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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute pancreatitis usually occurs as a result of alcohol abuse or bile duct obstruction. A careful review of the patient's history and appropriate laboratory studies can help the physician identify the etiology of the condition and guide management. Serum amylase and lipase levels are still used to confirm the diagnosis of acute pancreatitis. Although not routinely available, the serum trypsin level is the most accurate laboratory indicator for pancreatitis. Ultrasonography, computed tomography and endoscopic retrograde cholangiopancreatography are additional modalities that can help the family physician choose the best treatment approach. Prompt identification of patients who need intensive care referral or subspecialty consultation is crucial. The APACHE II and the multiple organ system failure scales provide prognostic information at the time of admission and may be repeated daily to monitor disease progression. Therapies such as nasogastric suctioning, anticholinergics and histamine H2-receptor blockers have not been shown to decrease symptoms or hospital stays in patients with acute pancreatitis. Systemic antibiotics have been found to improve outcome in patients with severe disease. With supportive care, most patients have a good clinical outcome.
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PMID:Diagnosis and management of acute pancreatitis. 1147 69

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

Lateral pancreaticojejunostomy (LPJ) is the cornerstone of surgical management of pain associated with chronic pancreatitis (CP) and ductal dilation. The pathologic key to failure of LPJ is disease confined to the head of the pancreas. Intraoperative pancreatoscopy with electrohydraulic lithotripsy (EHL) is a novel technique that avoids resection and eradicates intraductal lithiasis in the head of the gland. This study was undertaken to compare outcome of LPJ alone and LPJ with intraoperative EHL in the surgical management of CP. The records of patients undergoing LPJ with intraoperative EHL between 1996 and 1998 (Group A) were reviewed and compared with our historical data of patients who underwent LPJ alone from 1977 through 1991 (Group B). Quality-of-life questionnaires were administered in person or by telephone. Fisher's exact and Mann-Whitney statistical tests were used where appropriate. Twenty patients (12 men, 8 women; mean age 51 years, range 29-68) in Group A underwent LPH with EHL versus 85 patients in Group B (65 men, 20 women; mean age 43.6 years, range 24-73) who had LPJ only. The etiology of CP was attributed to alcohol abuse in 85 per cent of patients in Group A and 96 per cent in Group B. Mean follow-up for Group A was 2.7 years (range 1-4 years) and 6.3 years (range 1-15 years) for Group B. Complications occurred in four patients (Group A) and five patients (Group B) perioperatively. There were no deaths in either group in the early postoperative period. Subsequent operations for complications of CP were significantly fewer in Group A than in Group B (P < 0.05). Rehospitilizations were required in 35 and 60 per cent of patients in Group A and B respectively (P < 0.05). Postoperative insulin and enzyme supplementation requirements were unchanged in Group A and continued or worsened in Group B. Ninety per cent of patients in Group A viewed their health status as good or fair compared with 55 per cent in Group B (P < 0.05). Postoperative narcotic use was present in both groups, although the number of pain pills used decreased considerably from 25 per week to fewer than five in Group A. Intraoperative EHL may represent an alternative to resection of the head of the pancreas or may be used as an adjunct to LPJ in the surgical management of chronic fibrocalcific pancreatitis.
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PMID:Does intraoperative electrohydraulic lithotripsy improve outcome in the surgical management of chronic pancreatitis? 1140

Acute recurrent pancreatitis (ARP) results most commonly from alcohol abuse or gallstone disease. Initial evaluation fails to detect the cause of ARP in 10-30% of patients, and as a result the diagnosis of "idiopathic" ARP is given. In these patients, a more extensive evaluation including specialized labs, ERCP, endoscopic ultrasound, or magnetic resonance cholangiopancreatography typically leads to a diagnosis of microlithiasis, sphincter of Oddi dysfunction, or pancreas divisum. Less commonly, hereditary pancreatitis, cystic fibrosis, a choledochocele, annular pancreas, an anomalous pancreatobiliary junction, pancreatobiliary tumors, or chronic pancreatitis are diagnosed. Determining the etiology is important, as it helps to direct therapy, limits further unnecessary evaluation, and may improve a patient's long term prognosis.
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PMID:Idiopathic acute recurrent pancreatitis. 1156 74

