Severe Acute Alcoholic Pancreatitis Research Articles

Severe acute alcoholic pancreatitis complicated by distributive shock, abdominal compartment syndrome, and black pleural effusion

Severe acute pancreatitis (SAP) is a life-threatening medical emergency that can lead to multi-system organ failure and mortality. Here, we highlight a case of SAP complicated by a black pleural effusion (BPE), distributive shock, and acute abdominal compartment syndrome (ACS) requiring emergent decompressive laparotomy. BPE fluid analysis was consistent with previously reported exudative effusions from a pancreatic pseudocyst, though the computed tomography (CT) of abdomen and pelvis did not show definitive evidence of a pseudocyst. In addition, black fluid was also discovered during decompressive laparotomy for ACS. It is possible that the severely elevated intra-abdominal pressure contributed to a temporary translocation/transudation of this fluid from the abdominal cavity into the pleural space, as no re-accumulation of the BPE was observed on a follow-up CT after thoracostomy tube removal.

PFKFB3 controls acinar IP3R-mediated Ca2+ overload to regulate acute pancreatitis severity.

Acute pancreatitis (AP) is among the most common hospital gastrointestinal diagnoses; understanding the mechanisms underlying the severity of AP is critical for development of new treatment options for this disease. Here, we evaluate the biological function of phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3) in AP pathogenesis in 2 independent genetically engineered mouse models of AP. PFKFB3 was elevated in AP and severe AP (SAP), and KO of Pfkfb3 abrogated the severity of alcoholic SAP (FAEE-SAP). Using a combination of genetic, pharmacological, and molecular studies, we defined the interaction of PFKFB3 with inositol 1,4,5-trisphosphate receptor (IP3R) as a key event mediating this phenomenon. Further analysis demonstrated that the interaction between PFKFB3 and IP3R promotes FAEE-SAP severity by altering intracellular calcium homeostasis in acinar cells. Together, our results support a PFKFB3-driven mechanism controlling AP pathobiology and define this enzyme as a therapeutic target to ameliorate the severity of this condition.

S1894 A Case of Severe Acute Alcoholic Pancreatitis Complicated With Abdominal Compartment Syndrome

Introduction: Abdominal compartment syndrome (ACS) is a sustained intra-abdominal pressure (IAP) above 20mmHg with associated new-onset organ dysfunction. Even though it is rarely seen in clinical practice, up to 15% of patients with severe acute pancreatitis (SAP) develop ACS and have a mortality rate of up to 49%. Given that delayed treatment of ACS is associated with high mortality and adverse outcome, a higher clinical suspicion is needed to aid diagnosis. We present a case of severe pancreatitis complicated with ACS. Case Description/Methods: A 29-year-old man with a history of alcohol abuse presented with five days of severe abdominal pain. He was diagnosed with SAP. About 8 hours into admission to the ICU and resuscitation, he began having worsening work of breathing and persistent severe abdominal pain despite being on adequate opioid analgesic. Physical examination revealed tachycardia, diffuse peritoneal signs, guarding, and shock. Repeat labs revealed worsening leukocytosis, thrombocytopenia, hyperkalemia, hypocalcemia, lactic acidosis, and elevated creatinine kinase. There was also evidence of renal failure. An edematous pancreas with some peripancreatic fluid collection was evident on the CT abdomen (Figure). The abdominal x-ray was unremarkable. Indirect intra-abdominal pressure (IAP) by intravesical catheter pressure measurement was 35mmHg. He commenced medical management with neuromuscular paralysis and mechanical ventilatory support. A repeat IAP was 24mmHg. He then got surgical decompression by full-thickness midline laparotomy with wound vac placement which further reduced the IAP to 10mmHg. He received serial dialysis, correction of abnormal electrolytes, and serial transfusion with blood products as required. He remained critically ill on a mechanical ventilator and vasopressors, with a poor prognosis at the time of this writing. Discussion: The pathophysiology of elevated IAP in SAP is multifactorial. These include retroperitoneal inflammation, ascites, acute peripancreatic fluid collections, visceral edema, and aggressive fluid resuscitation. We believe some of the above listed had ensued in our patient for days before he presented to the hospital. Physical examination is inaccurate in diagnosing ACS. The first-line treatment is medical paralysis followed by surgical decompression if ineffective. We are writing this case to recommend early serial IAP measurements in patients with SAP.Figure 1.: CT abdomen showing edematous pancreas with some peripancreatic fluid collection.

Ulinastatin in the Management of Severe Acute Alcoholic Pancreatitis: A Case Series.

