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Background: Soluble urokinase plasminogen activator receptor (suPAR) is a biomarker associated with inflammatory and certain malignancies. Earlier we have shown that plasma suPAR (P-suPAR) predicts severity of acute alcohol-induced pancreatitis (AAP) on admission. Our aim was to investigate whether P-suPAR levels predict AAP recurrences or mortality during long-term follow-up after first AAP., Methods: Eighty-three patients (median age 47.5, range 25-71 years) suffering their first AAP during 2001-2005 were recruited and followed prospectively for 9 years with a median follow-up time of 7.0 (range 0.3-9.8) years. P-suPAR was measured by enzyme-linked immunosorbent assay (ELISA) from the samples taken at follow-up visits. Survival was registered in November 2014., Results: P-suPAR level on admission or after recovery of the first AAP did not predict the recurrence of AAP. However, higher P-suPAR measured after recovery of first AAP (3.6 vs. 2.9 ng/mL) predicted mortality during follow-up period (hazard ratio 1.48, p = .008). Cut-off value for P-suPAR indicating a higher risk for 10-year mortality resulted a value of ≥3.4 ng/mL. When adjusted for other covariates, P-suPAR above cut-off level retained its statistical significance as an independent factor., Conclusions: P-suPAR level on admission or after recovery of the first AAP does not predict the recurrence of AAP during long-term follow-up. However, P-suPAR ≥3.4 mg/mL measured after recovery from first AAP is associated with an increased risk of 10-year mortality as an independent factor. This can be used to detect patients with highest risk after AAP, in order to focus the preventive healthcare actions., (Copyright © 2018. Published by Elsevier B.V.)

Background: Data on the prevalence of pancreatic dysfunction after an episode of acute pancreatitis are conflicting. Our aim was to evaluate the natural course of endocrine and exocrine pancreatic function in the long-term follow-up after the first episode of acute alcoholic pancreatitis (AAP)., Methods: A total of 77 patients who survived their first episode of AAP between January 2001 and February 2005 were prospectively followed up for a maximum of 13 years. During the follow-up, patients were repeatedly interviewed and monitored for recurrences, new diabetes, and chronic pancreatitis. The pancreatic function was evaluated repeatedly during the follow-up., Results: Of the patients, 35% had ≥1 recurrent acute pancreatitis (RAP) episodes during the follow-up. New pancreatogenic diabetes developed in 19% of the previously nondiabetic patients, but only in patients with RAP (13/26 vs. 0/42; OR=39; 95% CI, 4.6-327.1). In addition, 55% of the patients developed new prediabetes or diabetes, and even this was more frequent in patients with RAP (86% vs. 42%; OR=8.2; 95% CI, 1.2-54.3). Exocrine dysfunction developed in 24% of the patients and was associated with abnormal findings in the endocrine function (P=0.003). Patients with RAP had a higher overall mortality compared with patients without RAP episodes during the follow-up (36% vs. 13%; HR=4.0; 95% CI, 1.4-11.0)., Conclusions: The risk for pancreatic endocrine dysfunction, pancreatogenic diabetes and mortality increases significantly if the patient has recurrent episodes of AAP. The risk of developing pancreatic dysfunction after AAP should be recognized and pancreatic function should be screened routinely during the years after the first episode of AAP.

