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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The etiology of acute pancreatitis, apart from alcohol abuse and cholelithiasis may also include a vascular component responsible for pancreatic ischemia. It is now acknowledged that chronic pancreatitis may be a consequence of the acute variant, but it remains unclear what factors influence this sequence of morphological changes. In order to clarify this issue we proposed a model of experimental acute pancreatitis in rats induced by a 30 min reduction of blood flow in inferior splenic artery followed by reperfusion. Rats were sacrificed at 1 h, 12 h, 24 h, and 2, 3, 5, 7, 14, 21, 28 days after cessation of ischemia. We performed histopathological examination of pancreatic tissue and measured pancreatic blood flow, plasma amylase activity and interleukin-1 beta concentration. The present findings indicate that transient pancreatic ischemia leads to the development of acute necro-haemorrhagic pancreatitis. The morphological features of acute inflammation are correlated positively with functional disorders. In some cases the features of chronic pancreatitis may appear transiently after the acute phase, whereas the repair of postinflammatory injury involves the regeneration of acinar cells.
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PMID:Morphological changes and morphological-functional correlations in acute experimental ischemia/reperfusion pancreatitis in rats. 1124 88

Some clinical cases published in literature show that angiotensin-converting enzyme (ACE)-inhibitor administration may cause acute pancreatitis. In this work, the authors report a case of a patient affected by hypertension. Upon admission, the authors started antihypertensive therapy using captopril, which caused an important amylase and lipase rise within 13 days. When the ACE-inhibitor therapy was stopped, a rapid decrease of the serum enzyme was observed within 3 days. The high levels of serum amylase and lipase were linked to neutrophilia but were not associated with relevant symptomatic findings or features of pancreatopathy. The absence of the usual conditions that may cause pancreatitis, such as biliary stasis, hypercalcemia, or alcohol abuse, and the rapid decrease of serum enzyme levels after drug suspension suggested an ACE-inhibitor-induced pancreatitis. This is the first clinical report of an ACE-inhibitor-induced pancreatitis in which captopril administration was found after hospitalization. The drug suspension probably prevented other complications. This case report suggests that, when ACE-inhibitor administration is started, serum amylase and lipase should be monitored in order to prevent acute pancreatitis without waiting for clinical evidence of a pancreatopathy.
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PMID:Angiotensin-converting-enzyme inhibitor administration must be monitored for serum amylase and lipase in order to prevent an acute pancreatitis: a case report. 1157 Jun 65

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

Acute pancreatitis is caused by acute or chronic alcohol intake or choledocholithiasis in approximately 80% of cases. In the absence of alcohol abuse or gallstones, a variety of established and putative factors must be considered, any of which can cause a single or recurrent attacks of acute pancreatitis. When the underlying cause eludes detection following an initial thorough search and leads to a second attack, the term idiopathic acute recurrent pancreatitis (IARP) is applied. This article discusses IARP and its work-up.
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PMID:Approach to idiopathic recurrent pancreatitis. 1498 94

The aim of this study was to investigate the association between H(2)-receptor antagonists and acute pancreatitis. The automated database of the Medicines Monitoring Unit (MEMO) was used to carry out a case-control study, supplemented with information on possible confounding factors from hospital and GP medical records. Cases were patients hospitalized with a computerized diagnosis of acute pancreatitis, and two sets of controls were drawn from (1) the study population and from (2) the same GP practice as the case. Current or 60-day exposure to cimetidine and ranitidine was analysed. In adjusted analyses, cimetidine exposure and ranitidine exposure were associated with an increased risk of hospitalization for acute pancreatitis, as were alcohol abuse and cholelithiasis. The risks were lower in unadjusted analyses, suggesting that the association is confounded, although they did not disappear completely. A possible explanation is that data on confounding were incomplete. This study cannot discount the existence of an association between H(2)-antagonists and acute pancreatitis, and highlights the difficulties involved in obtaining complete and accurate data on confounding factors that are not collected routinely.
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PMID:Do H2-receptor antagonists cause acute pancreatitis? 1507 67

Alcohol abuse is often associated with acute pancreatitis. The pathogenesis of alcoholic pancreatitis remains poorly understood, in part because of the lack of a suitable animal model to study the mechanism or mechanisms of this disease. It has been proposed that ethanol predisposes or sensitizes the pancreas to the effects of co-factors, and the combination of the effects of ethanol on the pancreas and the actions of these co-factors results in alcoholic pancreatitis. A number of viruses are known to infect the pancreas, and we have suggested that one co-factor that could be involved in the development of alcoholic pancreatitis is a viral infection. One of the most-studied groups of viruses that infect the pancreas and cause pancreatitis in human beings is the coxsackieviruses. We have shown that short-term (5-14 days) and subchronic (>28 days) administration of ethanol to mice increases the severity of coxsackie B3-induced pancreas damage. We hypothesize that consumption of ethanol would result in an impairment of pancreas regeneration after injury, similar to the effect of ethanol on liver regeneration. With the use of the murine model of coxsackie B3-mediated alcoholic pancreatitis we have obtained preliminary data to support the hypothesis. Specifically, consumption of ethanol by mice is associated with changes in the replication of acinar cells and their organization into acini after viral-mediated injury. We believe that this model will be a valuable tool to study the biochemical and molecular mechanisms involved in alcoholic pancreatitis.
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PMID:Ethanol consumption potentiates viral pancreatitis and may inhibit pancreas regeneration: preliminary findings. 1559 86

