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© Borgis - Postępy Nauk Medycznych 11/2017, s. 619-624 | DOI: 10.25121/PNM.2017.30.11.619
*Marcin Jadam, Grzegorz Oracz
Small intestine bacterial overgrowth in chronic pancreatitis
Przerost bakteryjny jelita cienkiego w przewlekłym zapaleniu trzustki
Department of Gastroenterology, Hepatology, Feeding Disorders and Pediatrics, The Children’s Memorial Health Institute, Warsaw
Head of Department: Professor Marek Woynarowski, MD, PhD
Streszczenie
Przewlekłe zapalenie trzustki (PZT) jest poważną chorobą, która ma istotny wpływ na jakość życia. Konsekwencją niewydolności zewnątrz- i wewnątrzwydzielniczej trzustki są: ból brzucha, cukrzyca i niedożywienie. Czynniki predysponujące do PZT, przebieg choroby oraz czynniki jatrogenne mogą prowadzić do zaburzeń mikrobioty jelitowej. Bakteryjny przerost jelita cienkiego (ang. small intestine bacterial overgrowth – SIBO) to zwiększona liczba bakterii w jelicie cienkim. Częstość jego występowania u pacjentów z PZT wynosi około 36%. W jego przebiegu występuje wiele nieswoistych objawów, a w ciężkich przypadkach może dochodzić do biegunki tłuszczowej, niedożywienia i utraty masy ciała. Ponadto, objawy nie tylko imitują te występujące w PZT, ale często nasilają je, utrudniając leczenie. „Złotym standardem” w diagnostyce SIBO jest jakościowa i ilościowa ocena aspiratu z jelita cienkiego, ale procedura ta jest inwazyjna, kosztowna i nie wszędzie dostępna. Odpowiedzią są szeroko stosowane wodorowe testy oddechowe z glukozą. Choroba dotyczy mikrobioty jelitowej, dlatego leczenie opiera się głównie na jej modyfikacji. Rifaksymina jest najlepiej zbadanym antybiotykiem stosowanym w SIBO. Probiotyki pomagają walczyć z oportunistycznymi patogenami jelitowymi, nie powodując jednocześnie zakłóceń w ekosystemie jelit. Równie ważne jest leczenie zaburzeń odżywienia związanych z SIBO. Niezależnie od terapii, zawsze należy rozważyć ryzyko nawrotu przerostu bakteryjnego. Ze względu na rosnącą świadomość wpływu mikrobioty na przebieg wielu chorób, konieczny jest dalszy rozwój diagnostyki i leczenia jej zaburzeń, także w przewlekłym zapaleniu trzustki.
Summary
Chronic pancreatitis (CP) is a serious disease that has a significant impact on the quality of life. The consequence of exocrine and endocrine pancreatic insufficiency is an abdominal pain, diabetes mellitus and malnutrition. Factors predisposing to CP, course of disease, as well as iatrogenic factors may lead to disorders in intestinal microbiota. Small intestine bacterial overgrowth (SIBO) is excess of bacteria in the small intestine. Its prevalence in adult patients with CP is approximately 36%. Many non-specific symptoms occur in SIBO, and in severe cases, it can lead to steatorrhea, malnutrition and weight loss. Furthermore, symptoms not only imitate those occurring in CP, but often aggravate them and hinder the treatment. “Golden standard” in SIBO diagnostics is a qualitative and quantitative assessment of aspirate from the small intestine, but this procedure is invasive, expensive and not widely available. The response are commonly used hydrogen breath tests with glucose. The disorder concerns intestinal microbiota, therefore the treatment is mainly based on its modification. Rifaximin is the best studied antibiotic, used in SIBO. Probiotics help to fight opportunistic intestinal pathogens, not causing disruption in gut ecosystem. It is equally important to treat nutritional disorders associated with SIBO. Regardless of therapy, the risk of bacterial overgrowth recurrence should always be considered. Due to the increasing awareness of microbiota’s influence on the course of many diseases, it is necessary to further develop diagnostics and treatment of its disorders, also in chronic pancreatitis.



Introduction
Chronic pancreatitis (CP) is an serious inflammatory process that develops in individuals with genetic, environmental and other risk factors, leading to progressive, irreversible organ injury. The disease proceeds with periods of remission and exacerbation. Gradual changes in the form of atrophy and fibrosis of pancreatic parenchyma are the cause of exocrine and subsequent endocrine pancreatic dysfunction. The consequence of this is recurring abdominal pain, which in advanced chronic pancreatitis may be constant, diabetes mellitus and malnutrition. Patients life expectancy and its quality are reduced due to progression of the disease, its association with other systemic illnesses and pancreatic cancer (1, 2).