Objectives: Systemic levels of soluble urokinase-type plasminogen activator receptor (suPAR) are increased in various inflammatory and infectious diseases. We investigated the activation and prognostic value of plasma suPAR (P-suPAR) in patients experiencing their first acute alcohol pancreatitis (AAP)., Methods: From prospectively collected data, we measured P-suPAR concentrations in 104 patients with AAP during hospitalization and again after discharge., Results: According to the revised Atlanta classification, pancreatitis was moderately severe in 29 (28%) and severe in 6 (6%) patients and these severities were combined for further analysis (non-mild AAP, n = 35; 34%). Median P-suPAR levels were significantly higher in patients with AAP during hospitalization than after discharge (4.8 vs 3.1 ng/mL; P < 0.001) and in non-mild compared to mild AAP (6.2 vs 4.2 ng/mL; P < 0.001). When the analysis was made 1 to 4 days after admission (n = 68), the area under the curve was 0.81 (95% confidence interval, 0.70-0.92). P-suPAR was found to be a better prognostic marker in AAP than C-reactive protein, hematocrit, or creatinine., Conclusions: P-suPAR concentrations are elevated in AAP and correlate with the severity of the disease. These results suggest that P-suPAR may have potential to serve as a novel prognostic marker for AAP severity on admission.

Objective: The long-term morphological changes induced by a single episode of alcoholic pancreatitis are not known. Our aim was to study these morphological changes in secretin-stimulated magnetic resonance cholangiopancreatography (S-MRCP) after the first episode of alcohol-associated acute pancreatitis and to evaluate the risk factors and possible protective factors potentially associated with later chronic findings. We have previously reported 2-year follow-up results in pancreatic morphology. This study extends the follow-up to 9 years., Patients and Methods: In this prospective follow-up study, S-MRCP imaging was performed for 44 (41 M, 3 F; mean age, 46 (25-68) years) patients after their first episode of alcohol-associated pancreatitis. Pancreatic morphology was evaluated at 3 months and at 2, 7, and 9 years after hospitalization. Recurrent attacks of pancreatitis were studied and pancreatic function was monitored by laboratory tests. Patients' alcohol consumption was evaluated with questionnaires, laboratory markers, and self-estimated alcohol consumption via interview. Smoking and body mass index were annually recorded., Results: At 3 months, 32 % of the patients had normal findings in S-MRCP, 52 % had acute, and 16 % had chronic changes. At 7 years, S-MRCP was performed on 36 patients with normal findings in 53 %, the rest (47 %) having chronic findings. Pancreatic cyst was present in 36 %, parenchymal changes in 28 %, and atrophy in 28 % of the cases. There were no new changes in the pancreas in the attending patients between 7 and 9 years (18 patients). Of the patients with only acute findings at 3 months, 60 % resolved to normal in 7 years, but the rest (40 %) showed chronic changes later on. The initial attack was mild in 65 %, moderate in 25 %, and severe in 10 % of the patients. Patients with mild first attack had fewer chronic changes at 7 years compared to patients with moderate or moderate and severe together (p = 0.03, p = 0.01). Of the patients in the seventh year of S-MRCP, 22 % had suffered a recurrent episode of acute pancreatitis (mean, 22 (2-60) months) and 11 % had a clinical diagnosis of chronic pancreatitis. At 7 years, 88 % of the patients with recurrences had chronic findings in S-MRCP versus 36 % with nonrecurrent pancreatitis (p = 0.02). Six (17 %) patients abstained from alcohol throughout follow-up (mean, 8.7 (7-9.1) years), but even one of these developed pancreatic atrophy. Out of the non-abstinent patients who did not suffer recurrences, 4/22 (18 %) had developed new findings during at follow-up S-MRCP (NS). In univariate analysis, heavy smoking showed no correlation with increased chronic changes compared to nonsmoking., Conclusions: Morphological pancreatic changes increase with recurrent episodes of acute pancreatitis. Patients with mild first attack have fewer chronic changes in the pancreas in the long term. However, even a single episode of acute alcoholic pancreatitis may induce chronic morphological changes in long-term follow-up.

