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

We developed an assay for methemalbumin in biological fluids by using diethylaminoethyl-Sephadex ion-exchange chromatography to separate this protein from interfering components, including hemopexin, transferrin, hemoglobin, and haptoglobin/hemoglobin complex. Initial screening of the samples requires measurement of A280/A405 ratios of the peak tubes of the isolated albumin fraction. Values exceeding 30 indicate that methemalbumin is absent, and no further work is required. Values of less than 30 suggest that methemalbumin is present in the original sample, whereupon the presence and amount of methemalbumin can be ascertained by coloremetric assay for iron with use of ferrozine. Results may be expressed either in terms of micrograms of methemalbumin iron per gram of albumin or in milligrams of methemalbumin per liter. The reproducibility of the method is of the order of +/- 7% (SD). Normal persons have essentially no methemalbumin iron in their serum. Three individuals with hemorrhagic pancreatitis showed values of 65, 98, and 198 mug of methemalbumin Fe per gram of albumin.
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PMID:Clinical determination of methemalbumin. 115 22

This study investigates the role of platelet-activating factor (PAF) in experimental pancreatitis. The concentration of PAF quantified in ascites of bile-induced pancreatitis by radioimmunoassay (RIA) ranged from 3.67 +/- 0.39 pmol/mL 2 h to 0.954 +/- 0.39 pmol/mL 10 h after injection of taurocholate. Administration of a potent PAF antagonist, WEB-2170, prior to injection of taurocholate prolonged mean survival time in rats receiving i.v. camostate and albumin (46.4 h, n = 15, vs controls 38.3 h, n = 13). However, the survival rate after 72 h was not improved. The histologically estimated severity of pancreatitis and pancreatic enzymes in blood, tissue, or ascites was not affected. WEB-2170 had no effect on survival when injected simultaneously with taurocholate into the pancreatic duct or given i.v. after induction of pancreatitis (1, 0.1, or 0.01 mg/kg WEB-2170 vs controls). Subcutaneous injection of 10 mg/kg WEB-2170 also did not improve survival in pancreatitis induced by choline-deficient, ethionine-supplemented diet in mice. It is concluded that administration of a PAF antagonist after the onset of severe experimental pancreatitis does not influence its outcome, although activation of PAF may play a role in the pathogenesis of pancreatitis.
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PMID:Influence of a platelet-activating factor antagonist on severe pancreatitis in two experimental models. 146 Mar 31

The possible risk factors for failure of medical therapy were examined in 23 patients with pancreatic ascites or effusion. The ascites or effusion resolved completely in 10 patients after a mean (+/- SEM) of 30 +/- 2 days of conventional medical treatment. In five patients in whom conventional medical therapy failed, the addition of an octreotide (SMS 201-995) analogue to the medical therapy led to a resolution of the ascites (three patients) or effusion (two patients). Six patients underwent surgery after failed medical therapy, one patient died while receiving conservative therapy, and one patient refused hospital treatment. Serum sodium and albumin levels were significantly lower, and the ratio of total fluid protein to total serum protein was significantly higher in the group that failed to heal in response to conventional medical therapy. Nine of 11 patients with mild to moderately severe chronic pancreatitis healed in response to conservative therapy. Only one of 10 patients with advanced pancreatitis healed in response to conventional medical therapy. Our results suggest that a selective surgical approach is warranted to treat pancreatic ascites and effusion. In patients with mild or moderately severe pancreatitis, medical therapy is recommended. Patients with advanced pancreatic disease should be selected for early surgery. Octreotide may be useful in the patient in whom surgery may be associated with a prohibitive morbidity or mortality.
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PMID:Pancreatic ascites and effusion. Risk factors for failure of conservative therapy and the role of octreotide. 159 72

The nutritional assessment by 24 hour-dietary recall, anthropometry and blood-components measurements was undertaken in 23 adult patients, 17 males and 6 females suffering of chronic diarrhea from pancreatitis (30%), inflammatory bowel disease (22%), short intestine syndrome (9%) and unknown diarrhea (35%). The nutritional assessment was done at the entry and repeated at the discharge of the hospitalization that averaged 35 days, during which the patients received specific medical treatment along with obstipating diets. The hospitalization resulted in overall improvement of the patients either clinically by reducing their defecation rate or nutritionally by increasing their protein-energy intake and the values of anthropometry and blood components (albumin, free-tryptophan and lymphocytes). When the patients where divided into two groups based on their fecal-fat output one could note the better nutritional response of the group showing steatorrhea than the non-steatorrhea group, with the serum albumin and the arm-muscle circumference being discriminatory between groups. However even in the better recovered patients the indicative values of a satisfactory nutritional status were not accomplished. Thus, these data suggest that besides the overall nutritional improvement seen in the studied chronic diarrhea patients the full-nutrition recovering would demand either or both a longer hospitalization and/or an early-aggressive nutritional support.
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PMID:[Nutritional implications on treatment and recovery of adult patients with chronic diarrhea]. 184 43