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

Although alcohol is well recognized as a systemic toxin, the enteric manifestations of alcohol abuse have only recently begun to be elucidated at the cellular and microvascular levels. Since the microvascular mechanism of the toxicity of alcohol has progressively been revealed, clinical applications of this research field should increase the availability of therapeutic options for alcohol-induced injuries of liver, pancreas and gastrointestinal (GI) tract. A high concentration of ethanol reduces GI and pancreas blood flow. Ethanol-induced GI hemorrhage, GI ulcer, and pancreatitis are initiated by the microcirculatory disturbance of GI mucosa and pancreas. Ethanol administration induces an increase in vasoactive agents such as endothelin and nitric oxide and oxidative stress. They appear to be involved in ethanol-induced GI and pancreatic injury. Regarding the effects of ethanol on the liver, small amount of ethanol increases hepatic blood flow, and prevents gut ischemia/reperfusion (I/R)-induced hepatic microvascular dysfunction and subsequent liver injury. While large amount of ethanol itself causes hepatic microvascular dysfunction, and aggravates the gut I/R-induced hepatic microvascular dysfunction and subsequent liver injury. Vasoactive agents and oxidative stress also appear to be involved in the liver injury. In endotoxemic animals, even small amount of ethanol causes hepatic microvascular dysfunction. Chronic ethanol consumption aggravates endotoxin-induced hepatic microvascular dysfunction. Chronic ethanol consumption aggravates gut I/R-induced leukostasis in the liver and hepatocellular injury associated with an enhanced expression of adhesion molecules, while it prevents the gut I/R-induced sinusoidal perfusion injury. Thus, effects of chronic ethanol consumption on the I/R injury are still controversial.
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PMID:[Effect of alcohol on organ microcirculation: its relation to hepatic, pancreatic and gastrointestinal diseases due to alcohol]. 1172 32

The recent genetic discoveries in CP support the hypothesis that inappropriate intrapancreatic activation of zymogens by trypsin results in autodigestion and pancreatitis. Two different protective mechanisms prevent activation of the pancreatic digestive enzyme cascade. First, SPINK1 inhibits up to 20% of potential trypsin activity and, second, trypsin itself activates trypsin-like enzymes readily degrading trypsinogen and other zymogens. Pancreatitis may therefore be the result of an imbalance between proteases and their inhibitors within the pancreatic parenchyma. The discovery of PRSS1 mutations in families with CP was the first breakthrough in the understanding of the underlying genetic mechanisms. Enhanced trypsinogen activation may be the common initiating step in pancreatitis caused by these mutations. The discovery of SPINK1 mutations underlines the importance of the protease inhibitor system in the pathogenesis of CP. Thus, gain-of-function in the cationic trypsinogen resulting in an enhanced autoactivation, or loss-of-function mutations in SPINK1 leading to decreased inhibitory capacity, may similarly disturb the delicate intrapancreatic balance of proteases and their inhibitors. The recent findings of SPINK1, CFTR, and PRSS1 mutations in CP patients without a family history have challenged the concept of idiopathic CP as a non-genetic disorder and the differentiation between HP and ICP. There is a clear mode of autosomal dominant inheritance for some mutations (R122H, N291, possibly MIT), whereas the inheritance pattern (autosomal recessive, complex, or modifying) of other mutations (A16V, N34S) is controverted or unknown. The lack of mutations in the above-mentioned genes in many patients suggests that CP may also be caused by genetic alterations in yet unidentified genes. Evaluation of CP patients without an obvious predisposing factor, e.g. alcohol abuse, should include genetic testing even in the absence of a family history of pancreatitis. Finally, identification of further disease-causing genes will create a better understanding of pathogenesis and may help to develop specific preventive and therapeutic strategies.
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PMID:Genetic aspects of chronic pancreatitis: insights into aetiopathogenesis and clinical implications. 1177 91

Although the three leading symptoms of chronic pancreatitis, pain, exocrine and endocrine pancreatic insufficiency, are well known, only a few long-term studies have correlated these symptoms with the natural course of the disease. Besides these symptoms, numerous pancreatic complications and/or pancreatitis-associated diseases may affect the course and determine the prognosis of chronic pancreatitis. Their influence, however, has not been studied in detail. This review has two major aims: The first one is to give an up-to-date survey of present knowledge on the natural course of the disease with a view to the leading symptoms under special consideration of how the duration of the disease, continual alcohol abuse as well as endoscopic procedures and surgical treatment affect pain. Included is also what is known about chronic pancreatitis as a precondition of pancreatic and extrapancreatic carcinoma. The effect of chronic pancreatitis on the socio-economic status of patients is discussed and the mortality rate of the disease. The second aim of this review is to stimulate pancreatologists from different centers to consolidate resources in order to perform larger controlled studies than any one single center can undertake and work out common criteria for the diagnosis of chronic pancreatitis and follow-up of its course.
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PMID:Natural course of chronic pancreatitis. 1212 Feb 64

This paper reports one case of pancreatitis and duodenal obstruction that occurred following repair of an abdominal aortic aneurysm. The patient had neither antecedent biliary or pancreatic disease nor alcohol abuse. The presentation was mild and the patient had an uneventful recovery without surgery. We present this uncommon entity and review the available literature.
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PMID:Pancreatitis and duodenal obstruction following abdominal aortic aneurysm repair. 1223 34

A 50-year-old man with a history of alcohol abuse had recurring severe epigastric pain. He suffered from chronic recurrent pancreatitis; the CT-scan showed a chain-of-lakes pattern of the pancreatic duct.
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PMID:[Diagnostic image (118). A man suffering from severe abdominal pain. Chronic recurrent pancreatitis]. 1251 20


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