Π‘ΠΏΠΈΡΠ°Π½ΠΈΠ΅ "Π Π΅Π²ΠΌΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΡ" / Journal "Rheumatology" - Sofia
ΠΠΎΡΡΠΎΡΠ½Π½ΠΈ Π°Π΄ΡΠ΅ΡΠΈ Π½Π° ΡΠ°Π·ΠΈ ΠΊΠΎΠ»Π΅ΠΊΡΠΈΡ
Π‘ΠΏΠΈΡΠ°Π½ΠΈΠ΅ΡΠΎ ΠΎΡΡΠ°Π·ΡΠ²Π° ΡΠ°Π·Π²ΠΈΡΠΈΠ΅ΡΠΎ Π½Π° ΡΠ΅Π²ΠΌΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΡΠ½Π°ΡΠ° Π½Π°ΡΠΊΠ° ΠΈ ΡΠ²ΡΡΠ·Π°Π½ΠΈΡΠ΅ Ρ Π½Π΅Ρ ΡΠΏΠ΅ΡΠΈΠ°Π»Π½ΠΎΡΡΠΈ. ΠΠΊΠ»ΡΡΠ΅Π½ΠΎ Π΅ ΠΈ ΡΠ΅ ΠΎΠ±ΡΠ°Π±ΠΎΡΠ²Π° Π² EMBASE/ExcerptaMedicaDatabase. Π’ΠΎ Π΅ ΠΈΠ·Π΄Π°Π½ΠΈΠ΅ Π½Π° ΠΠ°ΡΡΠ½ΠΎΡΠΎ Π΄ΡΡΠΆΠ΅ΡΡΠ²ΠΎ ΠΏΠΎ ΡΠ΅Π²ΠΌΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΡ ΠΈ ΠΏΡΠ΅Π΄ΡΡΠ°Π²Π»ΡΠ²Π° ΠΈΠ½ΡΠ΅ΡΠ΅Ρ Π·Π° ΡΠΈΡΠΎΠΊ ΠΊΡΡΠ³ ΠΌΠ΅Π΄ΠΈΡΠΈΠ½ΡΠΊΠΈ ΡΠΏΠ΅ΡΠΈΠ°Π»ΠΈΡΡΠΈ: ΠΈΠ½ΡΠ΅ΡΠ½ΠΈΡΡΠΈ, ΠΈΠΌΡΠ½ΠΎΠ»ΠΎΠ·ΠΈ, Π½Π΅Π²ΡΠΎΠ»ΠΎΠ·ΠΈ, ΠΎΡΡΠΎΠΏΠ΅Π΄ΠΈ-ΡΡΠ°Π²ΠΌΠ°ΡΠΎΠ»ΠΎΠ·ΠΈ, ΡΠΈΠ·ΠΈΠΎΡΠ΅ΡΠ°ΠΏΠ΅Π²ΡΠΈ, Π³Π°ΡΡΡΠΎΠ΅Π½ΡΠ΅ΡΠΎΠ»ΠΎΠ·ΠΈ ΠΈ Π΄Ρ. ΠΡΠ±Π»ΠΈΠΊΡΠ²Π°Ρ ΡΠ΅ Π½Π°ΡΡΠ½ΠΈ ΠΎΠ±Π·ΠΎΡΠΈ ΠΈ ΠΎΡΠΈΠ³ΠΈΠ½Π°Π»Π½ΠΈ Π±ΡΠ»Π³Π°ΡΡΠΊΠΈ ΡΡΠ°ΡΠΈΠΈ, ΡΠ΅Π·ΡΠΌΠ΅ΡΠ° ΠΎΡ ΠΊΠΎΠ½Π³ΡΠ΅ΡΠΈ ΠΈ ΠΊΠΎΠ½ΡΠ΅ΡΠ΅Π½ΡΠΈΠΈ Π½Π° ΠΠ°ΡΡΠ½ΠΎΡΠΎ Π΄ΡΡΠΆΠ΅ΡΡΠ²ΠΎ ΠΏΠΎ ΡΠ΅Π²ΠΌΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΡ, ΠΊΠ°ΠΊΡΠΎ ΠΈ ΡΠ΅ΡΠ΅Π½Π·ΠΈΠΈ Π·Π° Π½ΠΎΠ²ΠΎΠΈΠ·Π»Π΅Π·Π»ΠΈ ΠΊΠ½ΠΈΠ³ΠΈ. ***** ΠΠΎΠ΄ΠΈΡΠ½ΠΈΠ½Π° β Π₯VVΠ/2013 ***** ISSN 1310-0505 ***** Π Π΅Π΄Π°ΠΊΡΠΈΠΎΠ½Π½Π° ΠΊΠΎΠ»Π΅Π³ΠΈΡ: ΠΠ»Π°Π²Π΅Π½ ΡΠ΅Π΄Π°ΠΊΡΠΎΡ: Π΄ΠΎΡ. Π . Π‘ΡΠΎΠΈΠ»ΠΎΠ², Π΄.ΠΌ., ΠΠ»ΠΈΠ½ΠΈΠΊΠ° ΠΏΠΎ ΡΠ΅Π²ΠΌΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΡ, ΠΠ£ β Π‘ΠΎΡΠΈΡ, ΡΠ». βΠ£ΡΠ²ΠΈΡβ β 13, 1612 Π‘ΠΎΡΠΈΡ, ΡΠ΅Π». 858-50-86. ***** ΠΡΠ³Π°Π½ΠΈΠ·Π°ΡΠΈΠΎΠ½Π΅Π½ ΡΠ΅ΠΊΡΠ΅ΡΠ°Ρ: ΠΠ΅ΡΠ΅Π»ΠΊΠ° Π¦ΡΠΊΠ»Π΅Π²Π°
ΠΡΠ΅Π³Π»Π΅ΠΆΠ΄Π°Π½Π΅
Π’ΡΡΡΠ΅Π½Π΅ Π‘ΠΏΠΈΡΠ°Π½ΠΈΠ΅ "Π Π΅Π²ΠΌΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΡ" / Journal "Rheumatology" - Sofia ΠΎΡ ΠΠ²ΡΠΎΡ "ΠΠ²Π°Π½ΠΎΠ²Π°/Ivanova, Π./M."
