ALCOHOLIC VS. NON-ALCOHOLIC CHRONIC PANCREATITIS: SURGEONS’ PERSPECTIVE FROM A TERTIARY CENTRE IN INDIA

ABSTRACT Background: Although alcohol is the most common cause for chronic pancreatitis worldwide, idiopathic type is prevalent in India. Natural history and disease progression are different between these two groups. There is paucity of data comparing surgical outcome and quality of life in these patients. Aim: To evaluate clinical features, surgical outcome and quality of life between these two groups of patients. Method: All patients with chronic pancreatitis who underwent surgery were prospectively reviewed. Results: From 98 patients, 42 were alcoholic. Number of male and the mean age at the time of operation was significantly more in alcoholic patients. Smoking, preoperative hospital admission rate and the prevalence of local complications like inflammatory pancreatic head mass, biliary stricture and left sided portal hypertension were distinctly more common in alcoholic group. Frey procedure was required more commonly in alcoholic group. Mean postoperative hospital stay and overall postoperative complication rate were comparable between the two groups. Over a median follow up of 18 months there was significant improvement in quality of life and pain score in both the groups. Improvement of physical functioning score at follow-up was significantly more in alcoholic group but the requirement for analgesic medications were significantly more in alcoholic group. However, appetite loss was more perceived by non-alcoholic group. Conclusion: Alcoholic chronic pancreatitis presents with more local complications associated with chronic pancreatitis. Frey procedure is a safe and well accepted surgery in this group. Though they required more analgesic requirement in short term follow up, other aspects of quality of life are similar to non-alcoholic group.

Role of the Common PRSS1-PRSS2 Haplotype in Alcoholic and Non-Alcoholic Chronic Pancreatitis: Meta- and Re-Analyses

The association between a common PRSS1-PRSS2 haplotype and alcoholic chronic pancreatitis (ACP), which was revealed by the first genome-wide association study of chronic pancreatitis (CP), has been consistently replicated. However, the association with non-ACP (NACP) has been controversial. Herein, we sought to clarify this basic issue by means of an allele-based meta-analysis of currently available studies. We then used studies informative for genotype distribution to explore the biological mechanisms underlying the association data and to test for gene-environment interaction between the risk haplotype and alcohol consumption by means of a re-analysis. A literature search was conducted to identify eligible studies. A meta-analysis was performed using the Review Manager software. The association between the risk genotypes and NACP or ACP was tested for the best-fitting genetic model. Gene-environment interaction was estimated by both case-only and multinomial approaches. Five and eight studies were employed for the meta-analysis of ACP and NACP findings, respectively. The risk allele was significantly associated with both ACP (pooled odds ratio (OR) 1.67, 95% confidence interval (CI) 1.56–1.78; p < 0.00001) and NACP (pooled OR 1.28, 95% CI 1.17–1.40; p < 0.00001). Consistent with a dosage effect of the risk allele on PRSS1/PRSS2 mRNA expression in human pancreatic tissue, both ACP and NACP association data were best explained by an additive genetic model. Finally, the risk haplotype was found to interact synergistically with alcohol consumption.

Role of the common PRSS1-PRSS2 haplotype in alcoholic and non-alcoholic chronic pancreatitis: meta- and re-analyses

The association between a common PRSS1-PRSS2 haplotype and alcoholic chronic pancreatitis (ACP), which was revealed by the first genome-wide association study of chronic pancreatitis (CP), has been consistently replicated. However, the association with non-ACP (NACP) has been controversial. Herein, we sought to clarify this basic issue by means of an allele-based meta-analysis of currently available studies. We then used studies informative for genotype distribution to explore the biological mechanisms underlying the association data and to test for gene-environment interaction between the risk haplotype and alcohol consumption by means of a re-analysis. A literature search was conducted to identify eligible studies. Meta-analysis was performed using the Review Manager software. The association between the risk genotypes and NACP or ACP was tested for the best-fitting genetic model. Gene-environment interaction was estimated by both case-only and multinomial approaches. Five and eight studies were employed for the meta-analysis of ACP and NACP findings, respectively. The risk allele was significantly associated with both ACP (pooled OR 1.67, 95% CI 1.56–1.78; P<0.00001) and NACP (pooled OR 1.28, 95% CI 1.17–1.40; P<0.00001). Consistent with a dosage effect of the risk allele on PRSS1/PRSS2 mRNA expression in human pancreatic tissue, both ACP and NACP association data were best explained by an additive genetic model. Finally, the risk haplotype was found to interact synergistically with ACP.

Associated Liver Disease in Alcoholic Chronic Pancreatitis

Background: Alcohol is a common etiological factor in the pathogenesis of both pancreatic and liver disease. The frequencies of associated liver histological change in patients with alcoholic chronic pancreatitis (AICP) vary from series to series. Significant proportion of patients with alcoholic pancreatitis does have histological changes in liver. Subjects and Methods: The study was conducted at Narayana Medical College & Hospital, Chintareddy Palem, Nellore, Andhra Pradesh on liver-biopsy specimens from 23 patients with chronic alcoholic pancreatitis subjected to operation for pain, from August 2015 to July 2016 and all the patients had undergone liver biopsy at the time of surgery for AICP. The patients were followed as part of a prospective study of 33 patients who had been treated for chronic pancreatitis. The pathologists were requested to report on alcohol related histological changes in the specimen. Results: There were 23 patients and all were men. Chronic pancreatitis was due to alcohol abuse in all patients. The median age at surgery was 39.8 years. The mean duration of alcohol abuse was 20.5 years (range 6-29 years).The average alcohol intake was 122gm 36gms/day. Three patients had jaundice for 3-6 months duration. None of the patients had any other risk factor for liver disease and none of them had clinical or biochemical evidence of liver disease. The histological reports were, 4 patients had alcoholic hepatitis, 2 severe steatohepatitis, 1 granulomatous hepatitis, 3 cholestasitc changes, one fatty liver and 12 had no significant pathology. None of the patients had cirrhosis. Thus significant alcoholic liver disease was present in 30.4% (7/23) of the patients. There was no increased incidence of post-operative mortality and morbidity in patients with liver pathology. Conclusion: As reported in many other series, chronic alcoholic pancreatitis is associated with histological changes in liver in significant proportion of patients. However its clinical significance and prognosis of these patients are unknown.