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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some patients with hypertriglyceridemia and acute pancreatitis have marked hypocalcemia and high levels of plasma free fatty acids (FFAs). This study tests the hypothesis that increased plasma FFAs can significantly reduce the calcium level in vivo, a phenomenon which is different from local formation of calcium soaps due to lipolysis of adipose tissue lipids. Free fatty acid elevation was induced in rats by the administration of heparin and by the infusion of triglycerides. The results show that, compared with controls, induction of elevated FFA (from 1.57 +/- 0.08 mEq/L to 5.64 +/- 0.35, mean +/- SEM) causes the concentration of calcium to fall rapidly (from 9.04 +/- 0.06 mg/dl to 8.42 +/- 0.10, p less than 0.001). There is a significant (p less than 0.001) positive correlation between spontaneous baseline concentration of FFA and the responsiveness of calcium concentration to FFA challenge. At near-normal levels of FFA there is a significant (p less than 0.001) correlation between the magnitude of increased FFA concentration and decreased calcium concentration. Additional studies in vivo and in vitro show that elevated plasma triglycerides per se did not interfere with measurement of calcium concentration; however, FFA-albumin complexes bind calcium and lower its measured value. These findings suggest that (a) changes in the concentration of FFA occurring spontaneously may affect measured serum calcium concentration; (b) the observed depression of serum calcium concentration may be due in part to intravascular sequestration of calcium by FFA, but increased flux of circulating calcium-FFA complexes into extravascular and intracellular sites may also be important; (c) the markedly increased FFA concentration in some patients with acute pancreatitis may contribute significantly to hypocalcemia and calcium flux in these patients. As parathyroid hormone secretion, function, or integrity may be impaired in pancreatitis, the depressant effect of FFA could be even greater in that disease than in this model.
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PMID:Depression of serum calcium by increased plasma free fatty acids in the rat: a mechanism for hypocalcemia in acute pancreatitis. 402 61

Calcium homeostasis was studied serially in six patients admitted to the surgical intensive care unit because of acute pancreatitis. All developed ionized hypocalcemia. Serial assays of serum parathyroid hormone (PTH) revealed a prompt response to this hypocalcemia (1143 +/- 239 versus 574 +/- 24 pg/ml, P less than 0.05). Serum 1,25-dihydroxyvitamin D (1,25(OH)2D) levels rose from 26 +/- 8 to 104 +/- 17 pg/ml (P less than 0.01) in the expected time frame subsequent to the PTH peak, confirming the biologic significance of the PTH increases observed. Despite these significant elevations of PTH and 1,25(OH)2D, the expected prompt return of ionized calcium concentrations to normal levels was not seen. Also, urinary cyclic adenosine monophosphate production was not stimulated. These results suggest an acute functional resistance of bone to physiologic levels of PTH stimulation during the acute phase of pancreatitis. Fluid sequestration and hypovolemia are marked at this time. We suggest that pancreatitic hypocalcemia may occur when oligemic bone cannot respond normally to PTH and 1,25(OH)2D stimulation. As such, it may represent an end organ failure syndrome associated with shock and poor tissue perfusion.
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PMID:Calcium homeostasis in patients with acute pancreatitis. 619 46

Six patients receiving total parenteral nutrition (TPN) developed hypercalcemia and acute pancreatitis. Four were long-term home TPN patients, and two were short-term hospital TPN patients. Causes of pancreatitis other than hypercalcemia were not found. The etiology of the hypercalcemia remained unclear and in particular was not due to calcium infusion or hyperparathyroidism. In 4 patients in whom it was measured, the plasma parathyroid hormone was normal (in 2) or nondetectable (in 2). Hypercalcemia and pancreatitis subsided with discontinuation of TPN. Thus, some patients receiving TPN develop hypercalcemia, and in some of these pancreatitis ensues.
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PMID:Pancreatitis in association with hypercalcemia in patients receiving total parenteral nutrition. 677 4