Aims: To determine the recurrence of pancreatitis and subsequent pancreatic function in patients who stop drinking after the first episode of alcohol-associated pancreatitis., Methods: Of a total of 118 patients suffering from their first alcohol-associated pancreatitis, 18 (all men, age median 47 (27-71) years) met the inclusion criterion for abstinence during follow-up. The criterion for abstinence was alcohol consumption <24 g per 2 months (self-estimated), which is in line with questionnaires eliciting alcohol consumption and dependency (Alcohol Use Disorders Identification Test < 8 and Short Alcohol Dependence Data < 9). Recurrent attacks of acute pancreatitis were studied. Smoking, body mass index and laboratory tests detecting heavy consumption of alcohol were recorded. Blood and faecal tests were studied to assess endocrine and exocrine pancreatic function., Results: During a mean follow-up time of 5.15 (1.83-9.13) years and a total of 92.7 patient-years, there were no recurrent attacks of acute pancreatitis among the 18 abstainers. Two patients had diabetes prior to and one was diagnosed immediately after the first episode of acute pancreatitis. One patient had impaired glucose metabolism at 2 years. Two patients had low insulin secretion in glucagon-C-peptide test, one at 4 years and the other at 5 years. Only one patient (6%) maintained low elastase-1 activity during the abstinence follow-up. Of the 100 non-abstainers, 34% had at least one recurrence during the follow-up., Conclusion: Regardless of the mediator mechanisms of acute alcoholic pancreatitis, abstinence after the first episode protects against recurrent attacks. Pancreatic dysfunction is also rare among abstinent patients.

Aim: To investigate whether enteroviral infection might trigger acute pancreatitis in patients made susceptible due to high alcohol consumption., Methods: Patients with alcohol-induced acute pancreatitis were analyzed for signs of simultaneous or preceding enteroviral infection. We studied the serum samples of 40 patients hospitalized for alcohol-induced acute pancreatitis and 40 controls recruited from an alcohol detoxification center. Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect enterovirus RNA and diagnose acute viremia. Immunoglobulin G (IgG), immunoglobulin A (IgA) and immunoglobulin M (IgM) enteroviral antibodies were measured using enzyme immunoassay to detect subacute and previous infections. The samples were considered positive when the antibody titers were ≥ 15 IU. Furthermore, using RT-PCR, we studied pancreatic biopsy samples obtained during surgery from nine patients with chronic pancreatitis, one patient with acute pancreatitis and ten control patients with pancreatic carcinoma for evidence of persisting enteroviral RNA in the pancreatic tissue., Results: No enterovirus RNA indicating acute viremia was detected by RT-PCR in the serum samples of any patient or control. A high incidence of positive antibody titers was observed in both study groups: IgM antibodies had positive titers in 5/40 (13%) vs 4/40 (10%), P = 0.723; IgG in 15/40 (38%) vs 19/40 (48%), P = 0.366; and IgA in 25/40 (63%) vs 33/40 (83%), P = 0.045, patients and controls, respectively. Ten (25%) patients had severe pancreatitis and two (5%) required treatment in intensive care. The median length of hospitalization was 7 d (range: 3-47 d). The severity of acute pancreatitis or the length of hospitalization was not associated with enteroviral IgM, IgG or IgA antibodies. Five pancreatic biopsy samples tested positive with RT-PCR, three (8%) in the control group and two (5%) in the patient group (P = 0.64)., Conclusion: The rate of enteroviral infection is not increased in patients with alcohol-induced acute pancreatitis when compared to alcoholics with similar high alcohol use.

Background/aims: Hyperlipidemia is one known etiology of acute pancreatitis. Alcohol use is known to induce changes in lipid metabolism and might alter the serum lipid and fatty acid profile. We hypothesized that these changes may explain individual susceptibility of developing acute pancreatitis. We compared lipid and fatty acid profiles of patients with acute alcoholic pancreatitis and alcoholic controls., Methods: 19 patients with their first alcoholic pancreatitis and 20 controls were included. Late follow-up samples were obtained from 16 patients. Serum lipids were analyzed enzymatically and the fatty acid profile using gas chromatography., Results: The concentrations of serum total cholesterol, LDL-cholesterol and HDL-cholesterol were markedly lower in patients than in controls during the acute disease but normalized after follow-up. Patients had statistically significantly lower fatty acid proportions of saturated C14:0, polyunsaturated C18:2, C18:3 and C20:3 of the n-6-series and C18:3 of the n-3-series than controls. In contrast, patients had higher percentages of saturated C16:0 and monounsaturated C18:1n9 fatty acids than controls. Mead acid, C20:3n9, marker of essential fatty acid deficiency, was lower in patients than in controls. C14:0, C20:3n6, C18:3n3 and C20:3n9 remained altered after follow-up., Conclusion: Serum lipid and fatty acid levels were significantly altered during the acute disease and returned toward normal after 18-24 months, suggesting that the changes are secondary to acute pancreatitis. They are unlikely to be the much sought 'trigger factor' of pancreatic necro-inflammation. However, further studies are warranted to fully establish this point., (Copyright © 2012. Published by Elsevier B.V.)

