Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The major complications of chronic pancreatitis are malabsorption, diabetes mellitus, pancreatic calcification and pseudocysts. Sinistral portal hypertension due to splenic vein thrombosis, obstructive jaundice and duodenal stricture have also been reported as complications of chronic pancreatitis. However, a case having all these three complications at the same time is relatively rare. We present a case of chronic alcoholic pancreatitis complicated with simultaneous multiple severe complications. Although biliary drainage is usually a useful treatment for reducing the bilirubin level in the patients with obstructive jaundice, jaundice was hardly improved by the percutaneous transhepatic cholangio-drainage (PTCD) in this case. We discussed the cause of the failure in reducing the jaundice and reviewed the previous reports of complications of pancreatitis.
 ...
PMID:Alcoholic chronic pancreatitis with simultaneous multiple severe complications--extrahepatic portal obliteration, obstructive jaundice and duodenal stricture. 1600 77

Acute pancreatitis is a common disease with an annual incidence of between 5 and 80 people per 100,000 of the population. The two major etiological factors responsible for acute pancreatitis are alcohol and cholelithiasis (gallstones). The proportion of patients with pancreatitis caused by alcohol or gallstones varies markedly in different countries and regions. The incidence of acute alcoholic pancreatitis is considered to be associated with high alcohol consumption. Although the incidence of alcoholic pancreatitis is much higher in men than in women, there is no difference in sexes in the risk involved after adjusting for alcohol intake. Other risk factors include endoscopic retrograde cholangiopancreatography, surgery, therapeutic drugs, HIV infection, hyperlipidemia, and biliary tract anomalies. Idiopathic acute pancreatitis is defined as acute pancreatitis in which the etiological factor cannot be specified. However, several studies have suggested that this entity includes cases caused by other specific disorders such as microlithiasis. Acute pancreatitis is a potentially fatal disease with an overall mortality of 2.1%-7.8%. The outcome of acute pancreatitis is determined by two factors that reflect the severity of the illness: organ failure and pancreatic necrosis. About half of the deaths in patients with acute pancreatitis occur within the first 1-2 weeks and are mainly attributable to multiple organ dysfunction syndrome (MODS). Depending on patient selection, necrotizing pancreatitis develops in approximately 10%-20% of patients and the mortality is high, ranging from 14% to 25% of these patients. Infected pancreatic necrosis develops in 30%-40% of patients with necrotizing pancreatitis and the incidence of MODS in such patients is high. The recurrence rate of acute pancreatitis is relatively high: almost half the patients with acute alcoholic pancreatitis experience a recurrence. When the gallstones are not treated, the risk of recurrence in gallstone pancreatitis ranges from 32% to 61%. After recovering from acute pancreatitis, about one-third to one-half of acute pancreatitis patients develop functional disorders, such as diabetes mellitus and fatty stool; the incidence of chronic pancreatitis after acute pancreatitis ranges from 3% to 13%. Nevertheless, many reports have shown that most patients who recover from acute pancreatitis regain good general health and return to their usual daily routine. Some authors have emphasized that endocrine function disorders are a common complication after severe acute pancreatitis has been treated by pancreatic resection.
 ...
PMID:JPN Guidelines for the management of acute pancreatitis: epidemiology, etiology, natural history, and outcome predictors in acute pancreatitis. 1646 7