Microvascular permeability was studied in the isolated perfused rat pancreas using a rapid multiple indicator-dilution technique. Capillary extractions, permeability-surface area products (PS), and extravascular volumes of distribution (EVV) were determined for 22Na+, 51Cr-labeled EDTA, [57Co]-cyanocobalamin (B12), and 125I-labeled insulin at various perfusion flows. Permeability to albumin was negligible. PS for Na+ and EDTA increased with increasing flow, whereas PS for cyanocobalamin and insulin approached diffusion-limited exchange at flows greater than 3 ml.min-1.g-1. Permeability coefficients for Na+, EDTA, B12, and insulin were 36, 22, 11, and 3.48 x 10(-5) cm/s, respectively, and the permeability ratio for B12/insulin (3.16) indicated restricted diffusion to insulin. In the presence of unlabeled B12 and insulin EVV (0.15-0.19 ml/g) for EDTA, B12 and insulin approximated the interstitial volume. Caerulein-induced pancreatitis or treatment with the synthetic protease inhibitor camostate had no significant effects on permeability. In caerulein-treated rats, EVV for B12 was elevated (0.17 +/- 0.01 vs. 0.28 +/- 0.06; P less than 0.01), reflecting the interstitial edema associated with this model of pancreatitis. Permeability of the rat pancreatic microvasculature is similar to that of other fenestrated tissues, but it is 10- to 20-fold greater than that of continuous capillaries. Contrary to previous assumptions, permeability does not appear to be increased after induction of acute interstitial pancreatitis.
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PMID:Pancreatic microvascular permeability in caerulein-induced acute pancreatitis. 192 54

Indirect evidence suggests a causative role for intraperitoneal free fatty acids (FFA) in hypocalcemia associated with pancreatitis. We examined the effects of intraperitoneal injection of four naturally occurring FFAs on serum calcium in rats. Two saturated FFAs, stearate and palmitate, induced little or no hypocalcemia. Two unsaturated FFAs, oleate and linoleate, caused dramatic hypocalcemia in treated versus control rats (6.3 +/- 1.4 and 5.3 +/- 0.7 mg/dl, respectively, versus 10.1 +/- 0.6). Dose-response studies demonstrated that minute quantities of oleate (100 microliters per 250 g rat) caused marked hypocalcemia (7.2 +/- 0.3 mg/dl). Treated versus control rats also revealed a decrease in ionized calcium (3.15 +/- 0.2 versus 5.6 +/- 0.05 mg/dl) and magnesium (1.4 +/- 0.15 versus 2.0 +/- 0.10), an appropriate increase in PTH levels (1670 +/- 451 versus 396 +/- 235 pg/ml), and a fall in calcitonin levels (70.4 +/- 21.3 versus 47.5 +/- 16.4 pg/ml) but no change in albumin or phosphate levels. In vitro, the Ksp of calcium dioleate was shown to be 5.3 x 10(-8) m3/liter3; thus under physiologic conditions 100 microliters oleate binds 7.2 mg calcium, or approximately twice the total ECF ionized calcium in the rat. The amounts of intraperitoneal FFA that can easily be achieved in pancreatitis complex pathophysiologically significant amounts of calcium and may lead to severe hypocalcemia.
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PMID:Intraperitoneal free fatty acids induce severe hypocalcemia in rats: a model for the hypocalcemia of pancreatitis. 207 38

Much clinical and experimental evidence suggests that pancreatic ischaemia in the early phase of acute pancreatitis is important in the development of pancreatic necrosis. While depletion of intravascular volume has often been assumed to be the main circulatory defect, an additional disturbance of pancreatic microcirculation has been demonstrated experimentally. Possible contributory mechanisms include chemical-induced vasoconstriction, direct injury of vessel wall, intravascular coagulation and increased endothelial permeability resulting in pancreatic oedema, haemoconcentration and impaired venous drainage. Pancreatic ischaemia as a consequence of these local effects seems to be responsible for the transition of mild pancreatitis to parenchymal necrosis. In experimental models the beneficial effect of various drugs and of sympathetic blockade has been ascribed to an improvement in pancreatic perfusion. Although effective volume therapy is generally accepted as the mainstay of conservative treatment in acute pancreatitis, the efficacy of different fluid preparations is still controversial, and simple fluid resuscitation has not been shown to prevent the development of parenchymal necrosis. The specific impairment of pancreatic microcirculation cannot be prevented merely by replenishment of intravascular volume with crystalloids, albumin or plasma despite normalization of macrohaemodynamics. In contrast, partial replacement of blood by dextran preparations has been shown to increase pancreatic perfusion by improving blood fluidity. Isovolaemic haemodilution in conjunction with conventional fluid therapy may provide a new and effective means of protecting the pancreas from secondary injury due to the early ischaemic phase of acute pancreatitis.
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PMID:Pancreatic ischaemia in experimental acute pancreatitis: mechanism, significance and therapy. 225 94

