Acute pancreatitis (AP) is an acute inflammation of the pancreas caused by the activation of digestive enzymes in the pancreatic tissue. The main causes of AP are cholelithiasis and alcohol abuse; less commonly, it can be caused by drugs, with a prevalence of up to 5%. Causal associations between drugs and pancreatitis are largely based on case reports or case series with limited evidence. We reviewed the available data on drug-induced AP, focusing on antimicrobial drugs and antivirals, and discussed the current evidence in relation to the classification systems available in the literature. We found 51 suspected associations between antimicrobial and antiviral drugs and AP. The drugs with the most evidence of correlation are didanosine, protease inhibitors, and metronidazole. In addition, other drugs have been described in case reports demonstrating positive rechallenge. However, there are major differences between the various classifications available, where the same drug being assigned to different probability classes. It is likely that the presence in multiple case reports of an association between acute pancreatitis and a drug should serve as a basis for conducting prospective randomized controlled trials to improve the quality of the evidence.

With over 100000 hospital admissions per annum, acute pancreatitis remains the leading gastrointestinal cause of hospitalization in the United States and has far-reaching impact well beyond. It has become increasingly recognized that drug-induced pancreatitis (DIP), despite accounting for less than 3% of all cases, represents an important and growing though often inconspicuous cause of acute pancreatitis. Nevertheless, knowledge of DIP is often curtailed by the limited availability of evidence needed to implicate given agents, especially for non-prescription medications. Indeed, the majority of available data is derived from case reports, case series, or case control studies. Furthermore, the mechanism of injury and causality for many of these drugs remain elusive as a definitive correlation is generally not established (< 10% of cases). Several classification systems have been proposed, but no single system has been widely adopted, and periodic updates are required in light of ongoing pharmacologic expansion. Moreover, infrequently prescribed medications or those available over-the-counter (including herbal and other alternative remedies) are often overlooked as a potential culprit of acute pancreatitis. Herein, we review the ever-increasing diversity of DIP and the potential mechanisms of injury with the goal of raising awareness regarding the nature and magnitude of this entity. We believe this manuscript will aid in increasing both primary and secondary prevention of DIP, thus ultimately facilitating more expedient diagnosis and a decrease in DIP-related morbidity.

A current assessment of case reports of possible drug-induced pancreatitis is needed. We systematically reviewed the case report literature to identify drugs with potential associations with acute pancreatitis and the burden of evidence supporting these associations.

A protocol was developed a priori (PROSPERO CRD42017060473). We searched MEDLINE, Embase, the Cochrane Library, and additional sources to identify cases of drug-induced pancreatitis that met accepted diagnostic criteria of acute pancreatitis. Cases caused by multiple drugs or combination therapy were excluded. Established systematic review methods were used for screening and data extraction. A classification system for associated drugs was developed a priori based upon the number of cases, re-challenge, exclusion of non-drug causes of acute pancreatitis, and consistency of latency.

Seven-hundred and thirteen cases of potential drug-induced pancreatitis were identified, implicating 213 unique drugs. The evidence base was poor: exclusion of non-drug causes of acute pancreatitis was incomplete or poorly reported in all cases, 47% had at least one underlying condition predisposing to acute pancreatitis, and causality assessment was not conducted in 81%. Forty-five drugs (21%) were classified as having the highest level of evidence regarding their association with acute pancreatitis; causality was deemed to be probable or definite for 19 of these drugs (42%). Fifty-seven drugs (27%) had the lowest level of evidence regarding an association with acute pancreatitis, being implicated in single case reports, without exclusion of other causes of acute pancreatitis.

Much of the case report evidence upon which drug-induced pancreatitis associations are based is tenuous. A greater emphasis on exclusion of all non-drug causes of acute pancreatitis and on quality reporting would improve the evidence base. It should be recognized that reviews of case reports, are valuable scoping tools but have limited strength to establish drug-induced pancreatitis associations.

CRD42017060473.