Aims: Between 1970 and 1989 the incidence of pancreatitis increased in Finland in association with increased alcohol consumption. During the1990s there was a temporary decrease in alcohol consumption. We examined the trends in the amount of alcohol consumed in Finland and the incidence of hospital admissions for acute alcoholic pancreatitis and liver cirrhosis., Patients and Methods: The data on hospital admissions and annual alcohol consumption between 1987 and 2007 were obtained from the Finnish National Agency for Welfare and Health., Results: Alcohol consumption increased from 8.2 litres of ethanol per inhabitant per year in 1987 to 10.5 litres in 2007, but during the economic recession in the country there was a temporary decrease in alcohol consumption between 1992 and 1994, with the lowest consumption of 8.0 litres in 1994. The incidence of hospitalizations for acute alcoholic pancreatitis in the whole population increased significantly during the study period among both men (from 57 to 69/100,000/year) and women (from 7 to 12/100,000/year). However, there was a significant decrease in hospitalizations in 1996 and 1997 correlating with alcohol consumption three years earlier. The incidence of hospitalizations due to liver cirrhosis increased in the age groups over 45 years in both genders throughout the study period. A temporary decrease was observed in 1994, when alcohol consumption was at its lowest. Interestingly, there was a trend from pancreatitis to cirrhosis during the last six years, when the hospitalizations for acute pancreatitis decreased, although the hospitalizations for liver cirrhosis increased following increased alcohol consumption. During the study period the female-to-male ratio for liver cirrhosis was twice as high as for acute alcoholic pancreatitis, but the relative portion of females increased by 50% in both diagnoses., Conclusions: In contrast to liver cirrhosis, the hospital admissions for which followed the national alcohol consumption, admissions for acute alcoholic pancreatitis ceased to show a connection with the national alcohol consumption during the past several years.

Background & Aims: In the long term, half of patients with their first alcohol-associated acute pancreatitis (AP) develop acute recurrence, alcohol consumption being the main risk factor. None of the recent national or international guidelines for treatment include recommendations aimed to decrease recurrences, possibly because of a lack of studies. This study investigated whether AP recurrences can be reduced., Methods: One hundred and twenty patients admitted to a university hospital for their first alcohol-associated AP were randomized either to repeated intervention (n = 59) or initial intervention only (n = 61). The patients in the 2 groups did not differ. A registered nurse performed an intervention in both groups before discharge, after which it was repeated in the study group at 6-month intervals at the gastrointestinal outpatient clinic. Acute recurrences during the next 2 years were monitored., Results: There were 9 recurrent AP episodes in 5 patients in the repeated-intervention group compared with 20 episodes (P = .02) in 13 patients (P = .04) in the control group. The recurrence rates were similar during the first 6 months (4 vs 5 episodes), after which the repeated-intervention group had fewer recurrences than the control group (5 vs 15 episodes; P = .02)., Conclusions: The repeated visits at 6-month intervals at the gastrointestinal outpatient clinic, consisting of an intervention against alcohol consumption, appear to be better than the single standardized intervention alone during hospitalization in reducing the development of recurrent AP during a 2-year period.

