Recurrent Attacks Of Acute Pancreatitis Research Articles

Pancreaticobiliary malunion and incomplete pancreas divisum: an unusual cause of common bile duct obstruction

Pancreaticobiliary malunion (PBM) is a distinct disease entity of the pancreatic and biliary ductal system defined as a condition in which the junction of the pancreatic and biliary ducts occurs above the duodenal wall. PBM may be combined with a stenosis of the distal common bile duct and pathological changes in the common bile duct wall (congenital cyst of bile duct), being a potentially malignant condition. Pancreas divisum, resulting from a fusion failure of the ventral and dorsal pancreatic buds, and characterized by a dominant Santorine duct, is considered to be a predisposing factor to recurrent attacks of acute pancreatitis. In incomplete pancreas divisum, the ventral and dorsal pancreas are connected by a segmental branch. We report a case of a 33-year-old female patient with PBM associated with incomplete pancreas divisum, who had presented episodes of acute cholangitis due to a benign distal common bile duct stricture. Treatment with choledochoduodenostomy and cholecystectomy provided thorough relief and resolution of symptoms. This is the first report of coexistent PBM and incomplete pancreas divisum in a Caucasian patient with unusually late clinical manifestation.

Recurrent acute pancreatitis: From the editor

This special issue of World Journal of Gastroenterology contains a number of articles focusing on acute recurrent pancreatitis, a clinical entity that still remains a complex diagnostic and therapeutic challenge in clinical practice. Recurrent bouts of pancreatitis mainly occur in a gland which shows a normal morphology of both parenchyma and pancreatico-biliary ductal system at the time of diagnosis, when standard investigation is used; however, the introduction of ultrasound endoscopy (EUS) in clinical practice allowed us to identify mild to moderate ductal and parenchymal alterations in a relevant part of these patients, suggesting a chronic process, observed either at the onset of the disease or during the follow-up period. These pancreatic abnormalities can either suggest the presence of an underlying chronic process which evolves over time with recurrent attacks of acute pancreatitis or can be the consequence of multiple, self-limiting acute inflammatory episodes that induce persistent lesions within the gland with time. It is generally believed that, in about 70% of cases, a correct aetiological diagnosis is achieved by means of clinical history, laboratory tests, and standard imaging techniques, including CT scan, magnetic resonance cholangio-pancreatography (MRCP), and endoscopic retrograde cholangio-pancreatography (ERCP). Another significant improvement in the knowledge of aetiological factors has been achieved by the introduction of sphincter of Oddi manometry, microscopic search for bile crystals in the collected bile, and testing for cystic fibrosis transmembrane conductance regulator-gene (CFTR) and other genetic (SPINK1, PRSS1) mutations. Sphincter of Oddi manometry and the search for bile crystals may improve the diagnostic yield in patients in whom both pancreatico-biliary junction and ductal system have a normal appearance. By these techniques, the major role played by the sphincter of Oddi dysfunction, either of the biliary or pancreatic segment, and bile sludge or microlithiasis has been revealed in the occurrence of idiopathic recurrent pancreatitis. However, manometric investigation of the sphincter of Oddi may fail to document some dysfunction in a progressively increased percentage of patients in type 2 and 3 dysfunction, respectively, when the need for definite findings is highest. The introduction of the Secretin test, done by either MRCP or EUS investigation, has been documented to provide a more detailed visualization of the pancreatic ductal system and indirect information about the sphincter of Oddi function, avoiding ERCP-related risks. The aim of the present topic highlights is to provide a comprehensive overview of the current knowledge and unsettled issues on recurrent acute pancreatitis, including aetiological factors, diagnostic and therapeutic procedures, and clinical management. 995 Is acute recurrent pancreatitis a chronic disease? Mariani A, Testoni PA 999 Acute recurrent pancreatitis: An autoimmune disease? Pezzilli R 1007 Diagnostic approach to patients with acute idiopathic and recurrent pancreatitis, what should be done? Al-Haddad M, Wallace MB 1011 Role of genetic disorders in acute recurrent pancreatitis Keim V 1016 Endoscopic ultrasonography for evaluating patients with recurrent pancreatitis Petrone MC, Arcidiacono PG, Testoni PA 1023 Sphincter of Oddi dysfunction and bile duct microlithiasis in acute idiopathic pancreatitis Elta GH 1027 Pancreatic ductal system obstruction and acute recurrent pancreatitis Delhaye M, Matos C, Arvanitakis M, Deviere J 1034 Endoscopic therapy in acute recurrent pancreatitis Baillie J 1038 Diagnosis and management of relapsing pancreatitis associated with cystic neoplasms of the pancreas Brugge WR

