7 research outputs found
ΠΠ΅Π½Ρ Π΄Π΅ΡΠΎΠΊΡΠΈΠΊΠ°ΡΠΈΠΈ ΠΊΡΠ΅Π½ΠΎΠ±ΠΈΠΎΡΠΈΠΊΠΎΠ² ΠΈ ΠΈΡ ΡΠΎΠ»Ρ Π² ΡΠ°Π·Π²ΠΈΡΠΈΠΈ ΠΏΠ½Π΅Π²ΠΌΠΎΠ½ΠΈΠΈ
Objective: to analyze DNA polymorphism in inpatients with pneumonia. Subjects and methods. Group 1 consisted of 99 patients with acute community-acquired pneumonia (CAP). Group 2 included 95 patients with severe concomitant injury, including wounds (n=63) and generalized peritonitis (n=32). Among Group 2 patients, the authors singled out two subgroups: 2A comprising 57 patients with nosocomial pneumonia (NP) and 2B including 38 patients without NP. A control group was composed of 160 apparently healthy individuals. Polymerase chain reaction genotyping was carried out for the polymorphic genes controlling xenobiotic detoxification (such as GSTM1, GSTT1, GSTP1, and CYP1A1) and the MTHFR gene that is responsible for DNA synthesis and methylation. Results. Predisposition to acute CAP has been shown for the carriers of a minor allele (4889G) at the CYP1A1 locus: 12.7% versus 5.4% in the controls (p=0.034; OR=2.6); In Group 1 patients, the development of complications (toxic myocarditis, pleuritis, pleural empyema, toxic nephropathy) is most probable for a combination of GSTT1 + GSTM1 0/0 genotypes (OR=3.2; p=0.010 versus the control group). It has been established that in severe injury, peritonitis (2B), NP does not develop statistically significantly in 61.1% of cases with the GSTM1 + GSTT1 + genotype versus 38.8% in the controls (p=0.022) or versus 37.5% in subgroup 2A (p=0.045; OR=2.6). Key words: acute community-acquired pneumonia, nosocomial pneumonia, gene polymorphism.Π¦Π΅Π»Ρ β Π°Π½Π°Π»ΠΈΠ· ΠΏΠΎΠ»ΠΈΠΌΠΎΡΡΠΈΠ·ΠΌΠ° ΠΠΠ Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
ΠΏΠ½Π΅Π²ΠΌΠΎΠ½ΠΈΠ΅ΠΉ, Π½Π°Ρ
ΠΎΠ΄ΠΈΠ²ΡΠΈΡ