Disturbed secretion of pancreatic juice, which apart from its essential digestive function also acts antibacterially, altered gastrointestinal motility, alcohol abuse and medicines taken in the course of CP leads to the proliferation of pathogens in the intestinal lumen. Disorders of composition, amount of bacteria in the small intestine and accompanying symptoms are defined as small intestine bacterial overgrowth (SIBO). Manifestation of this disorder include non-specific gastrointestinal symptoms such as abdominal pain, flatulence, bloating, diarrhoea and more severe complications such as vitamins and other microelements deficiencies as well as growth disorders in children. Furthermore, symptoms caused by bacterial fermentation in SIBO not only imitate those occurring in chronic pancreatitis, but often aggravate them and hinder the treatment. The problem of bacterial overgrowth affects about 1/3 of people suffering from CP (3-5).
Chronic pancreatitis
Chronic pancreatitis is a serious disease that has a significant impact on the quality of life, which exacerbations and late sequelae can endanger patient life. In Europe, the incidence of CP range from 5 to 10 cases per 100,000 inhabitants. With median survival of 20 years, the prevalence is about 120 cases per 100,000 inhabitants. Pancreatitis is a rare childhood disease, but recent years have seen an increase in its incidence, which is explained by increased recognition (6, 7).
The causes of chronic pancreatitis, according to the TIGAR-O system, include toxic/metabolic, idiopathic, genetic, autoimmune, recurrent and severe acute pancreatitis and obstructive aetiology. Alcohol abuse remains the dominant cause of chronic pancreatitis in adults. In Western countries, it is attributed to 40-70% of all cases. Smoking is also an independent risk factor for chronic pancreatitis. Other than alcohol and tobacco etiologic factors of CP are responsible for 20-50% of remaining cases of the disease. In the paediatric population, the most common causes of CP are gene mutations, anatomical defects of the pancreatic duct, and dyslipidemia (2, 8, 9).
Recurrent episodes of acute pancreatitis and chronic inflammation cause persistent damage to the exocrine and endocrine tissues, which is the basis of chronic pancreatitis. The greater the severity of the disease, the more intense is fibrosis process and the calcification of the pancreatic parenchyma. There is a distortions of the pancreatic ducts in the form of stricture and dilatation. Regardless of origin, injury to exocrine tissue is associated with an increase in intracellular levels of activated pancreatic enzymes (also in the blood). The accompanying inflammation and stenosis of ducts can damage the surrounding endocrine cells leading to the development of carbohydrate metabolism disorders, including diabetes mellitus eventually. The consequences of exocrine insufficiency are maldigestion and malabsorption. They manifest i.a. with abdominal pain, bloating, steatorrhea, weight loss, vitamin and microelements deficiencies. In addition to the clinical picture of exocrine and endocrine failure, pain is the most debilitating and disabling symptom that occurs in the majority of patients with chronic pancreatitis.
Symptomatic treatment in CP is of primary importance. The aim of therapy is also to prevent further progression of the disease and complications. CP significantly increases the probability of developing pancreatic tumors. Where possible, risk factors that may aggravate the course of illness such as alcohol consumption or cigarette smoking should be modified. Nutritional therapy aims to improve the general condition of the patient. Changing habits will help to avoid exacerbations caused by dietary errors. In the treatment of pain apply i.a. drugs throughout the analgesic ladder, procedures to reduce the pressure in the pancreatic duct and parenchyma, invasive endoscopic and surgical methods. The latter two are also used in the prevention and treatment of complications of CP. Digestive disorders caused by exocrine insufficiency require pancreatic enzyme replacement therapy administered with meals. Carbohydrate metabolism disorders, initially, can be controlled with the help of oral hypoglycaemic drugs such as metformin. Usually, however, for the treatment of diabetes type 3c, which is associated with injury to the pancreas, insulin supplementation is required. It is recommended to use long-acting preparations along with on-demand short acting insulins (8, 10, 11).