This paper reviews the current literature on chronic pancreatitis (CP). Despite marked progress in diagnostic tools, predominately imaging methods, no consensus has been reached on the nomenclature of CP, ie diagnosis, classification, staging, pathomechanisms of pain and its optimal treatment. A major problem is that no single reliable diagnostic test exists for early-stage CP except histopathology (rarely available). This stage is characterised typically by recurrent acute pancreatitis +/- necrosis (eg pseudocysts). Acute pancreatitis is a well-defined condition caused in 80% of cases by gallstones or alcohol abuse. Alcoholic pancreatitis, in contrast to biliary pancreatitis, progresses to CP in the majority of patients. However, a definite CP-diagnosis is often delayed because progressive dysfunction and/or calcification, the clinical markers of CP, develop on average 5 years from disease onset. The progression rate is variable and depends on several factors eg aetiology, smoking, continued alcohol abuse. Repeated function testing eg by the faecal elastase test, is the best alternative for histology to monitor progression (or non-progression) of suspected (probable) to definite CP. The pathomechanism of pain in CP is multifactorial and data from different series are hardly comparable mainly because insufficient data of the various variables ie diagnosis, classification, staging of CP, pain pattern and presumptive pain cause, are provided. Pain in CP is rarely intractable except in the presence of cancer, opiate addiction or extra-pancreatic pain causes. Local complications like pseudocysts or obstructive cholestasis are the most common causes of severe persistent pain which can be relieved promptly by an appropriate drainage procedure. Notably, partial to complete pain relief is a common feature in 50-80% of patients with late-stage CP irrespective of surgery and about 50% of CP-patients never need surgery (or endoscopic intervention). The spontaneous "burn-out" thesis of CP is in accordance with this observation although precise data of this phenomenon are scarce. Recent observations indicate that the progression to late-stage CP is markedly delayed in non-alcoholic compared to alcoholic CP. Therefore, spontaneous pain relief is also delayed but it occurs in close association with severe exocrine insufficiency suggesting that aetiology has a major impact on the duration of early-stage CP and that the "burn-out" thesis appears valid both in uncomplicated alcoholic and nonalcoholic late-stage CP. For treatment of steatorrhea and diabetes the reader is referred to recent reviews. Mortality and survival are closely related to aetiology with an increased death rate of about 50% within 20 years from onset in alcoholic CP compared to a markedly better prognosis in hereditary and idiopathic "juvenile" CP. The risk of pancreatic cancer is increased particularly in nonalcoholic CP based on the longer survival, whereas the risk of extra-pancreatic (smoking-related) cancer is about 12-fold higher in alcoholic CP.
 ...
PMID:Diagnosis and management of chronic pancreatitis: current knowledge. 1663 63

In the last few years, reports of pancreatic inflammatory diseases caused by immunological mechanisms and with good response to steroid treatment have increased. Although this entity has been known by a number of names, at present the most widely accepted is that of autoimmune chronic pancreatitis (ACP). The present report describes the clinical, immunological, morphological, functional and pathological characteristics of two patients recently studied at our unit and discusses currently used diagnostic tests. The two patients had a complete response to steroid therapy. In our opinion, ACP is probably underdiagnosed in Spain. The availability of morphological, pathological and serological diagnostic tools developed in recent years will help to precisely determine the epidemiology of this process. Thus, quantification of serum levels of anti-carbonic anhydrase II and IgG4 has greatly contributed to the diagnosis of ACP. These tests should be performed in patients with a possible diagnosis of ACP, those suffering from diabetes mellitus type I with impairment of exocrine function, and those with alcoholic pancreatitis and a poor response to alcohol elimination. Once we are able to diagnose and determine the real prevalence of ACP in our setting, the most appropriate therapy and prognosis of this disease can be established.
 ...
PMID:[Autoimmune pancreatitis. An infrequent or underdiagnosed entity? Pathological, clinical and immunological characteristics]. 1673 37

A 40-year old male residing in the Mediterranean region and afflicted with chronic pancreatitis and diabetes is presented. This is a case of chronic calcific non-alcoholic pancreatitis with characteristic intraductal calculi on abdominal X-ray. Five years following the initial episode of pancreatitis, the patient developed insulin-requiring diabetes mellitus. This case accords with the criteria for fibrocalculous pancreatic diabetes with the unique feature of the patient having been born in Greece and being a resident of Greece.
 ...
PMID:Fibrocalculous pancreatic diabetes in patient residing in the Mediterranean region. 1674 87

Tropical pancreatitis was described 50 years ago as a disease of the tropical regions, particularly southern India, with young age at onset, malnutrition, rapid progression, severe pancreatic damage with multiple large ductal calculi, and absence of history of alcoholism or biliary tract disease as its hallmarks. Over the years, chronic pancreatitis in southern India has shown a change, with increase in older patients, occurrence of milder disease including milder diabetes, increasing longevity, and increasing association with alcoholism and smoking. This article looks at changes in the disease and in dietetic, environmental and socioeconomic factors over the years, in an attempt to understand the environment-gene interactions in its causation. This analysis shows that tropical pancreatitis may represent one end of the wide spectrum of chronic pancreatitis in the tropics, with alcoholic pancreatitis representing the other extreme.
 ...
PMID:Tropical pancreatitis - a distinct entity, or merely a type of chronic pancreatitis? 1854 43

