Acute pancreatitis during the treatment of relapsed acute promyelocytic leukemia with As2O3

A 77-year-old man suffered from acute pancreatitis during the treatment of relapsed acute promyelocytic leukemia with As2O3. He presented with epigastralgia on day 25 during the treatment with As2O3. Pancreatic enzyme levels were elevated and the computed tomography scan of the abdomen showed swelling of the pancreas. As acute pancreatitis due to As2O3 was suspected, As2O3 was discontinued. Intravenous gabexate mesilate was administered, and the pancreatitis improved. Acute pancreatitis should be considered as a possible complication during treatment with As2O3.     

Mortality in acute pancreatitis in Turku University Central Hospital 1971-1995.

BACKGROUND/AIMS: The role of surgical procedures in the treatment of acute pancreatitis is still unclear. The aim of the present study was to analyze the mortality in acute pancreatitis in Turku University Central Hospital during the last quarter century with special reference to the prevailing surgical treatment trends. METHODOLOGY: A total of 3921 patients with acute pancreatitis were treated 1971-1995. We analyzed the mortality in acute pancreatitis and the number of patients treated in the intensive care unit as well as the number of various surgical procedures used in the treatment of acute pancreatitis in each year 1971-1995. RESULTS: The most conspicuous finding was that the mortality in acute pancreatitis has not decreased any more during the last 15 years. Neither pancreatic resections nor peritoneal lavages seem to decrease the mortality. CONCLUSIONS: We conclude that despite various surgical procedures used in the treatment of acute pancreatitis the mortality in acute pancreatitis has not decreased any more during the last 15 years. Because of the retrospective nature of the current study the present results do not justify drawing any strict conclusions concerning the treatment of acute pancreatitis. However, the present results support the view that conservative treatment in the intensive care unit is justified as an initial therapy even in the fulminant attacks of acute pancreatitis.     

Azathioprine-Associated acute pancreatitis in the course of chronic active hepatitis

We have described a 22-year-old man with an HBsAg-positive chronic active hepatitis who developed an attack of pancreatitis during the course of treatment with prednisone and azathioprine. Clinical and biochemical abnormalities subsided when azathioprine was stopped and reappeared after rechallenge with the drug. Azathioprine-associated acute pancreatitis is well recognized mostly during treatment of Crohn's disease and after renal transplantation. This adverse effect should, therefore, also be kept in mind during the treatment of chronic active hepatitis.     

Recurrent acute pancreatitis and its relative factors

AIM: To evaluate the causes and the relative factors of recurrent acute pancreatitis. METHODS: From 1997 to 2000, acute pancreatitis relapsed in 77 of 245 acute pancreatitis patients. By reviewing the clinical treatment results and the follow-up data, we analyzed the recurrent factors of acute pancreatitis using univariate analysis and multivariate analysis. RESULTS: Of the 245 acute pancreatitis patients, 77 were patients with recurrent acute pancreatitis. Of them, 56 patients relapsed two times, 19 relapsed three times, each patient relapsed three and four times. Forty-seven patients relapsed in hospital and the other 30 patients relapsed after discharge. Eighteen patients relapsed in 1 year, eight relapsed in 1-3 years, and four relapsed after 3 years. There were 48 cases of biliary pancreatitis, 3 of alcohol pancreatitis, 5 of hyperlipidemia pancreatitis, 21 of idiopathic pancreatitis. Univariate analysis showed that the patients with local complications of pancreas, obstructive jaundice and hepatic function injury were easy to recur during the treatment period of acute pancreatitis (P= 0.022<0.05, P= 0.012<0.05 and P= 0.002<0.05, respectively). Multivariate analysis showed that there was no single factor related to recurrence. Of the 47 patients who had recurrence in hospital, 16 had recurrence in a fast period, 31 after refeeding. CONCLUSION: Acute pancreatitis is easy to recur even during treatment. The factors such as changes of pancreas structure and uncontrolled systemic inflammatory reaction are responsible for the recurrence of acute pancreatitis. Early refeeding increases the recurrence of acute pancreatitis. Defining the etiology is essential for reducing the recurrence of acute pancreatitis.     