Severe acute alcoholic pancreatitis is a second common form of pancreatitis that requires intensive care unit care and has high morbidity and mortality due to lacking specific treatment. Management of alcoholic pancreatitis is generally non- specific and supportive. We hereby present a case-series of three patients that describes the successful treatment of severe acute alcoholic pancreatitis with ulinastatin and other supportive treatment. From this we want to emphasize that ulinastatin a protease inhibitor can be used in the treatment of alcoholic pancreatitis.

Short- and long-term survival after severe acute pancreatitis: A retrospective 17 years' cohort study from a single center

PurposeTo study mortality in severe acute pancreatitis (SAP) and to identify risk factors for mortality. Materials and methodsA retrospective 17-years' cohort study of 435 consecutive adult patients with SAP treated at intensive care unit of a university hospital. ResultsOverall, 357 (82.1%) patients survived at 90 days follow-up. Three-hundred six (89.5%) patients under 60 years, 38 (60.3%) patients between 60 and 69 years, and 13 (43.3%) patients over 69 years of age survived at 90 days follow-up. Independent risk factors for death within 90-days were: 60 to 69 years of age (odds ratio [OR] 5.1), >69 years of age (OR 10.4), female sex (OR 2.0), heart disease (OR 2.9), chronic liver failure (OR 12.3), open abdomen treatment (OR 4.4) and sterile necrosectomy within 4 weeks (OR 14.7). The 10-year survival estimate was <70% in patients under 60 years and <30% in patients over 60 years. Underlying cause of death after the initial 90-day follow-up period was alcohol-related in 48 (57.1%) patients, and all of them had suffered from alcoholic SAP. ConclusionsAlthough younger patients have excellent short-term survival after SAP, the long-term survival estimate is disappointing mostly due to alcohol abuse.

An unusual esophageal endoscopic appearance

A 44-year-old man, with medical history of chronic alcoholic intoxication and smoking, presented with suspicion of infected pancreatic necrosis, 5 weeks after severe acute alcoholic pancreatitis. The physical examination revealed asthenia, diffuse abdominal pain and fever (38.4 °C). Laboratory results showed elevated inflammatory markers, anemia (hemoglobin 8.5 g/dL) and malnutrition with hypoalbuminemia (25 g/L). Abdominal CT-scan showed a 8 cm walled-off pancreatic necrosis. A necrosis puncture was positive for Escherichia coli. Before initiation of treatment of the infection, the patient experienced melena. Upper gastrointestinal endoscopy (UGE) showed pale and necrotic esophageal mucosa with coffee-ground exudates, from 28 cm from dental arches (DA) to the gastro-esophageal junction (Fig. 1). Proton pump inhibitor has been introduced; then, treatment of the infected pancreatic necrosis was performed by endoscopic transgastric drainage and antibiotic. Three weeks later, dysphagia for solids occurred. A new upper endoscopy showed impassable esophageal stricture with inflammatory mucosa and fibrinous exudates. Balloon dilation was performed 3 times during 4 months whit good clinical efficacy. What is the diagnosis? Answer: Acute esophageal necrosis or “Black esophagus”. The acute esophageal necrosis (AEN) or “black esophagus” is a rare disease, with a low incidence, estimated about 0,2% in a prospective study, diagnosing 8 patients from 3900 UGE [[1]Ben Soussan E. Savoye G. Hochain P. Hervé S. Antonietti M. Lemoine F. et al.Acute esophageal necrosis: a 1-year prospective study.Gastrointest Endosc. 2002 Aug; 56: 213-217Abstract Full Text Full Text PDF PubMed Google Scholar]. A recent literature review including 112 cases, reported a mean age at diagnosis of 68 years; with a male to female ratio of 4:1 [[2]Day A. Sayegh M. Acute oesophageal necrosis: a case report and review of the literature.Int J Surg. 2010; 8 ([Epub 2009 Oct 1]): 6-14https://doi.org/10.1016/j.ijsu.2009.09.014Crossref PubMed Scopus (35) Google Scholar]. AEN occurred generally in patients with significant comorbidities including cardiovascular risk factors, cancer, chronic pulmonary disease, alcohol abuse or liver cirrhosis [[3]Gurvits G.E. Shapsis A. Lau N. Gualtieri N. Robilotti J.G. Acute esophageal necrosis: a rare syndrome.J Gastroenterol. 2007 Jan; 42 ([Epub 2007 Feb 16]): 29-38Crossref PubMed Scopus (155) Google Scholar]. Acute conditions are often associated including shock and hypotension, acute liver failure or infection. The main clinical presentation includes upper gastrointestinal bleeding (hematemesis or coffee ground vomit) occurring in two third of cases. Melena, epigastric pain, and dysphagia are less common. Endoscopic examination reveals diffuse necrotic mucosa affecting, in most cases, the lower third of the esophagus with respect of gastro-esophageal junction [[2]Day A. Sayegh M. Acute oesophageal necrosis: a case report and review of the literature.Int J Surg. 2010; 8 ([Epub 2009 Oct 1]): 6-14https://doi.org/10.1016/j.ijsu.2009.09.014Crossref PubMed Scopus (35) Google Scholar]. The mechanism of AEN remains unclear, probably multifactorial where hypoperfusion in patients with comorbidities seems the key factors. Associated gastric outlet obstruction could also increase lesions by prolonged esophageal acid reflux (cardia preserved) [1Ben Soussan E. Savoye G. Hochain P. Hervé S. Antonietti M. Lemoine F. et al.Acute esophageal necrosis: a 1-year prospective study.Gastrointest Endosc. 2002 Aug; 56: 213-217Abstract Full Text Full Text PDF PubMed Google Scholar, 2Day A. Sayegh M. Acute oesophageal necrosis: a case report and review of the literature.Int J Surg. 2010; 8 ([Epub 2009 Oct 1]): 6-14https://doi.org/10.1016/j.ijsu.2009.09.014Crossref PubMed Scopus (35) Google Scholar, 3Gurvits G.E. Shapsis A. Lau N. Gualtieri N. Robilotti J.G. Acute esophageal necrosis: a rare syndrome.J Gastroenterol. 2007 Jan; 42 ([Epub 2007 Feb 16]): 29-38Crossref PubMed Scopus (155) Google Scholar]. Reported mortality rate of 38% is probably overestimated because occurring in patients with acute and severe life-threatening failure. Mucosal healing is observed in the most of cases but stricture can occurred and is reported in less than 10% of cases, accessible to endoscopic dilatation [[2]Day A. Sayegh M. Acute oesophageal necrosis: a case report and review of the literature.Int J Surg. 2010; 8 ([Epub 2009 Oct 1]): 6-14https://doi.org/10.1016/j.ijsu.2009.09.014Crossref PubMed Scopus (35) Google Scholar].