Drug-induced acute pancreatitis (DIAP) is a rare entity that is often challenging for clinicians. The aim of our study was to provide updated DIAP classes considering the updated definition of acute pancreatitis (AP) and in light of new medications and new case reports. A MEDLINE search (1950-2018) of the English language literature was performed looking for all adult (≥17 years old) human case reports with medication/drug induced as the cause of AP. The included case reports were required to provide the name of the drug, and diagnosis of AP must have been strictly established based on the revised Atlanta Classification criteria. A total of 183 medications were found to be implicated in 577 DIAP cases. A total of 78 cases were excluded because of minimal details or lack of definite diagnosis of AP. Drug-induced AP is rare, and most drugs cause mild DIAP. Only 2 drugs are well described in the literature to explain causation rather than association (azathioprine and didanosine). Larger case-control studies and a formal standardized DIAP reporting system are essential to study the true potential of the DIAP-implicated drugs described in this review.

Acute pancreatitis is a frequent reason for patient presentation to the emergency department (ED) and the most common gastrointestinal disease resulting in admission. Emergency clinicians are often responsible for the diagnosis and initial management of acute pancreatitis.

This review article provides emergency clinicians with a focused overview of the diagnosis and management of pancreatitis.

Pancreatitis is an inflammatory process within the pancreas. While the disease is often mild, severe forms can have a mortality rate of up to 30%. The diagnosis of pancreatitis requires two of the following three criteria: epigastric abdominal pain, an elevated lipase, and imaging findings of pancreatic inflammation. The most common etiologies include gallbladder disease and alcohol use. After the diagnosis has been made, it is important to identify underlying etiologies requiring specific intervention, as well as obtain a right upper quadrant ultrasound. The initial management of choice is fluid resuscitation and pain control. Recent data have suggested that more cautious fluid resuscitation in the first 24 h might be more appropriate for some patients. Intravenous opiates are generally safe if used judiciously. Appropriate disposition is a multifactorial decision, which can be facilitated by using Ranson criteria or the Bedside Index of Severity in Acute Pancreatitis score. Complications, though rare, can be severe.

Pancreatitis is a potentially deadly disease that commonly presents to most emergency departments. It is important for clinicians to be aware of the current evidence regarding the diagnosis, treatment, and disposition of these patients.

A 32-year-old man presented with epigastric pain. He had a previous episode of acute pancreatitis of undetermined cause 2 years earlier. The patient had taken trimethoprim (80 mg) and sulfamethoxazole (400 mg) twice daily because of acute urethritis 3 days prior to admission. No definite cause of acute pancreatitis could be identified on baseline studies. A thorough history-taking revealed that the patient had an episode of acute pancreatitis while taking trimethoprim (80 mg) and sulfamethoxazole (400 mg) twice daily for 2 weeks for prostatitis prior to the previous admission. Therefore, a cause-and-effect relationship between trimethoprim-sulfamethoxazole (TMP-SMX) and repeated episodes of pancreatitis was highly suggested. The patient was presumably diagnosed as TMP-SMX-induced pancreatitis. The final diagnosis was TMP-SMX-induced pancreatitis. Since drugs are rare causes of acute pancreatitis and the diagnosis of drug-induced pancreatitis is difficult to establish, we report this interesting case along with a review of medical literature.

To assess the incidence of and risk factors for acute pancreatitis in HIV-infected patients in the contemporary highly active antiretroviral therapy (HAART) era, we evaluated all cases of acute pancreatitis requiring hospitalization between 1996 and 2006 in patients followed at Johns Hopkins Hospital's HIV clinic. A nested, case-control analysis was employed for initial episodes of acute pancreatitis, and conditional logistic regression was used to assess risk factors. Of 5970 patients followed for 23,460 person-years (PYs), there were 85 episodes of acute pancreatitis (incidence: 3.6 events/1000 PYs). The incidence of pancreatitis from 1996 to 2000 was 2.6 events/1000 PYs; the incidence from 2001 to 2006 was 5.1 events/1000 PYs (p = 0.0014, comparing rates in two time periods). In multivariate regression, factors associated with pancreatitis included female gender (adjusted odds ratio [AOR] 2.96 [1.69, 5.19]; p < 0.001); stavudine use (AOR 2.19 [1.16, 4.15]; p = 0.016); aerosolized pentamidine use (OR 6.27; [1.42, 27.63]; p = 0.015); and CD4 count less than 50 cells/mm(3) (AOR 10.47 [3.33, 32.90]; p < 0.001). Race/ethnicity, HIV risk factor, HIV-1 RNA, and newer non-nucleoside reverse transcriptase inhibitors (NNRTI)- and protease inhibitor (PI)-based HAART regimens were not associated with an increased risk of pancreatitis after adjustment for the above factors. Pancreatitis remains a significant cause of morbidity in the HIV population in the HAART era. Acute pancreatitis is associated with female gender, severe immunosuppression, and stavudine and aerosolized pentamidine usage. Of note, newer antiretrovirals, particularly atazanavir, lopinivir/ritonavir, tenofovir, abacavir, and efavirenz, were not associated with an increased risk of pancreatitis.