复发性急性胰腺炎42例临床分析

目的探讨复发性急性胰腺炎的病因及诊治。方法回顾性分析42例复发性急性胰腺炎的病因及诊治情况。结果 42例复发病例中,胆源性25例,特发性9例,乙醇性6例,高脂血症、胰腺肿瘤各1例。42例均先行内科保守治疗,其中中转手术治疗14例(均治愈,愈后无复发);28例坚持内科治疗,愈后再次复发9例。本组死亡4例(手术、非手术各2例)。结论急性胰腺炎愈后复发的病因复杂,与疾病及多种药物使用有关,最常见的病因为胆石症、酗酒和暴饮暴食及特发性胰腺炎等有关。明确病因,积极恰当治疗,可减少复发性急性胰腺炎的发生。     

妊娠与急性胰腺炎

妊娠期女性因激素水平的改变易出现胃肠道症状,其中妊娠合并急性胰腺炎尤为严重,可能会危及母婴安全。妊娠期急性胰腺炎在诊断、治疗等方面具有特殊性。本文就妊娠期急性胰腺炎的病因、对母婴的影响、诊断、治疗等相关问题作一综述,以期能提高消化科医师和产科医师对本病的认识。     

Biliary microcrystals in idiopathic acute pancreatitis: clue for occult underlying biliary etiology

The main causes of pancreatic inflammation worldwide are biliary lithiasis and alcoholism. However, 10 to 30% of patients have been considered to have "idiopathic" acute pancreatitis. Recently, some studies showed that a significant rate of the so called idiopathic pancreatitis are caused by microlithiasis and/or biliary sludge, identified by the presence of cholesterol monohidrate and/or calcium bilirubinate microcrystals in the biliary sediment. In the present study, the analysis of microcrystals from bile obtained during endoscopic retrograde cholangiopancreatography was done in patients with pancreatitis (idiopathic, biliary or alcoholic--20 in each group). Patients with idiopathic pancreatitis and microcrystals in the bile underwent cholecystectomy whenever possible. Those who refused or were inapt to surgery underwent endoscopic sphincterotomy or received continuous therapy with ursodeoxycholic acid. Patients with idiopathic pancreatitis without biliary crystals did not receive any specific treatment. The prevalence of biliary microcrystals in patients with idiopathic pancreatitis (75%) and biliary pancreatitis (90%) was significantly higher than in those with alcoholic pancreatitis (15%). In the identification of the etiology of biliary pancreatitis, the presence of microcrystals had a sensitivity of 90%, specificity of 85%, positive predictive value of 85.7%, negative predictive value of 89.4% and accuracy of 87.5%. In the patients with recurrent idiopathic pancreatitis, with biliary crystals, there was an statistically significant reduction in the number of pancreatitis episodes after specific treatment. In the follow-up of this group during 23.3 +/- 4.8 months, recurrence of pancreatitis occurred only in patients with "persistent biliary factor" (choledocholithiasis and/or persistence of cholesterol monohidrate). All patients with idiopathic pancreatitis who underwent cholecystectomy had chronic cholecystitis. Moreover, cholelithiasis was present in one case. In the ultrassonographic follow-up of the patients with idiopathic acute pancreatitis with microcrystals in the bile, cholelithiasis was detected in one case. In the subgroup of five patients with idiopathic pancreatitis without biliary microcrystals recurrence occurred in one case. Ultrassonographic study during follow-up did not reveal biliary stones in any of these patients. We concluded that the detection of biliary microcrystals in "idiopathic" pancreatitis suggested an underlying biliary etiology, even if occult. What's more, early specific therapeutic procedure (cholecystectomy, endoscopic sphincterotomy or ursodeoxycholic acid) in patients with recurrent idiopathic pancreatitis with microcrystals in the bile reduced significantly the recurrence during the follow-up. Finally, acute pancreatitis (specially recurrent) should not be called idiopathic before the microscopic analysis of the bile, aiming to detect or exclude the presence of microcrystals.     

A randomized double-blind study using CaNa2EDTA, a phospholipase A2 inhibitor, in the management of human acute pancreatitis

In a randomized double-blind study the effect of CaNa2EDTA, a phospholipase A2 inhibitor, was tested as a treatment for acute pancreatitis. CaNa2EDTA was infused intravenously during the first 2 days after admission to hospital, in addition to normal conservative treatment. CaNa2EDTA decreased the serum phospholipase A2 activity and appeared to promote recovery from the illness. To what extent the inhibition of serum phospholipase activity may prevent the progress of severe haemorrhagic pancreatitis or diminish mortality and morbidity in acute pancreatitis should be investigated in further studies.     