Biliary T-Tube Remnant As the Cause of Microlithiasis and Recurrent Acute Pancreatitis, Detected By a New Per Oral Cholangioscopy System (SpyGlass)

A 62 year old female s/p cholecystectomy for cholelithiasis a year ago, with recurrent acute pancreatitis and mildly elevated LFTs with dilated biliary tree underwent ERCP that showed long cystic duct stump and dilated biliary tree without filling defects. Balloon sweep of CBD after sphinterotomy yielded only sludge. She developed another attack of acute pancreatitis after few months. MRCP showed a filling defect in the distal CBD. Repeat ERCP was done with sludge extraction. After few months, she had acute pancreatitis again and MRCP showed new distal CBD stone. An ERCP with cholangioscopy using the new per oral cholangioscopy system (SpyGlass) was done. Cholangiogram showed a filling defect in distal CBD but no filling defects in the cystic duct stump. Cholangioscopy confirmed the presence of the filling defect in distal CBD as microlithiasis, and in addition showed a tubular structure covered with sludge in the cystic duct. Balloon sweep of the cystic duct yielded a foreign body that was found to be remnant of a T-tube used during patient's cholecystectomy (picture). Presence of a foreign body in biliary tree is known to act as a nidus for sludge and microlithiasis formation. Recurrent attacks of acute pancreatitis in our patient were attributed to microlithiasis and sludge as a result of presence of T-tube remnant. Due to its hollow structure, the tube would fill with contrast and could not be visualized during ERCP. Filling with bile prevented visualization on MRCP. Being made up of radiolucent plastic material it also had evaded detection on CT scan. Direct cholangioscopy was the only diagnostic technique that enabled the detection of T-tube remnant in the cystic duct stump and subsequent removal.

Recurrent Attacks of Acute Pancreatitis from Ascaris in the Common Bile Duct

Journal of the American College of Surgeons 203(4):p 580-581, October 2006. | DOI: 10.1016/j.jamcollsurg.2006.03.026

Pancreatitis hereditaria causada por una nueva mutación en el gen del tripsinógeno. Presentación de una familia

Hereditary pancreatitis is an uncommon autosomal dominant disease secondary to a mutation normally located in the trypsinogen gene, preventing trypsin deactivation. This mutation translates clinically into recurrent attacks of acute pancreatitis and an increased risk of pancreatic cancer. We report a case of acute hereditary pancreatitis due to a trypsinogen mutation that has previously been described in only one family.

Gallbladder cholesterolosis: An aetiological factor in acute pancreatitis of uncertain origin

To investigate the possible relationship between gallbladder cholesterolosis and acute pancreatitis, we studied 3797 cholecystectomy specimens and found 55 cases of gallbladder cholesterolosis unassociated with biliary lithiasis. From the reviewed case notes, 27 of these patients presented with recurrent attacks of acute pancreatitis which disappeared after cholecystectomy (follow-up 65.1 months). A microscopic study revealed frank cholesterolosis in all cases with a pseudopolyp transformation of the mucosa, some polyps reaching a diameter of 2 mm. We postulate that the mechanism could be temporary impaction of cholesterolosis polyps at the sphincter of Oddi and suggest that patients with recurrent attacks of acute pancreatitis and negative aetiological investigation must be considered as at high risk of having gallbladder cholesterolosis and that they could benefit from cholecystectomy.

Accessory sphincterotomy (endoscopic and surgical) in patients with pancreas divisum.