Small intestine bacterial overgrowth
The number of microorganisms that colonize the digestive tract significantly exceeds the number of human body cells (1014 and 1013 cells, respectively). The greatest bacterial concentration is in the terminal section of the small intestine and colon (even 1012 bacteria per ml of intestinal contents). Due to the presence of mechanisms protecting against excessive microflora growth, the upper gastrointestinal tract (stomach, duodenum) has a significantly lower bacterial count (up to 103 bacteria per ml of intestinal contents). The further down, through alimentary tract, the greater the number of bacterial cells. Different conditions in each segment of the intestine cause differences not only in the number but also the type of microorganisms that inhabit them. Upper digestive tract is occupied by gastric acid-resistant organisms, such as Helicobacter pylori or Lactobacillus. Coliforms, which are Gram-negative, non-spore-forming, lactose-fermenting bacteria, are characteristic for the colon. Disorders in intestinal microbiota are called dysbiosis. Changes in the number of microorganisms, their location, or changes in the proportion of particular types of bacteria can contribute to the development of certain diseases. The definition of SIBO still evolves, but it is usually referred to as the excess of bacteria in the small intestine. A total of 105 CFU/ml (colony-forming units per ml) of aspirate is generally accepted, although some postulate lower values. Due to the imperfection of diagnostic tests, “discussion” on the diagnostic criteria is still ongoing. Prevalence of bacterial overgrowth is not easy to determine. It is detected in up to 15.6% of healthy individuals, and this number increases with age and associated illnesses (12-14).

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Piśmiennictwo
1. Yang D, Forsmark CE: Chronic pancreatitis. Curr Opin Gastroenterol 2017; 33(5): 396-403.
2. Oracz G: Przewlekłe zapalenie trzustki. [W:] Socha P, Lebensztejn DM, Kamińska D (red.): Gastroenterologia dziecięca: podręcznik do specjalizacji. Media-Press, Warszawa 2016: 378-381.
3. Signoretti M, Stigliano S, Valente R et al.: Small intestinal bacterial overgrowth in patients with chronic pancreatitis. J Clin Gastroenterol 2014; 48: S52-S55.
4. Capurso G, Signoretti M, Archibugi L et al.: Systematic review and meta-analysis: small intestinal bacterial overgrowth in chronic pancreatitis. United Eur Gastroenterol J 2016; 4(5): 697-705.
5. Sieczkowska A, Landowski P, Kaminska B, Lifschitz C: Small bowel bacterial overgrowth in children. J Pediatr Gastroenterol Nutr 2016; 62(2): 196-207.
6. Löhr JM, Dominguez-Munoz E, Rosendahl J et al.: United European Gastroenterology evidence-based guidelines for the diagnosis and therapy of chronic pancreatitis (HaPanEU). United Eur Gastroenterol J 2017; 5(2): 153-199.
7. Oracz G, Wejnarska K, Kołodziejczyk E, Kierkuś J: Pediatric acute and chronic pancreatitis increase in incidence or increasing awareness? Pancreas 2017; 46(6): e55-e56.
8. Kleeff J, Whitcomb DC, Shimosegawa T et al.: Chronic pancreatitis. Nat Rev Dis Primer 2017; 3: 17060.
9. Etemad B, Whitcomb DC: Chronic pancreatitis: diagnosis, classification, and new genetic developments. Gastroenterology 2001; 120(3): 682-707.
10. Kirkegård J, Mortensen FV, Cronin-Fenton D: Chronic pancreatitis and pancreatic cancer risk: a systematic review and meta-analysis. Am J Gastroenterol 2017; 112(9): 1366-1372.
11. Lindkvist B: Diagnosis and treatment of pancreatic exocrine insufficiency. World J Gastroenterol 2013; 19(42): 7258.
12. Ghoshal UC, Ghoshal U: Small intestinal bacterial overgrowth and other intestinal disorders. Gastroenterol Clin North Am 2017; 46(1): 103-120.
13. Krajicek EJ, Hansel SL: Small intestinal bacterial overgrowth. Mayo Clin Proc 2016; 91(12): 1828-1833.
14. Sekirov I, Russell SL, Antunes LCM, Finlay BB: Gut microbiota in health and disease. Physiol Rev 2010; 90(3): 859-904.
15. Ponziani FR, Gerardi V, Gasbarrini A: Diagnosis and treatment of small intestinal bacterial overgrowth. Expert Rev Gastroenterol Hepatol 2016; 10(2): 215-227.
16. Sachdev AH, Pimentel M: Gastrointestinal bacterial overgrowth: pathogenesis and clinical significance. Ther Adv Chronic Dis 2013; 4(5): 223-231.
