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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Familial benign hypercalcemia, or hypocalciuric hypercalcemia, may be defined as a dominantly inherited disorder of calcium and magnesium metabolism, characterized by lifelong hypercalcemia and hypermagnesemia (both of variable degree), that usually is not associated with any symptoms, physical signs, reduced vitality, or ill health. Chondrocalcinosis, pancreatitis, gallstones, and neonatal primary hyperparathyroidism are possible rare associations, but findings differ among various studies. The biochemical findings are bland, with "normal" values for serum PTH by many techniques, modest hypophosphatemia, and other findings usually normal. A low calcium:creatinine clearance ratio is suggestive of, but not diagnostic for, FBH; urinary calcium excretion less than 100 mg per day may be just as helpful. The diagnosis should not be made casually or without family screening, because the findings in a given patient may be identical to those in mild primary hyperparathyroidism. The major rationale for careful evaluation is to diagnose the syndrome of FBH and to help affected family members avoid needless expense and the risk of further evaluation and treatment.
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PMID:Familial benign (hypocalciuric) hypercalcemia. A troublesome mimic of mild primary hyperparathyroidism. 267 70

Calcium homeostasis and exocrine pancreas interact on several levels under both physiologic and pathophysiologic conditions. (1) Calcium ions are important intracellular mediators of cholinergic and hormonal stimulation of the pancreatic acinar cell, and thus play a central role in the stimulus-secretion coupling of ecbolic pancreatic function. (2) The calcium concentration in pancreatic juice is lower than in the interstitial fluid: pancreatic juice calcium is composed of two fractions, one of which is secreted together with enzyme proteins and the other diffuses along paracellular pathways dependent on serum calcium. Disturbed calcium secretion in pancreatic juice can be observed even following slight pancreatic alteration; conversely, disturbed calcium secretion may be of importance in the pathogenesis of chronic calcifying pancreatitis. (3) Hypocalcemia is an important symptom of acute pancreatitis whose pathogenesis has not been fully elucidated. (4) On the other hand, pancreatitis complicates chronic and acute hypercalcemic syndromes though the pathogenic mechanisms is uncertain. Experimental chronic hypercalcemia in animal models causes characteristic pancreatic secretory changes and disturbs the diffusion barrier for calcium. Experimental acute hypercalcemia causes stimulation of pancreatic enzyme secretion and cholecystokinin release. In addition, extracellular calcium has a direct stimulatory effect on pancreatic acinar cells in vitro.
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PMID:[Calcium homeostasis and exocrine pancreas: physiological ans pathological interrelations]. 268 7

In chronic pancreatitis with moderate derangements of carbohydrate tolerance (detected by the double glucose test), the basal concentrations of insulin and C-peptide in blood are normal whereas in patients with secondary diabetes mellitus are lowered. Glucagonemia is increased in patients of both groups. Euphylline (applied as an inhibitor of nucleotide phosphodiesterase), calcium gluconate and the adrenomimetic drug isadrin consistently increased insulinemia and the blood level of C-peptide in patients with chronic pancreatitis both with moderate and appreciable derangements of glucose tolerance. In patients with secondary diabetes that developed in the presence of pancreatitis, these drugs did not influence glucagonemia. The clinical prospects of the making use of the stimulating action of euphylline, calcium gluconate and isadrin on the function of beta-cells of the pancreas in chronic pancreatitis patients are under discussion.
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PMID:[The effect of pharmacological agents on pancreatic incretory activity in patients with chronic pancreatitis]. 269 52

