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Acute pancreatitis remains the commonest complication of ERCP (endoscopic retrograde cholangiopancreatography) with published incidence rates that have changed little over 30 years despite significant advances in endoscope and ERCP accessory technology and the introduction of structured ERCP training. Technique related risk factors for post ERCP pancreatitis have been recognised for many years and have been recently refined via large prospective audits. These studies have also revealed the importance of patient related factors and highlighted the high incidence of post ERCP pancreatitis in women being investigated for acalculus biliary pain or idiopathic recurrent acute pancreatitis. Sphincter of Oddi hypertension is often found to be present in this group of patients. Methods of preventing post ERCP pancreatitis have been sought for many years and numerous drugs have been tried using a variety of regimes with heterogeneous groups of patients. At present pancreatic duct stenting looks to be the most efficacious prophylactic method but is not for the beginner endoscopist. It is possible, however, by using a simple strategy to minimise the incidence of post ERCP pancreatitis and modulate its severity.
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PMID:Reducing the incidence and severity of post ERCP pancreatitis. 1611 Oct 92

Acute pancreatitis develops immediately after the causative impulse, while chronic pancreatitis develops after the long-term action of the noxious agent. A typical representative of acute pancreatitis is biliary pancreatitis, chronic pancreatitis develops in alcoholism and has a long latency. As alcoholic pancreatitis is manifested at first as a rule by a potent attack, it is classified in this stage as acute pancreatitis. The most frequent etiological factors in our civilization are thus cholelithiasis and alcoholism (both account for 20-50% in different studies). The assumed pathogenetic principles in acute biliary pancreatitis are the common canal of both efferent ducts above the obturated papilla, duodenopancreatic reflux and intrapancreatic hypertension. A detailed interpretation is however lacking. The pathogenesis of alcoholic pancreatitis is more complicated. Among others some part is played by changes in the calcium concentration and fusion of cellular membranes. Idiopathic pancreatitis occurs in up to 10%, part of the are due to undiagnosed alcoholism and cholelithiasis. Other etiologies are exceptional. Similarly as in cholelithiasis pancreatitis develops also during other pathological processes in the area of the papilla of Vater such as dysfunction of the sphincter of Oddi, ampulloma and juxtapapillary diverticulum, it is however usually mild. The incidence of postoperative pancreatitis is declining. Its lethality is 30% and the diagnosis is difficult. In the pathogenesis changes of the ion concentration are involved, hypoxia and mechanical disorders of the integrity of the gland. Pancreatitis develops in association with other infections--frequently in mumps, rarely in hepatitis, tuberculosis, typhoid and mycoses. Viral pancreatitis is usually mild. In parasitoses pancreatitis develops due to a block of the papilla Vateri. In hyperparathyroidism chronic pancreatitis is more likely to develop, recent data are lacking. As to dyslipoproteinaemias, pancreatitis develops in the Ist, IVth and Vth type of Frederikson's classification, in rare recessive disorders and other conditions such as hypothyroidism, renal insufficiency, oestrogen substitution and others. In pancreas divisum chronic pancreatitis is more likely to develop. In exotic countries tropical pancreatitis is most frequent. It is however similarly as alcoholic pancreatitis primarily chronic. A very serious course is usual in traumatic pancreatitis. Risk factors of pancreatitis after ERCP are in particular undilated biliary pathways, dysfunction of the sphincter of Oddi and the use of a needle knife (bistoury). Medicamentous prevention is not substantiated. Drug induced pancreatic damage is much rarer than hepatotoxicity. Pancreatitis is caused most frequently by immunosuppressives, methyldopa, corticoids and oestrogens. The question remains to what extent the course of pancreatitis is influenced by its etiology. Biliary, alcoholic, traumatic and postoperative pancreatitis is usually severe, pancreatitis associated with viroses and induced by drugs is usually mild.
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PMID:[Etiological factors of acute pancreatitis]. 1673 20

