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 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).

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).