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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An analysis of 89 cases with chronic pancreatitis revealed 56% of chronic alcoholic pancreatitis (AP). The sex ratio was 47 males to 3 females and the mean age at onset was 42.4 years in AP and 49.3 years in chronic non-alcoholic pancreatitis (NAP). The 'total amount' of alcohol consumption was correlated to the onset. In AP, the abdominal pain was apt to relapse and severe in nature, furthermore painless pancreatitis was seen in 6%. The association with diabetes or calcification (38%) were more frequently seen in AP. The calcifications in AP appeared to be smaller in size and distributed diffusely or localized in cephalic portion. A striking frequency of liver dysfunctions (39 cases) were demonstrated, however, cirrhosis was rare in AP. The P-S test dysunctions in NAP were frequently reversible in the follow up study, while even some of chronic asymptomatic alcoholics developed clinical signs of pancreatitis during the observed period and proceeded to definite AP, of whom pancreatic dysfunctions showed fluctuation and eventual progression. In other words, even pain free intervals the pancreatic inflammation in susceptible persons may proceed to ultimated destruction of the pancreas. The fatality from chronic pancreatitis was rare (12.3%), which was related diabetes mellitus.
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PMID:A clinical investigation of chronic pancreatitis--comparative study between alcoholic pancreatitis and non-alcoholic pancreatitis--. 66 97

Two studies investigating the association of liver disease with acute and chronic pancreatitis in alcoholics are presented. In a retrospective study of 50 patients, no clinical liver disease was found in 9 patients with acute pancreatitis, while 23 (56%) of 41 patients with chronic pancreatitis had liver disease by clinical criteria. Of this latter group, 8 were confirmed histologically; thus 19% of patients with chronic pancreatitis had biopsy-proven cirrhosis. Fifty alcoholic patients with pancreatitis were prospectively evaluated. All who had clinical evidence of liver disease were biopsied. No cases of liver disease were encountered in the 4 patients with acute pancreatitis. Although 28 (60%) cases of clinically diagnosed liver disease were present in 46 patients with chronic pancreatitis, only 20 of these seemed significant (cirrhosis, alcoholic hepatitis, severe fatty liver), for an incidence of 43%. Thus, clinically significant alcoholic liver disease occurs quite frequently in association with alcoholic pancreatitis. This association is meaningful in more effective management of these patients in general and in preoperative assessment of the risk of surgery in particular.
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PMID:Associated liver disease in alcoholic pancreatitis. 68 26

Sequential standard (1.0 U./kg.) and augmented (4.0-5.0 U./kg.) secretin response to the pancreas has been briefly compared in normal subjects and in patients with combinations of alcoholism, cirrhosis and alcoholic pancreatitis. The results of sequential testing led to the conclusion that, for clinical purposes, the standard test is adequate for the diagnosis of well established pancreatic pathologies causing gross destruction of the parenchyma. The augmented test is of particular value when the response to 1 U./kg. produced equivocal results, inasmuch as augmented stimulation enhances the masked secretory deficiency. The administration of the augmented stimulus to alcoholic patients yielded data which suggest a new hypothesis of pathogenesis for alcoholic pancreatitis, e.g., the postsecretin response pattern of minimal pancreatic inflammatory pathology is hypersecretion. Alcohol is thought to induce fatty degeneration of the pancreatic cell initially. Continued injury leads to necrosis and fibrosis.
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PMID:Standard and augmented secretin testing in chronic pancreatic alcoholic disease. 118 15

