Effect of type of alcoholic beverage in causing acute pancreatitis

Sir,

Thank you for your valuable comments. As you have noticed the association between spirit consumption and the risk of acute pancreatitis attenuated after exclusion of patients with gallstone-related acute pancreatitis. This resulted, as expected, in loss of statistical precision of the analyses resulting in a wider range of confidence interval. However, as shown in figure 2, the linear trend for the association between spirit consumption and acute pancreatitis remained unchanged. This support the fact the observed association was not due to chance.

The occurrence of recurrent acute pancreatitis after gallstone surgery was beyond the scope of the current study and was not assessed. Previous reports have estimated this proportion to about 10%.1-2

Although the peak of incidence for alcohol-related acute pancreatitis occurs at the age of 39, there is no reason to believe that age alters the association between spirit and of alcohol-related acute pancreatitis differently.

Sincerely

Omid Sadr-Azodi
MD, PhD
Karolinska University Hospital,
Stockholm, Sweden
omid.sadr-azodi@ki.se

References

1. Lankisch PG, Breuer N, Bruns A, Weber-Dany B, Lowenfels AB, Maisonneuve P. Natural history of acute pancreatitis: a long-term population-based study. Am J Gastroenterol. 2009 Nov;104(11):2797-805; quiz 2806. Epub 2009 Jul 14.

2. Lund H, Tønnesen H, Tønnesen MH, Olsen O. Long-term recurrence and death rates after acute pancreatitis. Scand J Gastroenterol. 2006 Feb;41(2):234-8.

• Commentor: Omid Sadr-Azodi - Stockholm, Sweden
• Date: Nov 16, 2011

Sir,

We read with interest this article by Sadr Azodi et al. Many excellent research reports have been published using the Swedish Patient Registry. Aspects of this paper are intriguing such as the cohort size and the 10-year follow-up achieved. There are some important weaknesses. The authors indeed show a significant association between the amount of spirits consumed on a single occasion and the risk of acute pancreatitis. This was emphasized as the ‘headline’ finding. However, it should be realised that this relationship becomes non-significant when the analysis is confined to cases of alcoholic pancreatitis i.e. excluding cases of gallstone pancreatitis from the analysis.

Secondly, there are a proportion of patients who develop recurrent pancreatitis following definitive treatment for gallstones. It may have been interesting to identify this group. Finally, the median age of the cohort studied here was over 60 years. However, the peak incidence of alcohol-related pancreatitis has a median age of 39 years and the incidence decreases with age (1). The study aim was to investigate the association between types of alcoholic beverage and the risk of pancreatitis. Therefore, the age range of the study group was not ideal to answer the main question posed by this study.

Ravinder Vohra PhD, MRCS, Glenn Miller MD, FRCS
York Teaching Hospitals NHS Foundation Trust
ravsvohra@hotmail.com

References

1. Lindkvist B, et al. Trends in incidence of acute pancreatitis in a Swedish population: is there really an increase? Clin Gastroenterol Hepatol 2004;2:831-7.

• Commentor: RS Vohra PhD, MRCS; GV Miller MD, FRCS - York Teaching Hospitals NHS Foundation Trust
• Date: Nov 14, 2011

Sir,

Thank you indeed for highlighting the essence of our results. Unfortunately, we did not have any information on the type of spirit consumed which limits the conclusions from the present study. However, as indicated by you, future studies to clarify the role of constituents of spirits on the development of acute pancreatitis are warranted and important for understanding the pathophysiology of acute pancreatitis.

Omid Sadr Azodi MD, PhD
Karolinska University Hospital
Stockholm, Sweden
omid.sadr-azodi@ki.se

• Commentor: Omid Sadr Azodi - Karolinska University Hospital
• Date: Oct 11, 2011

Sir,

We read with interest the article by Sadr Azodi et al. The article adds useful epidemiological evidence to further our understanding of alcohol-related acute pancreatitis (AP). An important finding is the lack of influence of frequency of consumption of spirits on the development of AP. One potential conclusion is that the actual contents of the spirits may be disturbing the homeostasis in the pancreas. While the authors attribute the increased risk of AP in people consuming spirits to oxidative state, it needs to be highlighted that this is but one of the possible mechanisms by which spirits could influence the development of AP (1).

We have previously appreciated a high incidence of alcohol-induced AP (2) amongst patients who reported a high consumption of country-made spirits. Based on the historical accounts of the patients, chemical analysis (using gas chromatography/mass spectrometry) of the consumed alcohols revealed the presence of other constituents (besides ethanol and water) which could potentially injure the pancreas but, to date, remain largely unexplored (3)!

It would be interesting to know the type of spirits consumed in the present study and if there was an increased risk with certain spirits. A further chemical analysis of the contents of the spirits may certainly be worth looking into. We hope this study, as well as, the accumulating data from similar studies (2,3) will direct further research in alcohol-induced AP towards analysing the role of the constituents in spirits and their impact on the pancreas (4).

Savio G. Barreto, Thomas Paxton, Michael Whitlaw
Modbury Hospital, South Australia
georgebarreto@yahoo.com

References

1. Barreto SG, Saccone GT. Alcohol-induced acute pancreatitis: the 'critical mass' concept. Med Hypotheses 2010;75(1): 73-76.

2. Barreto SG, Rodrigues J. Acute pancreatitis in Goa--a hospital-based study. J Indian Med Assoc 2008;106(9): 575-576, 578.

3. Barreto SG, Jardine D, Phillips P, Bhatia M, Saccone GT. Can by-products in country-made alcohols induce acute pancreatitis? Pancreas 2010;39(8): 1199-1204.

4. Barreto S, Jardine D, Phillips P, Bhatia M, Saccone G. Alcohol and the pancreas - we need to look beyond our noses! Pancreas 2011;40:1144-1145.

• Commentor: Savio G. Barreto, Thomas Paxton, Michael Whitlaw - Modbury Hospital
• Date: Oct 04, 2011