9 research outputs found
EFFECT OF PRIORITY DRINKING WATER CONTAMINANTS ON THE QUALITY INDICATORS OF BEVERAGES DURING THEIR PRODUCTION AND STORAGE
Currently, water from the centralized domestic drinking water supply system is mainly used to make non- alcoholic carbonated beverages and nectars. The classical technology does not always provide the purification of water from organic compounds. In addition, during water preparation, at the primary chlorination stage, chlorine-containing organic compounds (chloroform, dichloroethane, trichlorethylene, etc.) are formed due to the interaction of chlorine with natural organic substances. The by-products of natural water treatment by chloragents, in addition to the toxic and carcinogenic effects, can interact with the main components of products reducing their quality. Such water cannot be used for drinking purposes and in food production without the additional post-treatment. The results of the study of the effect of organic impurities present in water (chloroform, trichlorethylene and dichloroethane) on the stability of the components of non-alcoholic carbonated beverages (sodium benzoate, sucrose, citric acid, natural and synthetic dyes and vanillin) and nectars (color stability, vitamins A, C, group B) have been provided. The studies were carried out in the Kemerovo region using gas-liquid chromatography, molecular absorption spectroscopy, refractometry and capillary electrophoresis. The concentration of the main components of non-alcoholic carbonated beverages, nectars and priority contaminants (trichlorethylene and dichloroethane) has been reduced. It has been shown that chloroform does not come into chemical interaction with the components of beverages. The mechanism of interaction of sucrose, citric acid, sodium benzoate, vanillin, vitamins in non-alcoholic carbonated beverages and nectars with trichlorethylene and dichloroethane has been theoretically justified. It has been established that dichloroethane and trichlorethylene have a significant effect on the resistance of the main components of non-alcoholic carbonated beverages, with the exception of dyes, and also on the intensity of color and the preservation of vitamins of nectars, reducing the quality characteristics of beverages during production and storage
Π‘Π²ΡΠ·Ρ ΠΏΠΎΠ»ΠΈΠΌΠΎΡΡΠΈΠ·ΠΌΠ° Π³Π΅Π½ΠΎΠ² ΡΠ΅Π½ΠΈΠ½-Π°Π½Π³ΠΈΠΎΡΠ΅Π½Π·ΠΈΠ½ΠΎΠ²ΠΎΠΉ ΡΠΈΡΡΠ΅ΠΌΡ ΠΈΒ ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΠ°Π»ΡΠ½ΠΎΠΉ Π΄ΠΈΡΡΡΠ½ΠΊΡΠΈΠΈ ΡΒ ΡΠΎΡΠΌΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ΠΌ ΠΈΒ ΡΡΠΆΠ΅ΡΡΡΡ ΠΏΠΎΡΡΠ°Π»ΡΠ½ΠΎΠΉ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΠΈ ΡΒ Π±ΠΎΠ»ΡΠ½ΡΡ Ρ ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΈΠΌ Π³Π΅ΠΏΠ°ΡΠΈΡΠΎΠΌ Π‘