The pancreatic functions (PFD test and 75g GTT), pancreatic enzymes (serum-amylase, urine-amylase, serum-elastase I and serum-lipase), alcohol consumption histories, clinical symptoms, histological findings in the liver and ERP findings have been examined in 66 alcoholic patients. Fourty two out of 66 cases (64%) showed abnormal ERP findings which were compatible with chronic pancreatitis. But among these 42 cases, only 9 cases (21%) showed clinical symptoms such as epigastralgia, back pain, diarrhea and emaciation which suggest the existence of chronic pancreatitis. The degree of liver damage, alcohol consumption have no significant correlation with ERP findings. Furthermore, the severe alcoholic pancreatitis occurred in patients having mild liver injury more than those having severe liver injury such as cirrhosis. And the data of pancreatic functions and enzymes could not confirm ERP findings especially in patients with mild and moderate pancreatic injury when compared to normal ERP findings. We concluded that asymptomatic alcoholic pancreatitis occurred more frequently in painless alcoholic. It may be not suitable for only using the normal pancreatic functions test to diagnose the alcohol induced chronic pancreatitis.
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PMID:[Clinical study on alcoholic pancreatitis in alcoholics (especially in ERP findings)]. 275 67

In order to elucidate the functional states of the pancreas in the asymptomatic latent stage of chronic alcoholic pancreatitis, 45 chronic alcoholics with no obvious pancreatic structural abnormalities judged by endoscopic pancreatography were studied by pancreozymin-secretin test. We found three patterns of exocrine pancreatic function in alcoholics with or without cirrhosis: normal secretion (40%), hyposecretion (29%) and hypersecretion (31%). In the hyposecretory group, the amylase output proved to be impaired more frequently. In the hypersecretory group increases were observed in one or more of the following parameters, volume, bicarbonate output and amylase output. However, increase in volume was a fundamental condition in this hypersecretion. This study confirmed that exocrine pancreatic hyposecretion and hypersecretion were almost equally frequent in asymptomatic chronic alcoholics with no obvious pancreatographic abnormalities. These results suggest that ongoing exocrine pancreatic dysfunctions exist in the subclinical stage of chronic alcoholic pancreatitis.
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PMID:Exocrine pancreatic function in asymptomatic chronic alcoholics without structural pancreatic disease. 402 49

Seventy-two chronic alcoholics, 40 (all males) with chronic pancreatitis and 32 (23 males and nine females) with liver cirrhosis, were submitted to liver biopsy, endoscopic retrograde cholangiopancreatography and secretin-caerulein test in order to assess a possible liver involvement in chronic pancreatitis and viceversa, and to evaluate the existence of any relationship between the diseases of these two organs. Chronic pancreatitis patients were younger than cirrhotic patients and drank more than the cirrhotic females. Twenty-nine of the 40 patients had abnormal liver histology, five had micronodular cirrhosis and were older than the others. No relationship was found between the degree of pancreatic impairment and the type of liver injury. Five liver cirrhosis patients had an endoscopic retrograde cholangiopancreatography picture consistent with chronic pancreatitis; two were females with an alcohol intake lower than the one of the other females. In conclusion the association of chronic pancreatitis and liver cirrhosis was observed in a minority of cases, with the same percentage in the two groups, even if the cirrhotic subjects were older than the pancreatitics. Therefore we can postulate that different factors have roles in the pathogenesis of alcoholic cirrhosis and of chronic alcoholic pancreatitis. The association of the two diseases in two women with a relatively low alcohol intake supports this hypothesis.
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PMID:Association of chronic alcoholic liver and pancreatic disease: a prospective study. 407 7

The reason why similar amounts of alcohol consumption cause different types of organ damage in alcoholics is obscure. Recent studies indicate that hepatitis B virus infection may influence the development of liver cirrhosis in alcoholics. We investigated the prevalence of markers of viruses known to cause hepatitis (HAV, HBV, EBV, CMV) in two groups of patients, one with alcoholic pancreatitis without known liver cirrhosis and one with alcoholic liver cirrhosis without known pancreatitis. We found signs of past infection with HAV and HBV more often in alcoholics with liver cirrhosis than in patients with alcoholic pancreatitis or in age-matched controls.
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PMID:Prevalence of markers of hepatotrophic viruses in alcoholics with symptomatic liver cirrhosis or pancreatitis. 608 3