Sixteen patients with the congenital anomaly of pancreas divisum have been treated by enlarging the orifice of the accessory papilla. Attempts to do this at duodenoscopy succeeded in only 5 of 12 patients, and only one had a good clinical result. Sphincteroplasty was performed surgically in seven patients; five had a good or fair result. Most patients with poor results have undergone pancreatic resection. One patient died post-operatively; the remaining 15 divide equally as good (5), fair (5) and poor (5) results at follow-up after periods ranging from 7 months to 5 years. Results appear to be better in patients presenting with recurrent attacks of acute pancreatitis than in those with chronic pain. The preferred management for these patients remains unclear.

A prospective study of acute pancreatitis.

All 78 patients with acute pancreatitis admitted to one hospital in a 2-year period were included in a prospective survey of conservative management. The overall mortality rate was 11.5 per cent, being 46 per cent for 11 patients subjected to early laparotomy and only 6 per cent for patients managed without operation. Twenty-six patients were considered to have severe acute pancreatitis and all 9 deaths occurred in this group. Biliary disease was present in 51 per cent of patients, and the majority of those with biliary disease were over 60 years old. Alcohol-related acute pancreatitis occurred in 26 per cent of the total patients, and none of this group was over 60 years old. Acute pancreatitis was considered idiopathic in origin in only 13 per cent of the patients. Elective biliary surgery in 30 patients resulted in freedom from recurrent attacks of acute pancreatitis for the follow-up period (12-30 months). The results compare favourably with those in which glucagon and high dosage aprotinin (Trasylol) have been utilized in the management of acute pancreatitis.

Approach to idiopathic recurrent pancreatitis.

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.

Hereditary pancreatitis.

Hereditary pancreatitis is an autosomal dominant condition, which results in recurrent attacks of acute pancreatitis, progressing to chronic pancreatitis often at a young age. The majority of patients with hereditary pancreatitis express one of two mutations (R122H or N29I) in the cationic trypsinogen gene (PRSS1 gene). It has been hypothesised that one of these mutations, the R122H mutation causes pancreatitis by altering a trypsin recognition site so preventing deactivation of trypsin within the pancreas and prolonging its action, resulting in autodigestion. Families with these two mutations have been identified in many countries and there are also other rarer mutations, which have also been linked to hereditary pancreatitis. Patients with hereditary pancreatitis present in the same way as those with sporadic pancreatitis but at an earlier age. It is common for patients to remain undiagnosed for many years, particularly if they present with non-specific symptoms. Hereditary pancreatitis should always be considered in patients who present with recurrent pancreatitis with a family history of pancreatic disease. If patients with the 2 common mutations are compared, those with the R122H mutation are more likely to present at a younger age and are more likely to require surgical intervention than those with N29I. Hereditary pancreatitis carries a 40 % lifetime risk of pancreatic cancer with those patients aged between 50 to 70 being most at risk in whom screening tests may become important.

Acute recurrent pancreatitis.

History, physical examination, simple laboratory and radiological tests, and endoscopic retrograde cholangiopancreatography (ERCP) are able to establish the cause of recurrent acute pancreatitis in 70% to 90% of patients. Dysfunction of the biliary and/or pancreatic sphincter, as identified by sphincter of Oddi manometry, accounts for the majority of the remaining cases. The diagnosis may be missed if the pancreatic sphincter is not evaluated. Pancreas divisum is a prevalent congenital abnormality that is usually innocuous but can lead to recurrent attacks of acute pancreatitis or abdominal pain. In select cases, endoscopic sphincterotomy of the minor papilla can provide relief of symptoms and prevent further attacks. A small proportion of patients with idiopathic pancreatitis have tiny stones in the common bile duct (microlithiasis). Crystals can be visualized during microscopic analysis of bile that is aspirated at the time of ERCP. Neoplasia is a rare cause of pancreatitis, and the diagnosis can usually be established by computerized tomography or ERCP. A wide variety of medications can also cause recurrent pancreatitis. ERCP, sphincter of Oddi manometry, and microscopy of aspirated bile should be undertaken in patients with recurrent pancreatitis in whom the diagnosis is not obvious.