Impact of etiology on course and outcomes of severe acute pancreatitis

Background and objectiveSince the influence of etiological factors on the course and outcomes of acute pancreatitis (AP) is not fully understood yet, the aim of the study was to compare the outcomes of alcoholic and biliary severe acute pancreatitis (SAP). Materials and methodsWe investigated 81 patients with alcoholic and biliary SAP. Demographic data, etiologic factors, severity scores, intra-abdominal pressure, imaging studies, interventions, and treatment outcomes were prospectively entered into specially maintained database and subsequently analyzed. ResultsNo statistically significant difference was observed in the prevalence of SAP in biliary and alcoholic AP groups (P=0.429). Although, in the biliary SAP group patients were predominantly elderly women (P=0.003), the total in-hospital stay was longer in alcoholic SAP patients (P=0.021). The abdominal compartment syndrome developed more frequently (P=0.041) and necrosectomy was more frequently performed in alcoholic SAP group (not statistically significant). Although not statistically significant, a lower mortality rate among biliary SAP patients (25.0% vs. 13.5%) was observed. ConclusionsWe defined a trend toward decreased incidence of infected necrosis in larger volume (≥30%) pancreatic necrosis, absence of abdominal compartment syndrome, lower rate of necrosectomies, shorter in-hospital stay, and an insignificantly reduced mortality rate in biliary SAP patients, indicating more favorable course of biliary SAP.

Alcoholic severe acute pancreatitis with positive culture of pancreatic juice treated by nasopancreatic drainage

BackgroundSevere acute pancreatitis (SAP) is a serious disease associated with alcoholism and has a high mortality rate. Effective treatments have not been established. MethodsA 58-year-old man was admitted due to alcoholic SAP. Endoscopic retrograde cholangiopancreatography revealed pancreatic calculi at the pancreas head and a stricture in the pancreatic duct from the pancreas head to the body. Endoscopically, nasopancreatic drainage (NPD) was placed through the minor papilla to the pancreas tail beyond the stricture. ResultsPancreatic juice culture was positive for Streptococcus and Enterobacter. The day after NPD, upper abdominal pain was relieved. After changing NPD to a pancreatic stent, the patient was discharged on day 21 post-NPD. ConclusionAlcoholic SAP may reflect aggravation of chronic pancreatitis. The possibility of acute bacterial inflammation should be considered in all cases of chronic alcoholic pancreatitis who present with severe features of inflammation, even in the early stages of an attack. Treatment of this subset of cases by drainage could be of great importance and NPD may be the preferred method.