Four families with familial hypocalciuric hypercalcaemia were studied. The probands presented with abdominal pain, which in three was due to acute pancreatitis; in two the condition was life threatening. Serum concentrations of calcium, magnesium, phosphate, and immunoassayable parathyroid hormone, urinary calcium excretion, and the rate of renal tubular reabsorption of phosphate were measured; the findings were compared with results in 10 patients with primary hyperparathyroidism matched for serum calcium concentration to establish differences between the diseases. Familial hypocalciuric hypercalcaemia should be suspected in patients with hypercalcaemia in whom daily urinary calcium excretion is below 5 mmol (200 mg) provided renal insufficiency, vitamin D deficiency, and ingestion of drugs that reduce calcium excretion have been excluded. Most cases appear to run a benign course, but some may suffer considerable morbidity. Surgical treatment should be reserved for patients with severe complications, when all parathyroid tissue should be removed.
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PMID:Familial hypocalciuric hypercalcaemia and acute pancreatitis. 678 29

In order to further investigate hormonal changes and possible metabolic consequences in acute pancreatitis, 10 cases with a mild form of the disease was studied. The influence of tissue injury per se on the hormones in question was assessed from comparison with the hormone levels in the course of myocardial infarction (MI) in 9 cases. Insulin and glucose showed no consistent changes. Glucagon was suppressed on admission, 22 +/- 10 pg . ml-1, compared with the ultimate concentration, 40 +/- 20 pg . ml-1 (p less than 0.05), and with the initial value in MI, 74 +/- 32 pg . ml-1 (p less than 0.01). Serum calcitonin (CT) was strongly elevated initially, 348 +/- 313 pg . ml-1, compared with the ultimate level, 24 +/- 7 pg . ml-1 (p less than 0.001), and with the normal initial level in MI, 43 +/- 44 pg . ml-1 (p less than 0.01). Serum CT elevations were time-related to a slight reduction in corrected serum Ca, which might reflect a biological expression of this substance. In pancreatitis, parathyroid hormone (PTH) remained normal and unchanged throughout the study, whereas patients with MI had an increased level of this hormone on admission, 0.19 +/- 0.08 microgramEq . 1(-1), compared with the ultimate concentration, 0.09 +/- 0.03 microgram/q . 1(-1) (p less than 0.02) and with the initial concentration in pancreatitis, 0.11 +/- 0.06 microgramEq . 1(-1) (p less than 0.05). Supranormal PTH levels were found in more than half of the infarction patients on days 0 and 1.
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PMID:Characteristic changes in the concentrations of some peptide hormones, in particular those regulating serum calcium, in acute pancreatitis and myocardial infarction. 701 27

The renal handling of calcium and phosphate, which normally reflects parathyroid hormone (PTH) activity, was studied during the first 5 days after admission to hospital in 18 patients with acute pancreatitis. The ionized calcium level in plasma was calculated from the total calcium, albumin, total protein and pH. Hypocalcaemia (Ca less than 1.08) was found in 6 patients and was associated with low urine calcium concentrations, hypophosphataemia and lower renal tubular reabsorption of phosphate. Although these changes were all consistent with an appropriate renal response to increased PTH production in the hypocalcaemic patients, measured levels of PTH were very variable. In one patient who developed tetany, calcium infusion resulted in a rise in plasma calcium and a reversal of renal changes, but had little influence upon PTH levels. We found no evidence that hypomagnesaemia or proteolytic degradation of PTH were factors in the aetiology of hypocalcaemia. The discrepancy between evidence of PTH activity from renal function and immunoassayable levels of PTH in plasma might indicate that the parathyroid response, although present, was inadequate to mobilize enough skeletal calcium to prevent hypocalcaemia; it underlines the need for caution in the interpretation of data fom radioimmunoassay techniques when taken in isolation in situations where they have not been fully evaluated.
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PMID:Parathyroid function during acute pancreatitis. 705 76

