Histopathologic and Immunohistochemical Studies on the Mechanism of Interlobular Fibrosis of the Pancreas

2000 ◽  
Vol 124 (9) ◽  
pp. 1302-1305
Author(s):  
Koichi Suda ◽  
Masaru Takase ◽  
Kazuo Takei ◽  
Toshio Kumasaka ◽  
Fujihiko Suzuki
Keyword(s):  
Pancreatic Duct ◽  
Main Pancreatic Duct ◽  
Smooth Muscle Actin ◽  
Marked Change ◽  
Pancreatic Tissue ◽  
Alcoholic Pancreatitis ◽  
Chronic Alcoholic Pancreatitis ◽  
Chronic Alcoholic ◽  
Tissue Samples ◽  
Immunohistochemical Studies

Abstract Objective.—To elucidate the mechanism of interlobular fibrosis of the pancreas, which is categorized as chronic alcoholic pancreatitis. Methods.—Forty pancreatic tissue samples from patients with ampullary carcinomas, which cause various degrees of stricture of the main pancreatic duct, and 20 patients with chronic alcoholic pancreatitis were studied histopathologically and immunohistochemically. Results.—Fibrosis was observed in 23 of 40 patients with ampullary carcinomas and was classified into 3 categories: mild changes (10 cases), moderate changes (9 cases), and marked changes (4 cases). In the mild change cases, mild fibrosis was diffusely distributed in the interlobular areas, with scant immunoreactivity of anti–α-smooth muscle actin (α-SMA) and an expansive lobular appearance, whereas moderate and marked change cases showed interlobular and intralobular fibrosis with marked anti–α-SMA immunoreactivity and lobular atrophy. By quantitative analysis, the mild change cases showed both higher MIB1-positive and lower apoptotic acinar cell ratios than those of moderate and marked changes. Anti–α-SMA immunoreactivity in the patients with chronic alcoholic pancreatitis was found in interlobular fibrosis. Hence, mild changes in cases of ampullary carcinomas had histologic findings similar to chronic alcoholic pancreatitis, except for excessive fibrosis cases with patchy distribution. Conclusion.—Incomplete obstruction of the main pancreatic duct caused the beginning of interlobular fibrosis, which is categorized as chronic alcoholic pancreatitis.

scholarly journals Screening for mutations of the cationic trypsinogen gene: are they of relevance in chronic alcoholic pancreatitis?

Gut ◽  
1999 ◽  
Vol 44 (3) ◽  
pp. 413-416 ◽  
Author(s):  
N Teich ◽  
J Mössner ◽  
V Keim
Keyword(s):  
Liver Cirrhosis ◽  
Pancreatic Juice ◽  
Pancreatic Tissue ◽  
Alcoholic Pancreatitis ◽  
Alcoholic Liver Cirrhosis ◽  
Hereditary Pancreatitis ◽  
Chronic Alcoholic Pancreatitis ◽  
Chronic Alcoholic ◽  
Cationic Trypsinogen ◽  
Allele Specific

BACKGROUNDIn hereditary pancreatitis mutations of exons 2 (N21I) and 3 (R117H) of the cationic trypsinogen gene have been described.AIMSTo investigate whether the same mutations can also be found in patients with chronic alcoholic pancreatitis.METHODSLeucocyte 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).RESULTSR117H 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.CONCLUSIONSThe 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.

scholarly journals A case of splenic artery pseudoaneurysm rupture presenting as rectal bleeding in a regional hospital

2020 ◽  
Vol 2020 (12) ◽  
Author(s):  
Jonathon N Holt ◽  
Heinrich E Schwalb
Keyword(s):  
Rectal Bleeding ◽  
Splenic Artery ◽  
Artery Aneurysm ◽  
Regional Hospital ◽  
Alcoholic Pancreatitis ◽  
Chronic Alcoholic Pancreatitis ◽  
Chronic Alcoholic ◽  
Artery Pseudoaneurysm ◽  
Previous Trauma ◽  
Splenic Artery Pseudoaneurysm

Abstract Splenic artery pseudoaneurysm is a rare phenomenon most associated with chronic pancreatitis or previous trauma. Complications can include erosion and rupture into local structures, a situation that carries a reported mortality of 10–40%. A 58-year-old male with chronic alcoholic pancreatitis and a known splenic artery pseudoaneurysm presented to the emergency department of a regional hospital with rectal bleeding and sepsis. Computed tomography revealed a peri-splenic mass communicating with the splenic flexure. The patient was taken for an emergency splenectomy and left hemicolectomy and was confirmed to have rupture of the splenic artery aneurysm into the large bowel. This case presented with comparable features reported in the literature and demonstrates that access to emergency specialist surgical services in a regional setting offers the capability to manage rare, life threatening surgical emergencies.

Pathogenesis of pancreatic fibrosis in chronic alcoholic pancreatitis

1998 ◽  
Vol 114 ◽  
pp. A503
Author(s):  
T. Tanaka ◽  
T. Fujii ◽  
Y. Matsugu ◽  
Y. Kodoh ◽  
K. Koide ◽  
...  
Keyword(s):  
Pancreatic Fibrosis ◽  
Alcoholic Pancreatitis ◽  
Chronic Alcoholic Pancreatitis ◽  
Chronic Alcoholic

scholarly journals Nutritional profile of asymptomatic alcoholic patients

2011 ◽  
Vol 48 (2) ◽  
pp. 112-118 ◽  
Author(s):  
Maria Beatriz Sobral-Oliveira ◽  
Joel Faintuch ◽  
Dulce Reis Guarita ◽  
Claudia P. Oliveira ◽  
Flair J. Carrilho
Keyword(s):  
Lean Body Mass ◽  
Body Mass ◽  
Alcoholic Pancreatitis ◽  
C Reactive Protein ◽  
Chronic Alcoholic Pancreatitis ◽  
Chronic Alcoholic ◽  
Vitamin Deficiencies ◽  
Reactive Protein ◽  
Amyloid A ◽  
Visceral Disease

CONTEXT: Alcoholism may interfere with nutritional status, but reports are often troubled by uncertainties about ingested diet and organ function, as well as by ongoing abuse and associated conditions. OBJECTIVE: To identify nutritional and body compartment changes in stable alcoholics without confounding clinical and dietetic variables, a prospective observational pilot study was designed. Three well-matched populations were considered: subjects with chronic alcoholic pancreatitis, alcoholics without visceral disease, and healthy never-drinking adults (controls). METHODS: Subjects (n = 60) were asymptomatic males with adequate diet, no superimposed disease or complication, and alcohol-free for at least 6 months. After exclusions, 48 patients were compared. Variables encompassed dietary recall, bioimpedance analysis, biochemical profile and inflammatory markers. Main outcome measures were body fat, lean body mass, serum lipids, C-reactive protein, and selected minerals and vitamins. RESULTS: Both alcoholic populations suffered from reduced lean body mass (P = 0.001), with well-maintained body fat.Magnesium was depleted, and values of vitamin D and B12 correlated with alcohol abuse. LDL and total cholesterol was increased in alcoholics without pancreatitis (P = 0.04), but not in those with visceral damage. C-reactive protein and serum amyloid A correlated with duration of excessive drinking (P = 0.01). CONCLUSIONS: Undernutrition (diminished lean body mass, risk of magnesium and vitamin deficiencies) contrasted with dyslipidemia and increased cardiovascular risk. This second danger was masked during chronic pancreatitis but not in alcoholics without visceral disease. Further studies should focus special requirements of this population.

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