70% of pancreatitis cases are considered to be induced by alcohol. Half of those fallen ill with alcohol-induced acute pancreatitis will have relapses. A prospective follow-up study showed that the level of dependence on alcohol constitutes the most important risk factor. Continued drinking was shown to be a dose-responsive risk factor for relapse; abstinence provided for a complete protection against renewed pancreatitis. In a randomized study, a semi-annual meeting with a healthcare professional specialized in substance abuse problems significantly reduced new episodes of acute pancreatitis. It is thus possible to at least reduce relapses by intervening in the risk factors.

Background and Aims: The objective of this study was to measure the association of Helicobacter pylori infection with alcoholic acute pancreatitis., Material and Methods: This study comprised of 50 patients with their first alcoholic pancreatitis and 50 alcoholic controls with no history of pancreatitis but similar alcohol use recruited from an alcohol rehabilitation center. Helicobacter infection was measured using Enzygnost EIA IgG-test. Complications and length of hospital stay were also recorded in patients with alcoholic pancreatitis., Results: The seroprevalence of Helicobacter pylori was 10/50 (20%) in the pancreatitis group and 15/50 (30%) in the control group (p = NS). The median length of hospital stay of pancreatitis patients was 7 days, 11 days for those tested positive (range 6-25) and 6 days for those tested negative (range 3-47) for Helicobacter pylori, p = 0.013. As determined with the Atlanta criteria, seropositive patients tended to have more often severe pancreatitis, 4/10 (40%) vs. 6/40 (15%), OR 3.78 (95% CI 0.815-17.52), p = 0.097., Conclusions: This study suggests that Helicobacter pylori infection is not associated clinically significantly with the development of alcoholic pancreatitis. However, Helicobacter pylori infection may be associated with longer hospital stay due to more severe disease, which needs to be studied in a larger series of patients.

Background: Acute alcoholic pancreatitis (AAP) recurs in up to half of the patients, continuous alcohol consumption being an important risk factor. Changes in pancreatic function and morphology after acute pancreatitis have been characterized previously, but their association with later recurrences has not been adequately studied., Patients and Methods: In this prospective follow-up study, the pancreatic function of 54 patients (47 males and 7 females) with a median age of 49 years (range 25-71) and morphology (35 patients) were evaluated. Pancreatic morphology was evaluated by secretin-stimulated magnetic resonance pancreatography (SMRP). Patients were evaluated early (baseline) and at 2 years after the first episode of AAP. In order to evaluate later recurrences, the patients were followed for a median of 47 (range 28-66) months., Results: Of the 46 patients without previous diabetes, 17 patients (37%) developed impaired glucose metabolism during the 2 years following the first AAP. The prevalence of exocrine dysfunction decreased from 39% at baseline to 9% at 2 years. Of the patients with severe pancreatitis (n = 13, 24%), 31% had elevated glycosylated haemoglobin levels compared to 7% in patients with mild pancreatitis [p = 0.05, odds ratio (OR): 5.5, 95% confidence interval (CI): 1.04-29.0]. Twenty percent (7/35) of the patients had changes consistent with chronic pancreatitis on baseline SMRP, which persisted in all cases. Of the 29% patients with acute changes on baseline SMRP, the acute changes resolved in 50% and chronic pancreatitis was detected in the remaining 50% at 2 years. Development of chronic changes did not depend on continued alcohol consumption, as it was also found in 3 patients practising complete abstinence following their first attack of AAP. The presence of a chronic pseudocyst at 2 years predicted pancreatitis when compared to patients lacking pseudocyst formation: 4 (80%) versus 5 (17%) (p = 0.01, OR: 20.0, 95% CI: 1.83-219)., Conclusion: The severity of the first episode of AAP was associated with deteriorated diabetes control, but not with pancreatic exocrine dysfunction at 2 years. The number of patients with chronic changes on SMRP increased independently of alcohol consumption. Chronic pseudocyst formation seen on SMRP 2 years after AAP was significantly associated with recurrence of pancreatitis., ((c) 2009 S. Karger AG, Basel.)