Acute pancreatitis was initiated in the isolated ex vivo, perfused canine pancreas preparation by exposing the gland to a 2 hour period of ischemia before a 4 hour perfusion period. The pancreatitis was manifested by edema formation, weight gain, and hyperamylasemia. When the osmotically active agent albumin was added to the perfusate at the end of the ischemic period, virtually no edema developed, weight gain was minimal, and the amylase level remained within normal limits during the subsequent 4 hour perfusion period. This suggests that a change in capillary permeability may be an early step in the pathogenesis of ischemia-induced pancreatitis in this experimental model.
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PMID:Experimental ischemic pancreatitis: treatment with albumin. 241 56

Serum calcium changes in severe pancreatitis were studied in 23 dogs. Twelve dogs underwent duodenotomy and served as controls. Pancreatitis was induced in the other 11 by autologous bile injection (1 ml/kg) into the pancreatic duct. Serum amylase, total calcium, ionized calcium, albumin, magnesium, chloride, phosphorous, parathyroid hormone (PTH), and calcitonin were measured at 0, 1/2, 1, 3, 6, 24, 48, and 72 hours after duodenotomy or bile injection. Serum amylase levels became significantly elevated in all dogs with pancreatitis at 30 minutes (p less than 0.01) and remained so throughout the entire experiment. Total calcium levels dropped significantly 30 minutes after pancreatitis was induced from 10.0 +/- 0.3 mg/dl compared with 8.8 +/- 0.4 mg/dl in control dogs (p less than 0.05) and remained statistically lower for as long as 1 hour. Ionized calcium levels were significantly lower than were those of control dogs at 1/2, 1, 3, and 6 hours (p less than 0.05). Serum magnesium and chloride levels showed no significant changes between both groups. The only significant difference in phosphorus values was at 6 hours when they were higher in dogs with pancreatitis than in controls (6.2 +/- 0.3 mg/dl versus 4.8 +/- 0.4 mg/dl; p less than 0.05). Serum albumin levels remained unchanged throughout the study except for 48 hours when they were significantly lower in animals with pancreatitis (p less than 0.02). PTH levels were significantly greater in dogs with pancreatitis than in controls at 1, 3, 6, and 24 hours (p less than 0.05). There was no significant difference in calcitonin levels between both groups. Ionized calcium is a more reliable indicator of calcium fluxes in acute experimental pancreatitis since it remains depressed longer than total serum calcium. The time course of PTH elevation indicates a reaction to hypocalcemia, and failure of PTH secretion is not the cause of hypocalcemia in pancreatitis. This study does not support elevation of calcitonin as a cause of hypocalcemia in acute pancreatitis.
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PMID:Serum calcium metabolism in acute experimental pancreatitis. 241 69

The use of total parenteral nutrition (TPN) in the treatment of 73 patients with acute severe pancreatitis was prospectively studied during a two year period. Patients were divided into three groups on the basis of calorie substrate used. Glucose and twice weekly lipid infusion (glucose based) were used in 60 per cent; 27 per cent required daily lipid infusion (lipid based), and 13 per cent received no lipid because of pre-existing hyperlipemia or thrombocytopenia (no lipid). Nutritional indices (albumin, transferrin and total lymphocyte count) were initially abnormal in more than 80 per cent of patients, and 50 per cent had three or more of Ranson's criteria. After TPN, 81 per cent had improved nutritional indices, and none had hypertriglyceridemia or aggravation of pancreatitis develop. Patients who received lipid based or no lipid had higher insulin requirements (p less than 0.01) than those receiving mainly glucose. Mortality was increased tenfold (2.5 versus 21.4 per cent, p less than 0.01) in patients who did not achieve positive nitrogen balance. We conclude that TPN, either lipid or glucose based, is a safe and effective therapy to reverse the malnutrition of acute pancreatitis and that failure to achieve positive nitrogen balance is associated with increased mortality.
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PMID:Total parenteral nutrition and alternate energy substrates in treatment of severe acute pancreatitis. 249 6


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