8 research outputs found

    Π₯Π°Ρ€Π°ΠΊΡ‚Π΅Ρ€ клиничСских проявлСний ΠΎΠΆΠΎΠ³ΠΎΠ² Π³Π»Π°Π· Ρƒ ΠΏΠ°Ρ†ΠΈΠ΅Π½Ρ‚ΠΎΠ² с Ρ€Π°Π·Π»ΠΈΡ‡Π½Ρ‹ΠΌ Ρ„Π΅Π½ΠΎΡ‚ΠΈΠΏΠΎΠΌ ацСтилирования ΠΏΡ€ΠΈ Π½ΠΎΡ€ΠΌΠ°Π»ΠΈΠ·ΠΎΠ²Π°Π½Π½ΠΎΠΌ Π²Π½ΡƒΡ‚Ρ€ΠΈΠ³Π»Π°Π·Π½ΠΎΠΌ Π΄Π°Π²Π»Π΅Π½ΠΈΠΈ

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    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 patient’s 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¦Π•Π›Π¬. Π˜Π·ΡƒΡ‡ΠΈΡ‚ΡŒ Ρ…Π°Ρ€Π°ΠΊΡ‚Π΅Ρ€ клиничСского тСчСния пораТСния Π³Π»Π°Π·Π° ΠΏΡ€ΠΈ химичСских ΠΎΠΆΠΎΠ³Π°Ρ… Π² зависимости ΠΎΡ‚ Ρ„Π΅Π½ΠΎΡ‚ΠΈΠΏΠ° ацСтилирования (ЀА) ΠΏΡ€ΠΈ Π½ΠΎΡ€ΠΌΠ°Π»ΠΈΠ·ΠΎΠ²Π°Π½Π½ΠΎΠΌ Π²Π½ΡƒΡ‚Ρ€ΠΈΠ³Π»Π°Π·Π½ΠΎΠΌ Π΄Π°Π²Π»Π΅Π½ΠΈΠΈ (Π’Π“Π”).ΠœΠ•Π’ΠžΠ”Π«. Π‘Ρ‹Π»ΠΈ обслСдованы 103 Π±ΠΎΠ»ΡŒΠ½Ρ‹Ρ… с ΠΎΠΆΠΎΠ³Π°ΠΌΠΈ Π³Π»Π°Π· (141 Π³Π»Π°Π·): ΠΏΡ€ΠΈ ΠΏΠ΅Ρ€Π²ΠΈΡ‡Π½ΠΎΠΌ ΠΎΠ±Ρ€Π°Ρ‰Π΅Π½ΠΈΠΈ, Π½Π° этапах Ρ‚Π΅Ρ€Π°ΠΏΠΈΠΈ (2, 5, 7, 12 сутки ΠΎΡ‚ ΠΌΠΎΠΌΠ΅Π½Ρ‚Π° обращСния Π² ΠΊΠ»ΠΈΠ½ΠΈΠΊΡƒ) ΠΈ ΠΏΡ€ΠΈ Π°ΠΊΡ‚ΠΈΠ²Π½ΠΎΠΉ диспансСризации Π² сроки 30 Π΄Π½Π΅ΠΉ ΠΈ 4 мСс. послС выписки. Π§Π΅Ρ€Π΅Π· 1-2 Π³ΠΎΠ΄Π° послС пСрСнСсСнной ΠΎΠΆΠΎΠ³ΠΎΠ²ΠΎΠΉ Ρ‚Ρ€Π°Π²ΠΌΡ‹ с Ρ†Π΅Π»ΡŒΡŽ выявлСния ΠΏΠΎΠ·Π΄Π½ΠΈΡ… послСоТоговых ослоТнСний ΠΈ ΠΈΡ… ΠΈΠ½Ρ‚Π΅Ρ€ΠΏΡ€Π΅Ρ‚Π°Ρ†ΠΈΠΈ с ΡƒΡ‡Π΅Ρ‚ΠΎΠΌ ЀА Ρ‚Π°ΠΊΠΆΠ΅ Π±Ρ‹Π»ΠΈ обслСдованы 44 ΠΏΠ°Ρ†ΠΈΠ΅Π½Ρ‚Π°. Из ΠΎΠ±Ρ‰Π΅Π³ΠΎ числа 103 обслСдованных Π»ΠΈΡ† (141 ΠΏΠΎΡ€Π°ΠΆΠ΅Π½Π½Ρ‹ΠΉ Π³Π»Π°Π·) β€” 52 (69 Π³Π»Π°Π·) Π±ΠΎΠ»ΡŒΠ½Ρ‹Ρ… Π±Ρ‹Π»ΠΈ с ΠΌΠ΅Π΄Π»Π΅Π½Π½Ρ‹ΠΌ Ρ‚ΠΈΠΏΠΎΠΌ Ρ„Π΅Π½ΠΎΡ‚ΠΈΠΏΠ° ацСтилирования (МА) ΠΈ 51 больной (72 Π³Π»Π°Π·Π°) β€” с быстрым Ρ‚ΠΈΠΏΠΎΠΌ ацСтилирования (БА).