The diagnosis of drug-induced acute pancreatitis often is difficult to establish. Although some medications have been shown to cause acute pancreatitis with a large body of evidence, including rechallenge, some medications have been attributed as a cause of acute pancreatitis merely by a single published case report in which the investigators found no other cause. In addition, some medications reported to have caused acute pancreatitis have obvious patterns of presentation, including the time from initiation to the development of disease (latency). There also appear to be patterns in the severity of disease. After reviewing the literature, we have classified drugs that have been reported to cause acute pancreatitis based on the published weight of evidence for each agent and the pattern of clinical presentation. Based on our analysis of the level of evidence, 4 classes of drugs could be identified. Class I drugs include medications in which at least 1 case report described a recurrence of acute pancreatitis with a rechallenge with the drug. Class II drugs include drugs in which there is a consistent latency in 75% or more of the reported cases. Class III drugs include drugs that had 2 or more case reports published, but neither a rechallenge nor a consistent latency period. Class IV drugs were similar to class III drugs, but only 1 case report had been published. Our analysis allows an evidence-based approach when suspecting a drug as causing acute pancreatitis.

Many frequently prescribed drugs are suspected to cause acute pancreatitis (AP). The goal of this paper is to bring to light the often occult but real problem of drug-induced pancreatitis (DIP).

We searched the National Library of Medicine/Pubmed for reported cases of DIP from 1966 to April 30, 2004. Medications implicated in AP are classified based on the strength of evidence into one of three classes of drugs associated with pancreatitis. We reviewed the top 100 prescription medications in the United States for their association with AP.

Class I medications (medications implicated in greater than 20 reported cases of acute pancreatitis with at least one documented case following reexposure): didanosine, asparaginase, azathioprine, valproic acid, pentavalent antimonials, pentamidine, mercaptopurine, mesalamine, estrogen preparations, opiates, tetracycline, cytarabine, steroids, trimethoprim/sulfamethoxazole, sulfasalazine, furosemide, and sulindac. Class II medications (medications implicated in more than 10 cases of acute pancreatitis): rifampin, lamivudine, octreotide, carbamazepine, acetaminophen, phenformin, interferon alfa-2b, enalapril, hydrochlorothiazide, cisplatin, erythromycin, and cyclopenthiazide. Class III medications (all medications reported to be associated with pancreatitis). Of the top 100 most frequently prescribed medications in the United States, 44 have been implicated in AP, 14 of them fall into either Class I or II of medications associated with AP.

Among adverse drug reactions, pancreatitis is often-ignored because of the difficulty in implicating a drug as its cause. The physician should have a high index of suspicion for DIP, especially in specific subpopulations such as geriatric patients who may be on multiple medications, HIV+ patients, cancer patients, and patients receiving immunomodulating agents.

Acute pancreatitis has multiple causes, an unpredictable course, and myriad complications. The diagnosis relies on a combination of history, physical examination, serologic markers, and radiologic findings. The mainstay of therapy includes aggressive hydration, maintenance of NPO, and adequate analgesia with narcotics. Antibiotic and nutritional support with total parenteral nutrition should be used when appropriate.

Acute pancreatitis is a clinical condition that develops when active pancreatic inflammation is induced by stimuli noxious to the pancreas. Patients infected with human immunodeficiency virus (HIV) often have histologic abnormalities of the pancreas, and acute pancreatitis is much more common in HIV-infected patients than in the general population. This article reviews the epidemiology and etiology of acute pancreatitis in HIV-infected patients. The clinical presentation and treatment of acute pancreatitis in HIV-infected patients are also reviewed.

We sought to study asymptomatic pancreatic enzyme abnormalities in patients with human immunodeficiency virus (HIV) infection.

Serial serum amylase and lipase determinations were performed in ambulatory HIV-seropositive patients in whom pancreatitis was not suspected.