Background: At present, much attention is paid to genetic factors explaining the clinical course of chronic hepatitis C. Aim: To evaluate an association of the gene polymorphisms involved in the formation of endothelial dysfunction (NOS3 894G/T, CYBA 242C/T, MTHFR 677C/T) and encoding components of the renin-angiotensin system (ATR1 1166A/C, AGT (-6)G/T and 235M/T) with development and severity of portal hypertension syndrome in patients with chronic hepatitis C. Materials and methods: 162 patients with chronic hepatitis C and HCV-related cirrhosis (114 women and 48 men) were divided into the following groups: no portal hypertension (n = 98), "compensated" (n = 19) and "decompensated" (n = 45) portal hypertension. The gene polymorphisms were assessed by molecular genetic methods. Results: TT genotype of CYBA was more common in patients with portal hypertension than in those without (odds ratio (OR) for TT = 3.59, p = 0.031). This difference becomes larger when comparing the decompensated portal hypertension group with the no portal hypertension group (OR TT = 5.46, p = 0.009). Other gene polymorphisms were not associated with development or decompensation of portal hypertension. Multivariate analysis of the impact of genetic, clinical and demographic factors showed that portal hypertension was associated primarily with patients age at the time of the study (Wald's Ρ
2 = 14.99) and with their body mass index (Wald's Ρ
2 = 4.35). After exclusion of these population-wide risk factors from the model, the development of portal hypertension correlated with the carriage of 235TT genotype of CYBA (Wald's Ρ
2 = 6.07, OR = 4.29) and (-6)AA genotype AGT (Wald's Ρ
2 = 4.73, OR = 4.13), as well as with the lack of protective 235TT genotype AGT (Wald's Ρ
2 = 4.06, OR = 0.33). The combined effects of the studied gene polymorphisms on decompensation of the portal hypertension in patients with chronic HCV infection were similar. Conclusion: The development and increase in severity of portal hypertension syndrome in patients with chronic hepatitis C is directly correlated with the carriage of AA genotype of AGT (-6)G/A and TT genotype CYBA 242C/T and the absence of TT genotype AGT 235M/T.ΠΠΊΡΡΠ°Π»ΡΠ½ΠΎΡΡΡ. Π‘Π΅Π³ΠΎΠ΄Π½Ρ Π±ΠΎΠ»ΡΡΠΎΠ΅ Π²Π½ΠΈΠΌΠ°Π½ΠΈΠ΅ ΡΠ΄Π΅Π»ΡΠ΅ΡΡΡ ΠΏΠΎΠΈΡΠΊΡ Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΠ°ΠΊΡΠΎΡΠΎΠ², ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΡΡΠΈΡ
Β ΡΠ΅ΡΠ΅Π½ΠΈΠ΅Β Ρ
ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎΒ Π³Π΅ΠΏΠ°ΡΠΈΡΠ° Π‘. Π¦Π΅Π»Ρ β ΠΎΡΠ΅Π½ΠΈΡΡΒ ΡΠ²ΡΠ·Ρ ΠΏΠΎΠ»ΠΈΠΌΠΎΡΡΠΈΠ·ΠΌΠ°Β Π³Π΅Π½ΠΎΠ², Π²ΠΎΠ²Π»Π΅ΡΠ΅Π½Π½ΡΡ
Β Π² ΡΠ°Π·Π²ΠΈΡΠΈΠ΅Β ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΠ°Π»ΡΠ½ΠΎΠΉ Π΄ΠΈΡΡΡΠ½ΠΊΡΠΈΠΈ (NOS3 894G/T, CYBA 242C/T, MTHFR 677C/T) ΠΈ ΠΊΠΎΠ΄ΠΈΡΡΡΡΠΈΡ
ΠΊΠΎΠΌΠΏΠΎΠ½Π΅Π½ΡΡ ΡΠ΅Π½ΠΈΠ½-Π°Π½Π³ΠΈΠΎΡΠ΅Π½Π·ΠΈΠ½ΠΎΠ²ΠΎΠΉΒ Β ΡΠΈΡΡΠ΅ΠΌΡΒ Β (ATR1 1166A/C,Β AGT (-6)G/A ΠΈ 235M/T), Ρ ΡΠΎΡΠΌΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ΠΌ ΠΈ Π½Π°ΡΠ°ΡΡΠ°Π½ΠΈΠ΅ΠΌ ΡΡΠΆΠ΅ΡΡΠΈ ΡΠΈΠ½Π΄ΡΠΎΠΌΠ° ΠΏΠΎΡΡΠ°Π»ΡΠ½ΠΎΠΉ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΠΈΒ Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
Β Ρ
ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΈΠΌΒ Π³Π΅ΠΏΠ°ΡΠΈΡΠΎΠΌΒ Π‘. ΠΠ°ΡΠ΅ΡΠΈΠ°Π» ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ.Β Π‘ΡΠΎ ΡΠ΅ΡΡΡΠ΄Π΅ΡΡΡ Π΄Π²Π° Π±ΠΎΠ»ΡΠ½ΡΡ
Ρ
ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΈΠΌ Π³Π΅ΠΏΠ°ΡΠΈΡΠΎΠΌ Π‘ ΠΈ ΡΠΈΡΡΠΎΠ·ΠΎΠΌ ΠΏΠ΅ΡΠ΅Π½ΠΈ Π‘ (114 ΠΆΠ΅Π½ΡΠΈΠ½ ΠΈ 48 ΠΌΡΠΆΡΠΈΠ½) Π±ΡΠ»ΠΈ ΡΠ°Π·Π΄Π΅Π»Π΅Π½Ρ Π½Π° Π³ΡΡΠΏΠΏΡ: Π±Π΅Π· ΠΏΡΠΈΠ·Π½Π°ΠΊΠΎΠ²Β ΠΏΠΎΡΡΠ°Π»ΡΠ½ΠΎΠΉ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΠΈΒ (n = 98), Ρ ΡΠΈΠ½Π΄ΡΠΎΠΌΠΎΠΌΒ ΠΏΠΎΡΡΠ°Π»ΡΠ½ΠΎΠΉ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΠΈ Π² ΠΊΠΎΠΌΠΏΠ΅Π½ΡΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ (n = 19) ΠΈ Π΄Π΅ΠΊΠΎΠΌΠΏΠ΅Π½ΡΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ (n = 45) ΡΠ°Π·Π΅. ΠΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΠ΅ ΠΏΠΎΠ»ΠΈΠΌΠΎΡΡΠΈΠ·ΠΌΠ° ΠΈΡΡΠ»Π΅Π΄ΡΠ΅ΠΌΡΡ
Π³Π΅Π½ΠΎΠ² ΠΏΡΠΎΠ²ΠΎΠ΄ΠΈΠ»ΠΎΡΡ ΠΌΠΎΠ»Π΅ΠΊΡΠ»ΡΡΠ½ΠΎ-Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ ΠΌΠ΅ΡΠΎΠ΄Π°ΠΌΠΈ. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ.Β Π£Β ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ²Β Ρ ΡΠΈΠΌΠΏΡΠΎΠΌΠ°ΠΌΠΈΒ ΠΏΠΎΡΡΠ°Π»ΡΠ½ΠΎΠΉΒ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΠΈΒ Β Π΄ΠΎΡΡΠΎΠ²Π΅ΡΠ½ΠΎΒ Β ΡΠ°ΡΠ΅,Β ΡΠ΅ΠΌ Π² Π³ΡΡΠΏΠΏΠ΅ Π±Π΅Π·Β ΠΏΠΎΡΡΠ°Π»ΡΠ½ΠΎΠΉΒ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΠΈ,Β Π²ΡΡΡΠ΅ΡΠ°Π»ΠΎΡΡ Π½ΠΎΡΠΈΡΠ΅Π»ΡΡΡΠ²ΠΎ Π³Π΅Π½ΠΎΡΠΈΠΏΠ° TT Π³Π΅Π½Π° CYBA (ΠΎΡΠ½ΠΎΡΠ΅Π½ΠΈΠ΅Β ΡΠ°Π½ΡΠΎΠ²Β (ΠΠ¨) TT = 3,59,Β Ρ = 0,031). ΠΡΠΈ ΡΡΠ°Π²Π½Π΅Π½ΠΈΠΈΒ Π³ΡΡΠΏΠΏ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ²Β Ρ Π΄Π΅ΠΊΠΎΠΌΠΏΠ΅Π½ΡΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉΒ ΠΏΠΎΡΡΠ°Π»ΡΠ½ΠΎΠΉ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΠ΅ΠΉΒ ΠΈ Π±Π΅Π· ΠΏΠΎΡΡΠ°Π»ΡΠ½ΠΎΠΉΒ Β Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΠΈΒ Β ΡΠ°Π·Π»ΠΈΡΠΈΡΒ Β Π½Π°ΡΠ°ΡΡΠ°Π»ΠΈ (ΠΠ¨ TT = 5,46, Ρ = 0,009). ΠΠ»Ρ ΠΎΡΡΠ°Π»ΡΠ½ΡΡ
Π³Π΅Π½ΠΎΠ²Β Π΄ΠΎΡΡΠΎΠ²Π΅ΡΠ½ΡΡ
Β Β ΡΠ°Π·Π»ΠΈΡΠΈΠΉΒ Β Π½Π΅Β ΠΎΠ±Π½Π°ΡΡΠΆΠ΅Π½ΠΎ. ΠΠ½ΠΎΠ³ΠΎΡΠ°ΠΊΡΠΎΡΠ½ΡΠΉ Π°Π½Π°Π»ΠΈΠ· ΡΠΎΠ²ΠΌΠ΅ΡΡΠ½ΠΎΠ³ΠΎ Π²Π»ΠΈΡΠ½ΠΈΡ Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΈ ΠΊΠ»ΠΈΠ½ΠΈΠΊΠΎ-Π΄Π΅ΠΌΠΎΠ³ΡΠ°ΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΠ°ΠΊΡΠΎΡΠΎΠ²Β Π²ΡΡΠ²ΠΈΠ»: ΠΏΠΎΡΡΠ°Π»ΡΠ½Π°ΡΒ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΡΒ Π°ΡΡΠΎΡΠΈΠΈΡΡΠ΅ΡΡΡ ΠΏΡΠ΅ΠΆΠ΄Π΅Β Π²ΡΠ΅Π³ΠΎ Ρ Π²ΠΎΠ·ΡΠ°ΡΡΠΎΠΌΒ Π±ΠΎΠ»ΡΠ½ΡΡ
Π½Π°Β ΠΌΠΎΠΌΠ΅Π½ΡΒ ΠΎΠ±ΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡΒ (ΡΡΠ°ΡΠΈΡΡΠΈΠΊΠ° ΠΠ°Π»ΡΠ΄Π° ΟΒ² = 14,99) ΠΈ Ρ ΠΈΡ
ΠΈΠ½Π΄Π΅ΠΊΡΠΎΠΌ ΠΌΠ°ΡΡΡ ΡΠ΅Π»Π° (ΡΡΠ°ΡΠΈΡΡΠΈΠΊΠ° ΠΠ°Π»ΡΠ΄Π° ΟΒ² = 4,35). ΠΠΎΡΠ»Π΅ ΠΈΡΠΊΠ»ΡΡΠ΅Π½ΠΈΡ ΠΈΠ· ΠΌΠΎΠ΄Π΅Π»ΠΈ ΡΡΠΈΡ
ΠΎΠ±ΡΠ΅ΠΏΠΎΠΏΡΠ»ΡΡΠΈΠΎΠ½Π½ΡΡ
Β ΡΠ°ΠΊΡΠΎΡΠΎΠ²Β ΡΠΈΡΠΊΠ° ΡΠ°Π·Π²ΠΈΡΠΈΠ΅ ΠΏΠΎΡΡΠ°Π»ΡΠ½ΠΎΠΉ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΠΈ ΠΊΠΎΡΡΠ΅Π»ΠΈΡΠΎΠ²Π°Π»ΠΎ Ρ Π½ΠΎΡΠΈΡΠ΅Π»ΡΡΡΠ²ΠΎΠΌ 235Π’Π’ Π³Π΅Π½ΠΎΡΠΈΠΏΠ° Π³Π΅Π½Π° CYBA (ΡΡΠ°ΡΠΈΡΡΠΈΠΊΠ° ΠΠ°Π»ΡΠ΄Π° ΟΒ² = 6,07, ΠΠ¨ = 4,29) ΠΈ (-6)ΠΠ Π³Π΅Π½ΠΎΡΠΈΠΏΠ° Π³Π΅Π½Π° AGT (ΡΡΠ°ΡΠΈΡΡΠΈΠΊΠ° ΠΠ°Π»ΡΠ΄Π° ΟΒ² = 4,73, ΠΠ¨ = 4,13) ΠΈ ΠΎΡΡΡΡΡΡΠ²ΠΈΠ΅ΠΌ ΠΏΡΠΎΡΠ΅ΠΊΡΠΈΠ²Π½ΠΎΠ³ΠΎ 235Π’Π’ Π³Π΅Π½ΠΎΡΠΈΠΏΠ° Π³Π΅Π½Π° AGT (ΡΡΠ°ΡΠΈΡΡΠΈΠΊΠ° ΠΠ°Π»ΡΠ΄Π° ΟΒ² = 4,06, ΠΠ¨ = 0,33). ΠΠ½Π°Π»ΠΎΠ³ΠΈΡΠ½ΡΠΌ Π±ΡΠ»ΠΎ ΡΠΎΡΠ΅ΡΠ°Π½Π½ΠΎΠ΅ Π²Π»ΠΈΡΠ½ΠΈΠ΅ ΠΊΠΎΠΌΠ±ΠΈΠ½Π°ΡΠΈΠΈ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½Π½ΡΡ
Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΡ
Π²Π°ΡΠΈΠ°Π½ΡΠΎΠ²Β Π½Π° Π΄Π΅ΠΊΠΎΠΌΠΏΠ΅Π½ΡΠ°ΡΠΈΡΒ ΠΏΠΎΡΡΠ°Π»ΡΠ½ΠΎΠΉΒ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΠΈ.Β ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅.Β Π Π°Π·Π²ΠΈΡΠΈΠ΅Β ΠΈ Π½Π°ΡΠ°ΡΡΠ°Π½ΠΈΠ΅Β ΡΡΠΆΠ΅ΡΡΠΈ ΡΠΈΠ½Π΄ΡΠΎΠΌΠ°Β ΠΏΠΎΡΡΠ°Π»ΡΠ½ΠΎΠΉΒ Π³ΠΈΠΏΠ΅ΡΡΠ΅Π½Π·ΠΈΠΈ Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
Ρ
ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΈΠΌ Π³Π΅ΠΏΠ°ΡΠΈΡΠΎΠΌ Π‘ ΠΏΡΡΠΌΠΎ ΠΊΠΎΡΡΠ΅Π»ΠΈΡΡΠ΅Ρ Ρ Π½ΠΎΡΠΈΡΠ΅Π»ΡΡΡΠ²ΠΎΠΌΒ (-6)ΠΠ Π³Π΅Π½ΠΎΡΠΈΠΏΠ° Π³Π΅Π½Π° AGT ΠΈ 242TΠ’ Π³Π΅Π½ΠΎΡΠΈΠΏΠ° Π³Π΅Π½Π° CYBA ΠΈ Ρ ΠΎΡΡΡΡΡΡΠ²ΠΈΠ΅ΠΌ 235Π’Π’ Π³Π΅Π½ΠΎΡΠΈΠΏΠ° Π³Π΅Π½Π° AGT
ΠΡΠΎΠ³Π½ΠΎΠ·ΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ ΡΠΊΠΎΡΠΎΡΡΠΈ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΡΠΈΠ±ΡΠΎΠ·Π° ΠΏΠ΅ΡΠ΅Π½ΠΈ ΡΒ Π±ΠΎΠ»ΡΠ½ΡΡ Ρ ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΈΠΌ Π³Π΅ΠΏΠ°ΡΠΈΡΠΎΠΌΒ Π‘Β Π½Π° ΠΎΡΠ½ΠΎΠ²Π΅ ΠΊΠΎΠΌΠ±ΠΈΠ½Π°ΡΠΈΠΈ Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΡ ΠΈΒ ΡΡΠ΅Π΄ΠΎΠ²ΡΡ ΡΠ°ΠΊΡΠΎΡΠΎΠ²
Rationale: Search for predictors of aggressive course of chronic hepatitis C virus (HCV) infection in individual patients, including genetic studies, is consideredΒ to be a major urgentΒ goal. High rates of fibrosis progressionΒ in chronic HCV infection is associated with several gene polymorphismsΒ coding for the components of renin-angiotensin system and involved in the formation of endothelial dysfunction and oxidative stress.Aim: To develop a predictiveΒ modelΒ toΒ assessΒ theΒ probabilityΒ of rapid fibrosis progressionΒ in patientsΒ with chronic HCV infection based on the combination of the known genetic markers, clinical and demographic parameters.Materials and methods:Β One hundredΒ andΒ nineΒ patientsΒ withΒ chronicΒ HCVΒ infection (79 womenΒ and 30 men) of known duration and liver fibrosis were categorizedΒ into the groups with βrapid fibrosisβ (n = 54, the rate of fibrosis progression β₯ 0.13 fibrosis units / year) and with βslow fibrosisβΒ (n = 55, theΒ rateΒ of progression 0.13Β fibrosis units / year). PolymorphismsΒ of the studied genes were assessed by molecular genetic assays. Multivariate analysis of the influence of combination of geneticΒ variants, as well as of the interaction of genetic, clinical and demographic factors on the rate of fibrosis progressionΒ in the patients with chronic HCV infection was performed by logisticΒ regressionΒ Β method.Β Results:Β TheΒ rapid rate of fibrosis progressionΒ was significantly associated with patient'sΒ age at the time of infection (Wald statisticsΒ 14.955;Β p = 0.00011), male gender (Wald statisticsΒ 6.787;Β p = 0.00918),Β (-6)ΠΠ genotypeΒ of theΒ AGTΒ geneΒ carriageΒ (Wald statistics 6.512;Β p = 0.01072), 242Π’Π’-genotypeΒ of theΒ CYBA geneΒ Β (WaldΒ statisticsΒ Β 4.347;Β Β p = 0.03708),Β Β and 235ΠΠ’ genotype of the AGT geneΒ (Wald statistics 4.306; p = 0.03799). The model to predict the probability of rapid fibrosis progressionΒ in individuals with chronic HCV infection included the above mentioned