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Abstract
In chronic pancreatitis (CP), a syndrome of impaired assimilation of the components of the chyme (malassimilation) develops. It consists of the symptoms of maldigestion and malabsorption.
When the number of functionally active acinar cells in the pancreas decreases (atrophy, fibrosis), the required amount of enzymes cannot be provided to the duodenum. A disorder of cavity digestion develops. Non-hydrolyzed nutrients are retained in the duodenum to compensate for the lack of enzymes. This is how duodenostasis and duodenal hypertension are formed in CP with exocrine insufficiency of the pancreas. The clinical result is heaviness, distension, and discomfort in the upper abdomen, i.e. gastric dyspepsia.
The key role in the development of membrane digestion disorders in CP belongs to the small intestinal bacterial overgrowth (SIBO) syndrome. Patients with CP develop SIBO, which is characterized by excessive growth of the intestinal microbiota, fermentation processes, and inflammation in the small intestine. According to the results of a meta-analysis of 13 studies, the prevalence of SIBO in CP is 38.6%. The products of bacterial breakdown of food in the intestine can lead to organic changes in the mucous membrane (dystrophy, inflammation), which can impair the absorption of the final products of food hydrolysis under the influence of enzymes of the pancreas and small intestine. This is also facilitated by deconjugated bile acids formed during bacterial colonization of the initial parts of the small intestine, which have a damaging effect on its mucous membrane.
The article presents the results of our studies of the function and morphological changes in the small intestine in CP.
In CP, intestinal dysfunction develops. Enzyme preparations containing not only pancreatic but also intestinal enzymes should be included in the treatment of CP. The enzyme preparation Fermentaza Duo, which is manufactured using modern technologies, contains α-galactosidase. The drug effectively eliminates the manifestations of intestinal dyspepsia.
References
2. Коротько Г. Ф. Физиология системы пищеварения. Краснодар: ООО БК «Группа Б»; 2009. 608 с.
3. Линевский Ю. В., Линевская К. Ю., Воронин К. А. Синдром мальассимиляции и его лечение у больных хроническим панкреатитом. Мистецтво лікування. 2006; 4: 13–15.
4. Парфенов А. И. Энтерология: Руководство для врачей. 2-е изд., перераб. и доп. М.: ООО «Медицинское информационное агентство»; 2009. 880 с.
5. Di Stefano M., Miceli E., Gotti S. et al. The effect of oral alpha-galactosidase on intestinal gas production and gas-related symptoms. Dig Dis Sci. 2007; 52(1): 78–83. https://doi.org/10.1007/s10620-006-9296-9.
6. Dominguez-Muñoz J., Vujasinovic M., de la Iglesia D. et al. European guidelines for the diagnosis and treatment of pancreatic exocrine insufficiency: UEG, EPC, EDS, ESPEN, ESPGHAN, ESDO, and ESPCG evidence-based recommendations. United European Gastroenterol J. 2025; 13(1): 125–172. https://doi.org/10.1002/ueg2.12674.
7. El Kurdi B., Babar S., El Iskandarani M. et al. Factors that affect prevalence of small intestinal bacterial overgrowth in chronic pancreatitis: a systematic review, meta-analysis, and meta-regression. Clin Transl Gastroenterol. 2019; 10(9): e00072. https://doi.org/10.14309/ctg.0000000000000072.
8. Fernández-Millán E., Guillén C. Multi-organ crosstalk with endocrine pancreas: a focus on how gut microbiota shapes pancreatic beta-cells. Biomolecules. 2022; 12(1): 104. https://doi.org/10.3390/biom12010104.
9. Guo Y., Cao F., Li F. Impacts of pancreatic exocrine insufficiency on gut microbiota. J Zhejiang Univ Sci B. 2024; 25(4): 271–279. https://doi.org/10.1631/jzus.B2300070.
10. Lee A., Baker J., Wamsteker E. et al. Small intestinal bacterial overgrowth is common in chronic pancreatitis and associates with diabetes, chronic pancreatitis severity, low zinc levels, and opiate use. Am J Gastroenterol. 2019; 114(7): 1163–1171. https://doi.org/10.14309/ajg.0000000000000200.
11. Ní Chonchubhair H., Bashir Y., Dobson M. et al. The prevalence of small intestinal bacterial overgrowth in non-surgical patients with chronic pancreatitis and pancreatic exocrine insufficiency (PEI). Pancreatology. 2018; 18(4): 379–385. https://doi.org/10.1016/j.pan.2018.02.010.
12. Nishiyama H., Nagai T., Kudo M. et al. Supplementation of pancreatic digestive enzymes alters the composition of intestinal microbiota in mice. Biochem Biophys Res Commun. 2018; 495(1): 273–279. https://doi.org/10.1016/j.bbrc.2017.10.130.
13. Pironi L., Cuerda C., Jeppesen P. et al. ESPEN guideline on chronic intestinal failure in adults — Update 2023. Clin Nutr. 2023; 42(10): 1940–2021. https://doi.org/10.1016/j.clnu.2023.07.019.
14. Ritz S., Hahn D., Wami H. et al. Gut microbiome as a response marker for pancreatic enzyme replacement therapy in a porcine model of exocrine pancreas insufficiency. Microb Cell Fact. 2020; 19(1): 221. https://doi.org/10.1186/s12934-020-01482-2.
15. Schepis T., De Lucia S., Nista E. et al. Microbiota in Pancreatic Diseases: A Review of the Literature. J Clin Med. 2021; 10(24): 5920. https://doi.org/10.3390/jcm10245920.
16. Temel H., Kaymak Ö., Kaplan S. et al. Role of microbiota and microbiota-derived short-chain fatty acids in PDAC. Cancer Med. 2023; 12(5): 5661–5675. https://doi.org/10.1002/cam4.5323.
17. Tuck C., Taylor K., Gibson P. et al. Increasing symptoms in irritable bowel symptoms with ingestion of galacto-oligosaccharides are mitigated by α-galactosidase treatment. Am J Gastroenterol. 2018; 113(1): 124–134. https://doi.org/10.1038/ajg.2017.245.
18. Yang Q., Zhang J., Zhu Y. Potential roles of the gut microbiota in pancreatic carcinogenesis and therapeutics. Front Cell Infect Microbiol. 2022; 12: 872019. https://doi.org/10.3389/fcimb.2022.872019.