Eighty-six patients were enrolled in the study. Fifty-two patients (60%) were found to have abnormal amylase or lipase values on at least one determination. Only 12 (14% of all patients) had a more than twofold elevation of pancreatic enzymes. Seven patients had transient elevations of lipase within 3 months after the initiation of antiretroviral therapy. Independent factors associated with abnormal pancreatic enzymes were: positive serology for chronic hepatitis B or C, history of intravenous cotrimoxazole administration for the treatment of Pneumocystis carinii pneumonia, stage B of HIV disease, and HIV risk factors other than male homosexuality (mainly intravenous drug use). None of the patients developed clinical pancreatitis.

Asymptomatic mild to moderate elevations of amylase or lipase are common in HIV-positive patients, and are usually associated with positive serology for chronic hepatitis B or C, and medications, especially antiretrovirals and intravenous cotrimoxazole.

A 34-yr-old woman developed simultaneous pancreatitis and hepatitis following exposure to trimethoprim-sulfamethoxazole (TMP/SMX). The episode occurred 4 yr after a previous episode of hepatitis associated with TMP/SMX. This patient represents the second case of concurrent TMP/SMX-induced pancreatitis and hepatitis reported in the literature. However, it is the first in which the adverse reaction was documented following an inadvertent rechallenge with the drug.

Although autopsy studies reveal significant pancreatic lesions in about 10% of AIDS patients, pancreatic lesions infrequently produce symptoms and are rarely recognized premortem. Patients with AIDS can develop pancreatic disease from causes not related to AIDS or AIDS-specific lesions. AIDS-specific causes include opportunistic infection, AIDS-associated neoplasia, and medications used to treat complications of AIDS. Pancreatic involvement is usually part of a widely disseminated tumor and rarely produces clinical symptoms.

Few data exist about the incidence of drug-induced pancreatitis in the general population. 20 cases of drug-related pancreatitis were reported in Switzerland over a period of 12 years. The proportion of cases of pancreatitis caused by drugs is estimated to be around 2% in the general population, with much higher proportions in specific subpopulations, such as children and patients who are HIV positive. The literature about drug-induced pancreatitis consists mainly of anecdotal case reports. Clear evidence of a definite association with pancreatitis, by means of rechallenge tests, or consistent case reports, supported by animal experiments or data on the incidence of acute pancreatitis in drug trials exists for didanosine, valproic acid (sodium valproate), aminosalicylates, estrogen, calcium, anticholinesterases and sodium stibogluconate. An association with drug-induced pancreatitis is likely but not definitely proven for thiazide diuretics, pentamidine, ACE inhibitors, asparaginase, vinca alkaloids, some nonsteroidal anti-inflammatory drugs and clozapine. Pancreatitis is possibly caused by azathioprine, furosemide (frusemide), tetracycline, metronidazole, isoniazid, rifampicin (rifampin), sulphonamides, cyclosporin and some antineoplastic drugs. Many drugs have been reported to be associated with acute pancreatitis. However, lack of rechallenge evidence, consistent statistical data, or evidence from experimental studies on a possible mechanism prohibit definitive conclusions about most of them. The high incidence of concurrent illnesses known to induce acute pancreatitis, makes a trigger role or co-factor role for the drug seem most likely.

Drugs are a relatively uncommon cause of pancreatitis in adult patients, but should be considered when other reasonable causes of pancreatitis are not present. A wide variety of drugs have been reported to cause pancreatitis. Drug-induced pancreatitis is almost always acute and may be mild to fatal in severity. Definite proof that a drug causes pancreatitis requires that pancreatitis develops during treatment with the drug, that other likely causes of pancreatitis are not present, that pancreatitis resolves upon discontinuing the drug, and that pancreatitis usually recurs upon readministration of the drug. For ethical reasons, rechallenge with the suspect drug can be done only if the drug is necessary to treat a serious condition; thus this highly convincing piece of evidence relating the drug to pancreatitis may not be available. Information about drug-related pancreatitis is often not readily available, particularly for newer drugs. Clinicians should consider obtaining information directly from regulatory agencies and manufacturers as well as the literature.

The pancreas is frequently involved during HIV infection, especially by disseminated infections or neoplasms. These lesions are generally asymptomatic and are discovered at autopsy. However, hypoglycaemia secondary to massive pancreatic infiltration by a tumour or tuberculous necrosis may occur. The most important cause of pancreatic dysfunction in HIV-infected patients is a drug toxic effect (intravenous pentamidine, didanosine, zalcitabine). Hypoglycaemia, which may or may not be followed by diabetes, can develop during intravenous pentamidine therapy. In cases with increased serum amylase and/or lipase levels, potentially toxic drugs must be promptly discontinued to avoid major pancreatic involvement.