Objective: In an earlier retrospective study we showed that 46% of patients with acute alcoholic pancreatitis had recurrent attacks within 10-20 years, about 30% having a recurrence during the first 3 years. The aim of this prospective follow-up study was to determine the risk factors associated with recurrences., Material and Methods: Sixty-eight patients, (59 M, 9 F, mean age 46 years, range 25-71 years) who survived their first acute alcohol-induced pancreatitis from January 2001 to January 2004 volunteered to participate in the study. The diagnostic criteria for acute pancreatitis were epigastric pain, serum amylase > 3 times the upper normal range, elevated serum C-reactive protein (CRP), and signs of acute pancreatitis in imaging. Other etiologies were excluded. Alcohol consumption and dependency were detected by the Alcohol Use Disorders Identification Test (AUDIT) and the Short Alcohol Dependence Data (SADD), respectively, and by attempting to evaluate recent use in grams of pure alcohol. Social and demographic data of the patients, smoking, body mass index, and the severity of the pancreatitis were recorded. Serum and fecal markers of the endocrine and exocrine function and secretin-stimulated MRCP were studied. The patients were followed for a median 38 (25-61) months for recurrences, and at the 2-year time-point had a follow-up visit to investigate any changes in alcohol consumption., Results: Seventeen (25%) patients had recurrences of acute alcoholic pancreatitis during the follow-up. Pre-illness alcohol consumption, the severity of the pancreatitis, patient's social or demographic data, pancreatic function tests or morphologic changes in MRCP, or smoking did not correlate with recurrence. None of the 13 patients with consistent total abstinence from alcohol at 2 years developed recurrent pancreatitis compared with 17 out of 51 (33%) patients with at least some alcohol consumption (p = 0.02). Use of other sedatives than alcohol before the first attack of pancreatitis was an independent risk factor associated with recurrence (HR = 6.95, 95% CI 2.45-19.72, p < 0.001). A lower reduction in dependency on alcohol (less decreased SADD points) during 2 years was associated with a higher recurrence rate (HR = 0.921/each reduced point, 95% CI 0.872-0.974, p=0.004)., Conclusions: Contrary to chronic pancreatitis, smoking was not found to be a risk factor for recurrent episodes after the first attack of acute alcoholic pancreatitis. Abstinence from alcohol protects against recurrent pancreatitis. Patients who developed recurrent acute pancreatitis had increased dependency on alcohol, demonstrated by the use of other sedatives in addition to alcohol and supported by the less decreased dependency during the follow-up.

Objective: After the first acute alcohol-induced pancreatitis (AAIP) episode 46 % of patients will have a recurrent attack, but the pathophysiology is unclear. The hyperstimulation of the pancreas with cholecystokinin (CCK) induces acute pancreatitis. Alcohol induces temporary stimulation of the pancreas and CCK could be a mediator. CCK is regulated by releasing peptides - diazepam-binding protein (DBI) being a possible candidate. The aim of this study was to investigate the possible association between CCK plasma levels and DBI expression in patients with AAIP or its recurrence., Material and Methods: The study comprised 44 subjects (mean age 42 years): A) Patients with a first episode of AAIP (n = 9); B) patients with three or more episodes of AAIP (n = 11); C) patients with a heavy alcohol consumption, with no detected AAIP (n = 11) and D) healthy controls (n = 13). CCK levels were measured by radioimmunoassay (RIA). Duodenal biopsies were analyzed for DBI mRNA and histology., Results: There was no significant difference in CCK plasma levels, DBI expression or CCK/DBI ratio between the groups., Conclusions: There were no changes in fasting CCK plasma levels or DBI expression. This may suggest that they do not play a major role as risk factors for alcohol-induced pancreatitis.