ΡΡ Π½Π° ΡΡΠ°ΡΠΈΠΎΠ½Π°ΡΠ½ΠΎΠΌ Π»Π΅ΡΠ΅Π½ΠΈΠΈ. ΠΠ°ΡΠ΅ΡΠΈΠ°Π» ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ: ΠΏΠ΅ΡΠ²ΡΡ Π³ΡΡΠΏΠΏΡ (I) ΡΠΎΡΡΠ°Π²ΠΈΠ»ΠΈ 99 ΡΠ΅Π»ΠΎΠ²Π΅ΠΊ Ρ ΠΎΡΡΡΠΎΠΉ Π²Π½Π΅Π±ΠΎΠ»ΡΠ½ΠΈΡΠ½ΠΎΠΉ ΠΏΠ½Π΅Π²ΠΌΠΎΠ½ΠΈΠ΅ΠΉ (ΠΠ), Π²ΡΠΎΡΡΡ Π³ΡΡΠΏΠΏΡ (II) β 95 ΡΠ΅Π»ΠΎΠ²Π΅ΠΊ (ΡΡΠΆΠ΅Π»Π°Ρ ΡΠΎΡΠ΅ΡΠ°Π½Π½Π°Ρ ΡΡΠ°Π²ΠΌΠ°, Π²ΠΊΠ»ΡΡΠ°Ρ ΡΠ°Π½Π΅Π½ΠΈΡ β 63, ΠΎΠ±ΡΠΈΠΉ ΠΏΠ΅ΡΠΈΡΠΎΠ½ΠΈΡ β 32). Π‘ΡΠ΅Π΄ΠΈ Π±ΠΎΠ»ΡΠ½ΡΡ
II Π³ΡΡΠΏΠΏΡ Π±ΡΠ»ΠΈ Π²ΡΠ΄Π΅Π»Π΅Π½Ρ Π΄Π²Π΅ ΠΏΠΎΠ΄Π³ΡΡΠΏΠΏΡ: ΠΠ β 57 ΡΠ΅Π»ΠΎΠ²Π΅ΠΊ Ρ Π½ΠΎΠ·ΠΎΠΊΠΎΠΌΠΈΠ°Π»ΡΠ½ΠΎΠΉ ΠΏΠ½Π΅Π²ΠΌΠΎΠ½ΠΈΠ΅ΠΉ (ΠΠ) ΠΈ 38 ΡΠ΅Π»ΠΎΠ²Π΅ΠΊ (ΠΠ) β Π±Π΅Π· ΠΠ. ΠΡΡΠΏΠΏΡ ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ (Π) ΡΠΎΡΡΠ°Π²ΠΈΠ»ΠΈ 160 ΠΎΡΠ½ΠΎΡΠΈΡΠ΅Π»ΡΠ½ΠΎ Π·Π΄ΠΎΡΠΎΠ²ΡΡ
Π»ΡΠ΄Π΅ΠΉ. ΠΠ¦Π -Π³Π΅Π½ΠΎΡΠΈΠΏΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ ΠΏΡΠΎΠ²ΠΎΠ΄ΠΈΠ»ΠΈ Π΄Π»Ρ ΠΏΠΎΠ»ΠΈΠΌΠΎΡΡΠ½ΡΡ
Π³Π΅Π½ΠΎΠ², ΠΊΠΎΠ½ΡΡΠΎΠ»ΠΈΡΡΡΡΠΈΡ
Π΄Π΅ΡΠΎΠΊΡΠΈΠΊΠ°ΡΠΈΡ ΠΊΡΠ΅Π½ΠΎΠ±ΠΈΠΎΡΠΈΠΊΠΎΠ² (GSTM1, GSTT1, GSTP1, CYP1A1) ΠΈ MTHFR-Π³Π΅Π½Π°, ΠΎΡΠ²Π΅ΡΡΡΠ²Π΅Π½Π½ΠΎΠ³ΠΎ Π·Π° ΡΠΈΠ½ΡΠ΅Π· ΠΈ ΠΌΠ΅ΡΠΈΠ»ΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ ΠΠΠ. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ. ΠΠΎΠΊΠ°Π·Π°Π½Π° ΠΏΡΠ΅Π΄ΡΠ°ΡΠΏΠΎΠ»ΠΎΠΆΠ΅Π½Π½ΠΎΡΡΡ ΠΊ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ ΠΎΡΡΡΠΎΠΉ ΠΠ Π΄Π»Ρ Π½ΠΎΡΠΈΡΠ΅Π»Π΅ΠΉ ΠΌΠΈΠ½ΠΎΡΠ½ΠΎΠ³ΠΎ Π°Π»Π»Π΅Π»Ρ (4889G) Π² Π»ΠΎΠΊΡΡΠ΅ CYP1A1 : 12,7% ΠΏΡΠΎΡΠΈΠ² 5,4% Π² ΠΊΠΎΠ½ΡΡΠΎΠ»Π΅ (p=0,034; OR=2,6); ΡΠ°Π·Π²ΠΈΡΠΈΠ΅ ΠΎΡΠ»ΠΎΠΆΠ½Π΅Π½ΠΈΠΉ Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
I Π³ΡΡΠΏΠΏΡ (ΡΠΎΠΊΡΠΈΡΠ΅ΡΠΊΠΈΠΉ ΠΌΠΈΠΎΠΊΠ°ΡΠ΄ΠΈΡ, ΠΏΠ»Π΅Π²ΡΠΈΡ, ΡΠΌΠΏΠΈΠ΅ΠΌΠ° ΠΏΠ»Π΅Π²ΡΡ, ΡΠΎΠΊΡΠΈΡΠ΅ΡΠΊΠ°Ρ Π½Π΅ΡΡΠΎΠΏΠ°ΡΠΈΡ) Π½Π°ΠΈΠ±ΠΎΠ»Π΅Π΅ Π²Π΅ΡΠΎΡΡΠ½ΠΎ Π΄Π»Ρ ΠΊΠΎΠΌΠ±ΠΈΠ½Π°ΡΠΈΠΈ Π³Π΅Π½ΠΎΡΠΈΠΏΠΎΠ² GSTT1 + GSTM1 0/0 (OR=3,2; p=0,010 ΠΎΡΠ½ΠΎΡΠΈΡΠ΅Π»ΡΠ½ΠΎ Π³ΡΡΠΏΠΏΡ ΠΊΠΎΠ½ΡΡΠΎΠ»Ρ). ΠΡΡΠ²Π»Π΅Π½ΠΎ, ΡΡΠΎ ΠΏΡΠΈ ΡΡΠΆΠ΅Π»ΠΎΠΉ ΡΡΠ°Π²ΠΌΠ΅, ΠΏΠ΅ΡΠΈΡΠΎΠ½ΠΈΡΠ΅ (ΠΠ) ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈ Π΄ΠΎΡΡΠΎΠ²Π΅ΡΠ½ΠΎ Π² 61,1% ΡΠ»ΡΡΠ°Π΅Π² Π½Π΅ ΡΠ°Π·Π²ΠΈΠ²Π°Π΅ΡΡΡ ΠΠ ΠΏΡΠΈ Π³Π΅Π½ΠΎΡΠΈΠΏΠ΅ GSTM1 + GSTT1 + ΠΏΡΠΎΡΠΈΠ² 38,8% Π² ΠΊΠΎΠ½ΡΡΠΎΠ»Π΅ (p=0,022) ΠΈΠ»ΠΈ ΠΏΡΠΎΡΠΈΠ² 37,5% Π²ΠΎ ΠΠ ΠΏΠΎΠ΄Π³ΡΡΠΏΠΏΠ΅ (p=0,045; OR=2,6). ΠΠ»ΡΡΠ΅Π²ΡΠ΅ ΡΠ»ΠΎΠ²Π°: Π²Π½Π΅Π±ΠΎΠ»ΡΠ½ΠΈΡΠ½Π°Ρ ΠΏΠ½Π΅Π²ΠΌΠΎΠ½ΠΈΡ, Π½ΠΎΠ·ΠΎΠΊΠΎΠΌΠΈΠ°Π»ΡΠ½Π°Ρ ΠΏΠ½Π΅Π²ΠΌΠΎΠ½ΠΈΡ, ΠΏΠΎΠ»ΠΈΠΌΠΎΡΡΠΈΠ·ΠΌ Π³Π΅Π½ΠΎΠ²
Genetic Polymorphism and the Rate of Development of Complications in Pneumonia of Varying Genesis
Objective: to study the genetic polymorphism of the genes of phase I and II xenobiotic detoxification (GSTM1, GSTP1, GSTT1, CYP1A1), as well as ACE, CCR5, MTHFR, and those of the cytokines IL-6 and TNF-a to reveal hereditary predisposition to pneumonia of varying genesis and its complications. Materials and methods. The frequency of the allele variants of 7 genes was studied in the groups of patients with pneumonia (n=524) and healthy donors (a control group (n=178). Results. There were are genotypes associated with predisposition to community-acquired and nosocomial pneumonia (CAP and NP): GSTM I*, CYP1A1 606T/T, ACE D/D and those associated with a higher risk for complicated CAP. There were effects of the allelic variants of the ACE gene in developing complications, such as acute respiratory distress syndrome, multiple organ dysfunction, and sepsis: ACEI/I insertion homozygotes linked to survival and the alternative ACE D/D genotype to mortality. Conclusion: The study revealed an association of detoxification gene polymorphism with predisposition to CAP and NP and with the development of complications in CAP. Key words: xenobiotic detoxification genes, key ACE renin-angiotensin system gene, chemokine receptor 5 (CCR5) gene, pneumonia, acute respiratory distress syndrome, sepsis, multiple organ dysfunction