The successful management of nocardial brain abscess remains problematic. The authors report 11 cases of nocardial brain abscess treated between 1971 and 1993 and review 120 cases reported since 1950. The clinical findings included focal deficits in 55 patients (42%), nonfocal findings in 36 (27%), and seizures in 39 (30%). Extraneural nocardiae were present in 66% of the cases; pulmonary (38%) and cutaneous/subcutaneous (20%) locations were the most frequent. The abscesses were single in 54% of the patients, multiple in 38%, and of unknown number in 8%. Forty-four of 131 patients (34%) were immunocompromised; since 1975, 18 of 40 immunocompromised patients (45%) were transplant recipients and six (15%) had human immunodeficiency virus. The mortality rate was 24% after initial craniotomy and excision (11/45), 50% after aspiration/drainage (17/34), and 30% after nonoperative therapy (7/23); 29 cases (22%) were diagnosed at autopsy. The mortality rate was 33% in patients with single abscesses and 66% in those with multiple abscesses (P < 0.0003). There was no difference in the mortality rates of immunocompromised and nonimmunocompromised patients treated before computed tomography (CT) was available; since the advent of CT, however, the mortality rate has been significantly higher in immunocompromised patients (55% vs. 20%, P < 0.05). Although the mortality rate for nocardial brain abscesses has dropped almost 50% since the advent of CT, it has remained virtually unchanged in immunocompromised patients and is three times higher than that of other bacterial brain abscesses (30% vs. 10%). The authors recommend image-directed stereotactic aspiration for diagnosis; however, craniotomy and total excision are necessary in most cases, because nocardial abscesses are usually multiloculated. Patients with minimal neurological deficits or small abscesses may be treated initially with antibiotics alone. Sulfonamides, alone or in combination with trimethoprim, are most effective and should be continued for at least 1 year. Minocycline, imipenem, or aminoglycoside in combination with a third-generation cephalosporin may be used with reasonably good success as second-line agents in cases of allergy or nonresponsiveness to sulfa agents.

Pancreatic damage has been well described in HIV+ patients and can occur both for therapy and opportunistic infections, but its prevalence is not clear. The aim of our study was to evaluate the prevalence of pancreatic damage in a cohort of HIV+ hemophiliacs together with the clinical and prognostic value of the diagnostic methods commonly used. We studied 75 HIV+ patients and 26 HIV- as a control group: they were evaluated by biochemical tests, indirect pancreatic functional tests, abdominal ultrasound (US) and computed tomography (CT). No differences were observed between HIV+ and HIV- in elevation of pancreatic enzymes. Eleven patients had slight CT alterations and none had abnormal US. In HIV+ there was no relationship between enzyme elevation and CDC group, CD4+ cell count or therapy. In conclusion, pancreatic disorders have a very low prevalence in HIV+ hemophiliacs and biochemical alterations we found had a doubtful clinical significance. Lipase and isoamylase are the more reliable tests and lipase, being the cheapest and easiest to perform, has to be considered as the first test of choice for monitoring pancreatic damage in HIV+ patients.

To report a case of probable pentamidine-induced acute pancreatitis.

A patient was hospitalized because of fever, dyspnea, and productive cough. Chest X-ray revealed diffuse alveolar infiltrates, and the examination of bronchoalveolar lavage demonstrated the presence of Pneumocystis carinii. Intravenous cotrimoxazole was administered but the patient's condition did not improve. As secondary leukopenia appeared, the treatment was changed to pentamidine isethionate 4 mg/kg/d i.v. On day 5 of this new therapy, the patient experienced abdominal pain, and both blood and urine amylase concentrations raised to 330 U/L and 3960 U/L, respectively. The patient died 48 hours later, and signs of acute pancreatitis were observed in necropsy.

With reference to a classical method for estimating the probability of adverse drug reactions, a probable relationship between pentamidine therapy and acute pancreatitis was found in this patient. Furthermore, no alternative causes of pancreatitis were present.

It is likely that pentamidine administration in our patient resulted in an acute episode of pancreatitis. Serum and urine amylase concentrations should be monitored in patients receiving this drug.

