8 research outputs found
Π₯Π°ΡΠ°ΠΊΡΠ΅Ρ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΡ ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΠΉ ΠΎΠΆΠΎΠ³ΠΎΠ² Π³Π»Π°Π· Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΡΠ°Π·Π»ΠΈΡΠ½ΡΠΌ ΡΠ΅Π½ΠΎΡΠΈΠΏΠΎΠΌ Π°ΡΠ΅ΡΠΈΠ»ΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΠΏΡΠΈ Π½ΠΎΡΠΌΠ°Π»ΠΈΠ·ΠΎΠ²Π°Π½Π½ΠΎΠΌ Π²Π½ΡΡΡΠΈΠ³Π»Π°Π·Π½ΠΎΠΌ Π΄Π°Π²Π»Π΅Π½ΠΈΠΈ
PURPOSE: To study the character of clinical manifestations of ocular burns in patients with normal IOP and different acetylation phenotypes (APh).METHODS: We examined 103 patients with ocular burns (141 eyes) during their primary visit to the Republican Clinical Eye Hospital of the Ministry of Health of Uzbekistan, on different time-points during therapy (on days 2, 5, 7, 12 after the beginning of treatment) and then during an active clinical examination 30 days and 4 months after discharge. 44 patients were examined 1-2 years after suffering a burn injury in order to identify the later post-burn complications and their interpretation according to the patientβs APh. 52 (69 eyes) patients out of 103 examined patients (141 affected eyes) had a slow acetylation phenotype (SA) and 51 patients (72 eyes) β a fast acetylation phenotype (FA).RESULTS: The results of these studies allow us to assert that patients with SA phenotype develop deeper ocular burns, with eye tissue damages less prone to treatment than in FA patients, where less pronounced changes lead to faster process normalization. APh determines the course of the manifestations, their severity and risk of complications in ocular burns patients. Fast acetylation phenotype may serve as a prognostic marker of faster pathological changes regression in ocular tissues, whereas the slow acetylation phenotype suggests the development of more severe disease forms, often requiring a prolonged and complex therapy.Β Π¦ΠΠΠ¬. ΠΠ·ΡΡΠΈΡΡ Ρ
Π°ΡΠ°ΠΊΡΠ΅Ρ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΡΠ΅ΡΠ΅Π½ΠΈΡ ΠΏΠΎΡΠ°ΠΆΠ΅Π½ΠΈΡ Π³Π»Π°Π·Π° ΠΏΡΠΈ Ρ
ΠΈΠΌΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΎΠΆΠΎΠ³Π°Ρ
Π² Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡΠΈ ΠΎΡ ΡΠ΅Π½ΠΎΡΠΈΠΏΠ° Π°ΡΠ΅ΡΠΈΠ»ΠΈΡΠΎΠ²Π°Π½ΠΈΡ (Π€Π) ΠΏΡΠΈ Π½ΠΎΡΠΌΠ°Π»ΠΈΠ·ΠΎΠ²Π°Π½Π½ΠΎΠΌ Π²Π½ΡΡΡΠΈΠ³Π»Π°Π·Π½ΠΎΠΌ Π΄Π°Π²Π»Π΅Π½ΠΈΠΈ (ΠΠΠ).ΠΠΠ’ΠΠΠ«. ΠΡΠ»ΠΈ ΠΎΠ±ΡΠ»Π΅Π΄ΠΎΠ²Π°Π½Ρ 103 Π±ΠΎΠ»ΡΠ½ΡΡ
Ρ ΠΎΠΆΠΎΠ³Π°ΠΌΠΈ Π³Π»Π°Π· (141 Π³Π»Π°Π·): ΠΏΡΠΈ ΠΏΠ΅ΡΠ²ΠΈΡΠ½ΠΎΠΌ ΠΎΠ±ΡΠ°ΡΠ΅Π½ΠΈΠΈ, Π½Π° ΡΡΠ°ΠΏΠ°Ρ
ΡΠ΅ΡΠ°ΠΏΠΈΠΈ (2, 5, 7, 12 ΡΡΡΠΊΠΈ ΠΎΡ ΠΌΠΎΠΌΠ΅Π½ΡΠ° ΠΎΠ±ΡΠ°ΡΠ΅Π½ΠΈΡ Π² ΠΊΠ»ΠΈΠ½ΠΈΠΊΡ) ΠΈ ΠΏΡΠΈ Π°ΠΊΡΠΈΠ²Π½ΠΎΠΉ Π΄ΠΈΡΠΏΠ°Π½ΡΠ΅ΡΠΈΠ·Π°ΡΠΈΠΈ Π² ΡΡΠΎΠΊΠΈ 30 Π΄Π½Π΅ΠΉ ΠΈ 4 ΠΌΠ΅Ρ. ΠΏΠΎΡΠ»Π΅ Π²ΡΠΏΠΈΡΠΊΠΈ. Π§Π΅ΡΠ΅Π· 1-2 Π³ΠΎΠ΄Π° ΠΏΠΎΡΠ»Π΅ ΠΏΠ΅ΡΠ΅Π½Π΅ΡΠ΅Π½Π½ΠΎΠΉ ΠΎΠΆΠΎΠ³ΠΎΠ²ΠΎΠΉ ΡΡΠ°Π²ΠΌΡ Ρ ΡΠ΅Π»ΡΡ Π²ΡΡΠ²Π»Π΅Π½ΠΈΡ ΠΏΠΎΠ·Π΄Π½ΠΈΡ
ΠΏΠΎΡΠ»Π΅ΠΎΠΆΠΎΠ³ΠΎΠ²ΡΡ
ΠΎΡΠ»ΠΎΠΆΠ½Π΅Π½ΠΈΠΉ ΠΈ ΠΈΡ
ΠΈΠ½ΡΠ΅ΡΠΏΡΠ΅ΡΠ°ΡΠΈΠΈ Ρ ΡΡΠ΅ΡΠΎΠΌ Π€Π ΡΠ°ΠΊΠΆΠ΅ Π±ΡΠ»ΠΈ ΠΎΠ±ΡΠ»Π΅Π΄ΠΎΠ²Π°Π½Ρ 44 ΠΏΠ°ΡΠΈΠ΅Π½ΡΠ°. ΠΠ· ΠΎΠ±ΡΠ΅Π³ΠΎ ΡΠΈΡΠ»Π° 103 ΠΎΠ±ΡΠ»Π΅Π΄ΠΎΠ²Π°Π½Π½ΡΡ
Π»ΠΈΡ (141 ΠΏΠΎΡΠ°ΠΆΠ΅Π½Π½ΡΠΉ Π³Π»Π°Π·) β 52 (69 Π³Π»Π°Π·) Π±ΠΎΠ»ΡΠ½ΡΡ
Π±ΡΠ»ΠΈ Ρ ΠΌΠ΅Π΄Π»Π΅Π½Π½ΡΠΌ ΡΠΈΠΏΠΎΠΌ ΡΠ΅Π½ΠΎΡΠΈΠΏΠ° Π°ΡΠ΅ΡΠΈΠ»ΠΈΡΠΎΠ²Π°Π½ΠΈΡ (ΠΠ) ΠΈ 51 Π±ΠΎΠ»ΡΠ½ΠΎΠΉ (72 Π³Π»Π°Π·Π°) β Ρ Π±ΡΡΡΡΡΠΌ ΡΠΈΠΏΠΎΠΌ Π°ΡΠ΅ΡΠΈΠ»ΠΈΡΠΎΠ²Π°Π½ΠΈΡ (ΠΠ).Π ΠΠΠ£ΠΠ¬Π’ΠΠ’Π«. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½Π½ΡΡ
ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠΉ ΠΏΠΎΠ·Π²ΠΎΠ»ΡΡΡ ΡΡΠ²Π΅ΡΠΆΠ΄Π°ΡΡ, ΡΡΠΎ ΠΏΡΠΈ ΠΎΠΆΠΎΠ³Π°Ρ
Π³Π»Π°Π· ΠΏΡΠΈ ΠΠ ΡΠ°Π·Π²ΠΈΠ²Π°ΡΡΡΡ Π±ΠΎΠ»Π΅Π΅ Π³Π»ΡΠ±ΠΎΠΊΠΈΠ΅, ΡΡΠΆΠ΅Π»ΠΎ ΠΏΠΎΠ΄Π΄Π°ΡΡΠΈΠ΅ΡΡ Π»Π΅ΡΠ΅Π½ΠΈΡ Π΄Π΅ΡΡΡΡΠΊΡΠΈΠ²Π½ΡΠ΅ Π½Π°ΡΡΡΠ΅Π½ΠΈΡ Π² ΡΠΊΠ°Π½ΡΡ
Π³Π»Π°Π·Π°, ΠΏΡΠΈ ΠΠ β ΠΌΠ΅Π½Π΅Π΅ Π²ΡΡΠ°ΠΆΠ΅Π½Π½ΡΠ΅ ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΡ, ΠΊΠΎΡΠΎΡΡΠ΅ Π² Π΄Π°Π»ΡΠ½Π΅ΠΉΡΠ΅ΠΌ Π±ΡΡΡΡΠ΅Π΅ ΠΏΡΠΈΠ²ΠΎΠ΄ΡΡ ΠΊ Π½ΠΎΡΠΌΠ°Π»ΠΈΠ·Π°ΡΠΈΠΈ ΠΏΡΠΎΡΠ΅ΡΡΠ°. Π€Π ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ΅Ρ Ρ
Π°ΡΠ°ΠΊΡΠ΅Ρ ΡΠ΅ΡΠ΅Π½ΠΈΡ, ΡΡΠΆΠ΅ΡΡΡ ΠΈ ΡΠΈΡΠΊ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΠΎΡΠ»ΠΎΠΆΠ½Π΅Π½ΠΈΠΉ ΠΏΡΠΈ ΠΎΠΆΠΎΠ³Π°Ρ
Π³Π»Π°Π·. ΠΠ ΠΌΠΎΠΆΠ΅Ρ ΡΠ»ΡΠΆΠΈΡΡ ΠΏΡΠΎΠ³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΈΠΌ ΠΌΠ°ΡΠΊΠ΅ΡΠΎΠΌ ΠΊ Π±ΠΎΠ»Π΅Π΅ Π±ΡΡΡΡΠΎΠΉ ΡΠ΅Π³ΡΠ΅ΡΡΠΈΠΈ ΠΏΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΠΉ Π² ΡΠΊΠ°Π½ΡΡ
Π³Π»Π°Π·Π°, ΠΠ ΠΏΡΠ΅Π΄ΠΏΠΎΠ»Π°Π³Π°Π΅Ρ ΠΊ ΡΠ°Π·Π²ΠΈΡΠΈΡ Π±ΠΎΠ»Π΅Π΅ ΡΡΠΆΠ΅Π»ΡΡ
ΡΠΎΡΠΌ Ρ Π·Π°ΡΡΠΆΠ½ΡΠΌ ΠΈ ΠΎΡΠ»ΠΎΠΆΠ½Π΅Π½Π½ΡΠΌ ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ΠΌ, ΡΡΡΠ΄Π½ΠΎ ΠΏΠΎΠ΄Π΄Π°ΡΡΠΈΡ
ΡΡ ΡΡΠ°Π΄ΠΈΡΠΈΠΎΠ½Π½ΠΎΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ.
Fibrin Clot Structure and Properties are Altered in Systemic Lupus Erythematosus
Β© 2016, Springer Science+Business Media New York.Thrombotic complications in systemic lupus erythematosus contribute significantly to the morbidity and mortality rates. Abnormal formation and structure of fibrin clots add substantially to hypercoagulability and thrombosis. We used dynamic turbidimetry to assess in vitro the kinetics of fibrin polymerization and t-PA-induced fibrinolysis in recalcified plasma of patients with systemic lupus erythematosus compared to healthy subjects. Fibrin structure was studied using scanning electron microscopy. Clots from the pathological plasma samples polymerized significantly slower, resulting in formation of fibrin with a higher optical density and less compact fibrin networks with larger pores. These changes were associated with a prolonged clot lysis time and reduced lysis rate. The results show that in the blood of patients with systemic lupus erythematosus fibrin clots have a pro-thrombotic phenotype that comprises an important mechanism underlying lupus-related thrombophilia
Hyperfibrinogenemia and Increased Stiffness of Plasma Clots in the Active Systemic Lupus Erythematosus