factors; its use was demonstrated with two clinical cases.Conclusion: The analysis of the AGTΒ geneΒ (M235T andΒ G-6A loci) andΒ theΒ Π‘YBA geneΒ (C242TΒ locus) polymorphismsΒ areΒ relevant toΒ identify patientsΒ atΒ risk of rapidΒ liver fibrosis progression. In this case, 242Π’Π’ genotype of the CYBA geneΒ andΒ (-6)AA andΒ 235MT genotypes of the AGT geneΒ are consideredΒ unfavorable. To refine the prognosis, it is necessary to take into accountΒ demographic parameters (genderΒ and age at the moment of infection contraction), because male gender and older age of getting the infection would increase the probability of rapidly progressive of hepatitis C.ΠΠΊΡΡΠ°Π»ΡΠ½ΠΎΡΡΡ. ΠΠΎΠΈΡΠΊ Ρ ΠΊΠΎΠ½ΠΊΡΠ΅ΡΠ½ΠΎΠ³ΠΎΒ Π±ΠΎΠ»ΡΠ½ΠΎΠ³ΠΎ ΠΏΡΠ΅Π΄ΠΈΠΊΡΠΎΡΠΎΠ² Π°Π³ΡΠ΅ΡΡΠΈΠ²Π½ΠΎΠ³ΠΎ ΡΠ΅ΡΠ΅Π½ΠΈΡ Ρ
ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π³Π΅ΠΏΠ°ΡΠΈΡΠ° Π‘ (Π₯ΠΠ‘), Π² ΡΠΎΠΌ ΡΠΈΡΠ»Π΅ Ρ ΠΏΠΎΠΌΠΎΡΡΡ Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠΉ, ΠΏΡΠ΅Π΄ΡΡΠ°Π²Π»ΡΠ΅ΡΡΡ Π°ΠΊΡΡΠ°Π»ΡΠ½ΠΎΠΉ Π·Π°Π΄Π°ΡΠ΅ΠΉ. ΠΡΡΡΡΡΠΉ ΡΠ΅ΠΌΠΏ ΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΡΠΎΠ²Π°Π½ΠΈΡΒ ΡΠΈΠ±ΡΠΎΠ·Π°Β ΠΏΡΠΈ Π₯ΠΠ‘ Π°ΡΡΠΎΡΠΈΠΈΡΡΠ΅ΡΡΡΒ Ρ ΠΏΠΎΠ»ΠΈΠΌΠΎΡΡΠΈΠ·ΠΌΠΎΠΌ ΡΡΠ΄Π° Π³Π΅Π½ΠΎΠ², ΠΊΠΎΠ΄ΠΈΡΡΡΡΠΈΡ
ΠΊΠΎΠΌΠΏΠΎΠ½Π΅Π½ΡΡΒ Β Β Β ΡΠ΅Π½ΠΈΠ½-Π°Π½Π³ΠΈΠΎΡΠ΅Π½Π·ΠΈΠ½ΠΎΠ²ΠΎΠΉΒ Β Β Β ΡΠΈΡΡΠ΅ΠΌΡ ΠΈ Π²ΠΎΠ²Π»Π΅ΡΠ΅Π½Π½ΡΡ
Β Π² ΡΠΎΡΠΌΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΠ°Π»ΡΠ½ΠΎΠΉΒ Β Π΄ΠΈΡΡΡΠ½ΠΊΡΠΈΠΈΒ ΠΈΒ ΠΎΠΊΠΈΡΠ»ΠΈΡΠ΅Π»ΡΠ½ΠΎΠ³ΠΎΒ Β ΡΡΡΠ΅ΡΡΠ°.Π¦Π΅Π»Ρ β ΡΠ°Π·ΡΠ°Π±ΠΎΡΠΊΠ°Β ΠΏΡΠΎΠ³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΌΠΎΠ΄Π΅Π»ΠΈ ΠΎΡΠ΅Π½ΠΊΠΈ Π²Π΅ΡΠΎΡΡΠ½ΠΎΡΡΠΈ Π±ΡΡΡΡΠΎΠ³ΠΎ ΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΡΠΎΠ²Π°Π½ΠΈΡΒ ΡΠΈΠ±ΡΠΎΠ·Π°Β Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
Β Π₯ΠΠ‘Β Π½Π°Β ΠΎΡΠ½ΠΎΠ²Π°Π½ΠΈΠΈ ΠΊΠΎΠΌΠ±ΠΈΠ½Π°ΡΠΈΠΈΒ Β ΠΈΠ·ΡΡΠ΅Π½Π½ΡΡ
Β Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΡ
Β Β ΠΌΠ°ΡΠΊΠ΅ΡΠΎΠ²Β ΠΈ ΠΊΠ»ΠΈΠ½ΠΈΠΊΠΎ-Π΄Π΅ΠΌΠΎΠ³ΡΠ°ΡΠΈΡΠ΅ΡΠΊΠΈΡ
Β Β ΠΏΠ°ΡΠ°ΠΌΠ΅ΡΡΠΎΠ².ΠΠ°ΡΠ΅ΡΠΈΠ°Π»Β ΠΈΒ ΠΌΠ΅ΡΠΎΠ΄Ρ.Β Π‘ΡΠΎ Π΄Π΅Π²ΡΡΡΒ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² ΡΒ Ρ
ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΎΠΉΒ Β HCV-ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠ΅ΠΉΒ Β (79Β ΠΆΠ΅Π½ΡΠΈΠ½ ΠΈ 30 ΠΌΡΠΆΡΠΈΠ½) Ρ ΠΈΠ·Π²Π΅ΡΡΠ½ΠΎΠΉΒ Π΄Π»ΠΈΡΠ΅Π»ΡΠ½ΠΎΡΡΡΡΒ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ ΠΈ ΡΡΠ°Π΄ΠΈΠ΅ΠΉ ΡΠΈΠ±ΡΠΎΠ·Π° ΠΏΠ΅ΡΠ΅Π½ΠΈ Π±ΡΠ»ΠΈ ΡΠ°Π·Π΄Π΅Π»Π΅Π½Ρ Π½Π° Π³ΡΡΠΏΠΏΡ Ρ Β«Π±ΡΡΡΡΡΠΌ ΡΠΈΠ±ΡΠΎΠ·ΠΎΠΌΒ» (n = 54, ΡΠΊΠΎΡΠΎΡΡΡ ΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΡΠΈΠ±ΡΠΎΠ·Π°Β β₯ 0,13 Π΅Π΄. ΡΠΈΠ±ΡΠΎΠ·Π° / Π³ΠΎΠ΄)Β Β ΠΈΒ Β ΡΒ Β Β«ΠΌΠ΅Π΄Π»Π΅Π½Π½ΡΠΌΒ Β ΡΠΈΠ±ΡΠΎΠ·ΠΎΠΌΒ» (n = 55,Β ΡΠΊΠΎΡΠΎΡΡΡΒ ΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΡΠΎΠ²Π°Π½ΠΈΡΒ 0,13Β Π΅Π΄. ΡΠΈΠ±ΡΠΎΠ·Π° / Π³ΠΎΠ΄).Β Β Β ΠΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΠ΅Β Β ΠΏΠΎΠ»ΠΈΠΌΠΎΡΡΠΈΠ·ΠΌΠ° ΠΈΡΡΠ»Π΅Π΄ΡΠ΅ΠΌΡΡ
Β Π³Π΅Π½ΠΎΠ²Β ΠΏΡΠΎΠ²ΠΎΠ΄ΠΈΠ»ΠΎΡΡΒ ΠΌΠΎΠ»Π΅ΠΊΡΠ»ΡΡΠ½ΠΎ-Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ ΠΌΠ΅ΡΠΎΠ΄Π°ΠΌΠΈ. ΠΠ½ΠΎΠ³ΠΎΡΠ°ΠΊΡΠΎΡΠ½ΡΠΉ Π°Π½Π°Π»ΠΈΠ· ΠΊΠΎΠΌΠΏΠ»Π΅ΠΊΡΠ½ΠΎΠ³ΠΎ Π²Π»ΠΈΡΠ½ΠΈΡ Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΡ
Π²Π°ΡΠΈΠ°Π½ΡΠΎΠ², Π°Β ΡΠ°ΠΊΠΆΠ΅Β ΡΠΎΠ²ΠΌΠ΅ΡΡΠ½ΠΎΠ³ΠΎΒ Π²ΠΎΠ·Π΄Π΅ΠΉΡΡΠ²ΠΈΡ Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΈ ΠΊΠ»ΠΈΠ½ΠΈΠΊΠΎ-Π΄Π΅ΠΌΠΎΠ³ΡΠ°ΡΠΈΡΠ΅ΡΠΊΠΈΡ
Β ΡΠ°ΠΊΡΠΎΡΠΎΠ² Π½Π° ΡΠΊΠΎΡΠΎΡΡΡ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΡΠΈΠ±ΡΠΎΠ·Π° Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
Π₯ΠΠ‘ ΠΏΡΠΎΠ²ΠΎΠ΄ΠΈΠ»ΠΈ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ Π»ΠΎΠ³ΠΈΡΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΡΠ΅Π³ΡΠ΅ΡΡΠΈΠΈ.Β Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ.Β Π‘ΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈ Π·Π½Π°ΡΠΈΠΌΠΎ Ρ Π±ΡΡΡΡΡΠΌ ΡΠ΅ΠΌΠΏΠΎΠΌ ΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΡΠΈΠ±ΡΠΎΠ·Π° ΠΊΠΎΡΡΠ΅Π»ΠΈΡΠΎΠ²Π°Π»ΠΈ Π²ΠΎΠ·ΡΠ°ΡΡ Π±ΠΎΠ»ΡΠ½ΡΡ
Π½Π° ΠΌΠΎΠΌΠ΅Π½Ρ ΠΈΠ½ΡΠΈΡΠΈΡΠΎΠ²Π°Π½ΠΈΡΒ Β Β Β (ΡΡΠ°ΡΠΈΡΡΠΈΠΊΠ°Β Β ΠΠ°Π»ΡΠ΄Π° = 14,955; p = 0,00011),Β Β Β Β Β Β ΠΌΡΠΆΡΠΊΠΎΠΉΒ Β Β Β Β Β ΠΏΠΎΠ»Β Β Β Β Β Β (ΡΡΠ°ΡΠΈΡΡΠΈΠΊΠ° ΠΠ°Π»ΡΠ΄Π° = 6,787; p = 0,00918), Π½ΠΎΡΠΈΡΠ΅Π»ΡΡΡΠ²ΠΎΒ (-6)ΠΠ Π³Π΅Π½ΠΎΡΠΈΠΏΠ°Β Π³Π΅Π½Π°Β AGT (ΡΡΠ°ΡΠΈΡΡΠΈΠΊΠ° ΠΠ°Π»ΡΠ΄Π° = 6,512; p = 0,01072),Β 242Π’Π’-Π³Π΅Π½ΠΎΡΠΈΠΏΠ°Β Π³Π΅Π½Π°Β CYBAΒ (ΡΡΠ°ΡΠΈΡΡΠΈΠΊΠ°Β ΠΠ°Π»ΡΠ΄Π° = 4,347;Β p = 0,03708)Β ΠΈΒ 235ΠΠ’Β Π³Π΅Π½ΠΎΡΠΈΠΏΠ°Β Β Π³Π΅Π½Π°Β Β AGT (ΡΡΠ°ΡΠΈΡΡΠΈΠΊΠ°Β ΠΠ°Π»ΡΠ΄Π° = 4,306; p = 0,03799). ΠΠΎΡΡΡΠΎΠ΅Π½Π° ΠΌΠΎΠ΄Π΅Π»Ρ, ΠΏΡΠ΅Π΄ΡΠΊΠ°Π·ΡΠ²Π°ΡΡΠ°Ρ Π²Π΅ΡΠΎΡΡΠ½ΠΎΡΡΡΒ Π±ΡΡΡΡΠΎΠ³ΠΎΒ ΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΡΠΈΠ±ΡΠΎΠ·Π°Β Ρ Π±ΠΎΠ»ΡΠ½ΠΎΠ³ΠΎΒ Π₯ΠΠ‘Β Π½Π° ΠΎΡΠ½ΠΎΠ²Π°Π½ΠΈΠΈΒ Π²ΡΡΠ΅ΠΏΡΠΈΠ²Π΅Π΄Π΅Π½Π½ΡΡ
Β ΡΠ°ΠΊΡΠΎΡΠΎΠ², ΠΏΡΠΎΠ΄Π΅ΠΌΠΎΠ½ΡΡΡΠΈΡΠΎΠ²Π°Π½ΠΎ Π΅Π΅ ΠΏΡΠΈΠΌΠ΅Π½Π΅Π½ΠΈΠ΅Β Π½Π° Π΄Π²ΡΡ
ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΏΡΠΈΠΌΠ΅ΡΠ°Ρ
.ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅. ΠΠ»Ρ Π²ΡΡΠ²Π»Π΅Π½ΠΈΡ Π±ΠΎΠ»ΡΠ½ΡΡ
Ρ ΡΠΈΡΠΊΠΎΠΌ Β«Π±ΡΡΡΡΠΎΠ³ΠΎΒ» ΡΠ°Π·Π²ΠΈΡΠΈΡΒ ΡΠΈΠ±ΡΠΎΠ·Π°Β ΠΏΠ΅ΡΠ΅Π½ΠΈΒ ΡΠ΅Π»Π΅ΡΠΎΠΎΠ±ΡΠ°Π·Π½ΠΎΒ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ΠΈΠ΅ Π°Π½Π°Π»ΠΈΠ·Π° ΠΏΠΎΠ»ΠΈΠΌΠΎΡΡΠΈΠ·ΠΌΠ° Π³Π΅Π½Π°Β AGT (Π»ΠΎΠΊΡΡΡ M235T ΠΈ G-6A) ΠΈ Π³Π΅Π½Π°Β Π‘YBA (Π»ΠΎΠΊΡΡ C242T). ΠΠ΅Π±Π»Π°Π³ΠΎΠΏΡΠΈΡΡΠ½ΡΠΌΠΈΒ Π² ΡΡΠΎΠΌ ΡΠ»ΡΡΠ°Π΅ ΡΠ²Π»ΡΡΡΡΡ Π³Π΅Π½ΠΎΡΠΈΠΏΡ 242Π’Π’ Π³Π΅Π½Π° CYBA, (-6)AA ΠΈ 235MT Π³Π΅Π½Π° AGT. ΠΠ»Ρ ΡΡΠΎΡΠ½Π΅Π½ΠΈΡ ΠΏΡΠΎΠ³Π½ΠΎΠ·Π°Β Π½Π΅ΠΎΠ±Ρ
ΠΎΠ΄ΠΈΠΌΠΎ ΡΡΠΈΡΡΠ²Π°ΡΡ Π΄Π΅ΠΌΠΎΠ³ΡΠ°ΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΏΠΎΠΊΠ°Π·Π°ΡΠ΅Π»ΠΈ (ΠΏΠΎΠ» ΠΈ Π²ΠΎΠ·ΡΠ°ΡΡΒ Π½Π° ΠΌΠΎΠΌΠ΅Π½Ρ ΠΈΠ½ΡΠΈΡΠΈΡΠΎΠ²Π°Π½ΠΈΡ) β ΠΌΡΠΆΡΠΊΠΎΠΉ ΠΏΠΎΠ» ΠΈ Π±ΠΎΠ»Π΅Π΅Β ΡΡΠ°ΡΡΠΈΠΉ Π²ΠΎΠ·ΡΠ°ΡΡ ΠΈΠ½ΡΠΈΡΠΈΡΠΎΠ²Π°Π½ΠΈΡΒ ΡΠ²Π΅Π»ΠΈΡΠΈΠ²Π°ΡΡ Π²Π΅ΡΠΎΡΡΠ½ΠΎΡΡΡΒ Π±ΡΡΡΡΠΎΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΡΡΡΡΠ΅Π³ΠΎ ΡΠ΅ΡΠ΅Π½ΠΈΡ Π₯ΠΠ‘
ΠΠ΅ΠΌΠΎΠ»ΠΈΡΠΈΠΊΠΎ-ΡΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΈΠΉ ΡΠΈΠ½Π΄ΡΠΎΠΌ. ΠΠΎΠ·ΠΌΠΎΠΆΠ½Π°Ρ ΡΡΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠ°Ρ ΡΠΎΠ»Ρ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ, Π²ΡΠ·Π²Π°Π½Π½ΠΎΠΉ Campylobacter