Hereditary pancreatitis: Clinical presentation, ERCP findings, and outcome of endoscopic therapy

Background: Hereditary pancreatitis (HP) is an autosomal dominant disorder characterized by the onset of recurrent attacks of acute pancreatitis in childhood and frequent progression to chronic pancreatitis. There are limited data on the role of diagnostic and therapeutic ERCP in patients with HP. The aims of this study were to describe the clinical presentation and findings on pancreatography and to evaluate the role of endoscopic and surgical intervention in patients with HP. Methods: Twenty-seven consecutive patients with HP were referred for ERCP at two centers in the midwest United States. Medical records and pancreatograms were reviewed. Results: Pancreatography was abnormal in all patients. The majority (70%) had severe (Cambridge Grade III) changes of chronic pancreatitis. Nineteen (70%) patients underwent endoscopic therapy and 8 (30%) surgical intervention. After endoscopic therapy (mean follow-up 32 months), 50% were symptom free, 38% had moderate improvement, and 12% had no or transient improvement in symptoms. After surgery (mean follow-up 32 months), 38% were symptom-free, 25% had moderate improvement, and 12% had transient improvement in symptoms. Two patients treated surgically died of pancreatic cancer. Conclusions: In the short-term, improving drainage of the pancreatic ductal system by endoscopic means effectively relieves pain and reduces the number of attacks of pancreatitis in the majority of patients with HP. (Gastrointest Endosc 2002;56:66-71.)

Long-term course following severe acute pancreatitis

Background Although improvements in intensive care have reduced the mortality rate of severe acute pancreatitis, limited attention has been paid to subsequent health and pancreatic function among survivors. Method A follow-up study was conducted among 54 patients who survived an attack of severe acute pancreatitis. The main outcome measures were general condition, pain, evidence of exocrine and endocrine dysfunction, alcohol consumption, recurrent attacks of acute pancreatitis, working capacity, late death and its cause. Results 27 patients developed recurrent attacks of acute pancreatitis, more often following alcohol-induced pancreatitis (p Pain was frequent during the first year after the severe acute pancreatitis, but diminished with time. Nine patients (17%) among long-term survivors developed chronic pancreatitis. Temporary exocrine dysfunction after pancreatitis was frequent and one-third of patients developed diabetes mellitus. A tendency towards a lower consumption of alcohol was noted. General condition improved with time and working capacity was retained in most patients. Discussion Patients surviving severe acute pancreatitis generally seem to regain a good quality of life, thereby justifying the extensive management efforts needed during the acute phase of their illness.

Recurrent acute pancreatitis induced by isoniazid

A 31-year-old man on haemodialysis who developed recurrent attacks of acute pancreatitis during the treatment of pulmonary tuberculosis is presented. The pancreatitis rapidly subsided once isoniazid was withdrawn, but the problem recurred again upon reintroduction of the drug. There was no further recurrence during successful treatment with full doses of rifampicin and pyrazinamide for 1 year.

Recurrent Acute Pancreatitis

A scant 10 years ago, the causes of recurrent attacks of acute pancreatitis in patients with no history of gallstones or heavy alcohol consumption would have remained undiagnosed and untreated. We now know that at least five other conditions should be considered and that most can be treated effectively. The fourth article in our pancreatitis series focuses on this subgroup.

Acute pancreatitis: a lethal disease of increasing incidence.

Between 1968 and 1979 650 patients in the Bristol clinical area suffered 737 attacks of acute pancreatitis. Sex distribution was approximately equal and mean age was 60 years. Comparison with the previous decade shows an increase in mean annual incidence of first attacks from 53.8 to 73.0 cases per million population. Case mortality was unchanged at 20%. In no less than 35% of fatal cases the diagnosis was first made at necropsy. Gall stones were detected in 50% of first attacks, predominantly in women. The proportion of alcoholics (8% overall) increased three-fold during the period of the study. In 23% of cases no aetiological cause was identified. Eighty patients suffered 99 recurrent attacks of acute pancreatitis, with a mortality rate (12%) that was not significantly lower than that of the first attack. Neglected gall stones accounted for 51% of these subsequent attacks.