Drinking and dietary habits and serum lipids were studied in two groups of chronic alcoholics, one with liver cirrhosis and the other with acute or recurrent pancreatitis, with the intention of investigating whether these factors could be of importance for the seemingly haphazard occurrence of different organ damages in chronic alcoholics. Our data show that patients with alcoholic pancreatitis have a more intermittent drinking pattern than patients with alcoholic cirrhosis. The amount of alcohol required to cause pancreatitis seems to be smaller than what is necessary to produce cirrhosis. Although none of the cirrhotics had clinical symptoms of pancreatitis, 58% of the autopsied cirrhotics had some pancreatic damage at autopsy. It may be that symptomatic pancreatitis prevents the patients from drinking the larger amounts of alcohol necessary to produce cirrhosis. Dietary habits or occurrence of lipid abnormalities during abstinence did not differ between the groups.
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PMID:Alcohol consumption pattern and serum lipids in alcoholic cirrhosis and pancreatitis. A comparative study. 647 79

The prevalence with which alcoholic pancreatitis is associated with alcoholic liver disease is unclear. To investigate this association further, we have reviewed the autopsy findings of 1022 patients who died from alcoholic liver disease and compared these findings with those from 352 patients who died from cardiac or pulmonary disease. All patients who died from liver disease had a history of chronic alcoholism with clinical and biochemical evidence of severe liver damage. Death resulted from hepatic coma, gastrointestinal bleeding, or infection. Liver disease patients were classified into two groups: (1) those with cirrhosis (77%) and (2) those without cirrhosis but with acute and/or chronic sclerosing hyaline necrosis (23%). Anatomic and histopathologic changes characteristic of chronic pancreatitis were found in 203 patients in approximately the same frequency (20% and 18%, respectively) in both groups. Acute pancreatitis without chronic lesions was observed in 8% and 10% of both groups, respectively. In the control group of 352 autopsies (122 cardiac and 230 pulmonary patients), the overall prevalence of pancreatitis, at 2.6%, was significantly (P less than 0.001) lower than that observed in the alcoholic liver disease groups. A total of 22 cases (50%) dying from acute or chronic sclerosing hyaline necrosis had severe chronic calcifying pancreatitis compared to 29 patients (18%) (P less than 0.001) dying from cirrhosis. By contrast, dense fibrosis was significantly (P less than 0.001) more commonly observed in patients with cirrhosis. We conclude that pancreatitis occurs frequently in patients dying from alcoholic liver disease but is an uncommon finding in patients dying from other causes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pancreatitis associated with alcoholic liver disease. A review of 1022 autopsy cases. 673 67

Controversial data have been reported on gastric acid secretion in patients with chronic pancreatitis. Moreover, studies on gastroduodenal morphological changes in patients with this disease and with other alcohol-related conditions have given different results. Basal and penta-gastrin-stimulated gastric secretion, histological changes of gastric and duodenal mucosa, and basal and meal-stimulated gastrin were measured in 21 patients with chronic alcoholic pancreatitis and in the following pair-matched groups: 21 chronic alcoholics and 21 control subjects (nonulcer dyspepsia), and in 19 patients with proven liver cirrhosis of alcoholic origin. No patient suffered from peptic ulcers. Moreover, gastric secretion was also measured in 51 patients with proven duodenal ulcers and in 34 healthy subjects. Basal acid output in patients with chronic pancreatitis was significantly higher (p less than 0.05) than in the other groups, except for the patients with duodenal ulcers. Peak acid output values in patient with chronic pancreatitis were similar to those measured in patients with duodenal ulcer, and they were higher than in the healthy subject group and in patients with liver cirrhosis, but statistical significance was not attained for patients with nonulcer dyspepsia. An increased frequency of duodenitis was found in patients with chronic pancreatitis, whereas an increased frequency of gastric metaplasia in the duodenal bulb was observed in all the patients with alcohol-related conditions considered. No relevant differences among the considered groups were found relating to gastric histological changes. Basal and meal-stimulated gastrin were similar in all the studied groups. This study suggests that in patients with chronic pancreatitis there is increased gastric secretion and probably an increased capacity for secretion of acid. Moreover, in patients with chronic pancreatitis, duodenitis seems to be frequent, but it probably is not directly related to chronic alcohol consumption.
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PMID:Gastric secretion, gastroduodenal histological changes, and serum gastrin in chronic alcoholic pancreatitis. 707 77


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