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Acute chronic pancreatitis

Guyan et al. 1990) have used several markers of lipid peroxidation (9-cis-, 11-tmns-isomer of linoleic acid, conjugated dienes and ultraviolet fluorescent products) to demonstrate significant increases in the duodenal aspirate after secretin stimulation in patients with acute and clinic pancreatitis. They interpreted this as indicating induction of hepatic and pancreatic drug-metabolizing enzymes in the face of a shortfidl of antioxidant defences, more marked in chronic pancreatitis. Subsequent studies in patients with chronic pancreatitis have confirmed decreased serum concentrations of selenium, -carotene and vitamin E compared with healthy controls (Uden et al., 1992). Basso aol. (1990) have measured increases in lipid peroxides in the sera of patients with chronic... [Pg.152]

Only one study to date has been conducted on the treatment of acute pancreatitis with antioxidants. Clemens et al. (1991) were unable to show any difference in the incidence or severity of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis in a prospective, randomized, double-blind, placebo-controlled trial of allopurinol. However, Salim (1991) performed a similar trial of the effect of allopurinol and DMSO in patients with pain from recurrent pancreatitis, and found significant benefit. On the basis that depletion of antioxidants is important in the pathogenesis of chronic pancreatitis, the administration of a cocktail of antioxidants was assessed for its effect on pain in this disease. Treatment with a combination of organic selenium, d-carotene, vitamins C and E, and methionine was of benefit in the initial pilot study, and in a placebo-controlled trial (San-dilands etal., 1990 Uden et al., 1990). [Pg.153]

Studies of both acute and chronic pancreatitis in humans and in animals support the hypothesis that free radicals are involved in the pathogenesis of pancreatitis. There is some conflicting data from the animal work, which may in part be due to differences in the models used. It does also indicate that free radicals are not the only factors involved and su ests that activation of pancreatic enzymes are also imprortant, particularly in the development of haemorrhagic pancreatitis (Sanfey, 1991). The findings of decreased antioxidant defences and the success of treatment reported in chronic pancreatitis with a cocktail of antioxidants and with allopurinol surest further studies are required to establish the role of antioxidants in pancreatic disease and its prevention. [Pg.153]

Differentiate the signs and symptoms of acute from chronic pancreatitis. [Pg.337]

O The most common causes of acute and chronic pancreatitis in adults are ethanol abuse and biliary stones. [Pg.337]

The incidence of chronic pancreatitis is approximately 1 in 10,000 people. O The most common cause of chronic pancreatitis in adults in Western countries is ethanol abuse. The most common cause in children is cystic fibrosis, due to preexisting pancreatic insufficiency inherent in the disease. Gallstones can occur at the same time as chronic pancreatitis but are not often implicated as the cause. Unlike acute pancreatitis, chronic pancreatitis has an unknown etiology in a significant number of cases (30%).29,3°... [Pg.341]

As patients lose exocrine function of the pancreas, they have decreased ability to absorb lipids and protein ingested with normal dietary intake. Weight loss from nutritional malabsorption is a common symptom of chronic pancreatitis not often seen in acute pancreatitis. Fatty- or protein-containing stools are also common carbohydrate absorption is usually unaffected. Even though patients with chronic pancreatitis have decreased ability to absorb lipid from the gastrointestinal tract, there does not appear to be an increased incidence of fat-soluble vitamin deficiency in these patients.34... [Pg.342]

The presentation of chronic pancreatitis can be similar to that of acute pancreatitis. [Pg.342]

Differentiating an episode of acute pancreatitis from chronic pancreatitis maybe difficult because the clinical presentations can be similar. The diagnosis of chronic pancreatitis is made by looking for the effects of chronic pancreatic inflammation and scarring on the pancreas and the patient as a whole. Computed tomography or ERCP will allow visualization of chronic calcified lesions in the pancreas when present.37... [Pg.342]

Banks PA. Epidemiology, natural history, and predictors of disease outcome in acute and chronic pancreatitis. Gastrointest Endosc 2002 56(6 Suppl) S226-S230. [Pg.344]

In addition to ANP where it is associated with GI dys-motility [198, 199], SIBO is present in a significant proportion of patients with chronic pancreatitis [200, 201], Short-term rifaximin therapy was able to normalize the hydrogen breath test and improve symptoms (i.e. diarrhea and fecal fat excretion) in all patients studied (fig. 9) [201]. Bowel decontamination via administration of this topical antibiotic could, therefore, be beneficial in both acute and chronic pancreatitis. Double-blind, placebo-controlled studies are to be performed to explore the rifaximin potential in this indication. [Pg.54]

Contraindications Acute pancreatitis, exacerbation of chronic pancreatitis, hypersensitivity to pork protein... [Pg.935]

