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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the study was to determine the late outcome of acute alcoholic pancreatitis (a.a.p.), as assessed by clinical examination, functional tests and imaging techniques. 47 patients, 4-7 years after a.a.p. of moderate clinical course underwent a secretin-cerulein test (SCT), glucose tolerance test (GTT), ultrasound (US) and computed tomography (CT) of the pancreas. Exocrine pancreatic function impairment was found in 63.8%, glucose impaired tolerance (GIT)-in 12.8% overt diabetes-in 17.0%. GIT and overt diabetes were found only in patients with severe exocrine function impairment requiring enzyme supplementation. Ultrasound revealed pancreatic structure abnormalities mostly pancreas enlargement, pseudocysts, structural heterogeneity, contour irregularity, Wirsung duct dilatation and calcifications in 36.21% patients and computed tomography in 44.7%. Out of 16 patients with concomittant pathology found in SCT, US and CT 14 (29.8%) suffered from attacks of abdominal pain. We conclude that, as reflected by clinical symptoms, exo- and endocrine pancreatic function tests and imaging techniques, in about one third of patients even a moderate attack of a.a.p may lead to chronic pancreatitis. We suggest that patients after acute alcoholic pancreatitis should undergo prospective evaluation including both the function and structure estimation in order to early recognize and treat the revealed changes.
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PMID:Acute alcoholic pancreatitis does not lead to complete recovery. 908 29

Fibrocalculous pancreatic diabetes (FCPD) is a type of diabetes secondary to tropical chronic non-alcoholic pancreatitis. Little is known about the aetiopathogenesis of FCPD. We studied glutamic acid decarboxylase antibodies (GAD-Ab) and islet cell antibodies (ICA) in patients with FCPD and compared the results with Type 1 (insulin dependent) diabetes mellitus, Type 2 (non-insulin-dependent) diabetes mellitus and non-diabetic subjects in Southern India. The prevalence of GAD-Ab was 7.0% (95% Confidence Interval (CI) 1.9-17.2) in FCPD, 47.5% (CI 31.4-64.0) in Type 1 (p < 0.001 compared to FCPD), 5.6% (CI 1.5-13.9) in Type 2 (non-significant (NS) compared to FCPD) and 0% in controls. The prevalence of ICA was 6.3% (CI 1.2-17.4) in FCPD, 53.8% (CI 37.1-70.0) in Type 1 (p < 0.001 compared to FCPD), 9.9% (CI 4.0-19.4) in Type 2 (NS compared to FCPD) and 4.7% (CI 0.4-16.1) in controls. The data suggest that in FCPD, the frequency of auto-antibodies is low and its aetiology is probably not linked to autoimmunity in the majority of the patients.
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PMID:Antibodies to pancreatic islet cell antigens in diabetes seen in Southern India with particular reference to fibrocalculous pancreatic diabetes. 950 18

Diabetes develops in more than half of the patients with chronic alcoholic pancreatitis (CAP), mostly due to increasing insulin deficiency. In this regard CAP-related diabetes (CAP-DM) is similar to the type 1 diabetes. Data on microvascular complications in CAP-DM are scarce. The aim of the study was the analysis of microvascular complications frequency in relation to metabolic control in comparison with type 1 diabetes mellitus. The study subjects were 50 patients divided into two groups: group 1-25 patients with CAP-DM (15 men, 10 women, mean age 44.6 +/- 8.4 yrs, duration of diabetes 3.7 +/- 2.1 yrs, body mass index (BMI) 22.4 +/- 2.9 kg/m2, duration of CAP 7.0 +/- 3.5 years), and group 2-25 well-matched type 1 diabetes patients (14 men, 11 women, mean age 42.3 +/- 7.6 yrs, duration of diabetes 4.1 +/- 2.8 yrs, BMI 24.0 +/- +/- 2.5 kg/m2). CAP was diagnosed on the basis of clinical examination, ultrasound and computed tomography scans, and in some cases upon the results of endoscopic retrograde pancreatography. Fasting plasma glucose, glycated hemoglobin (HbA1c), total serum cholesterol, triglycerides, urea and creatinine concentrations were measured. Fundoscopy was performed in all the subjects, in addition fluorescein examination was conducted in 15 and 18 patients from groups 1 as 2 respectively. Fasting plasma glucose, HbA1c level and insulin requirement were significantly lower in CAP-DM patients than in type 1 diabetes subjects (133 +/- 48 vs 174 +/- 59 mg/dl, p < 0.01; 8.3 +/- 2.0 vs 9.8 +/- 1.1%, p < 0.01; 36 +/- 15 vs 57 +/- 11 IU/day, p < 0.001 respectively). However, the prevalence of background retinopathy (group 1-13/25, group 2-11/25), and microalbuminuria (group 1-14/25, group 2-13/25) was similar in both groups. No statistically significant differences were found between CAP-DM and type 1 diabetic patients in regard to blood lipids, triglycerides, urea and creatinine concentrations. We conclude that microvascular complications may be encountered in pancreatic diabetes as often as in type 1 diabetes. Therefore this particular type of secondary diabetes should be regarded by no means as a "milder" type of the disease.
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PMID:[Microvascular complications in pancreatic diabetes]. 1186 77

