Relação entre biomarcadores inflamatórios, de adesão celular, de estresse oxidativo, de lesão endotelial, remodelamento tecidual e vascular e os diferentes estágios da doença venosa crônica primária (classes clínicas CEAP C0a, C2, C3, C4) / Relationship between biomarkers of inflammation, cell adhesion, oxidative stress, endothelial cell damage, vascular and tissue remodeling and the different stages of primary chronic venous disease (CEAP clinical classes C0a, C2, C3, C4)

A doença venosa crônica (DVC) é uma desordem complexa que compreende sinais e sintomas que variam das telangiectasias às úlceras ativas. A DVC é classificada de acordo com aspectos clínicos, etiológicos, anatômicos e fisiopatológicos (CEAP) em sete classes variando de C0 à C6. A principal causa da DVC é a hipertensão venosa que altera o fluxo venoso e, consequentemente, a força de cisalhamento que induz alterações fenotípicas nas células endoteliais que passam a expressar mediadores pró-inflamatórios e pró-trombóticos, que levam à adesão de leucócitos, ao aumento do estresse oxidativo, da permeabilidade vascular e do dano endotelial e ao remodelamento tecidual e vascular.Em virtude dos inúmeros mecanismos e da diversidade de moléculas envolvidas na patogênese e progressão da DVC, é essencial conhecer a interação entre elas e também saber quais são as moléculas (biomarcadores) que se correlacionam positivamente ou negativamente com a gravidade da doença. Foram avaliados os níveis de Interleucina-6 (IL-6), sL-selectina, sE-selectina, sP-selectina, molécula de adesão intercelular-1solúvel (sICAM-1), molécula de adesão das células vasculares-1 solúvel (sVCAM-1), ativador tecidual do plasminogênio (tPA), atividade do inibidor do ativador do plasminogênio-1 (PAI-1), trombomodulina solúvel (sTM), fator de von Willebrand (vWF), metaloproteinase de matriz (MMP)-2, MMP-3, MMP-9, inibidor tecidual das MMPs -1 (TIMP-1), angiopoietina-1 e -2, sTie-2 e s-Endoglina e fator de crescimento do endotélio vascular (VEGF) no sangue coletado da veia braquial de 173 mulheres com DVC primária divididas em grupos C2, C3, C4 e C4 menopausadas (C4m) e de 18 voluntárias saudáveis (grupo C0a). Foram também analisados os níveis urinários de ent-prostaglandina F2α nesses grupos. Não foram encontradas diferenças estatisticamente significativas com relação às concentrações sanguíneas e urinárias de sE-selectina, sP-selectina, sICAM-1, atividade de PAI-1, MMP-3, razão TIMP-1/MMP-3 ...

Chronic Venous Disease (CVD) is a complex disorder, which encompasses signs and symptoms that vary from telangiectasias to active ulcers. The CVD is classified according Clinical, Etiologic, Anatomical and Pathophysiological (CEAP) aspects into seven classes varying from C0 to C6. The main cause of CVD is venous hypertension, which alters venous flow and consequently, shear stress. Abnormal shear stress induces phenotypic changes in endothelial cells that start to express pro-inflammatory and pro-thrombotic mediators that lead to leukocyte adhesion, oxidative stress, increased vascular permeability and endothelial cell damage and tissue and vascular remodeling. Due to several mechanisms and the diversity of molecules involved in the pathogenesis and progression of CVD, is essential to know the interplay between them and which are the molecules (biomarkers) that correlate positively and negatively with the severity of the disease. We investigated the levels of interleukin-6 (IL-6), sL-selectin, sE-selectin, sP-selectin, soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), tissue plasminogen activator (tPA), plasminogen activator inhibitor-1 (PAI-1) activity, soluble thrombomodulin (sTM), von Willebrand factor (vWf), matrix metalloproteinase (MMP)-2, MMP-3, MMP-9, tissue inhibitor of metaloproteinases-1 (TIMP-1), angiopoietin-1 and -2, sTie-2, s-Endoglin, vascular endothelial growth factor (VEGF) in the blood taken from the brachial vein of 173 patients with primary CVD divided into C2, C3, C4 and menopaused C4 (C4m) groups and 18 healthy volunteers (C0a group).We also investigated the urinary levels of ent-prostaglandin F2α in these groups. There was no statistically significant difference between groups with respect to blood or urinary levels of sE-selectin, sP-selectin, sICAM-1, PAI-1 activity, MMP-3, TIMP-1/MMP-3 ratio, angiopoietin-2, angiopoietin-1/angiopoietin-2 ratio, s-Endoglin ...