超高齢女性のアルコール性重症急性膵炎の1例

症例は99歳，女性．2010年11月中旬，心窩部痛，吐気・嘔吐のため当科を受診した．血清アミラーゼ1,553IU/lと高値．CT所見と併せ，急性膵炎と診断した．膵体尾部実質造影不良と腎下極以遠までの広範な炎症波及を認め，厚労省重症度判定基準 造影CT Grade 3の重症膵炎と判定した．日本酒2～3合，毎日，35年間の飲酒歴があり，成因はアルコール性と考えられた．心不全が増悪して一時重篤な状態に陥ったが，徐々に病態が改善し，最終的には，膵炎に伴う重篤な後遺症を残すことなく第137病日に退院した（退院時年齢100歳）．我が国において飲酒習慣を有する高齢女性は少なく，高齢女性のアルコール性膵炎は稀である．本例は，超高齢女性に発症したアルコールが成因と考えられる重症急性膵炎であり，極めて稀な症例と考えられた．高齢者の急性膵炎では，重症化，既往合併症の増悪や廃用症候群の続発に特に留意が必要である．

Serum Proinflammatory Cytokine Levels and White Blood Cell Differential Count in Patients with Different Degrees of Severity of Acute Alcoholic Pancreatitis

Several studies suggest that cytokines and neutrophils play an important role in the pathogenesis of acute pancreatitis (AP). The AIM OF THE STUDY was to assess the systemic release of proinflammatory cytokines and WBC (white blood cells) count with differential in patients with acute alcoholic pancreatitis (AAP) and to characterize the differences between patients with mild and severe forms of the disease. Thirty-five patients with the mild form of acute alcoholic pancreatitis (MAAP) were compared to 11 patients with severe acute alcoholic pancreatitis (SAAP). Serum levels of IL-6, IL-8, IL-12p40 and WBC differential count were measured every second day during the first week after admission. During the course of the study, the average level of IL-6 was significantly (p<0.05) higher in patients with SAAP than in patients with the mild form of the disease (MAAP). Serum levels of IL-8 and IL-12p40 on admission were higher in patients with SAAP than in patients with MAAP but the difference was not statistically significant. Of all the types of WBCs, neutrophils were significantly (p<0.05) elevated the entire time in SAAP patients when compared to patients with MAAP on 5th and 7th day from admission to hospital. Patients with SAAP had significantly higher proinflammatory cytokine IL-6 levels and neutrophil counts than patients with MAAP. The results suggest that proliferation and overstimulation of this subset of leukocytes might contribute to the development of the systemic inflammatory response in patients with SAAP.

Long-Term Prognosis of Acute Pancreatitis in Japan

This study was undertaken to evaluate the long-term prognosis of acute pancreatitis (AP) in Japan and to identify factors that predict major complications. In 1987, 2533 patients with moderate or severe acute pancreatitis were registered in a national survey in Japan. Follow-up studies were done in 2000 and in 2004 to evaluate recurrence of acute pancreatitis, transition to chronic pancreatitis, development of diabetes mellitus, and mortality. The relationship between incidence of complications and alcohol consumption during follow-up period was also analyzed. Valid replies were obtained from 714 cases in 2000 and 450 cases in 2004. Recurrence of acute pancreatitis occurred in 145 cases, and the recurrence rate was significantly higher in alcoholic pancreatitis compared with other etiologies. A transition to chronic pancreatitis occurred frequently in alcoholic pancreatitis and inversely correlated with existence of pancreatic necrosis in the initial disease. Complication with diabetes mellitus and the transition to chronic pancreatitis strongly correlated with persistent alcohol intake during follow-up period. During the follow-up period, 199 patients died, and 43 died of malignant disease. Recurrence of acute pancreatitis and a transition to chronic pancreatitis frequently occurred in alcoholic pancreatitis. Transition to chronic pancreatitis was inversely correlated with the existence of pancreatic necrosis at the initial presentation. Mortality as a result of malignant disease was not excessive in the patients with history of acute pancreatitis.