Natural history of acute pancreatitis. A long-term study.

Detailed clinical and laboratory follow-up was made of 113 patients, two to 12 years after their first attack of acute pancreatitis, to assess complete recovery versus the development either of acute relapsing pancreatitis, or of chronic pancreatitis. Mortality was low in patients with recurrent attacks of acute pancreatitis. Complete recovery decreased wih increasing periods of follow-up. In the group of alcoholic patients, complete recovery decreased continuously with a corresponding increase in chronic pancreatitis. In the group of patients with gallstones, chronic pancreatitis developed up to about three years after the acute attack, after which the recovery rate remained steady. Chronic pancreatitis in the patients with gallstones was usually painless. In patients with idiopathic pancreatitis, a high incidence of acute relapsing pancreatitis was seen, but this rarely persisted after three years. Pancreas function rarely recovered completely after an attack of severe acute pancreatitis. Alcohol withdrawal decreased the pain syndrome, but not the development of chronic pancreatitis. Early removal of gallstones minimized the development of chronic pancreatitis. Complete recovery did occur after one attack of acute pancreatitis, but probably only when the aetiological antecedent (alcohol or gallstones) had not been operating for a long time, as it is the antecedent rather than the acute attack which determines the eventual outcome.

Pancreatic disease.

New tests and test methods aid in the diagnosis of pancreatic disorders. Pancreatic carcinoma, especially, may have an improved prognosis with earlier detection as a result of refinements in arteriography, cytology, pancreatic radioisotopic scanning, and endoscopic retrograde cholangiopancreatography. Acute pancreatitis results most commonly from alcoholism, biliary tract disease, and trauma. Management is directed primarily at decreasing pancreatic exocrine secretion. Surgery is usually best avoided in the acute phase. Chronic pancreatitis is most often a result of recurrent attacks of acute pancreatitis. Diabetes and malassimilation become manifest as pancreatic destruction progresses. Management consists of replacement of pancreatic enzymes and diet supplements. Once chronic pancreatitis is established, surgery can only be directed at complications of the disease. Pancreatic ascites is usually associated with a break in the pancreatic ductal system. Ascites caused by trauma responds well to surgical intervention, but the alcoholic type is less amenable to treatment.

Recurrent Acute Pancreatitis in Patients With Cystic Fibrosis With Normal Pancreatic Enzymes

Ten adolescent and young adults with cystic fibrosis (CF) have had well-documented recurrent attacks of acute pancreatitis. The diagnosis of CF in each patient was delayed because they did not have pancreatic insufficiency. The diagnosis of CF was documented by the typical pulmonary involvement and elevated sweat sodium and chloride levels in all cases and a positive family history in six of the ten patients. Two patients were diagnosed as having acute pancreatitis before the diagnosis of CF was made, thus indicating that acute pancreatitis may be the presenting complaint in the young adult with CF. The diagnosis of acute pancreatitis was based on the presence of severe abdominal pain, usually with vomiting, tenderness in the mid-epigastrium, elevated serum and urinary amylase and serum lipase. Attacks were precipitated by fatty meals, alcohol ingestion; postcholecystectomy and tetracycline administration. In some patients no precipitating event could be elicited. Intravenous secretin-pancreozymin stimulation tests revealed a diminished bicarbonate secretion with little effect on the secretion of the zymogen enzymes. A mild attack of pancreatitis occurred after secretin-pancreozymin stimulation. The endocrine pancreatic function tested in four patients was normal as revealed by the glucose tolerance tests and determinations of serum insulin, growth hormone and free fatty acid. Transduodenal pancreatograms were performed in three patients; one showed a normal pancreatic duct, one showed duct obstruction and in the third patient a beady type of narrowing was found. The selenomethionine Se 75 uptake of the pancreas was noted only in the head of the pancreas. This suggests that loss of function occurs initially to a greater extent in the tail and body of the pancreas. Three patients died and showed characteristic lesions of CF.