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

We studied nine consecutive hypocalcemic patients with acute pancreatitis to elucidate the mechanism of hypocalcemia. Mean serum ionized calcium, 0.97 mM, was below the normal mean of 1.16 mM (P less than 0.001). Seven of eight patients tested had normal parathyroid hormone levels. All responded to parenteral parathyroid extract by increasing serum ionized calcium and urinary cyclic AMP, indicating parathyroid-hormone-responsive target organs. Calcitonin and glucagon concentrations were increased above normal in some patients, but there was no relation with serum ionized calcium. Parenteral glucagon had no significant effect on serum ionized calcium or calcitonin concentrations. These findings suggest that neither glucagon nor calcitonin was primarily responsible for the hypocalcemia, which did not produce expected increases in serum parathyroid hormone concentrations. Relative parathyroid insufficiency may account for the persistent hypocalcemia frequently observed in patients with acute pancreatitis.
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PMID:Inadequate parathyroid response in acute pancreatitis. 17 71

A retrospective and prospective study was made of 82 attacks of acute pancreatitis occurring in 80 patients. Attacks were defined as mild (55) or severe (27) according to clinical criteria. Severe attacks were associated with significantly low levels of uncorrected calcium and calculated ionized calcium, both at the time of admission and 48 h later. Patients with severe attacks were found to have lower levels of parathyroid hormone than either those with mild attacks or other patients who had undergone an abdominal operation. These results indicate that severe pancreatitis is associated with true hypocalcaemia, and that deficiency of circulating parathyroid hormone may be a factor in its production.
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PMID:The nature of hypocalcaemia in acute pancreatitis. 63 40

Differences in metabolic homeostasis in 12 patients with initial vs. eight patients with repeated attacks of acute pancreatitis have been compared during the acute phase of the disease. As a group, subjects with a previous history of pancreatitis had significantly lower glucagon concentrations (P less than 0.002) for the over all 24-hour study period. Conversely, the serum concentrations of blood sugar, insulin, growth hormone, gastrin, cortisol, nonesterified fatty acids, triglycerides and cholesterol failed to distinguish between the two patient groups. Likewise, immunoreactive plasma parathyroid hormone and calcitonin levels were comparable in both patient populations. Of the measurements considered, it would appear therefore that plasma immunoreactive glucagon is the best indicator of previous pancreatic inflammation. Evaluation of parenchymal integrity during an episode of acute pancreatitis would be of prognostic and therapeutic value in this disease.
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PMID:First 24 hours of acute pancreatitis. A biochemical and endocrine evaluation of initial versus repeated attacks. 69 15

Sequential daily measurements of plasma parathyroid hormone (PTH) have been performed in 89 patients with acute pancreatitis. A total of 439 PTH assays was obtained during 98 episodes of the disease. Three main patterns of PTH response were found. These responses were correlated with severity of disease graded by objective criteria and also to corrected serum calcium levels. The first type of PTH response was characterized by significantly elevated PTH levels soon after hospitalization with a subsequent decrease in levels to within the normal range by the third or fourth day of illness. This type of response was specifically associated with transient severe hypocalcaemia (corrected calcium less than 2.0 mmol/l). It was also associated with the most severe forms of disease and 6 of the 7 deaths. The second type of PTH response revealed initial PTH values in the upper level of the normal range (400--600 ng/l) while persistently low PTH levels were characteristic of the third type of response. Persistently low PTH levels were associated with normocalcaemia, and no patient in this group died. None of a group of 14 control patients exhibited the type 1 PTH response. An effective PTH response to an unidentified hypocalcaemic stimulus results in satisfactory calcium homeostasis in most patients with acute pancreatitis.
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PMID:Parathyroid hormone and calcium homeostasis in acute pancreatitis. 70 81

Calcium enters the pancreatic juice from two sources, one fraction associated with enzyme protein and another small fraction presumably by diffusion. The calcium concentration in pancreatic juice is lower than in plasma. It decreases with high flow rates and increases asymptotically to plasma concentration with low rates. In chronic pancreatitis calcium concentration is raised in the secretin-stimulated juice. After pancreozymin in moderate chronic pancreatitis it is low but in severe stages of the disease it is high signalling total dissociation from the entrance of enzyme protein, which is very low in these cases. Hypercalcemia stimulates enzyme secretion in the pancreas, hypocalcemia inhibits it. Calcium is essential for intracellular processes associated with secretion, the exact place in the sequence of "stimulus-secretion-coupling" still being unknown. Calcitonin as one of the hormones which regulates calcium homeostasis, inhibits secretion of enzymes but not of fluid and bicarbonate. The action of the parathyroid hormone on the exocrine pancreas is unknown. In primary hyperparathyroidism with chronic hypercalcemia acute and chronic pancreatitis occur 10 to 20 times more frequently than in the general population. In acute pancreatitis of whatever origin hypocalcemia is atypical feature of the disease indicating bad prognosis. The mechanism of its development is still unclear. In chronic pancreatitis the forming of calcified stones in the ducts is typical in cases associated with alcoholism, with protein malnutrition and with primary hyperparathyroidism. But it occurs also in cases with unknown etiology signalling a more general pathophysiological phenomenon. The calcium salts form a precipitate on protein plugs in the juice, which have been observed even in early stages of the disease in the small and larger ducts of the gland.
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PMID:The role of calcium in pancreatic secretion and disease. 77 77