17. Gabbard SL, Lacy BE, Levine GM, Crowell MD: The impact of alcohol consumption and cholecystectomy on small intestinal bacterial overgrowth. Dig Dis Sci 2014; 59(3): 638-644.
18. Hauge T, Persson J, Danielsson D: Mucosal bacterial growth in the upper gastrointestinal tract in alcoholics (heavy drinkers). Digestion 1997; 58(6): 591-595.
19. Marotta F, Tajiri H, Li Z et al.: Pure pancreatic juice from patients with chronic pancreatitis has an impaired antibacterial activity. Int J Gastrointest Cancer 1997; 22(3): 215-220.
20. Kumar K, Ghoshal UC, Srivastava D et al.: Small intestinal bacterial overgrowth is common both among patients with alcoholic and idiopathic chronic pancreatitis. Pancreatology 2014; 14(4): 280-283.
21. Spiller RC, Trotman IF, Higgins BE et al.: The ileal brake inhibition of jejunal motility after ileal fat perfusion in man. Gut 1984; 25: 365-374.
22. Gotfried J, Priest S, Schey R: Diabetes and the small intestine. Curr Treat Options Gastroenterol 2017. http://link.springer.com/10.1007/s11938-017-0155-x.
23. Chonchubhair H, Bashir Y, Dobson M et al.: Small intestinal bacterial overgrowth in chronic pancreatitis patients with pancreatic exocrine insufficiency; a prospective cohort study. Gut 2017; 66 (suppl. 1): A1-A27.
24. Su T, Lai S, Lee A et al.: Meta-analysis: proton pump inhibitors moderately increase the risk of small intestinal bacterial overgrowth. J Gastroenterol 2017. http://link.springer.com/10.1007/s00535-017-1371-9.
25. Erdogan A, Rao SSC, Gulley D et al.: Small intestinal bacterial overgrowth: duodenal aspiration vs glucose breath test. Neurogastroenterol Motil 2015; 27(4): 481-489.
26. Grace E, Shaw C, Whelan K, Andreyev HJN: Review article: small intestinal bacterial overgrowth – prevalence, clinical features, current and developing diagnostic tests, and treatment. Aliment Pharmacol Ther 2013; 38(7): 674-688.
27. Khoshini R, Dai S-C, Lezcano S, Pimentel M: A systematic review of diagnostic tests for small intestinal bacterial overgrowth. Dig Dis Sci 2008; 53(6): 1443-1454.
28. Rezaie A, Buresi M, Lembo A et al.: Hydrogen and methane-based breath testing in gastrointestinal disorders: the North American consensus. Am J Gastroenterol 2017; 112(5): 775-784.
29. Gasbarrini A, Corazza GR, Gasbarrini G et al.: Methodology and indications of H2-breath testing in gastrointestinal diseases: the Rome Consensus Conference. Aliment Pharmacol Ther 2009; 29: 1-49.
30. Gottlieb K, Le C, Wacher V et al.: Selection of a cut-off for high- and low-methane producers using a spot-methane breath test: results from a large north American dataset of hydrogen, methane and carbon dioxide measurements in breath. Gastroenterol Rep 2017; pii: gow048.
31. Shah SC, Day LW, Somsouk M, Sewell JL: Meta-analysis: antibiotic therapy for small intestinal bacterial overgrowth. Aliment Pharmacol Ther 2013; 38(8): 925-934.
32. Gatta L, Scarpignato C: Systematic review with meta-analysis: rifaximin is effective and safe for the treatment of small intestine bacterial overgrowth. Aliment Pharmacol Ther 2017; 45(5): 604-616.
33. Zhong C, Qu C, Wang B et al.: Probiotics for preventing and treating small intestinal bacterial overgrowth: a meta-analysis and systematic review of current evidence. J Clin Gastroenterol 2017; 51(4): 300-311.
otrzymano: 2017-10-05
zaakceptowano do druku: 2017-10-25

Adres do korespondencji:
*Marcin Jadam
Klinika Gastroenterologii, Hepatologii, Zaburzeń Odżywiania i Pediatrii Instytut „Pomnik – Centrum Zdrowia Dziecka”
Al. Dzieci Polskich 20, 04-730 Warszawa
tel. +48 (22) 815-73-84
marcin.jadam@gmail.com

Postępy Nauk Medycznych 11/2017
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