Calprotectin (Cal) concentration is elevated in acute inflammatory reactions and its increase in the plasma suggests a diagnostic potential for Cal assay. This study aimed (a) to evaluate the Cal plasma levels in patients suffering from acute pancreatitis (AP) and (b) to assess whether early assay of Cal plasma levels can be helpful in assessment of the severity of AP. Forty-six consecutive patients, median age 45 years, suffering from a first attack of AP were recruited at two medical centers. Data collected on admission included age, sex, delay between pain onset and admission, and Glasgow score. A severe outcome was defined according to the Atlanta criteria. AP was defined as edematous or necrotic according to the CT findings. Plasma Cal and serum C reactive protein (CRP) were assayed in all patients within the first 24 hr after hospitalization. Sixty subjects suffering from blood hypertension were recruited as controls. Plasma Cal was measured by a commercial ELISA system. In all AP patients and in none of the controls, plasma Cal concentration was higher than the normal limit. Cal values in AP patients were significantly higher than in controls (P < 0.0001). There was not a statistically significant difference in Cal values between patients with severe and patients with mild AP. Plasma Cal values did not differ in necrotizing and edematous AP. During the follow-up plasma Cal was reassayed in six of the patients with abdominal fluid collection and the values were higher in the two patients with infected necrosis. We conclude that plasma Cal is elevated in patients with AP but it is not a useful marker for early prediction of pancreatitis severity. Further studies could evaluate its usefulness in pancreatic infected necrosis.
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PMID:Plasma calprotectin levels in patients suffering from acute pancreatitis. 1696 44

The role of endoscopic therapy in the management of pancreatic diseases is continuously evolving; at present, most pathological conditions of the pancreas are successfully treated by endoscopic retrograde cholangiopancreatography (ERCP), endoscopic ultrasound (EUS) or both. Endoscopic placement of stents has played and still plays a major role in the treatment of chronic pancreatitis, pseudocysts, pancreas divisum, main pancreatic duct injuries, pancreatic fistulae, complications of acute pancreatitis, recurrent idiopathic pancreatitis and in the prevention of post-ERCP pancreatitis. These stents are currently routinely placed to reduce intraductal hypertension, bypass obstructing stones, restore lumen patency in cases with dominant, symptomatic strictures, seal main pancreatic duct disruption, drain pseudocysts or fluid collections, treat symptomatic major or minor papilla sphincter stenosis, and prevent procedure-induced acute pancreatitis. The present review aims at updating and discussing techniques, indications and results of endoscopic pancreatic duct stent placement in acute and chronic inflammatory diseases of the pancreas.
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PMID:Endoscopic stenting in benign pancreatic diseases. 1722 46

Significant visceral edema associated with massive fluid resuscitation, paralytic ileus and formation of pancreatic ascites in patients with severe acute pancreatitis (SAP) can lead to abdominal compartment syndrome (ACS) that can contribute to the early development of multiple organ dysfunction syndrome (MODS), especially in the early stages of the disease. The prevalence of intra-abdominal hypertension (IAH) in SAP is about 40% and a manifest ACS occurs in about 10% of the patients warranting close monitoring of intra-abdominal pressure (lAP) in all patients with the severe form of the disease. Although nonsurgical management utilizing percutaneous drainage of ascites or continuous hemodiafiltration may decrease IAP, most patients require decompressive laparostomy and temporary abdominal closure. The primary aim in managing the ensuing open abdomen is delayed fascial closure during initial hospitalization. On many occasions a planned hernia approach, either with early skin grafting over the exposed bowel or managing the ASC primarily with a subcutaneous linea alba fasciotomy, is the only available option. The development of ACS in patients with SAP seems to be associated with increased mortality.
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PMID:Abdominal compartment syndrome and acute pancreatitis. 1746 10

The role of endoscopic therapy in the management of pancreatic diseases is continuously evolving; at present most pathological conditions of the pancreas are successfully treated by endoscopic retrograde cholangio-pancreatography (ERCP) or endoscopic ultrasound (EUS), or both. Endoscopic placement of stents has played and still plays a major role in the treatment of chronic pancreatitis, pseudocysts, pancreas divisum, main pancreatic duct injuries, pancreatic fistulae, complications of acute pancreatitis, recurrent idiopathic pancreatitis, and in the prevention of post-ERCP pancreatitis. These stents are currently routinely placed to reduce intraductal hypertension, bypass obstructing stones, restore lumen patency in cases with dominant, symptomatic strictures, seal main pancreatic duct disruption, drain pseudocysts or fluid collections, treat symptomatic major or minor papilla sphincter stenosis, and prevent procedure-induced acute pancreatitis. The present review aims at updating and discussing techniques, indications, and results of endoscopic pancreatic duct stent placement in acute and chronic inflammatory diseases of the pancreas.
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PMID:Endoscopic pancreatic duct stent placement for inflammatory pancreatic diseases. 1802 85