ΠΠΎΠΊΠ°Π·Π°Π½ΠΈ 1 - 4 ΠΎΡ 4
Π Π΅Π·ΡΠ»ΡΠ°ΡΠΈ Π½Π° Π²ΡΡΠΊΠ° ΡΡΡΠ°Π½ΠΈΡΠ°
ΠΠΏΡΠΈΠΈ Π·Π° ΡΠΎΡΡΠΈΡΠ°Π½Π΅
- ΠΠΎΠΊΡΠΌΠ΅Π½ΡΠΡΠΎΡΠΈΠ°ΡΠΈΠ²Π½ΠΎ ΠΏΡΠΎΡΡΠ²Π°Π½Π΅ Π½Π° ΡΡΠ½ΠΊΡΠΈΠΎΠ½Π°Π»Π΅Π½ ΠΏΠΎΠ»ΠΈΠΌΠΎΡΡΠΈΠ·ΡΠΌ Π² Π³Π΅Π½Π° Π·Π° ΡΡΠ°Π½ΡΡΠΎΡΠΌΠΈΡΠ°ΡΠΈΡ ΡΠ°ΡΡΠ΅ΠΆΠ΅Π½ ΡΠ°ΠΊΡΠΎΡ beta1ΠΏΡΠΈ ΡΠΈΡΡΠ΅ΠΌΠ΅Π½ Π»ΡΠΏΡΡ Π΅ΡΠΈΡΠ΅ΠΌΠ°ΡΠΎΠ΄Π΅Ρ Π² Π±ΡΠ»Π³Π°ΡΡΠΊΠ°ΡΠ° ΠΏΠΎΠΏΡΠ»Π°ΡΠΈΡ(Π¦Π΅Π½ΡΡΠ°Π»Π½Π° ΠΌΠ΅Π΄ΠΈΡΠΈΠ½ΡΠΊΠ° Π±ΠΈΠ±Π»ΠΈΠΎΡΠ΅ΠΊΠ°, ΠΠ£ Π‘ΠΎΡΠΈΡ / Central Medical Library, MU β Sofia, 2012-04) ΠΠ°Π½ΠΎΠ»ΠΎΠ²Π°/Manolova, Π./I.; ΠΠ²Π°Π½ΠΎΠ²Π°/Ivanova, Π./M.; ΠΠ»Π΅ΠΊΡΠ°Π½Π΄ΡΠΎΠ²Π°/Aleksandrova, Π./E.; ΠΠΈΡΠ΅Π²Π°/Miteva, Π./L.; Π‘ΡΠΎΠΈΠ»ΠΎΠ²/Stoilov, Π ./R.; Π Π°ΡΠΊΠΎΠ²/Rashkov, Π ./R.; Π‘ΡΠ°Π½ΠΈΠ»ΠΎΠ²Π°/Stanilova, Π‘./S.; ΠΡΠ»ΡΠ±ΠΎΠ²Π°/Gulubova, Π./M.Π Π΅Π·ΡΠΌΠ΅. Π¦Π΅Π»ΡΠ° Π½Π° ΠΏΡΠΎΡΡΠ²Π°Π½Π΅ΡΠΎ Π±Π΅ΡΠ΅ Π΄Π° ΠΈΠ·ΡΠ»Π΅Π΄Π²Π°ΠΌΠ΅ ΡΠΎΠ»ΡΡΠ° Π½Π° ΠΏΡΠΎΠΌΠΎΡΠΎΡΠ΅Π½ ΠΏΠΎΠ»ΠΈΠΌΠΎΡΡΠΈΠ·ΡΠΌ - 509C/T Π² TGFΠ1 Π³Π΅Π½Π° Π·Π° ΠΏΡΠ΅Π΄ΡΠ°Π·ΠΏΠΎΠ»ΠΎΠΆΠ΅Π½ΠΈΠ΅ΡΠΎ ΠΊΡΠΌ ΡΠΈΡΡΠ΅ΠΌΠ΅Π½ Π»ΡΠΏΡΡ Π΅ΡΠΈΡΠ΅ΠΌΠ°ΡΠΎΠ΄Π΅Ρ (Π‘ΠΠ) ΠΈ ΠΊΠΎΠ½ΠΊΡΠ΅ΡΠ½ΠΈΡΠ΅ ΠΊΠ»ΠΈΠ½ΠΈΡΠ½ΠΈ ΠΏΡΠΎΡΠ²ΠΈ Π½Π° Π·Π°Π±ΠΎΠ»ΡΠ²Π°Π½Π΅ΡΠΎ Π² Π±ΡΠ»Π³Π°ΡΡΠΊΠ°ΡΠ° ΠΏΠΎΠΏΡΠ»Π°ΡΠΈΡ. 149 Π»ΡΠΏΡΡΠ½ΠΎ Π±ΠΎΠ»Π½ΠΈ ΠΈ 134 Π·Π΄ΡΠ°Π²ΠΈ ΠΊΠΎΠ½ΡΡΠΎΠ»ΠΈ Π±ΡΡ Π° Π³Π΅Π½ΠΎΡΠΈΠΏΠΈΠ·ΠΈΡΠ°Π½ΠΈ ΠΏΠΎ ΡΠΎΠ·ΠΈ ΠΏΠΎΠ»ΠΈΠΌΠΎΡΡΠ΅Π½ ΠΌΠ°ΡΠΊΠ΅Ρ ΡΡΠ΅Π· Π°Π½Π°Π»ΠΈΠ· Π½Π° ΠΏΠΎΠ»ΠΈΠΌΠΎΡΡΠΈΠ·ΡΠΌ ΠΏΠΎ Π΄ΡΠ»ΠΆΠΈΠ½Π°ΡΠ° Π½Π° ΡΠ΅ΡΡΡΠΈΠΊΡΠΈΠΎΠ½Π½ΠΈΡΠ΅ ΡΡΠ°Π³ΠΌΠ΅Π½ΡΠΈ ΡΠ»Π΅Π΄ PCR ΡΠ΅Π°ΠΊΡΠΈΡ (RFLP-PCR). ΠΠ°ΠΊΠ°Ρ ΡΡΡΠ°Π½ΠΎΠ²Π΅Π½ΠΈΡΠ΅ Π°Π»Π΅Π»Π½ΠΈ ΡΠ΅ΡΡΠΎΡΠΈ ΠΏΠΎ ΠΏΠΎΠ»ΠΈΠΌΠΎΡΡΠΈΠ·ΠΌΠ° ο509C/T ΡΡΠ΅Π΄ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΈ ΡΡΡ Π‘ΠΠ ΠΈ ΠΏΡΠΈ Π·Π΄ΡΠ°Π²ΠΈΡΠ΅ ΠΊΠΎΠ½ΡΡΠΎΠ»ΠΈ Π΄Π° Π±ΡΡ Π° ΡΡ ΠΎΠ΄Π½ΠΈ, ΠΏΡΠΈ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΈΡΠ΅ Π±Π΅ΡΠ΅ Π½Π°Π±Π»ΡΠ΄Π°Π²Π°Π½Π° ΠΏΠΎ-Π²ΠΈΡΠΎΠΊΠ° ΡΠ΅ΡΡΠΎΡΠ° Π½Π° Ρ Π΅ΡΠ΅ΡΠΎΠ·ΠΈΠ³ΠΎΡΠ½ΠΈΡ Π³Π΅Π½ΠΎΡΠΈΠΏ (53%) Ρ Π±Π»ΠΈΠ·ΠΊΠ° Π΄ΠΎ ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠ°ΡΠ° Π·Π½Π°ΡΠΈΠΌΠΎΡΡ Π² ΡΡΠ°Π²Π½Π΅Π½ΠΈΠ΅ ΡΡΡ Π·Π΄ΡΠ°Π²ΠΈΡΠ΅ ΠΊΠΎΠ½ΡΡΠΎΠ»ΠΈ (42%) Ρ OR = 1.52; 95% CI, 0.96 plus/minus 2.59, P = 0.059. ΠΡΠΈ Π±ΠΎΠ»Π½ΠΈΡΠ΅ Ρ Ρ Π΅ΠΌΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΡΠ½ΠΈ ΠΏΡΠΎΡΠ²ΠΈ Π±Π΅ΡΠ΅ ΡΡΡΠ°Π½ΠΎΠ²Π΅Π½Π° Π·Π½Π°ΡΠΈΠΌΠΎ ΠΏΠΎ-Π²ΠΈΡΠΎΠΊΠ° ΡΠ΅ΡΡΠΎΡΠ° Π½Π° Ρ Π΅ΡΠ΅ΡΠΎΠ·ΠΈΠ³ΠΎΡΠ½ΠΈΡ Π³Π΅Π½ΠΎΡΠΈΠΏ (60%) Π² ΡΡΠ°Π²Π½Π΅Π½ΠΈΠ΅ Ρ ΡΠ΅Π·ΠΈ Π±Π΅Π· Ρ Π΅ΠΌΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΡΠ½ΠΈ ΠΏΡΠΎΡΠ²ΠΈ (38%) Ρ OR = 2.41; 95%CI: 1.1 plus/minus 5.32; p = 0.016. ΠΠΎΡΠΈΡΠ΅Π»ΡΡΠ²ΠΎΡΠΎ Π½Π° Ρ Π΅ΡΠ΅ΡΠΎΠ·ΠΈΠ³ΠΎΡΠ½ΠΈΡ Π³Π΅Π½ΠΎΡΠΈΠΏ Π±Π΅ Π°ΡΠΎΡΠΈΠΈΡΠ°Π½ΠΎ ΠΈ Ρ Π½Π°Π»ΠΈΡΠΈΠ΅ Π½Π° Π°Π½ΡΠΈ-Π΄Π²ΠΠΠ (OR = 2.108; 95%CI: 1.033 plus/minus 4.295; p = 0.04). Π Π·Π°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅,ο509C/T ΠΏΠΎΠ»ΠΈΠΌΠΎΡΡΠΈΠ·ΠΌΡΡ Π² TGF-beta-I Π³Π΅Π½Π° Π²Π»ΠΈΡΠ΅ Π²ΡΡΡ Ρ Π³Π΅Π½Π΅ΡΠΈΡΠ½ΠΎΡΠΎ ΠΏΡΠ΅Π΄ΡΠ°Π·ΠΏΠΎΠ»ΠΎΠΆΠ΅Π½ΠΈΠ΅ ΠΊΡΠΌ Π‘ΠΠ ΠΈ ΠΊΠ»ΠΈΠ½ΠΈΡΠ½ΠΈΡΠ΅ ΠΈΠ·ΡΠ²ΠΈ Π½Π° Π·Π°Π±ΠΎΠ»ΡΠ²Π°Π½Π΅ΡΠΎ Π² Π±ΡΠ»Π³Π°ΡΡΠΊΠ°ΡΠ° ΠΏΠΎΠΏΡΠ»Π°ΡΠΈΡ, ΠΊΠΎΠ΅ΡΠΎ Π³ΠΎ ΠΎΠΏΡΠ΅Π΄Π΅Π»Ρ ΠΊΠ°ΡΠΎ Π΅Π΄ΠΈΠ½ ΠΎΡ Π³Π΅Π½Π΅ΡΠΈΡΠ½ΠΈΡΠ΅ ΡΠ°ΠΊΡΠΎΡΠΈ, Π΄ΠΎΠΏΡΠΈΠ½Π°ΡΡΡΠΈ Π·Π° ΠΊΠ»ΠΈΠ½ΠΈΡΠ½ΠΎΡΠΎ ΡΠ°Π·Π½ΠΎΠΎΠ±ΡΠ°Π·ΠΈΠ΅ Π½Π° Π·Π°Π±ΠΎΠ»ΡΠ²Π°Π½Π΅ΡΠΎ. ***** Summary. The aim of this study was to evaluate the association of ο509C/T promoter polymorphism of TGF-beta1 gene with systemic lupus erythematosus (SLE) and clinical features in Bulgarian population. A total of 149 patients with SLE and 134 healthy controls were genotyped for the ο509C/T polymorphism of TGF-beta1 by restriction fragment length polymorphism (RFLP)οο PCR assay. There were no significant differences in allele frequencies of ο509C>T polymorphism of TGF beta1 gene between the SLE patients and healthy controls. However, the frequency of heterozygous genotype among the SLE patients (53%) was higher compared to healthy controls (42%) with borderline significance and OR = 1.52; 95% CI, 0.96 plus/minus 2.59, P =0.059. In addition, heterozygous genotype was significantly higher in the SLE patients with haematological disorders (60%) compared to patients without these clinical features (38%) with OR = 2.41; 95%CI: 1.1 plus/minus 5.32; p = 0.016. The heterozygous genotype was also found to be slightly associated with anti-DNA positivity (OR = 2.0; 95%CI: 0.96 plus/minus 4.2; p = 0.045). In conclusion,our results suggest that ο509C > T polymorphism of TGF beta 1 may play a role in the susceptibility to SLE in the Bulgarian population. Also, TGF-beta1 polymorphism was related to specific clinical manifestations of the disease pointing TGF beta1 polymorphism as one of the genetic factors that explain the heterogeneity seen in/with SLE.
- ΠΠΎΠΊΡΠΌΠ΅Π½ΡΠΠΈΠ»ΠΎΡΠ½ΠΎ ΠΏΡΠΎΡΡΠ²Π°Π½Π΅ Π½Π° Π°ΡΠΎΡΠΈΠ°ΡΠΈΡΡΠ° Π½Π° ΠΏΡΠΎΠΌΠΎΡΠΎΡΠ΅Π½ ΠΏΠΎΠ»ΠΈΠΌΠΎΡΡΠΈΠ·ΡΠΌ Π² Π³Π΅Π½Π° Π·Π° ΠΈΠ½ΡΠ΅ΡΠ»Π΅Π²ΠΊΠΈΠ½ (IL)-12Ρ40 ΠΈ ΡΠ΅ΡΡΠΌΠ½ΠΎΡΠΎ Π½ΠΈΠ²ΠΎ Π½Π° IL-12p40 ΠΏΡΠΈ Π°Π½ΠΊΠΈΠ»ΠΎΠ·ΠΈΡΠ°Ρ ΡΠΏΠΎΠ½Π΄ΠΈΠ»ΠΈΡ(Π¦Π΅Π½ΡΡΠ°Π»Π½Π° ΠΌΠ΅Π΄ΠΈΡΠΈΠ½ΡΠΊΠ° Π±ΠΈΠ±Π»ΠΈΠΎΡΠ΅ΠΊΠ°, ΠΠ£ Π‘ΠΎΡΠΈΡ / Central Medical Library, MU β Sofia, 2012-08) ΠΠ°Π½ΠΎΠ»ΠΎΠ²Π°/Manolova, Π./I.; ΠΠ²Π°Π½ΠΎΠ²Π°/Ivanova, Π./M.; Π‘ΡΠΎΠΈΠ»ΠΎΠ²/Stoilov, Π ./R.; Π‘ΡΠ°Π½ΠΈΠ»ΠΎΠ²Π°/Stanilova, Π‘./S.Π¦Π΅Π»ΡΠ° Π½Π° Π½Π°ΡΡΠΎΡΡΠΎΡΠΎ ΠΏΠΈΠ»ΠΎΡΠ½ΠΎ ΠΏΡΠΎΡΡΠ²Π°Π½Π΅ Π±Π΅ΡΠ΅ Π΄Π° ΠΈΠ·ΡΠ»Π΅Π΄Π²Π°ΠΌΠ΅ Π΅ΡΠ΅ΠΊΡΠ° Π½Π° ΠΏΠΎΠ»ΠΈΠΌΠΎΡΡΠΈΠ·ΠΌΠ° IL12Bpro Π·Π° Π³Π΅Π½Π΅ΡΠΈΡΠ½ΠΎ ΠΏΡΠ΅Π΄ΡΠ°Π·ΠΏΠΎΠ»ΠΎΠΆΠ΅Π½ΠΈΠ΅ ΠΊΡΠΌ Π°Π½ΠΊΠΈΠ»ΠΎΠ·ΠΈΡΠ°Ρ ΡΠΏΠΎΠ½Π΄ΠΈΠ»ΠΈΡ (ΠΠ‘) ΠΈ ΡΠ΅ΡΡΠΌΠ½ΠΈΡΠ΅ Π½ΠΈΠ²Π° Π½Π° IL-12Ρ40 Π² Π±ΡΠ»Π³Π°ΡΡΠΊaΡΠ° ΠΏΠΎΠΏΡΠ»Π°ΡΠΈΡ. 54 Π±ΠΎΠ»Π½ΠΈ Ρ ΠΠ‘ ΠΈ 83 Π·Π΄ΡΠ°Π²ΠΈ ΠΊΠΎΠ½ΡΡΠΎΠ»ΠΈ Π±ΡΡ Π° Π³Π΅Π½ΠΎΡΠΈΠΏΠΈΠ·ΠΈΡΠ°Π½ΠΈ ΠΏΠΎ ΡΠΎΠ·ΠΈ ΠΏΠΎΠ»ΠΈΠΌΠΎΡΡΠ΅Π½ ΠΌΠ°ΡΠΊΠ΅Ρ ΡΡΠ΅Π· Π°Π»Π΅Π»-ΡΠΏΠ΅ΡΠΈΡΠΈΡΠ΅Π½ PCR ΠΌΠ΅ΡΠΎΠ΄ (AS-PCR). ΠΠ°ΠΊΠ°Ρ Π³Π΅Π½ΠΎΡΠΈΠΏΠ½ΠΎΡΠΎ ΠΈ Π°Π»Π΅Π»Π½ΠΎ ΡΠ°Π·ΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΠ΅ ΠΏΠΎ IL12Bpro Π΄Π° Π½Π΅ ΠΏΠΎΠΊΠ°Π·Π° ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈ Π·Π½Π°ΡΠΈΠΌΠΈ ΡΠ°Π·Π»ΠΈΠΊΠΈ ΠΌΠ΅ΠΆΠ΄Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΈΡΠ΅ Ρ ΠΠ‘ ΠΈ Π·Π΄ΡΠ°Π²ΠΈΡΠ΅ ΠΊΠΎΠ½ΡΡΠΎΠ»ΠΈ, ΡΡΠ΅Π΄ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΈΡΠ΅ Π±Π΅ΡΠ΅ Π½Π°Π±Π»ΡΠ΄Π°Π²Π°Π½Π° ΠΏΠΎ-Π½ΠΈΡΠΊΠ° ΡΠ΅ΡΡΠΎΡΠ° Π½Π° Ρ ΠΎΠΌΠΎΠ·ΠΈΠ³ΠΎΡΠ½ΠΈΡ 1.1 Π³Π΅Π½ΠΎΡΠΈΠΏ (16.7%) ΠΈ ΠΏΠΎ-Π²ΠΈΡΠΎΠΊΠ° - Π½Π° Ρ Π΅ΡΠ΅ΡΠΎΠ·ΠΈΠ³ΠΎΡΠ½ΠΈΡ 1.2 Π³Π΅Π½ΠΎΡΠΈΠΏ (51.8%) Π² ΡΡΠ°Π²Π½Π΅Π½ΠΈΠ΅ ΡΡΡ Π·Π΄ΡΠ°Π²ΠΈΡΠ΅ ΠΊΠΎΠ½ΡΡΠΎΠ»ΠΈ -ΡΡΠΎΡΠ²Π΅ΡΠ½ΠΎ 24.1% Π·Π° Ρ ΠΎΠΌΠΎΠ·ΠΈΠ³ΠΎΡΠ½ΠΈΡ 1.1 Π³Π΅Π½ΠΎΡΠΈΠΏ ΠΈ 45.8% Π·Π° Ρ Π΅ΡΠ΅ΡΠΎΠ·ΠΈΠ³ΠΎΡΠ½ΠΈΡ Π³Π΅Π½ΠΎΡΠΈΠΏ. ΠΠΎΠ³ΠΈΡΡΠΈΡΠ½ΠΈΡΡ ΡΠ΅Π³ΡΠ΅ΡΠΈΠΎΠ½Π΅Π½ Π°Π½Π°Π»ΠΈΠ· ΠΏΠΎΠΊΠ°Π·Π°, ΡΠ΅ Π½ΠΎΡΠΈΡΠ΅Π»ΡΡΠ²ΠΎΡΠΎ Π½Π° Ρ ΠΎΠΌΠΎΠ·ΠΈΠ³ΠΎΡΠ½ΠΈΡ Π³Π΅Π½ΠΎΡΠΈΠΏ ΠΏΠΎ Π²Π°ΡΠΈΠ°Π½ΡΠ½ΠΈΡ Π°Π»Π΅Π» 1 Π½Π°ΠΌΠ°Π»ΡΠ²Π° 1.5 ΠΏΡΡΠΈ (OR-0.662; 95% CI 0.22Γ·2.01) ΡΠΈΡΠΊΠ° ΠΎΡ ΡΠ°Π·Π²ΠΈΡΠΈΠ΅ Π½Π° Π°Π½ΠΊΠΈΠ»ΠΎΠ·ΠΈΡΠ°Ρ ΡΠΏΠΎΠ½Π΄ΠΈΠ»ΠΈΡ Π² ΡΡΠ°Π²Π½Π΅Π½ΠΈΠ΅ Ρ Π½ΠΎΡΠΈΡΠ΅Π»ΡΡΠ²ΠΎΡΠΎ Π½Π° Ρ ΠΎΠΌΠΎΠ·ΠΈΠ³ΠΎΡΠ½ΠΈΡ Π³Π΅Π½ΠΎΡΠΈΠΏ ΠΏΠΎ βΠ΄ΠΈΠ²ΠΈΡβ Π°Π»Π΅Π» 2. Π Π΅ΡΠΏΠ΅ΠΊΡΠΈΠ²Π½ΠΎ ΡΠΈΡΠΊΡΡ ΠΎΡ ΡΠ°Π·Π²ΠΈΡΠΈΠ΅ Π½Π° Π°Π½ΠΊΠΈΠ»ΠΎΠ·ΠΈΡΠ°Ρ ΡΠΏΠΎΠ½Π΄ΠΈΠ»ΠΈΡ Π΅ 1.5 ΠΏΡΡΠΈ ΠΏΠΎ-Π²ΠΈΡΠΎΠΊ ΠΏΡΠΈ ΠΈΠ½Π΄ΠΈΠ²ΠΈΠ΄ΠΈΡΠ΅, Π½ΠΎΡΠΈΡΠ΅Π»ΠΈ Π½Π° Ρ ΠΎΠΌΠΎΠ·ΠΈΠ³ΠΎΡΠ½ΠΈΡ 2.2 Π³Π΅Π½ΠΎΡΠΈΠΏ (OR-1.511; 95% CI 0.5Γ·4.64) ΠΈ ΠΏΠΎΡΡΠΈ 2 ΠΏΡΡΠΈ ΠΏΠΎ-Π²ΠΈΡΠΎΠΊ ΠΏΡΠΈ ΠΈΠ½Π΄ΠΈΠ²ΠΈΠ΄ΠΈΡΠ΅, Π½ΠΎΡΠΈΡΠ΅Π»ΠΈ Π½Π° βΠ΄ΠΈΠ²ΠΈΡβ Π°Π»Π΅Π» 2 Π² Π³Π΅Π½ΠΎΡΠΈΠΏΠ° (1.2+2.2) (OR-1.89; 95% CI 0.72Γ·5.01) Π² ΡΡΠ°Π²Π½Π΅Π½ΠΈΠ΅ Ρ ΠΈΠ½Π΄ΠΈΠ²ΠΈΠ΄ΠΈΡΠ΅, Π½ΠΎΡΠΈΡΠ΅Π»ΠΈ Π½Π° Ρ ΠΎΠΌΠΎΠ·ΠΈΠ³ΠΎΡΠ½ΠΈΡ 1.1 Π³Π΅Π½ΠΎΡΠΈΠΏ. ΠΠΎΠ»ΠΈΡΠ΅ΡΡΠ²Π΅Π½ΠΎΡΠΎ ΠΈΠ·ΠΌΠ΅ΡΠ²Π°Π½Π΅ Π½Π° ΡΠ΅ΡΡΠΌΠ½ΠΈΡΠ΅ Π½ΠΈΠ²Π° Π½Π° IL-12p40 ΠΏΠΎΠΊΠ°Π·Π°, ΡΠ΅ Ρ ΠΎΠΌΠΎΠ·ΠΈΠ³ΠΎΡΠ½ΠΈΡΡ Π³Π΅Π½ΠΎΡΠΈΠΏ 1.1 ΡΠ΅ Π°ΡΠΎΡΠΈΠΈΡΠ° Ρ ΠΏΠΎΠ²ΠΈΡΠ΅Π½ΠΈ ΡΠ΅ΡΡΠΌΠ½ΠΈ Π½ΠΈΠ²Π° Π½Π° IL-12p40 Π² ΡΡΠ°Π²Π½Π΅Π½ΠΈΠ΅ Ρ Π³Π΅Π½ΠΎΡΠΈΠΏ 2.2 ΠΊΠ°ΠΊΡΠΎ ΠΏΡΠΈ Π·Π΄ΡΠ°Π²ΠΈΡΠ΅ Π»ΠΈΡΠ°, ΡΠ°ΠΊΠ° ΠΈ ΠΏΡΠΈ Π±ΠΎΠ»Π½ΠΈΡΠ΅ Ρ ΠΠ‘, Π½ΠΎ ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈ Π΄ΠΎΡΡΠΎΠ²Π΅ΡΠ½Π° ΡΠ°Π·Π»ΠΈΠΊΠ° Π±Π΅ΡΠ΅ Π½Π°ΠΌΠ΅ΡΠ΅Π½Π° ΡΠ°ΠΌΠΎ ΠΏΡΠΈ Π±ΠΎΠ»Π½ΠΈΡΠ΅ Ρ ΠΠ‘. Π Π·Π°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅, Π½Π°ΡΠΈΡΠ΅ Π΄Π°Π½Π½ΠΈ ΠΏΠΎΠ΄ΠΊΡΠ΅ΠΏΡΡ Ρ ΠΈΠΏΠΎΡΠ΅Π·Π°ΡΠ°, ΡΠ΅ Π³Π΅Π½Π΅ΡΠΈΡΠ½ΠΈΡΠ΅ Π²Π°ΡΠΈΠ°ΡΠΈΠΈ Π² Π³Π΅Π½Π° Π·Π° IL12B, Π²Π»ΠΈΡΠ΅ΡΠΈ Π½Π° ΠΈΠ½Π΄ΡΡΠΈΡΠ°Π½Π°ΡΠ° ΠΏΡΠΎΠ΄ΡΠΊΡΠΈΡ Π½Π° IL-12p40, ΠΌΠΎΠ³Π°Ρ Π΄Π° Π΄ΠΎΠΏΡΠΈΠ½Π΅ΡΠ°Ρ Π·Π° ΠΏΡΠ΅Π΄ΡΠ°Π·ΠΏΠΎΠ»ΠΎΠΆΠ΅Π½ΠΈΠ΅ΡΠΎ ΠΊΡΠΌ ΡΠ°Π·Π²ΠΈΡΠΈΠ΅ Π½Π° Π°Π½ΠΊΠΈΠ»ΠΎΠ·ΠΈΡΠ°Ρ ΡΠΏΠΎΠ½Π΄ΠΈΠ»ΠΈΡ Π² Π±ΡΠ»Π³Π°ΡΡΠΊΠ°ΡΠ° ΠΏΠΎΠΏΡΠ»Π°ΡΠΈΡ. ***** Summary. The aim of this pilot study was to investigate the effect of IL12Bpro polymorphism on genetic susceptibility to ankylosing spondylitis (AS) and the serum levels of IL-12p40 in the Bulgarian population. 