primary hyperparathyroidism. They emphasized the association of hyperparathyroidism and pancreatitis. Since then pancreatitis has become a diagnostic clue to primary hyperparathyroidism. We report herein a 39-year-old woman who had suffered from acute relapsing pancreatitis 3 times in the past 2 years. Hypercalcemia persisted throughout the course. A movable mass 3 x 3 cm in diameter was noted over the right thyroid area on physical examination. A hypoechogenic mass 3.5 x 2.7 x 1.4 cm was found between the right lobe of the thyroid and the carotid artery. Because of a persistently high serum level of Ca2+, normal saline and furosemide were infused; the serum Ca2+ decreased gradually. After aspiration of the suspected mass, the serum level of Ca2+ increased from 8.7 mg/dL to 18 mg/dL. Because of the impression of parathyroid adenoma, surgery was performed and a 3 x 2.5 x 1.5 cm well-encapsulated mass was excised without difficulty. Pathologic examination revealed a well-encapsulated parathyroid adenoma. This case reveals that primary hyperparathyroidism maybe one of the causes of pancreatitis, and aspiration cytology, although it may be helpful for the diagnosis, can aggravate the hypercalcemia.
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PMID:Acute relapsing pancreatitis in primary hyperparathyroidism with hypercalcemia aggravated after aspiration cytology: report of a case. 168 89

The effect of local and systemic calcium administration was tested on the pancreas of cat and guinea pig. After 3 h of local calcium infusion (0.6 mmol/kg x h) via the splenic artery of the cat hemorrhagic pancreatitis could be shown. Control animals treated with potassium (1.1 mmol/kg x h) or 0.9% NaCl alone showed no morphological change in the pancreas. Intravenous administration of calcium (0.6 mmol/kg x h) led to a 1.8-fold increase in serum ionized calcium levels in the cat and a 1.6-fold increase in levels in the guinea pig. The cat showed necrosis of acinar and ductal cells throughout the gland at 12 h. In the guinea pig, acinar cell vacuolisation and cell necrosis started at 3 h, and at 9 h degeneration of entire acini, hydropic swelling and degeneration of ductal cells, and perivascular leukocytic infiltration was present. In both species, a significant increase in the number of intraductal precipitates and a significant increase in urinary amylase output was present in calcium treated animals. The findings suggest that hypercalcemia has a deleterious effect on the pancreas that causes acinar and ductal cell necrosis and eventually pancreatitis.
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PMID:Acute hypercalcemia induces acinar cell necrosis and intraductal protein precipitates in the pancreas of cats and guinea pigs. 198 43

Historically, primary hyperparathyroidism during pregnancy was associated with significant risk of maternal morbidity and fetal death. Maternal hypercalcemia results in fetal hypercalcemia, leading to suppression of fetal parathyroid gland function. Neonatal hypocalcemia with tetany is a common occurrence after birth when maternal calcium flow is interrupted. From 1930 to 1990, 109 cases of women with primary hyperparathyroidism associated with pregnancy have been reported, 39 of whom were treated surgically before delivery. Although fetal mortality rates for medically treated women have improved, fetal morbidity continues to remain higher than in women who undergo surgical treatment of parathyroid disease during pregnancy. Of 850 patients treated surgically for primary hyperparathyroidism since 1960, 12 were pregnant. Four of the patients were treated medically during pregnancy and underwent surgery after delivery; all four infants had neonatal hypocalcemia and tetany. The remaining eight patients were treated surgically during pregnancy: six in the second trimester and two (one with associated pancreatitis and one with hypercalcemic crisis) during the first trimester. There was no fetal or maternal morbidity or death in the surgical group. Parathyroid adenomas were present in 10 of the patients, hyperplasia in one, and parathyroid carcinoma in one. The management of maternal primary hyperparathyroidism diagnosed during pregnancy should be based on the patient's symptoms and severity of disease. Hyperparathyroidism characterized by progressive symptoms should be treated surgically, preferably during the second trimester. Symptom-free patients and those with mild hypercalcemia diagnosed in the third trimester may be managed medically, postponing operation until after delivery.
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PMID:Primary hyperparathyroidism during pregnancy. 174 71


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