A 48-year-old male who had a past history of alcoholic pancreatitis and diabetes mellitus was admitted to our hospital due to chills and vomiting, on August 13, 1998. His body temperature was 38.0 degrees C, and he had the disturbance of consciousness, tachypnea, tachycardia and hepatomegaly with tenderness. Laboratory findings showed highly inflammatory reactions, DIC and hepatorenal dysfunction. Abdominal CT and US revealed multiple liver abscess with portal vein thrombus. Serratia rubidaea was detected in the blood culture. SBT/CPZ and TOB were administered and he recovered. This is a rare case of Serratia rubidaea sepsis. It is also necessary to pay attention to Serratia infections as well as S. marcescens.
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PMID:[Community acquired sepsis by Serratia rubidaea]. 1190 95

Alcoholic pancreatitis is a major complication of alcohol abuse. Until recently, it was generally accepted that alcoholic pancreatitis was a chronic disease from the outset. However, evidence is now emerging in support of the 'necrosis-fibrosis' hypothesis that alcoholic pancreatitis begins as an acute process and that repeated episodes of acute injury lead to the changes of chronic pancreatitis (acinar atrophy and fibrosis) resulting in exocrine and endocrine dysfunction. The treatment of acute pancreatitis follows the regimen of bed rest, nasogastric suction, analgesia and intravenous support. The role of additional therapeutic measures such as prophylactic antibiotics, antioxidants and enteral nutrition in severe cases has not yet been precisely defined. The treatment of chronic pancreatitis involves attention to its three cardinal features: pain, maldigestion and diabetes. With respect to the pathogenesis of alcoholic pancreatitis, the focus of research over the past 30 years has shifted from the sphincter of Oddi and ductular abnormalities to the acinar cell itself. It has now been established that the acinar cell is capable of metabolizing alcohol and that direct toxic effects of alcohol and/or its metabolites on acinar cells may predispose the gland to injury in the presence of an appropriate trigger factor. A significant recent development relates to the characterization of pancreatic stellate cells, increasingly implicated in alcoholic pancreatic fibrosis. This chapter summarizes the natural history, clinical features, current trends in treatment as well as recent advances in our understanding of the pathogenesis of alcoholic pancreatitis.
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PMID:Alcohol-induced pancreatic injury. 1282 57

Chronic Calcific Pancreatitis of Tropics is a disease of unknown aetiology and is characterised by chronic pancreatitis with calcification in young persons who present with pain, diabetes, and/or steatorrhoea. ERCP performed on 42 patients with this condition revealed changes compatible with chronic pancreatitis. These changes were however, more marked and somewhat different from those seen in the alcoholic chronic pancreatitis. Cystic dilatation, tortuosity, and obstruction of the main pancreatic duct were similar to that in alcoholic pancreatitis. The features of CCPT that were different from those of latter, were large pancreatic calculi, absence of strictures/stenosis and absence of irregularity of the ductal wall. The calculi were predominantly in the head region of the pancreas causing maximal dilatation of the main pancreatic duct in the head of pancreas. The secondary branches were stunted, short and scanty but revealed a lower grade of changes, than the changes documented in the main pancreatic duct. The pancreatic ductal changes in CCPT seems to be different from that seen in chronic alcoholic pancreatitis and may be due to the difference in the pathophysiology of the underlying disease.
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PMID:A pancreatography study of chronic calcific pancreatitis of the tropics. 1283 1

Long-term, heavy alcohol consumption is associated with both acute and chronic pancreatitis. Progression of pancreatitis may lead to multiple comorbidities including maldigestion, diabetes, and pancreatic cancer. Understanding the underlying molecular, biochemical, and cellular mechanisms by which alcohol ingestion leads to the development of pancreatitis may help to develop strategies for the treatment and prevention of the disease. The National Institute on Alcohol Abuse and Alcoholism and the Office of Rare Diseases of National Institutes of Health sponsored a satellite symposium on "Mechanisms of Alcoholic Pancreatitis" at the annual meeting of the American Pancreatic Association, Chicago, IL, November 2002. For this symposium, 8 speakers were invited to address the following issues: (1) epidemiology of alcoholic pancreatitis; (2) pathophysiology of alcoholic pancreatitis; (3) animal models of alcoholic pancreatitis--roles of cholecystokinin (CCK) and viral infections; (4) alcohol and zymogen activation in the pancreatic acinar cell; (5) role of alcohol metabolism in alcoholic pancreatitis; (6) pancreatic stellate cell activation in alcoholic pancreatitis; and (7) genetic predisposition to alcoholic chronic pancreatitis. It was concluded that alcohol abuse is a major contributory factor to the development of both acute and chronic pancreatitis. The injurious effects of ethanol on the pancreas may be mediated through (1) sensitization of acinar cells to CCK-induced premature activation of zymogens; (2) potentiation of the effect of CCK on the activation of transcription factors, nuclear factor kappaB (NF-kappaB) and activating protein-1 (AP-1); (3) generation of toxic metabolites such as acetaldehyde and fatty acid ethyl esters; (4) sensitization of the pancreas to the toxic effects of coxsackievirus B3; and (5) activation of pancreatic stellate cells by acetaldehyde and oxidative stress and subsequent increased production of collagen and other matrix proteins.
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PMID:Mechanisms of alcoholic pancreatitis. Proceedings of a conference. Chicago, Illinois, USA, November 2002. 1457 87