Severe acute pancreatitis is a clinical entity that can develop into multiple organ failure (MOF), and still has a poor prognosis. It is generally agreed that excessive humoral mediators such as pro-inflammatory cytokines play important roles in the pathogenesis of organ failure in patients with severe acute pancreatitis (SAP). Furthermore, it has been reported that continuous hemodiafiltration (CHDF) can remove the excess humoral mediators during the hypercytokinemic state of systemic inflammatory response syndrome (SIRS). We experienced a case of severe acute pancreatitis induced by alcohol abuse, on whom we performed cytokine apheresis. The patient was a 46 year-old male. He received 14 cytokine apheresis procedures, for about 4 hours in each session, using a CTR-001 direct hemoperfusion (DHP) cartridge. His serum levels of pro-inflammatory cytokines such as interleukin-6 (IL-6; 1649.1+/-667.1-1257.1+/-489.4 pg/mL, P=0.013) decreased significantly after the CTR-001 procedures. However tumor necrosis factor-alpha (TNF-alpha) (26.2+/-1.7-24.3+/-1.9 pg/mL, P=0.087), IL-1beta (6.1+/-2.9-3.49+/-1.1 pg/mL, P=0.477), IL-8 (192.5+/-33.4-229.5+/-51.8 pg/mL, P=0.754) and IL-10 (14.4+/-2.7-14.0+/-1.9 pg/mL, P=0.726) did not decrease statistically. Therefore, we conclude that in this case, cytokine apheresis using a CTR-001 cartridge was effective for reducing the pro-inflammatory cytokines during severe acute pancreatitis.
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PMID:A case of severe acute pancreatitis treated with CTR-001 direct hemoperfusion for cytokine apheresis. 1607 84

Hypertriglyceridemia (HTG) is a rare but well known cause of acute pancreatitis (AP), which can be a life- threatening complication if the degree of HTG is severe enough. It might be primary in origin or secondary to alcohol abuse, diabetes mellitus, pregnancy, or drugs. A serum triglyceride (TG) level of more than 1,000 to 2,000 mg/dL in patients with type I, IV, or V hyperlipidemia (Fredrickson's classification) is the identifiable risk factor. HTG-induced AP typically presents as an episode of AP or recurrent AP. The clinical course of HTG-induced AP is not different from other causes. Routine management of HTG-induced AP should be similar to other causes. A thorough family history of lipid abnormalities should be obtained, and an attempt to identify secondary causes should be made. The mainstay of treatment includes dietary restriction of fatty meal and lipid-lowering medications (mainly fibric acid derivatives). Although there are limited experiences with plasmapheresis, lipid apheresis, heparinization and insulin application, these can support the treatment of HTG- induced AP. We report two cases of HTG-induced AP which were successfully treated by plasmapheresis.
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PMID:Acute pancreatitis due to hypertriglyceridemia: report of 2 cases. 1637 23

The pancreas develops from ventral and the dorsal buds, which undergo fusion. Failure to fuse results in pancreas divisum, which is defined by separate pancreatic ductal systems draining into the duodenum. Risk of developing pancreatitis is increased in pancreas divisum because of insufficient drainage. MR cholangiopancreatography (MRCP) is the technique of choice for detecting pancreas divisum non-invasively. Annular pancreas is the result of incomplete rotation of the pancreatic bud around the duodenum with the persistence of parenchyma or a fibrous band encircling (and sometimes stenosing) the duodenum. Acute pancreatitis is usually caused by bile duct stones or alcohol abuse. The Atlanta classification differentiates between mild acute and severe acute pancreatitis associated with organ failure and/or local complications such as necrosis, abscess or pseudocyst. Contrast-enhanced multi-detector row CT is the method of choice to assess the extent of disease. Balthazar et al.'s CT severity index assesses the risk of mortality and morbidity. In acute pancreatitis, the role of MRCP is mainly limited to finding bile duct stones in patients with suspected biliary pancreatitis. Chronic pancreatitis results in relentless and irreversible loss of exocrine (and sometimes endocrine) function of the pancreas. MDCT even shows subtle calcifications. MRCP is the method of choice for non-invasive assessment of the duct. Inflammatory pseudotumor in chronic pancreatitis and groove pancreatitis are difficult to differentiate from pancreatic cancer. In these cases, multiple imaging methods such as MDCT, MRI and endosonography including biopsy may be used to make a diagnosis.
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PMID:[Pancreas. Part I: congenital changes, acute and chronic pancreatitis]. 1649 5

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.
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PMID:Diagnosis and management of chronic pancreatitis: current knowledge. 1663 63


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