The exact aetiology of chronic calcifying pancreatitis is unknown; several factors that lead to the development of this well-defined disease have been identified. Epidemiologic studies and careful analysis of nutritional data played an important role in precising the risk represented by alcohol consumption and dietary habits, and characterized the geographical distribution of the disease. At the same time, biochemical modifications of the pancreatic juice were described in alcoholics; later on, a new family of pancreatic secretory protein, the so-called "Pancreatic Stone Protein" was discovered. While its secretory form (PSP S2-5) prevents calcium crystal formation from the supersaturated pancreatic juice, its partially degraded form (PSP S1) is insoluble and probably the main protein of intraductal and intraacinar precipitates. Recent studies have confirmed that in chronic calcifying pancreatitis patients the mRNA encoding the synthesis of PSP S2-5 is decreased, and the protein is diminished both in the zymogen granules and in the pancreatic juice.
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PMID:Chronic calcifying pancreatitis: epidemiology and current concept of the lithogenesis. 269 18

Acute necrotising pancreatitis in rats was induced by injecting 5% sodium taurocholate into the pancreatic duct. Prostaglandin E2 (100 micrograms/kg subcutaneously twice) decreased the mortality rate from 100% to 60% (NS). When treatment with prostaglandin E2 was combined with simultaneous administration of either dazmegrel (UK 38,485, 50 mg/kg bodyweight) or Sibelium (Flunarizine R 14,950, 0.2 mg/kg body weight) a significant decrease in the mortality rate (p less than 0.05) was recorded. Dazmegrel is a selective thromboxane A2 synthetase inhibitor and prevents the formation of thromboxane A2. Flunarizine (a calcium entry blocker) decreases thromboxane A2 formation and also inhibits the effects of raised thromboxane A2 concentrations. As plasma thromboxane B2 (the stable metabolite of thromboxane A2) concentrations increase and the plasma prostaglandin E2 concentrations decrease in acute necrotising pancreatitis in rats, the results of the present study indicate that these prostaglandins play a role in the pathophysiology of the disease. It is suggested that restoration of the balance in prostanoid concentrations will have a beneficial effect on the course of acute necrotising pancreatitis.
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PMID:Significance of prostaglandin E2 in acute necrotising pancreatitis in rats. 273 61

Investigations were carried out in 1041 consecutive patients of acute pancreatitis, to correlate the prognosis with their symptoms and signs. It has been found that there were 15 symptoms and signs may be related to their prognosis; that is age over 60, high intake of fatty food immediately before attack, severe upper abdominal pain with vomiting, pulse rate over 100/min, pulse pressure below 2.6 kPa, peritoneal irritation, absence of peristaltic sounds, bloody ascites, serum electrolytes disorder, acidosis, more than 4000 ml of fluid were needed in first 24 h, serum calcium level below 1.9 mmol/L, blood glucose over 8.3 mmol/L, BUN over 7.0 mmol/L, and poor liver functions. If there are less than 4 positive signs, edematous pancreatitis may be present, 5 to 8 positive signs may be necrotizing pancreatitis with high risk of mortality and early operation is indicated, and more than 8 positive signs the prognosis will be very poor.
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PMID:[Diagnostic criteria and their relation to prognosis in acute pancreatitis]. 280 98

In a 14-years period (1970-1984) eight-three patients were operated on for primary hyperparathyroidism (pHPT) at the University Hospital of Erlangen. Special attention was paid to associated diseases, symptoms, preoperative diagnostic parameters were serum calcium, parathyroid hormone in venous blood, cyclic AMP in 24 h-urine. In 15.7% only borderline increased serum calcium values were measured. Ulcer incidence in pHPT was 19% as compared with approx. 7% in the general population. There was no increased incidence of pancreatitis in pHPT. The possibility of an association of pHPT with the Multiple Endocrine Neoplasia (MEN) syndrome was emphasized and measures of early diagnosis proposed.
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PMID:[Primary hyperparathyroidism--experiences with concomitant diseases, symptoms, preoperative diagnosis and surgical procedure over a period of 14 years]. 288 2