Absceso hepático y fístula biliar como complicaciones locales de una pancreatitis aguda: abordaje y tratamiento

Acute pancreatitis is frequently associated with the development of local complications: collections, necrosis, pseudocysts and abdominal abscesses. Although the development of liver abscesses has been linked to bile duct obstruction or abdominal surgery in patients with chronic pancreatitis, there are few descriptions of liver abscesses associated with an episode of acute pancreatitis. We report the case of a 45-year-old man with a first episode of severe acute alcoholic pancreatitis, complicated with thrombosis of the right portal branch, liver abscess and intrahepatic biliary fistula. The approach and treatment are described.

Long-term outcome of severe acute pancreatitis

This study was undertaken to evaluate the post-discharge outcome of severe acute pancreatitis (SAP) and to clarify the prognostic factors for poor outcome. In 45 patients, recurrence of acute pancreatitis (AP), transition to chronic pancreatitis (CP), and development of diabetes mellitus (DM) were evaluated. Relationships of the outcome with the findings on admission and the presence/absence of alcohol intake were analyzed. The mean follow-up period was 56+/-6 months. Recurrence of AP was noted in 19% of the patients. The recurrence rate was higher in patients with necrotizing pancreatitis than in those without this feature. C-reactive protein and white blood cell (WBC) count were higher in patients with recurrence of AP. Transition to CP was noted in 22% of patients. The transition rate was higher in those with alcoholic SAP than in those with biliary SAP. In patients with transition to CP, the WBC count, hematocrit, Ranson score, and Japanese severity score were higher, and base excess (BE) was lower, compared with these features in patients without this transition. Development of DM was noted in 39% of patients. Blood glucose and BE were higher in patients who developed DM than in those who did not. The degree of inflammation and pancreatic necrosis found on admission for SAP may be related to the recurrence of AP. Alcoholic SAP in which the disease is very severe may contribute to the transition to CP. Patients with impaired glucose tolerance readily develop DM after SAP.

C difficile Enteritis in Ileostomy Patients: Report of Three Cases and Review of the Literature

C. difficile (CD) is the most common cause of nosocomial infectious diarrhea and is generally considered a colonic pathogen. CD small bowel enteritis (CDSBE) has only rarely been reported. We describe the clinical course and treatment of 3 ileostomy patients with diarrhea due to CD. Case #1: 48 YOM s/p colectomy and ileostomy for Crohn's disease 2 yrs previously presented with fever, nausea, vomiting, abdominal pain, increased ileostomy output, and marked dehydration. Antibiotics had been administered 3 months previously. Ileostomy CD toxin was positive by ELISA. He responded to a standard course oral metronidazole and vancomycin with resolution of symptoms and negative repeat CD toxin after treatment. Case #2: 72 YOM s/p colectomy and ileostomy for ulcerative colitis 24 yrs earlier presented with a low-grade fever and non-bloody diarrhea of 1-month duration. There was no antecedent antibiotic use. Ileostomy CD toxin was positive by ELISA. He was initially treated with metronidazole, which was switched to oral vancomycin. He responded to 2 weeks of vancomycin, but relapsed following discontinuation and received a 1-month course of vancomycin with clearance of the toxin. Case #3: 39 YOM with severe acute alcoholic pancreatitis required a total abdominal colectomy and ileostomy for colonic ischemia. He required multiple courses of antibiotics and subsequently developed a high ileostomy output. Ileostomy fluid CD toxin was positive and he responded to a standard course oral metronidazole and vancomycin Discussion: CDSBE has been reported in 20 patients in the literature, but only previously in ten ileostomy patients, most of whom were detected in the early post-operative period ( < 90 days). In only 3 cases in the literature was CDSBE diagnosed > 90 d following surgery in ileostomy patients. We report 2 more such cases, and a third in the early post-operative period. Most patients have a history of antibiotic use and present with increased ileostomy output. Most respond to standard therapies (oral metronidazole or oral vancomycin). Relapses may occur. Conclusion: C. Difficile enteritis is a potential cause of high ileostomy output and should be in the differential diagnosis. Treatment with oral metronidazole or vancomycin is generally effective.