Hemolytic uremic syndrome (HUS), one of the forms of thrombotic microangiopathy, is a severe emergency with non-immune (Coombs negative) anemia, thrombocytopenia and acute renal injury. HUS is heterogeneous, and its most common form, the typical HUS, is associated with Shiga toxin (Stx) producing bacteria, such as Escherichia coli, Shigella dysenteriae, and Citrobacter freundii. Less frequent is HUS, caused by a neuraminidase producing streptococcus (pneumococcal HUS). The most uncommon form is the atypical HUS, which is a genetic orphan disease associated with an abnormality in the regulatory protein of the complement system. HUS has a fairly high mortality rate, amounting to 10β15% on average. The long-term outcomes of HUS depend on its type, as well as on the degree of the primary body tissue damage. According to the data from Novosibirsk Children's Municipal Clinical Hospital No 3 from 1991, 44 cases of HUS in children have been identified. Complete recovery, without any residual abnormalities, was registered in 25 children (56.8% of the cases). Nine children (20.5%) developed chronic kidney disease and 10 (22.7%) of all HUS cases were fatal. Early diagnosis, as well as the identification of pathogenetic mechanisms, is the basis for adequate therapy and outcome prediction. Campylobacter may be one of the causative agents of HUS. Despite new cases of Campylobacter-associated HUS being registered in the world, the very possibility of HUS induction by this pathogen and its pathophysiology are currently unclear. There is no convincing evidence for both Stx and the neuraminidase-related mechanism of HUS in Campylobacter infections. Given the high incidence of autoimmune disorders like Guillain-Barre syndrome and reactive arthritis in Campylobacter infections, it is currently impossible to exclude an autoimmune mechanism of HUS in these diseases. Thus, the role of Campylobacter, as a new potential bacterial agent of HUS, as well as the pathogenesis of such conditions in Campylobacter infections, requires further study.ΠΠ΄Π½Π° ΠΈΠ· ΡΠΎΡΠΌ ΡΡΠΎΠΌΠ±ΠΎΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΌΠΈΠΊΡΠΎΠ°Π½Π³ΠΈΠΎΠΏΠ°ΡΠΈΠΈ Π³Π΅ΠΌΠΎΠ»ΠΈΡΠΈΠΊΠΎ-ΡΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΈΠΉ ΡΠΈΠ½Π΄ΡΠΎΠΌ (ΠΠ£Π‘) ΠΏΡΠ΅Π΄ΡΡΠ°Π²Π»ΡΠ΅Ρ ΡΠΎΠ±ΠΎΠΉ ΡΡΠΆΠ΅Π»ΡΡ, ΡΡΠ³Π΅Π½ΡΠ½ΡΡ ΠΏΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΡ, Ρ
Π°ΡΠ°ΠΊΡΠ΅ΡΠΈΠ·ΡΡΡΡΡΡΡ ΡΠ°Π·Π²ΠΈΡΠΈΠ΅ΠΌ Π½Π΅ΠΈΠΌΠΌΡΠ½Π½ΠΎΠΉ (ΠΡΠΌΠ±Ρ-ΠΎΡΡΠΈΡΠ°ΡΠ΅Π»ΡΠ½ΠΎΠΉ) Π°Π½Π΅ΠΌΠΈΠΈ, ΡΡΠΎΠΌΠ±ΠΎΡΠΈΡΠΎΠΏΠ΅Π½ΠΈΠΈ ΠΈ ΠΎΡΡΡΠΎΠ³ΠΎ ΠΏΠΎΡΠ΅ΡΠ½ΠΎΠ³ΠΎ ΠΏΠΎΠ²ΡΠ΅ΠΆΠ΄Π΅Π½ΠΈΡ. ΠΠ»Ρ ΠΠ£Π‘ ΡΠ²ΠΎΠΉΡΡΠ²Π΅Π½Π½Π° Π³Π΅ΡΠ΅ΡΠΎΠ³Π΅Π½Π½ΠΎΡΡΡ ΡΠΎΡΠΌ. ΠΠ°ΠΈΠ±ΠΎΠ»Π΅Π΅ ΡΠ°ΡΡΠ°Ρ ΡΠΎΡΠΌΠ° β ΡΠΈΠΏΠΈΡΠ½ΡΠΉ ΠΠ£Π‘ β ΡΠ²ΡΠ·Π°Π½Π° Ρ Π±Π°ΠΊΡΠ΅ΡΠΈΡΠΌΠΈ, ΠΏΡΠΎΠ΄ΡΡΠΈΡΡΡΡΠΈΠΌΠΈ Π¨ΠΈΠ³Π°-ΡΠΎΠΊΡΠΈΠ½ (Stx), Escherichia coli, Shigella dysenteriae, Citrobacter freundii. Π Π΅ΠΆΠ΅ Π²ΡΡΡΠ΅ΡΠ°Π΅ΡΡΡ ΠΠ£Π‘, Π²ΡΠ·Π²Π°Π½Π½ΡΠΉ ΡΡΡΠ΅ΠΏΡΠΎΠΊΠΎΠΊΠΊΠΎΠΌ, ΠΏΡΠΎΠ΄ΡΡΠΈΡΡΡΡΠΈΠΌ Π½Π΅ΠΉΡΠ°ΠΌΠΈΠ½ΠΈΠ΄Π°Π·Ρ, β ΠΏΠ½Π΅Π²ΠΌΠΎΠΊΠΎΠΊΠΊΠΎΠ²ΡΠΉ ΠΠ£Π‘. ΠΠ°ΠΈΠ±ΠΎΠ»Π΅Π΅ ΡΠ΅Π΄ΠΊΠ°Ρ ΡΠΎΡΠΌΠ° β Π°ΡΠΈΠΏΠΈΡΠ½ΡΠΉ ΠΠ£Π‘, Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΎΠ΅ ΠΎΡΡΠ°Π½Π½ΠΎΠ΅ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠ΅, ΠΎΠ±ΡΡΠ»ΠΎΠ²Π»Π΅Π½Π½ΠΎΠ΅ Π½Π°ΡΡΡΠ΅Π½ΠΈΠ΅ΠΌ Π±Π΅Π»ΠΊΠ° ΡΠ΅Π³ΡΠ»ΡΡΠΎΡΠ° ΡΠΈΡΡΠ΅ΠΌΡ ΠΊΠΎΠΌΠΏΠ»Π΅ΠΌΠ΅Π½ΡΠ°. ΠΠ£Π‘ ΠΎΡΠ»ΠΈΡΠ°Π΅ΡΡΡ Π΄ΠΎΡΡΠ°ΡΠΎΡΠ½ΠΎ Π²ΡΡΠΎΠΊΠΎΠΉ Π»Π΅ΡΠ°Π»ΡΠ½ΠΎΡΡΡΡ, Π΄ΠΎΡΡΠΈΠ³Π°ΡΡΠ΅ΠΉ Π² ΡΡΠ΅Π΄Π½Π΅ΠΌ 10β15%. ΠΠΎΠ»Π³ΠΎΡΡΠΎΡΠ½ΡΠΉ ΠΏΡΠΎΠ³Π½ΠΎΠ· ΠΏΡΠΈ ΠΠ£Π‘ Π·Π°Π²ΠΈΡΠΈΡ ΠΎΡ Π΅Π³ΠΎ ΡΠΈΠΏΠ°, Π° ΡΠ°ΠΊΠΆΠ΅ ΠΎΡ Π³Π»ΡΠ±ΠΈΠ½Ρ ΠΏΠ΅ΡΠ²ΠΎΠ½Π°ΡΠ°Π»ΡΠ½ΠΎΠ³ΠΎ ΠΏΠΎΠ²ΡΠ΅ΠΆΠ΄Π΅Π½ΠΈΡ ΡΠΊΠ°Π½Π΅ΠΉ ΠΎΡΠ³Π°Π½ΠΈΠ·ΠΌΠ°. ΠΠΎ Π΄Π°Π½Π½ΡΠΌ ΠΠΠ£Π ΠΠ‘Π ΠΠΠΠ β 3 (ΠΠΎΠ²ΠΎΡΠΈΠ±ΠΈΡΡΠΊ, Π ΠΎΡΡΠΈΡ), Π½Π°ΡΠΈΠ½Π°Ρ Ρ 1991 Π³. ΡΡΡΠ°Π½ΠΎΠ²Π»Π΅Π½ΠΎ 44Β ΡΠ»ΡΡΠ°Ρ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΠΠ£Π‘ Ρ Π΄Π΅ΡΠ΅ΠΉ. ΠΠΎΠ»Π½ΠΎΠ΅ Π²ΡΠ·Π΄ΠΎΡΠΎΠ²Π»Π΅Π½ΠΈΠ΅, Π±Π΅Π· ΡΠ°Π·Π²ΠΈΡΠΈΡ ΠΊΠ°ΠΊΠΈΡ
-Π»ΠΈΠ±ΠΎ Π½Π°ΡΡΡΠ΅Π½ΠΈΠΉ, Π·Π°ΡΠΈΠΊΡΠΈΡΠΎΠ²Π°Π½ΠΎ Ρ 25 (56,8%) Π΄Π΅ΡΠ΅ΠΉ, ΡΠ°Π·Π²ΠΈΡΠΈΠ΅ Ρ
ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΎΠΉ Π±ΠΎΠ»Π΅Π·Π½ΠΈ ΠΏΠΎΡΠ΅ΠΊ ΠΎΡΠΌΠ΅ΡΠ΅Π½ΠΎ Ρ 9 (20,5%) ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ², Π»Π΅ΡΠ°Π»ΡΠ½ΠΎ Π·Π°Π²Π΅ΡΡΠΈΠ»ΡΡ ΠΠ£Π‘ Π² 10 (22,7%) ΡΠ»ΡΡΠ°ΡΡ
. Π Π°Π½Π½ΡΡ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠ°, Π° ΡΠ°ΠΊΠΆΠ΅ Π²ΡΡΠ²Π»Π΅Π½ΠΈΠ΅ ΠΏΠ°ΡΠΎΠ³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΌΠ΅Ρ
Π°Π½ΠΈΠ·ΠΌΠΎΠ² Π»Π΅ΠΆΠ°Ρ Π² ΠΎΡΠ½ΠΎΠ²Π΅ Π°Π΄Π΅ΠΊΠ²Π°ΡΠ½ΠΎΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ ΠΈ ΠΏΡΠΎΠ³Π½ΠΎΠ·ΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΠΈΡΡ
ΠΎΠ΄ΠΎΠ² Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ. ΠΠ΄Π½ΠΈΠΌ ΠΈΠ· Π½ΠΎΠ²ΡΡ
ΡΡΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΡ
Π°Π³Π΅Π½ΡΠΎΠ² ΠΠ£Π‘ ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ Campylobacter. ΠΠ΅ΡΠΌΠΎΡΡΡ Π½Π° ΡΠΎ ΡΡΠΎ Π² ΠΌΠΈΡΠ΅ ΡΠ΅Π³ΠΈΡΡΡΠΈΡΡΡΡΡΡ Π½ΠΎΠ²ΡΠ΅ ΡΠ»ΡΡΠ°ΠΈ ΠΠ£Π‘, ΡΠ²ΡΠ·Π°Π½Π½ΠΎΠ³ΠΎ Ρ Campylobacter, Π½Π° Π½Π°ΡΡΠΎΡΡΠ΅ΠΌ ΡΡΠ°ΠΏΠ΅ Π½Π΅ ΡΡΠ½Ρ Π½ΠΈ ΡΠ°ΠΌΠ° Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΠΎΡΡΡ ΠΈΠ½Π΄ΡΠΊΡΠΈΠΈ ΠΠ£Π‘ Π΄Π°Π½Π½ΡΠΌ Π²ΠΎΠ·Π±ΡΠ΄ΠΈΡΠ΅Π»Π΅ΠΌ, Π½ΠΈ ΠΏΠ°ΡΠΎΠ³Π΅Π½Π΅Π· ΡΡΠΎΠ³ΠΎ ΡΠΎΡΡΠΎΡΠ½ΠΈΡ. ΠΠ΅Ρ ΡΠ±Π΅Π΄ΠΈΡΠ΅Π»ΡΠ½ΡΡ
Π΄ΠΎΠΊΠ°Π·Π°ΡΠ΅Π»ΡΡΡΠ² ΠΊΠ°ΠΊ Stx, ΡΠ°ΠΊ ΠΈ Π½Π΅ΠΉΡΠ°ΠΌΠΈΠ½ΠΈΠ΄Π°Π·Π½ΠΎΠ³ΠΎ ΠΌΠ΅Ρ
Π°Π½ΠΈΠ·ΠΌΠ° ΡΠ°Π·Π²ΠΈΡΠΈΡ ΠΠ£Π‘ ΠΏΡΠΈ ΠΊΠ°ΠΌΠΏΠΈΠ»ΠΎΠ±Π°ΠΊΡΠ΅ΡΠ½ΡΡ
ΠΈΠ½ΡΠ΅ΠΊΡΠΈΡΡ
. Π£ΡΠΈΡΡΠ²Π°Ρ Π²ΡΡΠΎΠΊΡΡ ΡΠ°ΡΡΠΎΡΡ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΠΏΡΠΈ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΡΡ
, Π²ΡΠ·Π²Π°Π½Π½ΡΡ
Campylobacter, ΡΠ°ΠΊΠΈΡ
Π°ΡΡΠΎΠΈΠΌΠΌΡΠ½Π½ΡΡ
ΠΏΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΠΉ, ΠΊΠ°ΠΊ ΡΠΈΠ½Π΄ΡΠΎΠΌ ΠΠΈΠΉΠ΅Π½Π° β ΠΠ°ΡΡΠ΅, ΡΠ΅Π°ΠΊΡΠΈΠ²Π½ΡΠ΅ Π°ΡΡΡΠΈΡΡ, ΡΠ΅Π³ΠΎΠ΄Π½Ρ Π½Π΅ ΠΏΡΠ΅Π΄ΡΡΠ°Π²Π»ΡΠ΅ΡΡΡ Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΡΠΌ ΠΈΡΠΊΠ»ΡΡΠΈΡΡ Π°ΡΡΠΎΠΈΠΌΠΌΡΠ½Π½ΡΠΉ ΠΌΠ΅Ρ
Π°Π½ΠΈΠ·ΠΌ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΠΠ£Π‘ ΠΏΡΠΈ ΡΡΠΈΡ
Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡΡ
. Π’Π°ΠΊΠΈΠΌ ΠΎΠ±ΡΠ°Π·ΠΎΠΌ, ΡΠΎΠ»Ρ Campylobacter Π² ΠΊΠ°ΡΠ΅ΡΡΠ²Π΅ Π½ΠΎΠ²ΠΎΠ³ΠΎ ΠΏΠΎΡΠ΅Π½ΡΠΈΠ°Π»ΡΠ½ΠΎΠ³ΠΎ Π±Π°ΠΊΡΠ΅ΡΠΈΠ°Π»ΡΠ½ΠΎΠ³ΠΎ Π°Π³Π΅Π½ΡΠ° ΠΠ£Π‘, Π° ΡΠ°ΠΊΠΆΠ΅ ΠΏΠ°ΡΠΎΠ³Π΅Π½Π΅Π· ΠΏΠΎΠ΄ΠΎΠ±Π½ΡΡ
ΡΠΎΡΡΠΎΡΠ½ΠΈΠΉ ΠΏΡΠΈ ΠΊΠ°ΠΌΠΏΠΈΠ»ΠΎΠ±Π°ΠΊΡΠ΅ΡΠ½ΡΡ
ΠΈΠ½ΡΠ΅ΠΊΡΠΈΡΡ
Π½ΡΠΆΠ΄Π°ΡΡΡΡ Π² Π΄Π°Π»ΡΠ½Π΅ΠΉΡΠ΅ΠΌ ΠΈΠ·ΡΡΠ΅Π½ΠΈΠΈ