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Chronic pancreatitis (CP) is characterised by irreversible damage to the pancreas causing endocrine and exocrine dysfunction which results in decreased quality of life and reduced life expectancy.1
Adam et al recently published an interesting study on a possible diagnostic tool for CP based on metabolomic profiles of patients and controls.2
Our previous international cohort analysis showed that the proportion of patients developing CP is exponentially and directly associated with the number of acute pancreatitis (AP) episodes, thus strengthening the focus on the challenging task of diagnosing CP early.3 4 However, in addition to diagnosing early, we should also focus on preventive interventions, before the damage becomes irreversible.
Alcohol is the main aetiological factor for CP and both alcohol consumption and smoking increase the risk for recurrence of AP and the development of CP. According to Ahmed Ali et al, in a follow-up study of 669 AP patients, smoking represented the dominant risk factor for recurrent AP (RAP) and a combination of alcohol consumption and smoking was the main risk factor for the progression to CP.5 Therefore, cessation programmes and patient education are extremely important means to intervening and lowering the recurrence of AP and the progression to CP.6 7 However, total cessation and abstinence often seems impossible for patients and they do not even try. Is it also possible to reduce recurrence and progression by decreasing the amount consumed?
Basic research evidence clearly suggests that alcohol and smoking amplify each other’s harmful effects.8 9 However, large cohorts are lacking to determine whether smoking and alcohol consumption dose-dependently, mutually exacerbate the damage to the pancreas caused by each.
We have used the international cohort in the Acute Pancreatitis Registry initiated by the Hungarian Pancreatic Study Group. Data were collected from 13 countries and 30 medical centres, with 2441 cases included in the analysis. Further characteristics of the cohort and information on methods are available in online supplemental file 1.
Supplemental material
The patient population was divided into groups according to current amounts of smoking and alcohol consumption. We found that both smoking and alcohol consumption are dose-dependently associated with amylase and lipase levels and with the prevalence of RAP and CP among AP patients. Alcohol consumption was also linked to a higher rate of local complications (figure 1).
Dose dependency in alcohol consumption and smoking in AP. (A) Light and heavy alcohol consumption and smoking groups and definitions. (B, C) Amylase and lipase levels on admission. (D) Prevalence of RAP and CP (%). (E) Proportion of local complications (%). (F, G) Amylase and lipase levels on admission. (H) Prevalence of RAP and CP (%). *P<0.001, **p=0.003. Pearson’s χ2 test and the Kruskal-Wallis rank sum tests were used. AP, acute pancreatitis; CP, chronic pancreatitis; RAP, recurrent AP.
Second, we examined the possible synergistic effect of these two risk factors. We arranged the cohort population into four groups based on current smoking and alcohol consumption status (figure 2). Smoking and drinking together are associated with the male sex and linked to the first AP episode 15 years earlier than non-smoking and non-drinking are. Analysing on-admission and outcome parameters between groups, we found that amylase and lipase levels are the lowest and the proportion of moderately severe cases are the highest in the smoking–drinking group, suggesting the most pancreatic tissue damage and local complications here. The highest proportion of patients with RAP was found in both smoking groups, and the largest percentage of CP patients was observed in the smoking–drinking population, suggesting a clear synergising effect of alcohol consumption and smoking and a highlighted importance of smoking in progression.
Combined alcohol consumption and smoking groups in AP. (A) Groups. (B) Sex. *P<0.001 in all comparisons. (C) Age. *P<0.001 or p=0.001 in all comparisons. (D) Severity. Moderately severe *p=0.003 vs NS–ND. P=0.022 vs S–ND. (E) On admission amylase level. *P<0.001 vs NS–ND. **P<0.003 vs NS–ND. ***p<0.001 vs NS–ND, NS–D and S–ND. (F) On-admission lipase level. *P<0.003 vs NS–ND, p<0.006 vs NS–D. **P<0.001 vs NS–ND and NS–D. (G) Prevalence of recurrent AP. *P=0.003 vs NS–ND. **p=0.04 vs NS–D. p<0.001 vs NS–ND. (H) Prevalence of chronic pancreatitis. *P<0.001 vs NS–ND, NS–D. Pearson’s χ2 test and the Kruskal-Wallis rank sum tests were used. AP, acute pancreatitis; NS–D: non-smoking–drinking; NS–ND: non-smoking–non-drinking; S–D: smoking–drinking; S-ND: smoking–non-drinking.
Our analysis confirms in a clinical setting that both smoking and alcohol are dose-dependently associated with pancreatic tissue damage and the prevalence of RAP and CP. Moreover, they mutually exacerbate each other’s harmful effect. In addition to the development of prognostic and therapeutic measures, further clinical trials on cessation programmes and patient education are needed. Communication to all stakeholders of the importance of at least quitting smoking or cutting the amount of smoking and alcohol consumption is crucial.
Data availability statement
Original raw data are available from the corresponding author on reasonable request.
Ethics statements
Patient consent for publication
Ethics approval
The study was approved by the Scientific and Research Ethics Committee of the Medical Research Council and the National Public Health Centre under the following ID numbers: 22254-1/2012/EKU and 17787-8/2020/EÜIG.
Acknowledgments
We wish to thank all the contributing members of the Hungarian Pancreatic Study Group (HPSG) and the Centre of Excellence for Pancreatic Diseases (CEPD).The abstract for the analysis was published at conferences held by the European Pancreatic Club, United European Gastroenterology and the American Pancreatic Association.
Supplementary materials
Supplementary Data
This web only file has been produced by the BMJ Publishing Group from an electronic file supplied by the author(s) and has not been edited for content.
Footnotes
Collaborators Hungarian Pancreatic Study Group: Bálint Erőss, Péter Jenő Hegyi, Szilárd Váncsa, Rita Nagy, Katalin Márta, Klementina Ocskay, Márk Félix Juhász, Marcell Imrei, Mária Földi, Szabolcs Kiss, Balázs Csaba Németh, Tamás Takács, László Czakó, Szilárd Gódi, Judit Bajor, Patrícia Sarlós, László Gajdán, Mária Papp, József Hamvas, Márta Varga, Melania Macarie, Imola Török, János Novák, Artautas Mickevicius, Elena Ramirez Maldonado, Shamil Galeev, Ville Sallinen, Barnabás Bod, Ali Tüzün Ince, Tamás Nagy, Nándor Faluhelyi, Noémi Gede, Stefania Bunduc, Tamás Hussein, Mónika Lipp, Anna Németh, Orsolya Urbán, Dorottya Tarján, Simon Tóth, Dániel Pécsi, Péter Varjú, Noémi Zádori.
Contributors PH conceptualised the study. ÁV, FI, AS and AP contributed to the data collection and quality assurance. AS, ZS, PM and NF extracted and analysed the data. PH, AS, AP and NF interpreted the data. AS and PH wrote the manuscript. All the authors reviewed and contributed to the manuscript before finalisation and submission. Hungarian Pancreatic Study Group (full names are available in the Contributors section and affiliations are detailed in online supplemental file 1: BE, PJH, SV, RN, KM, KO, FJ, MF, SK, BN, TT, LC, SG, JB, PS, LG, MP, JH, MV, MM, IT, JN, AM, ERM, SG, VS, BB, ATI contributed to the data collection. TN, NF contributed to the interdisciplinary evaluation of the cases. NG conducted preliminary analyses. BE, PJH, SV, RN, KM, KO, FJ, MI, MF, SK, NG, SB, TH, ML, AN, OU, DT, ST, DP, PV and NZ ensured professional data quality control.
Funding The research was supported by project grant K131996 to PH and by funding from the University of Pécs Medical School Research Fund (300909) to AS.
Disclaimer The funders had no effect on the concept, data collection and analysis, and writing of the manuscript.
Competing interests None declared.
Provenance and peer review Not commissioned; internally peer reviewed.
Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.