Objective: Unlike patients with alcoholic hepatitis, patients with acute alcoholic pancreatitis seldom come into the hospital in an intoxicated state. Long-term history of heavy drinking induces increases in the serum pancreatic enzymes and pancreatitis-associated protein profiles during the withdrawal period. The aim of this study was to investigate the role of withdrawal in triggering acute alcoholic pancreatitis by studying the time-course of development of the first symptoms of the first acute alcoholic pancreatitis., Material and Methods: One hundred patients (85 M, 15 F, mean age 46, range 18-73 years) with the first acute alcoholic pancreatitis were asked three different questions in an attempt to clarify the same issue: Had you already stopped continuous drinking before the start of the acute abdominal pain that later led to hospitalization? Had you already stopped continuous drinking before you started to experience nausea or vomiting? How many hours after taking the last drop of alcohol did you start to feel pain (0 h, 1<6 h, 7-12 h, 13-24 h, 25-48 h, >48 h)? The amount of alcohol consumed was evaluated 1) during the past week and 2) during the past 2 months. The severity of the pancreatitis was assessed by serum C-reactive protein concentration, presence of necrosis, the development of pancreatic complications and the length of stay in hospital and in the intensive care unit., Results: Eighty-five patients were able to respond to the questions. Of these, 69% had developed pain and 91% nausea/vomiting only after they had already stopped continuous drinking. Whereas 29% of the patients developed some symptoms before stopping drinking, the majority of the patients developed symptoms during the first day after cessation (43%) or later (28%), mainly during the second day of cessation of drinking. In both the univariate analysis and the multivariate analysis the timing of the symptoms was dependent on the amount of alcohol consumed during the previous 2 months and in the past week., Conclusions: In the majority of patients with first acute alcoholic pancreatitis, the symptoms begin during the early withdrawal period. The withdrawal period might be more important than previously emphasized in the development of acute alcoholic pancreatitis.

Background: Alcohol is the most common cause of acute pancreatitis in Finland (70%). The amount of alcohol consumed has been shown to be associated with the prevalence of pancreatitis in the country, and also to be an important determinant of the severity of the first episode of acute alcoholic pancreatitis. We have a clinical suspicion that the use of alcohol and the incidence of pancreatitis are increased during holiday periods in summer, although no seasonal variations have been reported in a German population., Methods: Between 1972 and 1992 a total of 1556 episodes with acute alcoholic pancreatitis were treated at Tampere University Hospital; 552 were first episodes and 1004 were recurrent. For comparison, we investigated 297 episodes of acute biliary pancreatitis treated in that same time period. We investigated the monthly prevalence of acute alcoholic (first and recurrent) pancreatitis and compared this with the monthly absolute alcohol consumption., Results: Taking all alcoholic pancreatitis episodes into account, significant differences can be seen between prevalence and month of onset of the disease (P < 0.0001), whereas among biliary pancreatitis episodes there were no differences (P = 0.3). Prevalence of acute alcoholic pancreatitis was significantly higher than the expected prevalence in July and August, and the amount of alcohol consumption (100% alcohol, litres) was highest during these same months. Also during March, October and December the prevalence was higher than expected., Conclusion: Months with holiday seasons, Christmas, Easter, summer and autumn, are associated with the highest alcohol consumption and the highest prevalence of acute alcoholic pancreatitis.