Β© 2017, Springer Science+Business Media, LLC. Systemic lupus erythematosus (SLE) is an autoimmune disease associated with an increased risk of thrombosis. We hypothesized that inflammation-associated hyperfibrinogenemia can contribute to the prothrombotic phenotype of fibrin clots by changing their mechanical properties. Twenty-eight SLE patients were categorized based on their disease activity scores (SLEDAI) into the groups with inactive (SLEDAIΒ Β 4, nΒ =Β 14) forms of the disease. Clots from individual platelet-free plasma samples were probed using shear rheometry and viscoelastic properties of the fibrin gels were determined as the storage (Gβ²) and loss (Gβ³) moduli. A significant increase of Gβ² was revealed in the clots from the plasma of active SLE patients over inactive SLE, which correlated with elevated fibrinogen levels. Clots from the plasma of inactive SLE patients had the elasticity and fibrinogen levels indistinguishable from those in control plasma from healthy subjects. Thus, inflammatory hyperfibrinogenemia in the active SLE form makes fibrin clots stiffer which has been previously shown to be associated with a higher incidence of thrombotic disorders
Fibrin Clot Structure and Properties are Altered in Systemic Lupus Erythematosus
Β© 2016, Springer Science+Business Media New York.Thrombotic complications in systemic lupus erythematosus contribute significantly to the morbidity and mortality rates. Abnormal formation and structure of fibrin clots add substantially to hypercoagulability and thrombosis. We used dynamic turbidimetry to assess in vitro the kinetics of fibrin polymerization and t-PA-induced fibrinolysis in recalcified plasma of patients with systemic lupus erythematosus compared to healthy subjects. Fibrin structure was studied using scanning electron microscopy. Clots from the pathological plasma samples polymerized significantly slower, resulting in formation of fibrin with a higher optical density and less compact fibrin networks with larger pores. These changes were associated with a prolonged clot lysis time and reduced lysis rate. The results show that in the blood of patients with systemic lupus erythematosus fibrin clots have a pro-thrombotic phenotype that comprises an important mechanism underlying lupus-related thrombophilia
Fibrin Clot Structure and Properties are Altered in Systemic Lupus Erythematosus
Β© 2016, Springer Science+Business Media New York.Thrombotic complications in systemic lupus erythematosus contribute significantly to the morbidity and mortality rates. Abnormal formation and structure of fibrin clots add substantially to hypercoagulability and thrombosis. We used dynamic turbidimetry to assess in vitro the kinetics of fibrin polymerization and t-PA-induced fibrinolysis in recalcified plasma of patients with systemic lupus erythematosus compared to healthy subjects. Fibrin structure was studied using scanning electron microscopy. Clots from the pathological plasma samples polymerized significantly slower, resulting in formation of fibrin with a higher optical density and less compact fibrin networks with larger pores. These changes were associated with a prolonged clot lysis time and reduced lysis rate. The results show that in the blood of patients with systemic lupus erythematosus fibrin clots have a pro-thrombotic phenotype that comprises an important mechanism underlying lupus-related thrombophilia
Fibrin Clot Structure and Properties are Altered in Systemic Lupus Erythematosus