Acute pseudocyst A collection of pancreatic juice enclosed by a wall of fibrous or granulation tissue, which arises as a consequence of acute pancreatitis, pancreatic trauma, or chronic pancreatitis. [Pg.57]

The trypsin family of proteases plays a role in acute and chronic pancreatitis, as well as leads to its ultimate destruction [4, 105]. In pancreatitis, active exocrine enzymes are prematurely released inside the pancreatic duct. Various factors can contribute to the development of acute pancreatitis. Trypsinogen, chymotrypsinogen, procarboxypeptidase, and proelastase are inactive proforms of proteolytic enzymes produced by the pancreatic acinar cells. Following secretion these enzymes are activated in a cascade that converts trypsinogen to trypsin in the duodenum and/or small intestine. [Pg.239]

Qll The most useful tests in suspected pancreatitis are biochemical the tests involve measurements of the concentration of amylase and lipase in blood. Increased blood levels of a-amylase can be found in a number of other conditions, for example disease of the ovaries, but elevated amylase is most often seen in acute and chronic pancreatitis. During acute attacks, the blood can contain three to five times more amylase and lipase than normal and the pattern of change is characteristic. [Pg.270]

The course of pancreatic fibrosis in rats induced by dibutyltin dichloride was studied 2-36 weeks after single i.v. treatment of rats with dose of 6 or 8 mgkg . The pancreatic fibrosis induced by Bu2SnCl2 differs from other experimental models of acute pancreatitis. Extensive infiltration is present in fibrotic areas without pancreatic atrophy or lipomatosis. The presence of chronic inflammatory lesions characterized by the destruction of exocrine parenchyma and fibrosis, and in the later stages the endocrine parenchyma, indicates a chronic pancreatitis. ... [Pg.1688]

Schafer D F, Sorrell M F 1999 Hepatocellular carcinoma. Lancet 353 1253-1257 Steer M L et al 1995 Chronic pancreatitis. New England Journal of Medicine 332 1482-1490 Steinberg W, Tenner S1994 Acute pancreatitis. New England Journal of Medicine 330 1198-1210... [Pg.660]

A 32-year-old man, who had been in hospital for several months because of acute intermittent porphyria and chronic pancreatitis, had a seizure and an asystolic cardiac arrest. Resuscitation was unsuccessful. There was a suspicion of patient mistreatment by one of the attending nurses, and toxicological analyses showed high blood concentrations of lidocaine, diazepam, phenytoin, and promethazine. Diazepam and phenytoin... [Pg.2057]

The authors postulated the following mechanisms acute exacerbation of chronic pancreatitis, a direct effect of pentagastrin on the pancreas, increased pancreatic secretion due to stimulation by gastric acid, reflux of duodenal contents or bile, arterial hypotension with local acidosis in the pancreas. [Pg.2773]

The pancreas is uniquely susceptible to high concentrations of ethanol, which can induce an acute inflammatory response characterized by release of amylase into the circulation. If severe or if this evolves into chronic pancreatitis it may lead to autodigestion by exocrine enzymes and ultimately to secondary endocrine dysfunction. [Pg.1226]

The major exocrine pancreatic disorders presenting in adult life are acute pancreatitis, chronic pancreatitis, and carcinoma of the pancreas. The use of enzyme tests in the diagnosis of acute pancreatitis is discussed in Chapter 21. The etiologies of pancreatitis are given in Box 48-6. [Pg.1867]

Prolonged nasogastric suction Malabsorption syndromes Extensive bowel resection Acute and chronic diarrhea Intestinal and biliary fistulas Protein-calorie malnutrition Acute hemorrhagic pancreatitis Primary hypomagnesemia (neonatal)... [Pg.1909]

Abou-Assi S, Craig K, O Keefe SJD, et al. Hypocaloric jejunal feeding is better than total parenteral nutrition in acute pancreatitis Results of a randomized comparative study. Am J Gastroenterol 2002 97 2255-2262. Scolapio J, Malhi-Chowla N, Ukleja A. Nutrition supplementation in patients with acute and chronic pancreatitis. Gastroenterol Clin North Am 1999 28 695-707. [Pg.735]


See other pages where Acute chronic pancreatitis is mentioned: [Pg.210]    [Pg.337]    [Pg.166]    [Pg.248]    [Pg.248]    [Pg.53]    [Pg.79]    [Pg.414]    [Pg.86]    [Pg.73]    [Pg.83]    [Pg.571]    [Pg.1749]    [Pg.613]    [Pg.2222]    [Pg.721]    [Pg.722]    [Pg.734]   
See also in sourсe #XX -- [ Pg.92 ]




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Pancreatitis, acute

Pancreatitis, chronic

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