Screening for mutations of the cationic trypsinogen gene: are they of relevance in chronic alcoholic pancreatitis?
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BACKGROUND: In hereditary pancreatitis mutations of exons 2 (N21I) and 3 (R117H) of the cationic trypsinogen gene have been described. AIMS: To investigate whether the same mutations can also be found in patients with chronic alcoholic pancreatitis. METHODS: Leucocyte DNA was prepared from 23 patients with chronic alcoholic pancreatitis, 21 with alcoholic liver cirrhosis, 34 individuals from seven independent families with hereditary pancreatitis, and 15 healthy controls. DNA was also obtained from pancreatic tissue (n=7) and from pancreatic juice (n=5) of patients suffering from chronic alcoholic pancreatitis. R117H was detected by restriction digestion with Afl III. N21I was identified by an allele specific polymerase chain reaction (PCR). RESULTS: R117H was detected in four families with hereditary pancreatitis. The N21I mutation was identified in three families. All mutations were confirmed by sequencing of the corresponding DNAs. In patients with chronic alcoholic pancreatitis neither the exon 2 nor exon 3 mutations were present in blood leucocytes, pancreatic juice, or pancreatic tissue. DNA of the patients with alcoholic liver cirrhosis as well as all controls was of wild type. CONCLUSIONS: The allele specific PCR may be used to screen for the N21I mutation of cationic trypsinogen. Both trypsinogen mutations were found in hereditary pancreatitis but do not seem to be major pathogenic factors in chronic alcoholic pancreatitis. (+info)
Endoscopic ultrasonography: changes of chronic pancreatitis in asymptomatic and symptomatic alcoholic patients.
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Changes suggestive of chronic pancreatic damage by endoscopic ultrasonography were studied in 31 asymptomatic and symptomatic alcohol abusers. Fifteen additional patients who did not drink alcohol served as controls. Eighty-nine percent (17 of 19) of the alcohol abusers with chronic abdominal pain had chronic pancreatitis by endoscopic ultrasonography. Similarly, 58%, (7 of 12) asymptomatic alcoholic patients also had changes of chronic pancreatitis on endosonography. Endoscopic ultrasonography has thus detected changes suggestive of alcohol-induced chronic pancreatic damage in up to 58% of asymptomatic alcoholic persons and in 89% of alcoholic persons with pancreatic type pain. (+info)
Activation of pancreatic stellate cells in human and experimental pancreatic fibrosis.
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The mechanisms of pancreatic fibrosis are poorly understood. In the liver, stellate cells play an important role in fibrogenesis. Similar cells have recently been isolated from the pancreas and are termed pancreatic stellate cells. The aim of this study was to determine whether pancreatic stellate cell activation occurs during experimental and human pancreatic fibrosis. Pancreatic fibrosis was induced in rats (n = 24) by infusion of trinitrobenzene sulfonic acid (TNBS) into the pancreatic duct. Surgical specimens were obtained from patients with chronic pancreatitis (n = 6). Pancreatic fibrosis was assessed using the Sirius Red stain and immunohistochemistry for collagen type I. Pancreatic stellate cell activation was assessed by staining for alpha-smooth muscle actin (alphaSMA), desmin, and platelet-derived growth factor receptor type beta (PDGFRbeta). The relationship of fibrosis to stellate cell activation was studied by staining of serial sections for alphaSMA, desmin, PDGFRbeta, and collagen, and by dual-staining for alphaSMA plus either Sirius Red or in situ hybridization for procollagen alpha(1) (I) mRNA. The cellular source of TGFbeta was examined by immunohistochemistry. The histological appearances in the TNBS model resembled those found in human chronic pancreatitis. Areas of pancreatic fibrosis stained positively for Sirius Red and collagen type I. Sirius Red staining was associated with alphaSMA-positive cells. alphaSMA staining colocalized with procollagen alpha(1) (I) mRNA expression. In the rat model, desmin staining was associated with PDGFRbeta in areas of fibrosis. TGFbeta was maximal in acinar cells adjacent to areas of fibrosis and spindle cells within fibrotic bands. Pancreatic stellate cell activation is associated with fibrosis in both human pancreas and in an animal model. These cells appear to play an important role in pancreatic fibrogenesis. (+info)
Complicated chronic pancreatitis causing mycotic aortic aneurysm: in situ replacement with a cryopreserved aortic allograft.
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Mycotic aortic aneurysm, which resulted from infected pancreatic pseudocysts with retroperitoneal abscess, developed in a patient with chronic pancreatitis. The aorta was approached through median laparotomy. Necrotic material was debrided from the pancreatic pseudocysts, and the mycotic aneurysm was resected. The aorta was replaced in situ with a cryopreserved aortic allograft. This report discusses the rare complication of pancreatic pseudocysts, which affect the infrarenal abdominal aorta and cause a large mycotic aneurysm. This case suggests that the use of cryopreserved allografts is promising for in situ reconstruction, even in a grossly infected field. (+info)
Development of an animal model of chronic alcohol-induced pancreatitis in the rat.