Plasma calcitonin, glucagon and parathyroid hormone were measured in patients with acute pancreatitis. Plasma calcitonin was not detectable in 6 specimens obtained from the hypocalcaemic patients. Plasma glucagon values were similar in patients with acute pancreatitis and control subjects and were unrelated to hypocalcaemia, which was not even induced by glucagon infusion. High or rising parathyroid hormone levels were noted in association with hypo-and normocalcaemia, suggesting that parathyroid hormone rises and maintains plasma calcium within normal limits. Plasma parathyroid hormone was, however, undetectable in 8 patients with prolonged hypocalcaemia. Deficiency of parathyroid hormone due to its destruction by proteolytic enzymes or because of parathyroid gland exhaustion is suggested as the major factor inducing persistent hypocalcaemia in acute pancreatitis. Administration of parathyroid hormone should, therefore, be considered in patients with acute pancreatitis when hypocalcaemia does not respond to intravenous calcium therapy.
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PMID:The aetiology of hypocalcaemia in acute pancreatitis. 111 72

Variables of calcium metabolism were measured in 11 patients with clearly documented acute pancreatitis. Total and ionized calcium levels were either low or in the low-normal range as were phosphorus and total magnesium levels. Parathyroid hormone levels were high, and there was a significant inverse correlation with ionized calcium. Gastrin levels were normal, calcitonin values were uniformly below the detection limit of the assay, and pancreatic glucagon levels were elevated. The hypocalcemia of acute pancreatitis was probably not caused by abnormalities of glucagon, calcitonin, or gastrin secretion. Furthermore, parathyroid hormone secretion was apparently not impaired. Hypomagnesemia possibly played a minor role. This study suggests that the hypocalcemia of acute pancreatitis is secondary to extraskeletal calcium sequestration or an as yet unidentified defect of bone metabolism, or both.
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PMID:The hypocalcemia of acute pancreatitis. 114 52

To determine changes in parathyroid hormone secretion and target organ response caused by acute pancreatitis before the development of systemic toxic conditions, experimental acute pancreatitis was induced in rats with a choline-deficient, ethionine-supplemented diet. After 7 days, the rats were weighed and bled, and one kidney was assayed for 25-hydroxyvitamin D1 hydroxylase activity. Several manifestations of pancreatitis were observed in rats given the diet: weight loss (from 29.6 to 26.3 g vs that for control rats, from 29 to 52.8 g) and lower dietary intake (15.5 vs 47 g per rat per 7 days). Serum amylase levels fell from 1794 to 350 U/L in rats given the choline-deficient, ethionine-supplemented diet compared with levels of 1800 to 2100 U/L in control rats. The pancreases of rats given the choline-deficient, ethionine-supplemented diet showed degeneration, necrosis, and hemorrhaging. Serum levels of calcium, phosphorus, chloride, and parathyroid hormone did not change significantly throughout the experiment. Renal 25-hydroxyvitamin D1 hydroxylase activity was higher than in control rats (8.9 +/- 0.8 vs 7.6 +/- 0.6 fmol/mg of kidney per minute). Acute pancreatitis in this experimental animal model does not alter serum levels of calcium and parathyroid hormone or reduce target organ responsiveness to the hormone.
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PMID:Parathyroid hormone secretion and target organ response in experimental acute pancreatitis. 170 5

A case of acute pancreatitis associated with primary hyperparathyroidism is reported. There was none of usual causes of pancreatitis, which did not recur following the removal of a parathyroid adenoma. There are over one hundred of cases of acute or chronic pancreatitis associated with hyperparathyroidism in the literature, suggesting a causal relationship between the two entities. The pancreatic disease has been attributed either to the hypercalcemia or to the excess of circulating parathyroid hormone. However, some authors have recently questioned any link between these two diseases.
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PMID:[Acute pancreatitis associated with primary hyperparathyroidism]. 175 Oct 69

Patients with acute pancreatitis commonly manifest hypocalcemia for reasons which are unknown. We found that porcine pancreas extracts (PX) significantly decreased blood-ionized calcium in Balb/c mice. Partially-purified PX with a molecular mass of approximately 27 kDa decreased blood-ionized calcium in the mice. Partially-purified PX suppressed not only 45Ca release from fetal rat long bones which had been stimulated by parathyroid hormone, interleukin-1 alpha, tumor necrosis factor, transforming growth factor-alpha, 1,25-dihydroxyvitamin D3 and prostaglandin E2, but tartrate-resistant acid phosphatase-positive multinucleated cell formation in the presence of 1,25-dihydroxyvitamin D3 in mouse marrow cultures. The results suggest that there is an as yet-unidentified bone metabolism-regulating substance in porcine pancreas which might be responsible for the hypocalcemia associated with acute pancreatitis.
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PMID:Porcine pancreas extract decreases blood-ionized calcium in mice and inhibits osteoclast formation and bone resorption in culture. 199 7


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