54 patients with AS and 83 healthy controls were genotyped for this polymorphic marker by the allele-specific PCR assay (AS-PCR). Although there were no significant differences in the genotype and allele distribution of IL12Bpro polymorphism between the patients with AS and the healthy controls, a lower frequency of the homozygous genotype 1.1 (16.7%) and a higher frequency of the heterozygous genotype 1.2 (51.8%) were observed among the AS patients, compared with the healthy controls:ο 24.1% for the homozygous genotype 1.1 and 45.8% for the heterozygous genotype, respectively. The logistic regression analysis has shown that the carriers of IL12Bpro 1.1 are at a 1.5 times lower risk (OR-0.662; 95% CI 0.22Γ·2.01) of developing AS than the carriers of the homozygous genotype for the wild allele 2. Respectively, the risk of developing AS is 1.5 times higher for the individuals carrying the homozygous genotype 2.2 (OR-1.511; 95% CI 0.5 Γ· 4.64) and almost 2 times higher for these carrying the wild allele 2 in the genotype (1.2+2.2) (OR-1.89; 95% CI 0.72Γ·5.01), compared to the individuals, carrying the homozygous genotype 1.1. The quantitative measurement of the serum IL-12p40 levels has shown that the homozygous genotype 1.1 is associated with elevated levels of IL-12p40, compared with the genotype 2.2 in both healthy subjects and patients with AS, but a statistically significant difference was found only for the patients with AS. In conclusion, our data support the hypothesis that genetic variations in the gene for IL12B, affecting the inducible production of IL-12p40, may contribute to the AS susceptibility in the Bulgarian population.
- ΠΠΎΠΊΡΠΌΠ΅Π½ΡΠΠΈΠ»ΠΎΡΠ½ΠΎ ΠΏΡΠΎΡΡΠ²Π°Π½Π΅ Π½Π° ΡΠ΅ΡΡΠΌΠ½ΠΈΡΠ΅ Π½ΠΈΠ²Π° Π½Π° TNF-Ξ± Π²ΡΠ² Π²ΡΡΠ·ΠΊΠ° Ρ ΠΊΠ»ΠΈΠ½ΠΈΡΠ½ΠΈΡΠ΅ ΠΈ Π»Π°Π±ΠΎΡΠ°ΡΠΎΡΠ½ΠΈΡΠ΅ ΠΏΠ°ΡΠ°ΠΌΠ΅ΡΡΠΈ Π½Π° Π±ΠΎΠ»Π΅ΡΡΠ½Π°ΡΠ° Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡ ΠΏΡΠΈ Π±ΡΠ»Π³Π°ΡΡΠΊΠ° ΠΏΠΎΠΏΡΠ»Π°ΡΠΈΡ ΠΎΡ Π±ΠΎΠ»Π½ΠΈ Ρ Π°Π½ΠΊΠΈΠ»ΠΎΠ·ΠΈΡΠ°Ρ ΡΠΏΠΎΠ½Π΄ΠΈΠ»ΠΈΡ(Π¦Π΅Π½ΡΡΠ°Π»Π½Π° ΠΌΠ΅Π΄ΠΈΡΠΈΠ½ΡΠΊΠ° Π±ΠΈΠ±Π»ΠΈΠΎΡΠ΅ΠΊΠ°, ΠΠ£ Π‘ΠΎΡΠΈΡ / Central Medical Library, MU β Sofia, 2011-06) ΠΠ²Π°Π½ΠΎΠ²Π°/Ivanova, Π./M.; Π‘ΡΠΎΠΈΠ»ΠΎΠ²/Stoilov, Π ./R.; ΠΠ»Π°ΡΠΈΠΊΠ°Π½ΠΎΠ²Π°/Platikanova, Π./M.; ΠΠ°Π½ΠΎΠ»ΠΎΠ²Π°/Manolova, Π./I.Π Π΅Π·ΡΠΌΠ΅. Π¦Π΅Π»ΡΠ° Π½Π° Π½Π°ΡΠ΅ΡΠΎ ΠΏΡΠΎΡΡΠ²Π°Π½Π΅ Π±Π΅ΡΠ΅ Π΄Π° Π°Π½Π°Π»ΠΈΠ·ΠΈΡΠ°ΠΌΠ΅ ΡΠ΅ΡΡΠΌΠ½ΠΈΡΠ΅ Π½ΠΈΠ²Π° Π½Π° tumor necrosis factor-alpha (TNF-Ξ±) ΠΏΡΠΈ Π±ΠΎΠ»Π½ΠΈ Ρ Π°Π½ΠΊΠΈΠ»ΠΎΠ·ΠΈΡΠ°Ρ ΡΠΏΠΎΠ½Π΄ΠΈΠ»ΠΈΡ (ΠΠ‘) ΠΈ Π²ΡΡΠ·ΠΊΠ°ΡΠ° ΠΈΠΌ Ρ Π±ΠΎΠ»Π΅ΡΡΠ½Π°ΡΠ° Π°ΠΊΡΠΈΠ²- Π½ΠΎΡΡ. ΠΠ° ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ½Π΅ Π½Π° ΡΠ΅ΡΡΠΌΠ½ΠΈΡ ΡΠΈΡΠΎΠΊΠΈΠ½ TNF-Ξ± Π±Π΅ΡΠ΅ ΠΏΡΠΈΠ»ΠΎΠΆΠ΅Π½ ELISA ΡΠ΅ΡΡ ΠΏΡΠΈ 45 ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΈ Ρ ΠΠ‘. Π Π΅Π·ΡΠ»ΡΠ°ΡΠΈΡΠ΅ Π±ΡΡ Π° ΡΡΠ°Π²Π½Π΅Π½ΠΈ Ρ ΡΠ΅Π·ΠΈ Π½Π° 36 Π·Π΄ΡΠ°Π²ΠΈ ΠΊΠΎΠ½ΡΡΠΎΠ»ΠΈ. ΠΠ·ΡΠ»Π΅Π΄Π²Π°Ρ ΠΌΠ΅ ΡΡΡΠΎ Π²ΡΡΠ·ΠΊΠ°ΡΠ° ΠΌΠ΅ΠΆ- Π΄Ρ ΡΠ΅ΡΡΠΌΠ½ΠΈΡΠ΅ ΠΊΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΠΈ Π½Π° ΡΠΎΠ·ΠΈ ΡΠΈΡΠΎΠΊΠΈΠ½ ΠΈ ΠΏΠ°ΡΠ°ΠΌΠ΅ΡΡΠΈΡΠ΅ Π½Π° Π±ΠΎΠ»Π΅ΡΡΠ½Π°ΡΠ° Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡ ΠΏΡΠΈ ΠΠ‘. Π‘Π΅ΡΡΠΌΠ½Π°ΡΠ° ΠΊΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΡ Π½Π° TNF-Ξ± ΠΏΡΠΈ Π±ΠΎΠ»Π½ΠΈΡΠ΅ Ρ ΠΠ‘ (mean plus/minus SD, 7.37 plus/minus 17.69; range, 0.3-62.7) Π½Π΅ ΡΠ΅ ΡΠ°Π·Π»ΠΈΡΠ°Π²Π°ΡΠ΅ ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈ Π·Π½Π°ΡΠΈΠΌΠΎ ΠΎΡ ΡΠ°Π·ΠΈ Π½Π° Π·Π΄ΡΠ°Π²ΠΈΡΠ΅ ΠΊΠΎΠ½ΡΡΠΎΠ»ΠΈ (mean plus/minus SD, 1.03 plus/minus 0.47; range, 0.44-2.4) (p = 0.558). ΠΠ΅ Π½Π°ΠΌΠ΅ΡΠΈΡ ΠΌΠ΅ ΡΠ°Π·Π»ΠΈΠΊΠ° ΠΈ Π² ΡΡΠΎΠΉΠ½ΠΎΡΡΠΈΡΠ΅ Π½Π° ΡΠ΅ΡΡΠΌΠ½ΠΈΡΠ΅ Π½ΠΈΠ²Π° Π½Π° TNF-Ξ± ΠΌΠ΅ΠΆΠ΄Ρ Π±ΠΎΠ»Π½ΠΈΡΠ΅ Ρ Π°ΠΊΡΠΈΠ²Π΅Π½ ΠΏΠ΅ΡΠΈΡΠ΅ΡΠ΅Π½ Π°ΡΡΡΠΈΡ (mean plus/minus SD, 7.72 plus/minus 18.18; range, 0.5-62.7) ΠΈ ΡΠ΅Π·ΠΈ Ρ ΠΈΠ·ΠΎΠ»ΠΈΡΠ°Π½ΠΎ Π°Π½Π³Π°ΠΆΠΈΡΠ°Π½Π΅ Π½Π° Π³ΡΡΠ±Π½Π°ΠΊΠ° (mean plus/minus SD, 7.04 plus/minus 17.61; range, 0.3-62.6; p = 0.524). ΠΠ΅ ΡΡΡΠ°Π½ΠΎΠ²ΠΈΡ ΠΌΠ΅ ΠΊΠΎΡΠ΅Π»Π°ΡΠΈΡ ΠΌΠ΅ΠΆΠ΄Ρ TNF-Ξ± ΠΈ ΠΈΠ·ΠΌΠ΅ΡΠ΅Π½ΠΈΡΠ΅ ΠΊΠ»ΠΈΠ½ΠΈΡΠ½ΠΈ ΠΈ Π»Π°Π±ΠΎΡΠ°ΡΠΎΡΠ½ΠΈ ΠΏΠ°ΡΠ°ΠΌΠ΅ΡΡΠΈ Π½Π° Π±ΠΎΠ»Π΅ΡΡΠ½Π°ΡΠ° Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡ β BASDAI, ASDAS-CΠ Π, ASDAS-Π‘Π£Π, Π³Π»ΠΎΠ±Π°Π»Π½Π° ΠΎΡΠ΅Π½ΠΊΠ° Π½Π° Π»Π΅ΠΊΠ°ΡΡ ΠΈ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠ° Π·Π° Π±ΠΎΠ»Π΅ΡΡ- Π½Π°ΡΠ° Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡ, Π‘Π£Π ΠΈ CΠ Π. ***** Summary. The aim of our study was to analyse the serum tumor necrosis factor-alpha (TNF-alpha) levels in patients with AS and their relationship with disease activity. An ELISA test was used to analyse serum cytokine TNF-alpha levels in 45 patients with AS. Results were compared with those from 36 healthy controls. The relationship between serum concentrations of this cytokine and parameters of disease activity in AS patients was also evaluated. No significant difference was found between TNF-alpha serum levels in AS and in controls (mean plus/minus SD, 7.37 plus/minus 17.69; range, 0.3-62.7) and between patients with spinal involvement only (mean plus/minus SD, 7.04 plus/minus 17.61; range, 0.3-62.6; p = 0.524) and those who also had peripheral arthritis (mean plus/minus SD, 7.72 plus/minus 18.18; range, 0.5-62.7), as well. TNF-alpha did not correlate with laboratory or clinical parameters of disease activityο οο BASDAI, ASDAS-CRP, ASDAS-Π‘Π£Π, physicianβs and patient`s global assessment of disease activity, ESR and CRP.
- ΠΠΎΠΊΡΠΌΠ΅Π½ΡΠ Π°Π·Ρ ΠΎΠ΄ΠΈΡΠ΅ Π·Π° Π»Π΅ΡΠ΅Π½ΠΈΠ΅ΡΠΎ Π½Π° ΡΠ΅Π²ΠΌΠ°ΡΠΎΠΈΠ΄Π½ΠΈΡ Π°ΡΡΡΠΈΡ, Π°Π½ΠΊΠΈΠ»ΠΎΠ·ΠΈΡΠ°ΡΠΈΡ ΡΠΏΠΎΠ½Π΄ΠΈΠ»ΠΈΡ ΠΈ ΠΏΡΠΎΡΠΈΠ°ΡΠΈΡΠ½ΠΈΡ Π°ΡΡΡΠΈΡ ΡΡΡ ΡΠΈΠ½ΡΠ΅ΡΠΈΡΠ½ΠΈ ΠΈ Π±ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ½ΠΈ Π±ΠΎΠ»Π΅ΡΡΠΎΠΏΡΠΎΠΌΠ΅Π½ΡΡΠΈ Π°Π½ΡΠΈΡΠ΅Π²ΠΌΠ°ΡΠΈΡΠ½ΠΈ Π»Π΅ΠΊΠ°ΡΡΡΠ²Π΅Π½ΠΈ ΠΏΡΠΎΠ΄ΡΠΊΡΠΈ ΠΏΡΠ΅Π· 2010 Π³. Π² Π . ΠΡΠ»Π³Π°ΡΠΈΡ(Π¦Π΅Π½ΡΡΠ°Π»Π½Π° ΠΌΠ΅Π΄ΠΈΡΠΈΠ½ΡΠΊΠ° Π±ΠΈΠ±Π»ΠΈΠΎΡΠ΅ΠΊΠ°, ΠΠ£ Π‘ΠΎΡΠΈΡ / Central Medical Library, MU β Sofia, 2011-12) Π‘ΡΠΎΠΈΠ»ΠΎΠ²/Stoilov, Π ./R.; ΠΠ²Π°Π½ΠΎΠ²Π°/Ivanova, Π./M.; Π‘ΡΠΎΠΈΠ»ΠΎΠ²/Stoilov, Π./N.; ΠΠ°ΡΠΈΠ½ΡΠ΅Π²Π°/Marincheva, Π‘./S.