Background: Recent studies have shown that cholecystokinin (CCK) agonist, cerulein can induce acute pancreatitis in animals. The role of CCK in the induction of acute pancreatitis in humans is unclear. We investigated plasma CCK levels in alcoholic and biliary pancreatitis on admission and during the episode of acute pancreatitis., Methods: Plasma CCK concentrations were determined by a specific and sensitive radioimmunoassay using CCK antiserum (Euro-Diagnostica, Malmö, Sweden) in 35 patients with acute alcoholic pancreatitis, in 27 patients with acute biliary pancreatitis, in 34 patients with nonpancreatic acute abdominal pain, and in 43 healthy subjects. The mean time from the first symptoms to the plasma sample was 31 (+/- 3.7) h in alcoholic pancreatitis patients and 25 (+/- 5.1) h in biliary pancreatitis patients. We also determined CCK levels in 20 patients during the episode of acute pancreatitis. Normal fasting level of CCK is < or = 1.12 pmol/L according to manufacturer., Results: Basal plasma CCK concentrations were significantly lower both in alcoholic pancreatitis (mean +/- SEM, 0.04 +/- 0.03 pmol/L, p < 0.0001) and biliary pancreatitis patients (0.17 +/- 0.13 pmol/L, p < 0.0001) than in nonpancreatic acute abdominal pain patients (1.23 +/- 0.32 pmol/L) or healthy subjects (1.18 +/- 0.20 pmol/L). Plasma CCK levels also remained low until the patient was well-recovering and had started oral diet., Conclusion: Basal plasma CCK concentrations are significantly decreased in acute alcoholic and biliary pancreatitis after the first day from the beginning of the symptoms until the patient was well-recovering.

Background: Owing to the current lack of long-term follow-up data on the recurrence of alcohol-induced acute pancreatitis (AP), we studied the pattern of recurrence and determined the characteristics of the disease to predict the recurrence., Methods: Between 1972 and 1991, 2678 AP episodes were detected; 1555 were induced by alcohol, and 591 of them were the first episode. During the first alcohol-induced AP 29 patients died and were excluded from further analysis. Of the 562 included, 503 were men, and 59 women. Admission serum tests, severity index, development of complications, intensive care unit and hospital stay, and need for surgery were assessed. Case records were studied. The national database was used to detect admissions to other hospitals., Results: Overall, 260 (46%) developed recurrent disease. Of the first relapses, 80% developed during 4 years. The recurrence rate has not changed with time. Age less than 45 years increased the risk (odds ratio (OR) = 2.42; 95% confidence interval (CI), 1.30-4.50). The risk factors of the first alcohol-induced AP associated with the development of multi-recurring pancreatitis are age <45 years (OR, 2.42; 95% CI, 1.59-13.0), 0-2 positive Glasgow criteria (OR, 2.45; 95% CI, 1.16-5.19), and arterial oxygen tension >60 mmHg (OR, 9.90; 95% CI, 1.32-74.3)., Conclusions: Fewer than half of the patients develop recurrent alcohol-induced AP. Younger patients are at the highest risk of recurrence. Those whose first alcohol-induced pancreatitis episode was not severe are at a higher risk of developing multi-recurring pancreatitis.

Conclusion: There are differences in the microbiology of infected pancreatic necrosis in alcoholic and biliary pancreatitis. One possible explanation may be different routes of contamination., Background: Infection is a severe complication in acute pancreatitis. Bacteria are found in 40-70% of all patients suffering from necrotizing pancreatitis. We investigated whether there were any differences in microbes isolated from pancreatic necrosis in biliary and alcoholic pancreatitis., Methods: Microbiological tests were conducted on necrosis taken at the operation for pancreatitis with the etiology of (group A) alcoholic pancreatitis (n = 47) and (group B) biliary pancreatitis (n = 23). Patients with simultaneous cholecystitis were excluded. The time from the first symptoms to the operation or the extent of necrosis did not differ between the groups., Results: Microbes were isolated more often in the cultures from group B than group A (17/23 = 74% vs 15/47 = 32%, p = 0.001). The most common were Gram-positive bacteria in group A and Gram-negative bacteria in group B. From the first week, from the onset of symptoms to the operation. Gram-negative bacteria were isolated significantly more often in the cultures from group B patients than from group A patients (8/10 = 80% vs 1/5 = 20%, p = 0.04). In multivariate analysis, we found that biliary pancreatitis was an independent risk factor (adds ratio 5.5, 95% confidence interval [CI] 0.59-52.10) of contamination of necrosis with Gram-negative bacteria.