Bacterial overgrowth syndrome of upper parts of gastrointestinal tract in acute necrotizing pancreatitis
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acute pancreatitis, bacterial colonization, microflora, purulent septic complications, bacterial overgrowth syndrome

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Rotar, O. V., Khomiak, I. V., Polioviy, V. P., & Rotar, V. I. (2020). Bacterial overgrowth syndrome of upper parts of gastrointestinal tract in acute necrotizing pancreatitis. Herald of Pancreatic Club, 49(4), 55-58.

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Aim: to study the changes in the microflora of the upper part of digestive tract during acute necrotizing pancreatitis.

Material and methods. Acute necrotizing pancreatitis was induced in 42 white rats; changes in the mucous microflora of the upper part of digestive tract were studied. Bacteriological examination of the contents of the proximal small intestine was performed in 42 patients with acute necrotic pancreatitis during gastrofibroscopy.

Results and discussion. Induction of acute necrotic pancreatitis was accompanied by impaired colonization resistance of the intestinal mucosa due to the elimination of bifidobacteria and lactobacilli: the frequency of their growth from the mucosa decreased threefold (p<0.01), and the population level, respectively, by 25% (p<0.05) and by 36% (p<0.02). The mucosa was actively colonized by gram-negative pathogenic and conditionally pathogenic enterobacteria at high population level (3.07‒5.39 lg CFU/g), which allowed this microflora to overcome the damaged intestinal barrier and translocate. Pathogenic Escherichia spp. and Proteus spp. were cultivated from the mesenteric lymph nodes in 24 hours; Enterobacteria spp. and Staphylococci spp. were isolated from portal blood, pancreatic tissue, and peritoneal cavity 48 hours after induction of acute pancreatitis. Eight strains of gram-negative microorganisms were identified in small intestine in 69% of patients before surgery. Similar microflora was cultivated from pathological foci in 57.4% of patients after surgery.

Conclusion. Severe deficiency of autochthonous anaerobic microflora occurred in the upper parts of the digestive tract in acute necrotizing pancreatitis, causing excessive colonization by pathogenic and conditionally pathogenic microorganisms and promoting bacterial translocation.
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