Β© 2016, Springer Science+Business Media New York.Thrombotic complications in systemic lupus erythematosus contribute significantly to the morbidity and mortality rates. Abnormal formation and structure of fibrin clots add substantially to hypercoagulability and thrombosis. We used dynamic turbidimetry to assess in vitro the kinetics of fibrin polymerization and t-PA-induced fibrinolysis in recalcified plasma of patients with systemic lupus erythematosus compared to healthy subjects. Fibrin structure was studied using scanning electron microscopy. Clots from the pathological plasma samples polymerized significantly slower, resulting in formation of fibrin with a higher optical density and less compact fibrin networks with larger pores. These changes were associated with a prolonged clot lysis time and reduced lysis rate. The results show that in the blood of patients with systemic lupus erythematosus fibrin clots have a pro-thrombotic phenotype that comprises an important mechanism underlying lupus-related thrombophilia
Hyperfibrinogenemia and Increased Stiffness of Plasma Clots in the Active Systemic Lupus Erythematosus
Β© 2017, Springer Science+Business Media, LLC. Systemic lupus erythematosus (SLE) is an autoimmune disease associated with an increased risk of thrombosis. We hypothesized that inflammation-associated hyperfibrinogenemia can contribute to the prothrombotic phenotype of fibrin clots by changing their mechanical properties. Twenty-eight SLE patients were categorized based on their disease activity scores (SLEDAI) into the groups with inactive (SLEDAIΒ Β 4, nΒ =Β 14) forms of the disease. Clots from individual platelet-free plasma samples were probed using shear rheometry and viscoelastic properties of the fibrin gels were determined as the storage (Gβ²) and loss (Gβ³) moduli. A significant increase of Gβ² was revealed in the clots from the plasma of active SLE patients over inactive SLE, which correlated with elevated fibrinogen levels. Clots from the plasma of inactive SLE patients had the elasticity and fibrinogen levels indistinguishable from those in control plasma from healthy subjects. Thus, inflammatory hyperfibrinogenemia in the active SLE form makes fibrin clots stiffer which has been previously shown to be associated with a higher incidence of thrombotic disorders
RELATIONSHIP OF INFLAMMATORY ACTIVITY AND KIDNEY DAMAGES IN SYSTEMIC LUPUS ERYTHEMATOSUS
To solve the problems in the surveyed 45 patients: examination, laboratory complex, immune and instrumental methods. All 45 patients with SLE kidney disease manifested itself in the form of lupus nephritis. Syndrome hypertension met in 35.5% of cases, the syndrome of chronic renal failure in 37.7% of cases. Urinary syndrome characterized by moderate proteinuria (75.5%), hematuria (73.3%) and leukocyturia (73.3%). Positive correlation of tumor necrosis factor Ξ±, C-reactive protein level of creatinine, urea, ESR and SLE activity, which confirms the participation of the factors described in the immune process lupus inflammation