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This study was designed to develop an animal model of alcoholic pancreatitis and to test the hypothesis that the dose of ethanol and the type of dietary fat affect free radical formation and pancreatic pathology. Female Wistar rats were fed liquid diets rich in corn oil (unsaturated fat), with or without a standard or high dose of ethanol, and medium-chain triglycerides (saturated fat) with a high dose of ethanol for 8 wk enterally. The dose of ethanol was increased as tolerance developed, which allowed approximately twice as much alcohol to be delivered in the high-dose group. Serum pancreatic enzymes and histology were normal after 4 wk of diets rich in unsaturated fat, with or without the standard dose of ethanol. In contrast, enzyme levels were elevated significantly by the high ethanol dose. Increases were blunted significantly by dietary saturated fat. Fibrosis and collagen alpha1(I) expression in the pancreas were not detectable after 4 wk of enteral ethanol feeding; however, they were enhanced significantly by the high dose after 8 wk. Furthermore, radical adducts detected by electron spin resonance were minimal with the standard dose; however, the high dose increased carbon-centered radical adducts as well as 4-hydroxynonenal, an index of lipid peroxidation, significantly. Radical adducts were also blunted by approximately 70% by dietary saturated fat. The animal model presented here is the first to demonstrate chronic alcohol-induced pancreatitis in a reproducible manner. The key factors responsible for pathology are the amount of ethanol administered and the type of dietary fat. (+info)
The natural history of alcoholic chronic pancreatitis.
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An improved knowledge of the natural history is the indispensible basis for a rational concept in regard to the diagnosis, classification, understanding and management of pain in chronic pancreatitis. Unfortunately, data on the natural history of CP are scarce and conflicting. Some relevant observations of our prospective long-term study of a mixed medical-surgical cohort comprising 207 patients with alcoholic CP (mean follow-up 17 years from onset) are summarized. In early-stage CP, episodes of recurrent pancreatitis were predominant. Severe persistent pain was typically associated with local complications (mainly postnecrotic cysts in 54%; symptomatic cholestasis in 24%) relieved definitely by a drainage procedure. Lasting pain remission was documented in >80% of the whole cohort within 10 years from onset in association with marked pancreatic dysfunction. From our experience, the relief of "chronic" pain regularly follows selective surgery tailored to the presumptive pain cause or it occurs spontaneously in uncomplicated advanced CP (excluding narcotic addiction). (+info)
Effect of somatostatin on the sphincter of Oddi in patients with acute non-biliary pancreatitis.
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BACKGROUND: Somatostatin has been used to prevent pancreatitis after endoscopic retrograde cholangiopancreatography but its effect on acute non-biliary pancreatitis is still unclear. AIM: The purpose of this study was to evaluate the function of the sphincter of Oddi (SO) and the effect of somatostatin on patients with non-biliary pancreatitis. METHODS: Twenty patients (18 males, two females) with acute pancreatitis (alcoholic 18, idiopathic two) received SO manometry within one week after admission. After baseline measurement, a bolus dose of somatostatin (Stilamin, Serono) 250 microg was infused slowly, and SO manometry was repeated after five minutes. Continuous infusion of somatostatin 250 microg/h was given for 12 hours after SO manometry. Serum amylase, lipase, glucose, and C reactive protein (CRP) levels were examined before and after somatostatin infusion. RESULTS: SO manometry was unsuccessful in six patients due to contracted sphincter. In the remaining 14 patients, high SO basal pressure (SOBP >40 mm Hg) was found in seven patients. After somatostatin infusion, mean SOBP decreased from 48.8 (29) to 31.9 (22) mm Hg (p<0.01). One patient had a paradoxical reaction to somatostatin (SOBP increased from 30 to 50 mm Hg) while the other 13 patients had a fall in SOBP after somatostatin. One patient developed abdominal pain with a serum amylase level of 2516 IU/l after SO manometry. No other side effects or changes in amylase, lipase, glucose, or CRP levels were observed in the other 19 patients after SO manometry and somatostatin infusion. DISCUSSION: Sphincter of Oddi dysfunction is common in patients with acute non-biliary pancreatitis and in most cases somatostatin can relax the sphincter. (+info)
Severe hypophosphatemia in a patient with acute pancreatitis.
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CONTEXT: We describe a patient with alcohol-induced pancreatitis who developed severe life-threatening hypophosphatemia of multifactorial origin during hospitalization. CASE REPORT: Decreased phosphate levels along with urine phosphate wasting were already noticed on the patient's admission due to underlying chronic alcoholism. However, a further deterioration of hypophosphatemia appeared on the second day of hospitalization presumably resulting from an increased transfer of phosphate from extracellular to intracellular fluid. CONCLUSIONS: Phosphate deficiency is often overlooked in patients with acute pancreatitis. Our case emphasizes that serum phosphate levels should be checked along with serum calcium levels in patients with acute pancreatitis, especially in alcoholic patients. (+info)