Pancreatic morphological changes in long-term follow-up after initial episode of acute alcoholic pancreatitis.

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.

Goal-related outcome after acute alcohol-pancreatitis -- a two-year follow-up study.

The aim of this study was to find out if an acute pancreatitis leads the patients to reduce their alcohol consumption and if there are factors predicting the outcome. We also observed which factors affected the choice of patient's personal drinking goal, e.g., abstinence or moderate drinking, how this goal changed during the follow-up and how the goal affected the change in drinking habits. In 2001-2005, 120 patients treated in Tampere University Hospital for their first alcohol-related acute pancreatitis were interviewed before discharge from the hospital and at the two-year follow-up. All patients had at least one intervention session for their alcohol use. Of the patients 87 (72.5%) completed the study. The alcohol consumption level and its changes, personal drinking goal of the patients, the factors affecting the choice and the changes of the goal were observed. Most (96.4%) of the patients were willing to reduce their drinking. At follow-up, 34 (40.5%) patients succeeded in reducing their alcohol consumption under the pre-set moderate drinking level. The only factor predicting alcohol use was the number of hospitalization days due to the acute alcohol-related pancreatitis (p=0.015). Those who chose abstinence seemed to succeed more often in stopping drinking or reducing their drinking below risk levels as compared to those with moderation goal (47.9% vs. 28.6%, p=0.075). The only abstinence-goal predicting factor was the concern of the relatives, friends or doctors (p=0.001). All 6 patients who needed intensive care chose abstinence-goal. During the follow-up period the goal changed. At baseline, the majority chose abstinence but two years after pancreatitis, the majority was striving for moderate drinking. A serious illness seems to be a good opportunity to change and to motivate patients. Even if abstinence is recommended to patients with alcohol-related pancreatitis, communication of individual goals is important in the motivation process of the patients.

Is alcoholic pancreatitis associated with enteroviral infection?

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.

Abstinence after first acute alcohol-associated pancreatitis protects against recurrent pancreatitis and minimizes the risk of pancreatic dysfunction.

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.

Serum lipid and fatty acid profiles are highly changed in patients with alcohol induced acute pancreatitis.

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.

Pancreatic damage after the first episode of acute alcoholic pancreatitis and its association with the later recurrence rate.

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.

The recurrence of acute alcohol-associated pancreatitis can be reduced: a randomized controlled trial.

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.

Risk factors for recurrent acute alcohol-associated pancreatitis: a prospective analysis.

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.

Is it long-term continuous drinking or the post-drinking withdrawal period that triggers the first acute alcoholic 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.

Cutting down substance abuse--present state and visions among surgeons and nurses.

BACKGROUND: Although substance abuse is variably common among surgical patients, detection of the problem and brief interventions are seldom undertaken. The aim of the present study was to assess surgeons' and nurses' activity in screening substance abuse among their patients and obstacles concerning intervention of patients with substance abuse. METHODS: Surgeons and nurses of The Department of Surgery, Tampere University Hospital were asked to predict if the surgical patients treated during a 24-h period (n=211) had a substance abuse disorder. This was compared to the patients' self-reports based on the Alcohol Use Disorders Identification Test (AUDIT) and questions about use of other substances. The surgeons and the nurses were also asked to complete a questionnaire related to interventions of patients with substance abuse; perceived knowledge, skills, attitudes and obstacles. RESULTS: Of the surgical patients, 47 (22%) proved to be substance abusers. Out of them, 23% were detected by surgeons and nurses. Of the surgeons (n=44) 83% and of the nurses (n=332) 84% perceived responsibility for intervention but claimed many obstacles. Nurses reported the lack of knowledge as the main obstacle. Of the nurses 18% reported enough knowledge to conduct the whole brief intervention compared to 34% of surgeons (p=0.021). The main obstacle reported by surgeons was the lack of time. CONCLUSIONS: Surgeons and nurses detect only minority of the substance abusing surgical patients. Lack of knowledge and time prevent intervening in patients' substance abuse. These results may be utilized when developing a program to better involve surgeons and nurses in detection and intervention of surgical patients' substance abuse.