Autoimmune pancreatitis with evolution to cholangitis: a case report

We report the case of a 47-year-old Caucasian male patient who presented with obstructive jaundice and mild epigastric pain. Autoimmune pancreatitis was diagnosed based on magnetic resonance imaging, biopsy and clinical evolution, and the patient was successfully treated with corticosteroids. However, a few months later ERCP showed an image compatible with sclerosing cholangitis. Again, treatment with corticosteroids was given, after which the bile ducts became normal. A few months later, again there was a relapse and azathioprine was started. After decreasing the dose of immunesuppression, we saw relapses of cholangitis and pancreatitis, with eventually evolution to chronic calcifying pancreatitis. The aim of this report is to describe autoimmune pancreatitis as a cause of obstructive jaundice, and to illustrate that evolution to an immunesuppression-responsive cholangitis, with evolution to chronic calcifying pancreatitis is possible. Also, our patient had a small fluid collection, possibly a pseudocyst, an unusual finding in autoimmune pancreatitis, which disappeared during treatment.     

Acute pancreatitis as a possible consequence of metronidazole during a relapse of ulcerative colitis

We present the first case of metronidazole-related acute pancreatitis during a relapse of ulcerative colitis. A 31-year-old male patient, with inflammatory bowel disease on mesalamine treatment for the last 5 months, suffered from a 48-h abdominal pain and nausea. He was also administered metronidazole during a relapse 5 days before. Laboratory and imaging investigation revealed acute pancreatitis. Conservative measures and metronidazole as well as mesalamine withdrawal resulted in complete recovery. Clinical remission of ulcerative colitis was obtained by prednisolone administration. Mesalamine was reintroduced and no recurrence was noticed for a year. Acute pancreatitis was mainly attributed to metronidazole owing to the absence of recurrence after mesalamine readministration, the time of onset after the initiation of metronidazole and the lower typical range between its onset and mesalamine exposure. Identifying acute pancreatitis as a possible consequence of a certain medication in inflammatory bowel disease patients may be particularly important to determine further treatment of their disease.     

La pancréatite aiguë au cours de la rectocolite ulcérohémorragique : complication rare de la mésalazine

Acute pancreatitis secondary to mesalazine is rare. Thirty-nine cases were described. We report a new case of pancreatitis during treatment of distal ulcerative colitis (UC) with mesalazine in a 38-year-old woman, without alcohol consumption. Treatment with enema and oral mesalazine was started. One week later, the patient was admitted for pancreatic epigastric pain; lipasemia was raised to threefold the upper normal limit. Ultrasound and abdominal CT scan showed an enlarged heterogeneous pancreatic head without Wirsung or biliary ducts abnormalities; treatment was stopped with regression of symptomatology as well as normalization of lipasemia after 10 days. Acute pancreatitis secondary to mezalasine is a rare side effect in the treatment of chronic inflammatory bowel diseases. This diagnosis must be evoked in any patient receiving mesalazine and presents pancreatic epigastric pain after excluding other causes of pancreatitis, particularly autoimmune etiology.     

Stress kinase inhibition modulates acute experimental pancreatitis

AIM: To examine the role of p38 during acute experimental cerulein pancreatitis. METHODS: Rats were treated with cerulein with or without a specific JNK inhibitor (CEP1347) and/or a specific p38 inhibitor (SB203580) and pancreatic stress kinase activity was determined. Parameters to assess pancreatitis included trypsin, amylase, lipase, pancreatic weight and histology. RESULTS: JNK inhibition with CEP1347 ameliorated pancreatitis, reducing pancreatic edema. In contrast, p38 inhibition with SB203580 aggravated pancreatitis with higher trypsin levels and, with induction of acinar necrosis not normally found after cerulein hyperstimulation. Simultaneous treatment with both CEP1347 and SB203580 mutually abolished the effects of either compound on cerulein pancreatitis. CONCLUSION: Stress kinases modulate pancreatitis differentially. JNK seems to promote pancreatitis development, possibly by supporting inflammatory reactions such as edema formation while its inhibition ameliorates pancreatitis. In contrast, p38 may help reduce organ destruction while inhibition of p38 during induction of cerulein pancreatitis leads to the occurrence of acinar necrosis.     