Π Π΅Π·ΡΠΌΠ΅. Π Π°Π½Π½ΠΎΡΠΎ ΠΏΠΎΡΡΠ°Π²ΡΠ½Π΅ Π½Π° Π΄ΠΈΠ°Π³Π½ΠΎΠ·Π°ΡΠ° ΠΈ ΡΠ°Π½Π½ΠΎΡΠΎ ΠΈ Π°Π³ΡΠ΅ΡΠΈΠ²Π½ΠΎ Π»Π΅ΡΠ΅Π½ΠΈΠ΅ Π½Π° ΡΠ΅Π²ΠΌΠ°ΡΠΎΠΈΠ΄Π½ΠΈΡ Π°Ρ- ΡΡΠΈΡ (RA) ΡΠ° ΡΡΠ΅Π΄ ΠΎΡΠ½ΠΎΠ²Π½ΠΈΡΠ΅ ΡΠ°ΠΊΡΠΎΡΠΈ Π·Π° Π·Π°Π±Π°Π²ΡΠ½Π΅ ΡΠ΅ΠΌΠΏΠ° Π½Π° ΠΊΠΎΡΡΠ½ΠΎ-Ρ ΡΡΡΡΠ»Π½ΠΈΡΠ΅ Π΄Π΅ΡΡΡΡΠΊΡΠΈΠΈ, ΡΠ΅ΡΠΏΠ΅ΠΊΡΠΈΠ²Π½ΠΎ Π½Π° ΠΈΠ½Π²Π°Π»ΠΈΠ΄ΠΈΠ·Π°ΡΠΈΡΡΠ°. ΠΠΎΠ΄ΠΎΠ±Π½ΠΈ ΡΠ΅Π·ΡΠ»ΡΠ°ΡΠΈ ΡΠ° ΡΡΠΎΠ±ΡΠ΅Π½ΠΈ ΠΈ ΠΏΡΠΈ Π±ΠΎΠ»Π½ΠΈ Ρ Π°Π½ΠΊΠΈΠ»ΠΎΠ·ΠΈΡΠ°Ρ ΡΠΏΠΎΠ½Π΄ΠΈΠ»ΠΈΡ (AS) ΠΈ ΠΏΡΠΎΡΠΈΠ°ΡΠΈΡΠ΅Π½ Π°ΡΡΡΠΈΡ (PsA). ΠΠΎΠ»Π΅ΠΌΠΈ Π½Π°Π΄Π΅ΠΆΠ΄ΠΈ Π² ΡΠΎΠ²Π° ΠΎΡΠ½ΠΎΡΠ΅Π½ΠΈΠ΅ ΡΠ΅ Π²ΡΠ·Π»Π°Π³Π°Ρ Π½Π° Π±ΠΎΠ»Π΅ΡΡΠΎΠΏΡΠΎΠΌΠ΅Π½ΡΡΠΈΡΠ΅ Π°Π½ΡΠΈΡΠ΅Π²ΠΌΠ°ΡΠΈΡΠ½ΠΈ Π»Π΅ΠΊΠ°ΡΡΡΠ²Π΅Π½ΠΈ ΠΏΡΠΎΠ΄ΡΠΊΡΠΈ (Disease-modifying antirheumatic drugs, DMARDs) ΠΈ ΠΏΡΠ΅Π΄ΠΈ Π²ΡΠΈΡΠΊΠΎ Π½Π° Π±ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ½ΠΈΡΠ΅ ΡΡΠ΅Π΄ΡΡΠ²Π°. Π¦Π΅Π»ΡΠ° Π½Π° Π½Π°ΡΡΠΎΡΡΠΎΡΠΎ ΠΏΡΠΎΡΡΠ²Π°Π½Π΅ Π΅ Π΄Π° ΡΠ΅ ΡΡΡΠ°Π½ΠΎΠ²ΠΈ ΠΏΠΎΡΡΠ΅Π±Π»Π΅Π½ΠΈΠ΅ΡΠΎ Π½Π° ΡΠΈΠ½ΡΠ΅ΡΠΈΡΠ½ΠΈ ΠΈ Π±ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ½ΠΈ DMARDs Π² ΠΡΠ»Π³Π°ΡΠΈΡ ΠΏΡΠ΅Π· 2010 Π³. Π·Π° Π»Π΅- ΡΠ΅Π½ΠΈΠ΅ Π½Π° Π±ΠΎΠ»Π½ΠΈΡΠ΅ ΠΎΡ RA, AS ΠΈ PsA. ΠΡΠ΅Π· 2010 Π³. Π΅ Π½Π°ΡΠ°ΡΠ½Π°Π» Π±ΡΠΎΡΡ Π½Π° Π±ΠΎΠ»Π½ΠΈΡΠ΅ ΠΎΡ RA, Π»Π΅ΠΊΡΠ²Π°Π½ΠΈ ΡΡΡ ΡΠΈΠ½ΡΠ΅ΡΠΈΡΠ½ΠΈ DMARDs. Π£Π²Π΅Π»ΠΈΡΠ΅Π½ΠΈΠ΅ΡΠΎ Π΅ Π·Π° ΡΠΌΠ΅ΡΠΊΠ° ΠΏΡΠ΅Π΄ΠΈ Π²ΡΠΈΡΠΊΠΎ Π½Π° Leflunomide (Arava). Π’ΠΎΠ·ΠΈ ΡΠ°ΠΊΡ ΡΠ΅ ΠΎΠ±ΡΡΠ½ΡΠ²Π° Ρ ΠΊΠΎΠ½ΡΠ΅Π½ΡΡΡΠ° Π½Π° ΠΠΠ , ΡΠ΅ Π±ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ½ΠΎ ΡΡΠ΅Π΄ΡΡΠ²ΠΎ ΠΏΡΠΈ Π±ΠΎΠ»Π½ΠΈ ΠΎΡ RA ΡΠ΅ Π²ΠΊΠ»ΡΡΠ²Π° ΡΠ°ΠΌΠΎ ΡΠ»Π΅Π΄ Π½Π΅ΠΏΠΎΠ²Π»ΠΈΡΠ²Π°Π½Π΅ Π½Π° Π°ΡΡΡΠΈΡΠ° ΠΎΡ Methotrexate ΠΈ Leflunomid. Π Π°Π·Ρ ΠΎΠ΄ΠΈΡΠ΅ Π·Π° Π±ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ½ΠΈ DMARDs ΡΠ° ΠΏΠΎ- Π²Π΅ΡΠ΅ ΠΎΡ 5 ΠΏΡΡΠΈ ΡΠΏΡΡΠΌΠΎ ΠΏΡΠ΅Π΄Ρ ΠΎΠ΄Π½Π°ΡΠ° 2009 Π³ΠΎΠ΄ΠΈΠ½Π°. Π’ΠΎΠ·ΠΈ ΡΠ°ΡΡΠ΅ΠΆ Π΅ Π·Π° ΡΠΌΠ΅ΡΠΊΠ° ΠΏΡΠ΅Π΄ΠΈ Π²ΡΠΈΡΠΊΠΎ Π½Π° Π±ΠΎΠ»- Π½ΠΈΡΠ΅ ΠΎΡ RA ΠΈ AS. ΠΠΈΠΏΡΠ°ΡΠ° Π½Π° Π΄ΠΎΡΡΠ°ΡΡΡΠ½ΠΎ Π΅ΡΠ΅ΠΊΡΠΈΠ²Π½ΠΈ ΡΠΈΠ½ΡΠ΅ΡΠΈΡΠ½ΠΈ Π»Π΅ΠΊΠ°ΡΡΡΠ²Π΅Π½ΠΈ ΠΏΡΠΎΠ΄ΡΠΊΡΠΈ (NSAIDs ΠΈ DMARDs) Π·Π° Π»Π΅ΡΠ΅Π½ΠΈΠ΅ΡΠΎ Π½Π° AS ΡΡΠΈΠΌΡΠ»ΠΈΡΠ° ΠΏΠΎΡΡΠ΅Π±Π»Π΅Π½ΠΈΠ΅ΡΠΎ Π½Π° Π±ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ½ΠΈ ΡΡΠ΅Π΄ΡΡΠ²Π°. ΠΡΠΏ- ΡΠ΅ΠΊΠΈ Π½Π°ΡΠ°ΡΠ½Π°Π»ΠΎΡΠΎ ΠΏΠΎΡΡΠ΅Π±Π»Π΅Π½ΠΈΠ΅ Π½Π° Π±ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ½ΠΈ ΡΡΠ΅Π΄ΡΡΠ²Π° Π·Π° Π»Π΅ΡΠ΅Π½ΠΈΠ΅ΡΠΎ Π½Π° Π²ΡΠ·ΠΏΠ°Π»ΠΈΡΠ΅Π»Π½ΠΈΡΠ΅ ΡΡΠ°Π²Π½ΠΈ Π·Π°Π±ΠΎΠ»ΡΠ²Π°Π½ΠΈΡ Ρ Π½Π°Ρ, ΠΏΡΠΎΡΠ΅Π½ΡΡΡ Π½Π° ΠΎΠ±Ρ Π²Π°Π½Π°ΡΠΈΡΠ΅ Π΅ ΠΌΠ½ΠΎΠ³ΠΎ ΠΌΠ°Π»ΡΠΊ Π² ΡΡΠ°Π²Π½Π΅Π½ΠΈΠ΅ Ρ Π΄ΡΡΠ³ΠΈΡΠ΅ ΡΡΡΠ°Π½ΠΈ ΠΎΡ ΠΠ²ΡΠΎΠΏΠ΅ΠΉΡΠΊΠΈΡ ΡΡΡΠ·, ΠΊΡΠ΄Π΅ΡΠΎ ΡΡΠ΅Π΄Π½ΠΈΡΡ ΠΏΡΠΎΡΠ΅Π½Ρ Π΅ 12. Π£ Π½Π°Ρ Π½Π° TNF-Ξ± Π±Π»ΠΎΠΊΠ΅ΡΠΈ ΡΠ° 0.42% ΠΎΡ Π±ΠΎΠ»Π½ΠΈΡΠ΅ Ρ RA ΠΈ 0.40% ΠΎΡ Π±ΠΎΠ»Π½ΠΈΡΠ΅ Ρ AS. Π’ΠΎΠ²Π° ΠΏΠΎΠΊΠ°Π·Π²Π°, ΡΠ΅ Π΄ΠΎΡΡΡΠΏΡΡ Π΄ΠΎ ΡΠΊΡΠΏΠΎΡΡΡΡΠ²Π°ΡΠΎΡΠΎ ΠΈ Π²ΠΈΡΠΎΠΊΠΎΠ΅ΡΠ΅ΠΊΡΠΈΠ²Π½ΠΎ Π»Π΅ΡΠ΅Π½ΠΈΠ΅ Ρ Π±ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ½ΠΈ DMARDs Π² Π . ΠΡΠ»Π³Π°ΡΠΈΡ Π΅ ΡΠΈΠ»Π½ΠΎ ΠΎΠ³ΡΠ°Π½ΠΈΡΠ΅Π½. Π Π΅ΠΈΠΌΠ±ΡΡΡΠ½Π°ΡΠ° ΠΏΠΎΠ»ΠΈΡΠΈΠΊΠ° Π½Π° Π·Π΄ΡΠ°Π²Π½ΠΎΠΎΡΠΈΠ³ΡΡΠΈΡΠ΅Π»Π½Π°ΡΠ° ΡΠΈΡΡΠ΅ΠΌΠ° Π΅ ΠΊΠ»ΡΡΡΡ ΠΊΡΠΌ ΠΏΠΎΠ΄ΠΎΠ±ΡΡΠ²Π°Π½Π΅ Π΄ΠΎΡΡΡΠΏΠ° Π΄ΠΎ Π»Π΅ΡΠ΅Π½ΠΈΠ΅ Ρ Π±ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ½ΠΈ ΡΡΠ΅Π΄ΡΡΠ²Π°. Π Π΅ΠΈΠΌΠ±ΡΡΡΠΈΡΠ°Π½Π΅ΡΠΎ ΡΠ°ΠΌΠΎ Π½Π° 75% ΠΎΡ ΡΠ΅Π½Π°ΡΠ° Π½Π° ΡΠΎΠ²Π° Π»Π΅ΡΠ΅Π½ΠΈΠ΅ Π΅ Π½Π΅ΠΏΠΎΡΠΈΠ»Π½Π° ΡΠ΅ΠΆΠ΅ΡΡ Π·Π° Π±ΠΎΠ»Π½ΠΈΡΠ΅. ΠΡΠ΅ ΠΎΡΠ΅ Π΅ ΠΌΠ°Π»ΡΠΊ ΠΏΡΠΎΡΠ΅Π½ΡΡΡ Π½Π° Π±ΠΎΠ»Π½ΠΈΡΠ΅, Π»Π΅ΠΊΡΠ²Π°Π½ΠΈ ΡΡΡ ΡΠΈΠ½ΡΠ΅ΡΠΈΡΠ½ΠΈ DMARDs. Π Π΅ΠΈΠΌΠ±ΡΡ- ΡΠΈΡΠ°Π½Π΅ΡΠΎ, ΡΠ°Π·Π±ΠΈΡΠ° ΡΠ΅, Π΅ Π²Π°ΠΆΠ½ΠΎ, Π½ΠΎ ΡΠΎ Π½ΡΠΌΠ° ΡΠΎΠ»ΠΊΠΎΠ²Π° Π³ΠΎΠ»ΡΠΌΠ° ΡΠ΅ΠΆΠ΅ΡΡ ΠΊΠ°ΠΊΡΠΎ ΠΏΡΠΈ Π±ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ½ΠΈΡΠ΅ ΡΡΠ΅Π΄- ΡΡΠ²Π°. ΠΠΎ-Π²Π°ΠΆΠ½ΠΈ ΡΠ° ΠΏΠΎΠ·ΠΈΡΠΈΡΡΠ° Π½Π° ΡΠ΅Π²ΠΌΠ°ΡΠΎΠ»ΠΎΠ³Π° ΠΈ ΡΡΠ³Π»Π°ΡΠΈΠ΅ΡΠΎ Π½Π° ΡΠ°ΠΌΠΈΡ Π±ΠΎΠ»Π΅Π½. ***** Summary. Early diagnosis and early aggressive treatment of rheumatoid arthritis (RA) are among the major factors for delaying the rate of bone-tendon destructions and, respectively, of invalidism. Such observations have also been reported in patients with ankylosing spondylitis (AS) and psoriatic arthritis (PsA). Regarding this, great hopes are reposed in disease-modifying antirheumatic drugs (DMARDs) and, particularly, in biologic agents. The aim of this study was to determine and evaluate the utilization of synthetic and biologic DMARDs in the treatment of RA, AS and PsA for 2010 in Bulgaria. For 2010, an increase of the number of RA treatments with synthetic DMARDs was registered, predominantly attributed to treatments with leflunomide (Arava). This fact can be explained by the consensus achieved by the members of the Bulgarian Society for Rheumatology that a biologic agent is to be included in the treatment of RA, only after a lack of response to methotrexate and leflunomide. In 2010, expenditures for biologic DMARDs were 5 times higher compared with these for the preceding 2009. This increase was attributed mostly to RA and AS treatments. The lack of sufficiently effective synthetic medicinal products (NSAIDs and DMARDs) for the treatment of AS, has stimulated the use of biologic agents. Despite the increased utilization of biologic agents in the treatment of inflammatory joint diseases in Bulgaria, the proportion of their users is too small, compared with the average 12% in the other EU countries. In our country, 0.42% of the RA patients and 0.40% of the AS patients are on TNF-Ξ± blockers. This indicates that the access to expensive and highly effective treatments with biologic DMARDs is very limited in Bulgaria. The reimbursement policy of the health insurance system is the key to improving the access to biologic agent treatment. The reimbursement of only 75% of the cost of this treatment is still far beyond patient affordability. The proportion of patients treated with synthetic DMARDs is still too low. Of course, reimbursement of synthetic DMARDs is of importance, but it has no such heaviness as this of biologic agents. Rheumatologistβs opinion and patient's compliance are of greater importance.