The article reports the case of a 27-year old woman hospitalised in the internal medicine ward for acute pancreatitis after eating fat food and drinking alcohol. In addition to acute pancreatitis, the patient complained of vision problems. The ophthalmologist detected bilateral occurrence of large whitish nidi located primarily around the optic disc, intraretinal hemorrhage and a massive retinal oedema in the central field and diagnosed Purtscher-like retinopathy. After a month of treatment of acute pancreatitis, the clinical picture improved, the patient's vision sharpness improved and the laboratory parametres returned to normal. The finding on the ocular fundus also improved. Even though similar cases are rare, more patients with acute pancreatitis should be checked for eventual vision disorders. Ocular fundus examination should be included in the set of tests performed for acute pancreatitis, similarly to the practice in arterial hypertension or diabetes mellitus patients.
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PMID:[Purtscher-like retinopathy--a rare complication of acute pancreatitis]. 1852 97

Twenty-two patients diagnosed as having acute pancreatitis (AP) were examined to assess whether hyperbaric oxygen therapy (HBO) was an efficient and safe adjunct to the standardized treatment protocol in patients with AP. The impact of HBO on oxygenation in the splanchnic area, homeostasis, oxidative stress, and intraabdominal hypertension was evaluated. A treatment group consisted of 11 patients treated for 3 days (twice a day) using a monoplace chamber under pressures of 1.7-1.9 ATA. Patients (n = 11) in the control group were managed in accordance with the standardized treatment protocol. HBO improved oxygen delivery to the splanchnic area, positively affected homeostasis and induced no significant intraabdominal pressure changes. HBO demonstrated neither explicit prooxidative effect nor typical complications.
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PMID:[Use of hyperbaric oxygenation as a component of intensive care in acute pancreatitis and its impact on homeostasis and intensity of oxidative stress]. 1865 73

Acute intermittent porphyria (AIP) is an inherited metabolic disease that can affect the autonomic, peripheral and central nervous systems. Pancreatic diseases assocated with AIP is rarely reported. We report here a 60-year-old non-alcoholic male who had typical manifestations of AIP, including abdominal pain, constipation, tachycardia, hypertension, mental disturbances, psychiatric manifestations, seizures, peripheral neuropathy, and excessive excretion of porphyrin precursors in urine. Increases of serum amylase and lipase, as well as mild pancreatic edema on ultrasonography, were noted during the acute attack of AIP, suggesting concomitant acute pancreatitis. In this patient, brain magnetic resonance imaging revealed reversible multifocal cerebral lesions resembling a posterior reversible encephalopathy syndrome (PRES) during the acute attack of AIP. Because the clinical manifestations of acute pancreatitis could be present with an acute attack of AIP, early confirmation of diagnosis is mandatory to effectively manage the attack and avoid inappropriate treatment.
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PMID:Acute intermittent porphyria presenting as acute pancreatitis and posterior reversible encephalopathy syndrome. 1897 24

A 72-year-old woman was admitted to our hospital because of massive proteinuria of 2.2 g/day. She had seen a general practitioner for management of Basedow disease, diabetes mellitus and hypertension for 24 years. On admission, she complained of anorexia and nausea. Laboratory data showed serum creatinine of 3.62 mg/dL and MPO-ANCA of 68 EU. Renal biopsy revealed crescentic glomerulonephritis complicated with membranous nephropathy. Thiamazole (MMI), which was being given for Basedow disease for years, was withdrawn on the suspicion as a cause of MPO-ANCA. Three years after the withdrawal of MMI, renal failure slowly progressed to the end-stage, while MPO-ANCA was negative. She was introduced onto hemodialysis. At that time, MPO-ANCA became positive again, the titer being 12.9 EU. Therefore, we suspected a relapse of ANCA-related vasculitis and performed steroid pulse therapy on the patient with methylprednisolone at 0.5 g/day for 3 days. On hospital day 14, MPO-ANCA became negative. On day 25, however, severe acute pancreatitis developed and a pancreatic tumor lesion was found on CT. In spite of amelioration of the pancreatitis by medical treatment, the pancreatic tumor lesion did not show any significant change. On day 48, she died of multiple organ failure. Autopsy showed a mucinous cyst adenoma of pancreas and necrotizing pancreatitis. We suspected steroid therapy as the cause of the pancreatic lesions.
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PMID:[MPO-ANCA related vasculitis complicating mucinous cystadenoma of the pancreas and severe acute pancreatitis after steroid pulse therapy: a case report]. 1906 54


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