Pancreatitis and palindromic arthropathy with effusions associated with sodium stibogluconate treatment in a renal transplant recipient

We report the occurrence of two side effects, pancreatitis and palindromic arthropathy with effusions, associated with injections of sodium stibogluconate used in the treatment of kala-azar. No clear mechanism to account for the problems was identified despite extensive investigation. We suggest that when abdominal pain is experienced during treatment with antimonial drugs pancreatitis should be borne in mind as a possible cause.     

Acute pancreatitis associated with boceprevir: a case report

Approximately 170 million people are infected with hepatitis C, and the sustained virological response rate to treatment with pegylated interferon and ribavirin is 30–50%. In an attempt to improve the chances of cure, boceprevir is being added to therapy, but it is associated with an increased incidence of adverse events. We herein report a case of acute pancreatitis developed during treatment with pegylated interferon, ribavirin and boceprevir. Boceprevir was the most likely cause of drug-associated pancreatitis after the most common causes were ruled out, since this adverse event had not occurred when the patient had previously been exposed to pegylated interferon and ribavirin and there was no recurrence of the episode of pancreatitis when these two drugs were reintroduced. Acute pancreatitis is a rare adverse event associated with boceprevir therapy, but a potentially fatal event. Sequential determination of pancreatic enzymes should be considered during hepatitis C treatment with boceprevir.     

Endoscopic sphincterotomy in acute biliary pancreatitis: A question of anesthesiological risk

Two consecutive surveys of acute pancreatitis in Italy, based on more than 1000 patients with acute pancreatitis, reported that the etiology of the disease indicates biliary origin in about 60% of the cases. The United Kingdom guidelines report that severe gallstone pancreatitis in the presence of increasingly deranged liver function tests and signs of cholangitis (fever, rigors, and positive blood cultures) requires an immediate and therapeutic endoscopic retrograde cholangiopancreatography (ERCP). These guidelines also recommend that patients with gallstone pancreatitis should undergo prompt cholecystectomy, possibly during the same hospitalization. However, a certain percentage of patients are unfit for cholecystectomy because advanced age and presence of comorbidity. We evaluated the early and long-term results of endoscopic intervention in relation to the anesthesiological risk for 87 patients with acute biliary pancreatitis. All patients underwent ERCP and were evaluated according to the American Society of Anesthesiology (ASA) criteria immediately before the operative procedure. The severity of acute pancreatitis was positively related to the anesthesiological grade. There was no significant relationship between the frequency of biliopancreatic complications during the follow-up and the ASA grade. The frequency of cholecystectomy was inversely related to the ASA grade and multivariate analysis showed that the ASA grade and age were significantly related to survival. Finally, endoscopic treatment also appeared to be safe and effective in patients at high anesthesiological risk with acute pancreatitis. These results further support the hypothesis that endoscopic sphincterotomy might be considered a definitive treatment for patients with acute biliary pancreatitis and an elevated ASA grade.     

Spontaneous rupture of the spleen in chronic calcifying pancreatitis: report of three cases

Spontaneous rupture of the spleen is a rare complication of chronic calcifying pancreatitis. Anemia and hemorrhagic shock may not occur, making diagnosis more difficult. Favourable response to conservative treatment does not prevent the need for splenectomy, as calcifiying chronic pancreatitis may progress locally. We report three cases of spontaneous rupture of the spleen. In two cases, splenic rupture revealed calcifying chronic pancreatitis and both patients underwent urgent splenectomy. In the third case, the patient was known to have calcifying chronic pancreatitis, and splenectomy was performed because of unsuccessful conservative treatment. We discuss the role of distal pancreatectomy during splenectomy to reduce the rate of postoperative complications and additional surgery. We also discuss the role of arterial embolisation and laparoscopy in the management of this rare condition.     

Bulimia. An underlying behavioral disorder in hyperlipidemic pancreatitis: a prospective multidisciplinary approach

Between 1978 and 1985, we conducted a prospective study of 21 patients who survived several attacks of pancreatitis and were diagnosed as having primary hyperlipidemia. None of the patients suffered from chronic alcoholism, primary diabetes, or cholelithiasis or was receiving prolonged steroid therapy. Lowering of plasma lipid values toward normal was achieved in all patients following a program of combined dietary and drug (bezafibrate) therapy. Five patients had recurrent episodes of pancreatitis during the treatment program. These patients were diagnosed subsequently as suffering from bulimia and were all given cognitive behavioral therapy. One patient died following an attack of pancreatitis. An underlying eating disorder should be suspected in patients who relapse after treatment for pancreatitis and hyperlipidemia. Multidisciplinary treatment should be used in these patients to improve therapeutic efficacy and uncover behavioral patterns that have a direct impact on their life expectancy.     