Tropical chronic pancreatitis (TCP) is a juvenile form of chronic calcific non-alcoholic pancreatitis, seen almost exclusively in the developing countries of the tropical world. The classical triad of TCP consists of abdominal pain, steatorrhoea, and diabetes. When diabetes is present, the condition is called fibrocalculous pancreatic diabetes (FCPD) which is thus a later stage of TCP. Some of the distinctive features of TCP are younger age at onset, presence of large intraductal calculi, more aggressive course of the disease, and a high susceptibility to pancreatic cancer. Pancreatic calculi are the hallmark for the diagnosis of TCP and in non-calcific cases ductal dilation on endoscopic retrograde cholangiopancreatography, computed tomography, or ultrasound helps to identify the disease. Diabetes is usually quite severe and of the insulin requiring type, but ketosis is rare. Microvascular complications of diabetes occur as frequently as in type 2 diabetes but macrovascular complications are uncommon. Pancreatic enzyme supplements are used for relief of abdominal pain and reducing the symptoms related to steatorrhoea. Early diagnosis and better control of the endocrine and exocrine dysfunction could help to ensure better survival and improve the prognosis and quality of life of TCP patients.
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PMID:Tropical chronic pancreatitis. 1465 69

Diabetes mellitus (DM) in chronic pancreatitis (ChP) is considered a unique clinical and metabolic unit. Compared to type I DM it has many different properties: glycemic lability, more frequent hypoglycaemic episodes, and minimum incidence of ketoacidosis. The need of insulin administration to achieve satisfying diabetes mellitus compensation is significantly lower and response of peripheral tissues to endogenous and exogenous insulin significantly higher compared to type I diabetics. These clinical differences result from decreased but always preserved insulin secretion, decreased glucagon production, impaired external pancreatic secretion, and also excessive alcohol use or insufficient or irregular food intake of the patients. Secondary DM in ChP is accompanied by chronic, microangiopathic and neuropathic complications analogous to other DM types. Nonpharmacological treatment measurements of the first choice are elimination of alcohol, sufficient and adequate nutrition, and simultaneous treatment of impaired exocrinal secretion. A pharmacology treatment is insulin therapy! It is a substitution treatment for insulin deficiency. Insulin doses must be chosen very carefully because of the risk of hypoglycaemia. The most frequent cause of secondary diabetes mellitus in patients with pancreatic diseases in Europe is chronic alcoholic pancreatitis and in tropical countries and India non-alcoholic tropical calcific pancreatitis (TCP).
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PMID:[Diabetes mellitus in chronic pancreatitis]. 1530 35

Chronic pancreatitis is mostly caused by heavy alcohol consumption and is characterized by the onset of symptoms in the fourth and fifth decade. Beginning in patients older than 65 years of age is rare. Leading symptom is recurrent or persisting abdominal pain which is missed only in approximately 5% of the cases. Chronic pancreatitis is classified as idiopathic if there is no anamnesis of alcohol abuse or some rare specific causes. The Idiopathic Chronic Senile Pancreatitis (ICSP) is a subset of the non-alcoholic pancreatitis and is characterized by advanced age at the time of first manifestation. Although life expectancy especially in chronic alcoholic pancreatitis is reduced, there are many patients who reach older age. The natural history in all forms of chronic pancreatitis shows a decrease in pain and the manifestation of exocrine and endocrine insufficiency as late complications. Especially in the elderly loss of weight may occur with steatorrhea and pancreatic diabetes mellitus as the dominating clinical problem of chronic pancreatitis. If pain persists treatment is symptomatically with analgesics. The possibility of causal surgery or the indication for endoscopic treatment of painful chronic pancreatitis should be proven in every single case. Standard pancreatin treatment consisting of large amounts of enzymes will abolish maldigestion. Pancreatic diabetes requires often insulin, there is a tendency to hypoglycaemia. In contrast to chronic pancreatitis cancer of the pancreas is a typical and frequent disease of the elderly. The prognosis is bad and one year life expectancy is just about 11%. One of the reasons is, that the diagnosis is found lately because early symptoms are missing. Specific symptoms like pain, weight loss or jaundice occur lately. In suspicion of pancreatic cancer a lot of methods of morphological diagnostic are available such as CT, MRCP, ultrasound, ERCP and PET, in addition the specific tumor markers CA 19-9 and CEA. After diagnostic is completed, curative resection is possible in only a low percentage of all cases. Old age is no contraindication for surgery, prognosis and the risk of surgery don't differ to other age groups. In most cases palliative therapy is the only possible option because of an advanced tumor stage. Sufficient pain therapy, endoscopic stenting in case of obstructive jaundice or gastroenterostomy in case of duodenal are useful interventions.
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PMID:[Chronic pancreatis and pancreatic carcinoma in the elderly]. 1598 40


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