Elevation of plasma tissue factor levels in patients with severe acute pancreatitis

Coagulative disorders are known to occur in severe acute pancreatitis (SAP), and they are related to its severity and organ dysfunctions. Tissue factor (TF) is a transmembrane glycoprotein that activates the extrinsic pathway of the blood coagulation cascade. Plasma TF levels increase in patients with sepsis and acute coronary syndrome. However, plasma TF levels in SAP have not yet been reported. We measured plasma TF antigen levels by enzyme-linked immunosorbent assay in 36 patients with acute pancreatitis at the time of admission. The relationships between their plasma TF levels and various factors (severity, etiology, pancreatic necrosis, organ dysfunction, and prognosis) were analyzed. The utility of plasma TF as a clinical marker was evaluated. Plasma TF levels significantly increased in patients with SAP compared with healthy volunteers and drinkers, respectively. Plasma TF level in alcoholic SAP with pancreatic necrosis was significantly higher than that in alcoholic SAP without pancreatic necrosis or that in nonalcoholic SAP with pancreatic necrosis. The incidence of an abnormally high level of plasma TF was 63.6% in alcoholic SAP with pancreatic necrosis. The area under the ROC curve of plasma TF for detection of pancreatic necrosis in alcoholic SAP was 0.773 and was superior to those of Japanese severity score and lactate dehydrogenase. Plasma TF levels were elevated in patients with SAP, particularly in those with alcoholic SAP with pancreatic necrosis, suggesting that TF may be closely related to the development of pancreatic necrosis in alcoholic SAP and that the plasma TF level may be a useful marker for it.

The canine model of severe acute alcoholic pancreatitis

The canine model of severe acute alcoholic pancreatitis

Cimetidine in the treatment of acute alcoholic pancreatitis: A randomized, double-blind study

A double-blind study was made of the comparative effectiveness of cimetidine in the treatment of acute alcoholic pancreatitis. The study group was composed of 27 patients with acute episodes of alcoholic pancreatitis of mild to moderate severity. The patients were randomized into 2 groups, either receiving cimetidine, 300 mg four times daily or a placebo. Both groups were given intravenous fluids and meperidine hydrochloride (Demerol) as needed. There were no significant differences between the 2 groups as measured by a variety of clinical and laboratory parameters. The mean value of the daily serum amylase in the placebo group declined steadily to normal; hyperamylasemia in this group persisted for 52 ± 11 hr (mean ± SE). By contrast, serum amylase in the cimetidine group peaked at 24 hr after the start of treatment and remained abnormal slightly longer; the duration of hyperamylasemia in the group was 69 ± 10 hr. It is concluded that: (1) cimetidine is not superior to a placebo in the management of mild to moderately severe acute alcoholic pancreatitis and (2) serum amylase activity in patients with acute alcoholic pancreatitis given cimetidine tends to be greater and hyperamylasemia is of somewhat longer duration than in those treated with a placebo.

Cimetidine in the Treatment of Acute Alcoholic Pancreatitis

Abstract A double-blind study was made of the comparative effectiveness of cimetidine in the treatment of acute alcoholic pancreatitis. The study group was composed of 27 patients with acute episodes of alcoholic pancreatitis of mild to moderate severity. The patients were randomized into 2 groups, either receiving cimetidine, 300 mg four times daily or a placebo. Both groups were given intravenous fluids and meperidine hydrochloride (Demerol) as needed. There were no significant differences between the 2 groups as measured by a variety of clinical and laboratory parameters. The mean value of the daily serum amylase in the placebo group declined steadily to normal; hyperamylasemia in this group persisted for 52 ± 11 hr (mean ± SE). By contrast, serum amylase in the cimetidine group peaked at 24 hr after the start of treatment and remained abnormal slightly longer; the duration of hyperamylasemia in the group was 69 ± 10 hr. It is concluded that: (1) cimetidine is not superior to a placebo in the management of mild to moderately severe acute alcoholic pancreatitis and (2) serum amylase activity in patients with acute alcoholic pancreatitis given cimetidine tends to be greater and hyperamylasemia is of somewhat longer duration than in those treated with a placebo.

Nasogastric Suction in the Treatment of Alcoholic Pancreatitis

Twenty-nine patients with mild to moderately severe acute alcoholic pancreatitis were randomly allocated to treatment with or without nasogastric suction. Antibiotics, anticholinergics, and antacids were not used. No significant differences were found between the two groups in duration of the following: abdominal pain, abdominal tenderness, nausea, narcotic requirement, fever, and elevated serum and urine amylase levels. The data suggested that even though a larger proportion of patients treated with suction became pain-free within the first two days of treatment, treatment without suction was associated with earlier return of normal bowel sounds and smaller risk of prolonged hyperamylasemia. Because nasogastric suction provided no clear-cut advantages in this admittedly small group, it might be considered elective rather than mandatory in the treatment of mild to moderately severe acute alcoholic pancreatitis. (<i>JAMA</i>229:51-52, 1974)