Proteolytic enzymes, lipase, kinins, and other active peptides liberated from the inflamed pancreas convert inflammation of the pancreas, a single-organ disease of the retroperitoneum, to a multisystem disease. Adult respiratory distress syndrome, in addition to being secondary to microvascular thrombosis, may be the result of active phospholipase A (lecithinase), which digests lecithin, a major component of surfactant. Myocardial depression and shock are suspected to be secondary to vasoactive peptides and a myocardial depressant factor. Coagulation abnormalities may range from scattered intravascular thrombosis to severe disseminated intravascular coagulation. Acute renal failure has been explained on the basis of hypovolemia and hypotension. The renin-angiotensin alterations in acute pancreatitis (AP) as mediators of renal failure need to be studied. Metabolic complications include hypocalcemia, hyperlipemia, hyperglycemia, hypoglycemia, and diabetic ketoacidosis, of which hypocalcemia has been long recognized as an indicator of poor prognosis. The pathogenesis of hypocalcemia is multifactorial and includes calcium-soap formation, hormonal imbalances (e.g., parathyroid hormone, calcitonin, glucagon), binding of calcium by free fatty acid-albumin complexes, and intracellular translocation of calcium. Subcutaneous fat necrosis, arthritis, and Purtscher's retinopathy are rare. The various prognostic criteria of AP and other associated laboratory abnormalities are manifestations of systemic effects. Early recognition and appropriated management of these complications have resulted in improved prognosis of severe AP.
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PMID:Acute pancreatitis: a multisystem disease. 804 85

Serum levels of parathyroid hormone (PTH), calcium and albumin were measured daily for 5 days in 41 selected patients with moderate to severe acute pancreatitis. The PTH level was measured by means of a two-site immunoradiometric assay specific for the intact polypeptide. A rise in PTH level was observed more commonly in patients with a complicated or fatal outcome than in those with an uncomplicated course (14 of 16 versus six of 25 patients, P < 0.001). Although PTH levels were variable in the presence of hypocalcaemia, raised concentrations were found more frequently in patients with complications (seven of eight versus two of seven without complications, P = 0.035). This study confirms that an appropriate rise in PTH level occurs in response to the hypocalcaemic stimulus in patients with acute pancreatitis.
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PMID:Circulating intact parathyroid hormone levels in acute pancreatitis. 817 97

The cause and effect relationship between acute pancreatitis and primary hyperparathyroidism (pHPT) still evokes controversy. Our paper reviews the debate in the medical literature. In this controversy we add a case of a 49-year old non-alcoholic man presenting with recurrent attacks of acute pancreatitis. His raised serum calcium was realized rather late. Eventually, high intact parathyroid hormone levels led to open neck exploration and finding of a solitary parathyroid adenoma. Post-surgery, serum calcium returned to normal and abdominal symptoms disappeared. The case report and the accompanying literature review support our belief, that acute pancreatitis is one of the symptoms of pHPT often caused by a parathyroid adenoma and curable by its excision.
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PMID:Pancreatitis in primary hyperparathyroidism. 1519 Jun 38

Secondary hyperparathyroidism is highly prevalent in patients with end-stage renal disease. After successful kidney transplantation, however, parathyroid glands gradually involute to normal size with subsequent normalization of intact parathyroid hormone (PTH), serum calcium, and phosphorous concentrations. This report describes a 48-year-old diabetic end-stage renal disease patient who underwent a successful cadaveric kidney transplant. Serum calcium and phosphorous concentrations normalized within 6 months. Three years later, he presented with complaints of proximal muscle weakness that was progressively worsening. Physical examination revealed temporal wasting and proximal muscle weakness. Detailed neurologic examination was unremarkable except for decreased vibratory sensation in both feet. Laboratory data showed stable allograft function (serum creatinine, 1.3 mg/dL), hypocalcemia, and hypophosphatemia with markedly elevated alkaline phosphatase level (726 IU/L) and intact PTH level (947 pg/mL). Further laboratory evaluation revealed poor nutritional status and severe deficiency of 25(OH)D (4.0 ng/mL). Past medical history included remote episodes of acute pancreatitis due to prior alcohol abuse. Computed tomography of the abdomen showed calcific atrophic pancreas, and steatorrhea was confirmed on stool studies. Decreased bone mineral density was noted by computed tomography bone density scan. Secondary hyperparathyroidism and osteomalacia had developed due to severe vitamin D deficiency, occurring as a result of previously unrecognized, minimally symptomatic pancreatic exocrine insufficiency. Treatment with vitamin D, calcium, and pancreatic enzyme replacement led to remarkable resolution of clinical symptoms and secondary hyperparathyroidism (intact PTH, 65 pg/mL after therapy) and resulted in significant improvement in bone mineralization. Factors associated with vitamin D deficiency in the chronic kidney disease and post-transplant patient population are reviewed.
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PMID:Osteomalacia and secondary hyperparathyroidism after kidney transplantation: Relationship to vitamin D deficiency. 1722 Jun 96


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