РЕЗУЛЬВАВЫ. Π Π΅Π·ΡƒΠ»ΡŒΡ‚Π°Ρ‚Ρ‹ ΠΏΡ€ΠΎΠ²Π΅Π΄Π΅Π½Π½Ρ‹Ρ… исслСдований ΠΏΠΎΠ·Π²ΠΎΠ»ΡΡŽΡ‚ ΡƒΡ‚Π²Π΅Ρ€ΠΆΠ΄Π°Ρ‚ΡŒ, Ρ‡Ρ‚ΠΎ ΠΏΡ€ΠΈ ΠΎΠΆΠΎΠ³Π°Ρ… Π³Π»Π°Π· ΠΏΡ€ΠΈ МА Ρ€Π°Π·Π²ΠΈΠ²Π°ΡŽΡ‚ΡΡ Π±ΠΎΠ»Π΅Π΅ Π³Π»ΡƒΠ±ΠΎΠΊΠΈΠ΅, тяТСло ΠΏΠΎΠ΄Π΄Π°ΡŽΡ‰ΠΈΠ΅ΡΡ Π»Π΅Ρ‡Π΅Π½ΠΈΡŽ дСструктивныС Π½Π°Ρ€ΡƒΡˆΠ΅Π½ΠΈΡ Π² тканях Π³Π»Π°Π·Π°, ΠΏΡ€ΠΈ БА β€” ΠΌΠ΅Π½Π΅Π΅ Π²Ρ‹Ρ€Π°ΠΆΠ΅Π½Π½Ρ‹Π΅ измСнСния, ΠΊΠΎΡ‚ΠΎΡ€Ρ‹Π΅ Π² дальнСйшСм быстрСС приводят ΠΊ Π½ΠΎΡ€ΠΌΠ°Π»ΠΈΠ·Π°Ρ†ΠΈΠΈ процСсса. ЀА опрСдСляСт Ρ…Π°Ρ€Π°ΠΊΡ‚Π΅Ρ€ тСчСния, Ρ‚ΡΠΆΠ΅ΡΡ‚ΡŒ ΠΈ риск развития ослоТнСний ΠΏΡ€ΠΈ ΠΎΠΆΠΎΠ³Π°Ρ… Π³Π»Π°Π·. БА ΠΌΠΎΠΆΠ΅Ρ‚ ΡΠ»ΡƒΠΆΠΈΡ‚ΡŒ прогностичСским ΠΌΠ°Ρ€ΠΊΠ΅Ρ€ΠΎΠΌ ΠΊ Π±ΠΎΠ»Π΅Π΅ быстрой рСгрСссии патологичСских ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΠΉ Π² тканях Π³Π»Π°Π·Π°, МА ΠΏΡ€Π΅Π΄ΠΏΠΎΠ»Π°Π³Π°Π΅Ρ‚ ΠΊ Ρ€Π°Π·Π²ΠΈΡ‚ΠΈΡŽ Π±ΠΎΠ»Π΅Π΅ тяТСлых Ρ„ΠΎΡ€ΠΌ с затяТным ΠΈ ослоТнСнным Ρ‚Π΅Ρ‡Π΅Π½ΠΈΠ΅ΠΌ, Ρ‚Ρ€ΡƒΠ΄Π½ΠΎ ΠΏΠΎΠ΄Π΄Π°ΡŽΡ‰ΠΈΡ…ΡΡ Ρ‚Ρ€Π°Π΄ΠΈΡ†ΠΈΠΎΠ½Π½ΠΎΠΉ Ρ‚Π΅Ρ€Π°ΠΏΠΈΠΈ.

    Fibrin Clot Structure and Properties are Altered in Systemic Lupus Erythematosus

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    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

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    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 (Gβ€²) and loss (Gβ€³) moduli. A significant increase of Gβ€² 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

    No full text
    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

    No full text
    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

    Get PDF
    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

    No full text
    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 (Gβ€²) and loss (Gβ€³) moduli. A significant increase of Gβ€² 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

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    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
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