To search autoantigens in autoimmune pancreatitis (AIP), we have screened the human pancreas cDNA library with a patient's serum and obtained 10 positive clones. Seven out of 10 clones were amylase alpha-2A, the autoantibody to which was specifically detected in sera from patients with AIP and fulminant type 1 diabetes (FT1DM) [T. Endo, S. Takizawa, S. Tanaka, M. Takahashi, H. Fujii, T. Kamisawa, T. Kobayashi, Amylase alpha-2A autoantibodies: novel marker of autoimmune pancreatitis and fulminant type 1 diabetes mellitus, Diabetes 58 (2009) 732-737]. Sequencing of 1 out of remaining 3 positive clones revealed that it was identical to heat shock protein 10 (HSP 10) cDNA. Using a recombinant HSP 10, we have developed enzyme-linked immunosorbent assay (ELISA) system for detecting autoantibodies against HSP 10. We found that autoantibody against HSP 10 was also produced with high frequency in sera from patients with AIP (92%) and FT1DM (81%), but not in chronic alcoholic pancreatitis (8%) or healthy volunteers (1.4%). These results suggest that an autoantibody against HSP 10 is also a new diagnostic marker for both AIP and FT1DM.
 ...
PMID:HSP 10 is a new autoantigen in both autoimmune pancreatitis and fulminant type 1 diabetes. 1952 60

Alcohol and products of its metabolism lead to impairment of many organs functions, what cause systemic and local carbohydrates metabolism disturbances. Abusing of alcohol induces changes in pancreatic digestive enzymes secretion, what contributes to development of chronic alcoholic pancreatitis. Alcohol can cause secondary diabetes, what is result of pancreatic beta-cells damage and is a risk factor for type 2 diabetes. Alcohol cause liver cells degeneration and induction of many metabolic disturbances especially carbohydrates.
 ...
PMID:[The participation of ethanol in induction of carbohydrates metabolism disturbances]. 1965 Apr 35

This study was undertaken to evaluate the long-term prognosis of acute pancreatitis (AP) in Japan and to identify factors that predict major complications. In 1987, 2533 patients with moderate or severe acute pancreatitis were registered in a national survey in Japan. Follow-up studies were done in 2000 and in 2004 to evaluate recurrence of acute pancreatitis, transition to chronic pancreatitis, development of diabetes mellitus, and mortality. The relationship between incidence of complications and alcohol consumption during follow-up period was also analyzed. Valid replies were obtained from 714 cases in 2000 and 450 cases in 2004. Recurrence of acute pancreatitis occurred in 145 cases, and the recurrence rate was significantly higher in alcoholic pancreatitis compared with other etiologies. A transition to chronic pancreatitis occurred frequently in alcoholic pancreatitis and inversely correlated with existence of pancreatic necrosis in the initial disease. Complication with diabetes mellitus and the transition to chronic pancreatitis strongly correlated with persistent alcohol intake during follow-up period. During the follow-up period, 199 patients died, and 43 died of malignant disease. Recurrence of acute pancreatitis and a transition to chronic pancreatitis frequently occurred in alcoholic pancreatitis. Transition to chronic pancreatitis was inversely correlated with the existence of pancreatic necrosis at the initial presentation. Mortality as a result of malignant disease was not excessive in the patients with history of acute pancreatitis.
 ...
PMID:Long-term prognosis of acute pancreatitis in Japan. 1989 91

Hereditary pancreatitis shares a majority of clinical and morphologic features with chronic alcoholic pancreatitis, but may present at an earlier age. The term hereditary pancreatitis has primarily been associated with mutations in the serine protease 1 gene (PRSS1) which encodes for cationic trypsinogen. PRSS1 mutations account for approximately 68-81% of hereditary pancreatitis. Mutations in other genes, primarily serine protease inhibitor Kazal type 1 (SPINK1) and the cystic fibrosis transmembrane conductance regulator (CFTR) are also associated with hereditary pancreatitis. While chronic alcoholic pancreatitis may develop in the fourth or fifth decades, patients with hereditary pancreatitis may develop symptoms in the first or second decades of life. Hereditary pancreatitis is diagnosed either by detecting a causative gene mutation or by the presence of chronic pancreatitis in two first-degree or three second-degree relatives, in two or more generations, without precipitating factors and with a negative workup for known causes. Patients with hereditary pancreatitis may have recurrent acute pancreatitis and may develop pancreatic exocrine and endocrine insufficiency. Hereditary pancreatitis may involve premature trypsinogen activation or decreased control of trypsin. Recurrent inflammation can lead to acute pancreatitis and subsequently to chronic pancreatitis with parenchymal calcification. There is a markedly increased risk of pancreatic carcinoma compared with the general population. Patients are often referred for evaluation of pancreatitis, biliary or pancreatic ductal dilatation, jaundice, biliary obstruction, pancreatic duct stone or stricture, pancreatic pseudocysts, and for evaluation for malignancy. Medical treatment includes pancreatic enzyme supplementation, nutritional supplementation, diabetes management, and palliation of pain. Patients should avoid tobacco use and alcohol exposure. Hereditary pancreatitis is reviewed and recommendations for genetic testing are discussed.
 ...
PMID:Hereditary pancreatitis for the endoscopist. 2350 50


<< Previous 1 2 3 4 5 Next >>