Treatment with anti-factor VIIa in acute pancreatitis in rats: blocking both coagulation and inflammation?

OBJECTIVE: Acute pancreatitis starts as an autodigestive process restricted to the pancreas and progresses to a systemic inflammation via cytokine release into the blood stream. Several inhibitors of the coagulation cascade, including active-site-inactivated factor VIIa, have shown anti-inflammatory properties in other inflammatory models than acute pancreatitis. Free radical scavengers have proven useful in reducing the oxidative damage during hyperinflammatory conditions. The aim of this study was to investigate whether pretreatment with FVIIai would have any effect on the multiple organ dysfunction syndrome (MODS) in severe acute pancreatitis. MATERIAL AND METHODS: Experimental acute pancreatitis was induced by intraductal infusion of taurodeoxycholate in the pancreatic duct. The animals were pretreated with N-acetyl-cysteine and active-site-inactivated factor VIIa. Neutrophil infiltration in the lungs, ileum and colon was quantified by myeloperoxidase activity. Inflammatory markers, IL-6 and MIP-2, were measured using ELISA. RESULTS: Tissue infiltration of neutrophils in the lungs, ileum and colon significantly increased during acute pancreatitis as compared to sham operation. These levels were reduced by pretreatment with N-acetylcysteine and active-site-inactivated factor VIIa. Levels of interleukin-6 and macrophage inflammatory protein-2 increased significantly during acute pancreatitis. Pretreatment with NAC and FVIIai reduced these levels. CONCLUSIONS: Both N-acetylcysteine and active-site-inactivated factor VIIa showed powerful anti-inflammatory properties in experimental acute pancreatitis. As they exert their effects through different physiological mechanisms, they represent potential candidates for future multimodal treatment of acute pancreatitis.     

Case report: acute pancreatitis induced by Clozapine

Two percent of acute pancreatitis are drug induced. In the present paper, we reported the case of a 39 year-old patient with chronic-hallucinatory schizophrenia who developed symptomatic pancreatitis during the clozapine dose titration performed to reach the therapeutic range. Diagnosis of pancreatitis was suggested by clinical examination and abnormal laboratory values of pancreatic enzymes and confirmed by C-T scan and ultrasonography. The causal incrimination of clozapine in this case seems likely as all other possible causes of pancreatitis were excluded, as AP developed shortly after the introduction of the drug and as the pancreatic enzymes normalized after clozapine was stopped. No rechallenge to confirm the causal relationship was however attempted. So far, only eight cases of acute pancreatitis have been reported in association with clozapine use. Clozapine is an atypical antipsychotic drug which belongs to the chemical class of dibenzodiazepines. The mechanism by which clozapine could produce acute pancreatitis remained unclear. Nevertheless, we advocate a careful biological follow-up (measuring periodically the concentrations of amylase, lipase and triglycerides) during the treatment by clozapine.     

Pancreatic Sphincterotomy and Pure Pancreatic Juice Collection for Treatment of Chronic Pancreatitis

Abstract: After our introduction of endoscopic pancreatic sphincterotomy for treatment of chronic pancreatitis in 1985, our interest has been focused to the value of pure pancreatic juice collection with or without pancreatic sphincterotomy for management of chronic pancreatitis. Through pancreatic sphincterotomy, pain relief was obtained in 13 out of 16 cases with moderate and marked chronic pancreatitis. After pancreatic sphincterotomy extraction of pancreatic calculi using basket forceps was done successfully in 2 of these cases, Spontaneous stone passage occured in the other 2. In pure pancreatic juice collection without pancreatic sphincterotomy, pain relief was seen in 6 out of 13 cases with mild and moderate chronic pancreatitis. The protein plug was simultaneously aspirated during the procedure in 3 cases. Recently, we have indicated in these patients both pancreatic sphincterotomy and pure pancreatic juice collection and noted pain relief was obtained in all of the 8 cases with this approach. With an improvement in the technology of pancreatic drainage, these endoscopic treatment modalities may be possibly useful to stop the progression of chronic pancreatitis.