There are two different forms of chronic pancreatitis: one is obstructive pancreatitis which results from a pre-existing obstacle (usually a tumour or a scar) and the other, much more frequent, is chronic calcifying pancreatitis which seems to begin with the formation of precipitates in acini and ducts, later transformed into stones and calcifications made up of calcium carbonate, and therefore is a pancreatic lithiasis. Since the pancreatic juice is supersaturated in calcium carbonate, the presence of an inhibitor of crystallization must be postulated. This has now been identified as a 13500 daltons molecular weight protein: the pancreatic stone protein secreted by the acinar cells. This protein is decreased in chronic calcifying pancreatitis irrespective of its origin (alcoholic, hereditary, hypercalcaemic, tropical, idiopathic), although its reduction is unrelated to any of these aetiological factors. Chronic alcohol consumption may encourage calcium stone formation possibly by disturbing the cholinergic regulation of pancreatic secretion, with decrease in citrate secretion (citrate is a chelator of calcium) and increase in enzyme secretion. The diagnostic and therapeutic implications of these findings are already obvious.
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PMID:[Chronic calcifying pancreatitis, pancreatic calculi. New data]. 293 79

One hundred nineteen children, either French or from the Ivory Coast, aged 1-8 years, were submitted to pancreatic function testing by duodenal aspiration. Trypsin, chymotrypsin, lipase, phospholipase, amylase, volume, bicarbonate, chloride, and calcium were estimated before and after an intravenous injection of 1 CU secretin + 3 CHR units pancreozymin per kilogram of body weight. Sixty-two patients were normal European children, and 11 were normal African children. Twenty-five African children presented with kwashiorkor and 10 African children had presented with kwashiorkor but had recovered at the time of the test. Three cases of recurrent kwashiorkor are also included. In the normal group of African children, phospholipase concentration, volume, and bicarbonate were significantly decreased but chymotrypsin and trypsin concentrations were not, when compared to the normal European population. In kwashiorkor patients, lipase, amylase, phospholipase, and chymotrypsin concentration were significantly decreased compared to normal Africans. Trypsin, volume, and bicarbonate were not affected. These modifications disappeared after refeeding. In cases of recurrent kwashiorkor, all enzymes, including trypsin, were decreased. Calcium was never modified. These modifications were very different from those observed in chronic alcoholic and hypercalcemic pancreatitis. In a two-year study, chronic calcifying pancreatitis (CCP) was diagnosed in 14 patients (13 males), hospitalized in Abidjan. The mean age at onset of the disease was 41 years (SD 12.71), which is very similar to European cases. The most frequent cause was alcoholism, as in Occidental countries. The nutrition of the population was low in protein, calories being provided mostly by manioc, but no apparent symptoms of malnutrition were observed in the parents of our patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Exocrine pancreatic function of children from the Ivory Coast compared to French children. Effect of kwashiorkor. 300 10

This paper presents a review of the clinical significance of juxtapapillary duodenal diverticula in man. The incidence of such diverticula varies considerably in the literature, and possibly depends on the methods of investigation used. Studies show that the incidence of biliary calculi is significantly higher in patients with juxtapapillary diverticula as compared with patients without such diverticula. The assumed higher rate of diverticula in patients with pancreatitis is probably due to the presence of biliary calculi in these patients. Studies have shown that there is an insufficient choledochoduodenal sphincter in patients with diverticula, and also a higher rate of bacterial contamination of the duodenum and bile ducts in these patients. Fecal type flora has been found in most patients with juxtapapillary duodenal diverticula. Further, pigment gallstones have been found in most patients with diverticula, and analyses of these calculi showed that calcium bilirubinate was the main component. Further studies in our laboratory have shown that bacterial cultures produced beta-glucuronidase, a fact which may be connected with the increased frequency of pigment gallstones. Other studies have shown that there is a higher rate of diverticula in patients with recurrent biliary calculi who had undergone cholecystectomy. Recent data have also shown that there is a higher rate of common bile duct calculi in patients with diverticula, than in those without diverticula and without prior cholecystectomy--a fact supporting the theory on the pathogenesis of biliary calculi in patients with juxtapapillary diverticula. Other, and rare complications due to such diverticula are also mentioned.
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PMID:Juxtapapillary duodenal diverticula. 313 98


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