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EFFECTS OF NANOSILVER ON CLINICAL COURSE OF ACUTE INTESTINAL INFECTIONS, INTESTINAL MICROFLORA AND CYTOKINES
Lufunyo Edson Lihweuli, 5th year student
Scientific adviser – assist. K.S. Polov’yan
Sumy State University, infectious diseases and epidemiology department
The incidence of acute intestinal infections (AII), caused by conditionally pathogenic microorganisms has increased nowadays in Ukraine. As a result, widely used antibacterial drugs are forming resistance in microorganisms that needs to be reviewed etiotropic priority treatment at AII.
The purpose of research is to study clinical course, levels of cytokines and condition of intestinal microflora at AII caused by conditionally pathogenic microorganisms by using colloidal citrate of nanosilver.
40 patients hospitalized in Sumy regional infectious clinical hospital named after Z.Y. Krasovytskiy were examined, average age of (35,11±2,93) years. Men and women were under 20. Patients were hospitalized at (1,26±0,07) day of onset. Patients were divided into two groups of 20 persons each depending on the medical purpose. First group of patients received basic therapy – gastric and/or intestine lavage, diet, rehydration, enzymes and sorbents. The second – colloidal citrate of nanosilver 10 mg/l 100 ml three times a day for 5 days on the background of basic therapy. Intestinal microflora, cytokines IL-1β, IL 4, sIg A at hospitalization and on (5,94±0,18) day of disease were examined.
At the beginning of treatment group of patients were comparable for frequency of defecation (first group (8,13±1,74) and second (5,74±1,12) times a day, p>0,05), the body temperature rose (37,49±0,12) 0C and other clinical symptoms. After the therapy of 2nd group patients rather than 1st one abdominal pain disappeared, the (3,79±0,24) and (5,38±0,31) days respectively, p<0,001. Also, patients receiving colloidal citrate of nanosilver had earlier terms of normalization of defecation (1st and 2nd group (4,05±0,26) and (5,06±0,34) days respecticely, p<0,05), decreased patient length of stay in hospital ((5,53±0,18) and (6,44±0,3) days, p<0,01 respectively).
In the beginning of therapy all patients’ growth was established compared with the norm of sIg A (1st, 2nd and norm group (20,10±1,55), (19,62±1,57) respectively and (4,05±0,36) mg/l, p<0,001), IL-1β ((3,67±0,40), (3,22±0,26) respectively and (1,81±0,03) pg/l, p<0,001), IL 4 ((8,26±0,52), (8,24±0,53) respectively and (0,97±0,13) pg/l, p<0,001). In the early recovery period two groups IL-1β declined to normal (1,80±0,10) and (1,97±0,09) pg/l, p<0,001; IL 4 was less in dynamics (p<0,001), but higher then normal (1st group – (5,36±0,43), 2nd – (4,03±0,46), p<0,001). Lower concentrations of IL 4 in 2nd group in the early recovery period (p<0,05) points to reduce the risk of inflammatory response to normal flora and possible chronization of pathological process in the colon compared to the patients of 1st group. After discharge from hospital the level of sIg A of 1st and 2nd groups did not reach the norm ((19,62±1,57) and (14,38±1,16) respectively, p<0,001), but differed significantly between groups (p<0,05).
In the study of intestinal microflora on (5,94±0,18) day of disease decrease in the number of Bifidobacterium and Lactobacillus in both groups of patients were detected (in the 1st (3,50±1,02) and (4,13±0,94 ) in 2nd (4,89±0,88) respectively and (4,95±0,89) against normal (7,90±0,07) and (7,75±0,1) lg CFU/g p<0,001). In 2nd group, compared with 1st one the level of total E. coli was below ((7,47±0,06) and (7,66±0,07) lg CFU/g respectively, p<0,05), other members of the conditionally pathogenic microorganisms ((0,52±0,36) and (2,77±0,93) lg CFU/g respectively, p<0,05), indicating less severity of dysbacteriosis. The number of fungi Candida did not differ from normal in dynamics.
Thus, the use of colloidal citrate of nanosilver at AII leads to faster normalization of defecation, reduction of the pain syndrome duration and length of staying in the hospital; reduces the risk of inflammatory response to normal flora and progression of intestinal dysbacteriosis.
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