Serum concentrations of trypsin and elastase I were determined in 109 HIV Ab-positive patients (52 asymptomatic HIV-infected patients, 25 with lymphadenopathy syndrome, and 32 with acquired immunodeficiency syndrome) to assess the prevalence of possible pancreatic damage in these patients. Serum trypsin was abnormally elevated in 46 of the 109 patients (42.2%): 19 of the 52 asymptomatic HIV-infected patients (36.6%), 9 of the 25 with lymphadenopathy syndrome (36%), and 18 of the 32 with acquired immunodeficiency syndrome (56.3%). Serum elastase 1 was elevated in 14 of the 109 HIV Ab-positive patients (12.8%): 3 of the 52 asymptomatic HIV-infected patients (5.8%), 3 of the 25 with lymphadenopathy syndrome (12%), and 8 of the 32 with acquired immunodeficiency syndrome (25%). None of the patients with abnormally high serum pancreatic enzyme concentrations had clinically evident pancreatic disease. There was no statistically significant difference in serum levels of trypsin and elastase I between drug addicts and nonaddicts, between alcoholics and nonalcoholics, or between those with cytomegalovirus infection and those without. A significant inverse relationship was found between serum enzyme concentrations and the number of CD4+ lymphocytes. The results of this study show that high levels of serum trypsin and elastase are present in an elevated percentage of patients with acquired immunodeficiency syndrome, suggesting that the pancreas is frequently damaged in this disease. The finding of abnormally high serum enzyme concentrations not only in patients with AIDS, but also in asymptomatic carriers and in patients with lymphadenopathy syndrome suggests an association between HIV infection and the development of pancreatic lesions.

Two patients without risk factors or a prior history of pancreatitis developed acute pancreatitis soon after initiating pentamidine isethionate therapy for Pneumocystis carinii pneumonia associated with the acquired immunodeficiency syndrome. In both patients the pancreatitis improved following medication cessation. One patient did not redevelop pancreatitis when he subsequently received inhaled pentamidine. Review of the literature revealed five previously reported cases of this drug reaction. Pentamidine-associated pancreatitis appears to develop within three weeks of initiating therapy and after receiving more than 1 g in cumulative dosage. Glucose abnormalities, renal insufficiency, and non-specific abdominal pain may be early warning signs of pentamidine-associated pancreatitis.

Acute pancreatitis has a high morbidity and significant mortality. Among its many causes ethanol is pre-eminent, but many other drugs have also been incriminated. This article begins with a definition of the mechanisms, pathogenesis and clinical features of acute pancreatitis; it then critically reviews the evidence for drugs, excluding ethanol, as being causative. The drugs which have been implicated are considered under 3 headings: definite associations, probable associations and unlikely associations. A brief outline of possible treatment, strategies and prognosis associated with acute pancreatitis concludes the article.

We reviewed the English-language literature pertaining to drug-induced pancreatitis and attempted to determine whether the reported association between each drug and pancreatitis was valid. The following drugs seem to cause pancreatitis: azathioprine, chlorothiazide and hydrochlorothiazide, oestrogens, frusemide, 6-mercaptopurine, methyldopa, sulphonamides, sulindac, tetracycline and valproic acid. Less convincing but suggestive evidence exists for colaspase, chlorthalidone, combination cancer chemotherapy, cimetidine, cisplatin, corticosteroids, cytosine arabinoside, diphenoxylate, ethacrynic acid, iatrogenic hypercalcaemia, methandienone, metronidazole, nitrofurantoin, pentamidine, phenformin, piroxicam and procainamide. In general, pancreatitis is a very rare complication of treatment with these drugs. The pathogenesis of the pancreatitis is usually obscure, but is probably mediated by an immune response. Certain drugs such as oestrogens cause hypertriglyceridaemia, which in turn may lead to pancreatitis.

A young woman who developed acute pancreatitis coincident with Crohn's disease is presented. The pancreatitis was documented by pancreatic hyperamylasemia, elevated urine amylase activity, abdominal sonogram, computed tomography, and laparotomy. A cause-and-effect relationship has not been established, however; no etiology other than the Crohn's disease, which was confined to the ileum and colon, could be identified. Surgical removal of the severely involved ileum led to the resolution of the pancreatitis. A possible relationship between acute pancreatitis and Crohn's disease is proposed, although potential pathophysiologic mechanisms are unknown. The diagnosis of pancreatic involvement in such cases may make an important contribution to therapy.