A Comparison of the Efficacy of Cataract Surgery Using Aqualase(R) with Phacoemulsification Using MicroFlow(R) System

PURPOSE: To compare the outcomes after phacoemulsification performed with the AquaLase(R) and phacoemulsification in MicroFlow(R) system, including surgically induced astigmatism (SIA), corneal endothelial cell damage and postoperative recovery of visual acuity. METHODS: The cataracts of Lens Opacities Classification System, version III (LOCS III) nuclear grade below 2 were subjected in this study. Nineteen eyes underwent cataract operation using AquaLase(R) (Alcon Laboratories, Fort Worth, Texas, U.S.A.). A control group (19 eyes) used the MicroFlow(R) system (Millenium, Stortz, U.S.A.) and was selected by matching age, sex, systemic disease, corneal astigmatism and corneal endothelial cell density. All the surgeries were performed by the same operator. SIA, corneal endothelial cell loss, visual acuity, and corneal thickness were evaluated postoperatively. RESULTS: SIA in the group using AquaLase(R) was less than that of the group using MicroFlow(R) system (P=0.022) at 2 months postoperatively. Evaluation of corneal endothelial cell loss, recovery of visual acuity and corneal thickness found no statistically significant differences between the two groups. CONCLUSIONS: Cataract surgery using AquaLase(R) induces less surgically induced astigmatism in mild to moderate cataracts.

Endothelial Cell Damage in Microincison Cataract Surgery and Coaxial Phacoemulsification

PURPOSE: To evaluate the damage to corneal endothelial cells following coaxial phacoemulsification and bimanual microincision cataract surgery (MICS). METHODS: We measured and compared the changes in the corneal endothelial mean cell density, cell size variation coefficient, hexagonality, and central corneal thickness in senile cataract patients who had received either coaxial phacoemulsification (Group 1, n=20), MICS using ultrasound (Group 2, n=20), and MICS using laser (Group 3, n=20). The endothelial cell parameters and corneal thickness were evaluated preoperatively and at 1 week, 1 month, and 2 months postoperatively. RESULTS: There was no significant difference among the three groups in terms of the endothelial cell parameters and corneal thickness during two months (p>0.05). CONCLUSIONS: MICS is a safe technique that does not appear to be associated with more damage to the corneal endothelium than coaxial phacoemulsification. A longer follow-up study is necessary to investigate its potential benefits for replacing conventional surgery.

Comparison of the Phaco Chop and the Mini Chop Methods in Cataract Surgery

PURPOSE: To compare effective phacoemulsification time (EPT), the severity of corneal swelling and corneal endothelial cell density after cataract surgery between the phaco chop method and the mini chop method. METHODS: Cataract surgery was performed by phaco chop (15 eyes) or by mini chop (13 eyes) method in 28 eyes of 27 patients. The nuclear opacity of cataract grade was more than 5 on LOCS (Lens opacities classification system) III. EPT and the amount of irrigated BSS solution were measured during the operation. Corneal thickness (preoperative, immediate postoperative, postoperative 1 day, 1 week, 1 month, and 3 months) and corneal endothelial cell density (preoperative, postoperative 1month and 3 months) were measured. RESULTS: The EPT of phaco chop group was 5.2 sec and that of mini chop was 1.0 sec (p=0.000). The amount of irrigated BSS was 193.7 ml and 170.4 ml in the phaco chop group and the mini chop group, respectively. The increase in corneal thickness was 3.2% and 0.9% at immediately after surgery (p=0.128), 19.0% and 10.5% at postoperative 1 day (p=0.088), 5.7% and 1.5% at postoperative 1 week (p=0.080), 0% and -1.3% at postoperative 1 month (p=0.717), and -0.4% and -0.6% at postoperative 3 months (p=0.890) in the phaco chop group and the mini chop group, respectively. Corneal endothelial cell density decreased 23.0% in the phaco chop group and 9.4% in the mini chop group at postoperative 1 month (p=0.005) and 22.9%, 12.6%, at 3 months respectively (p=0.036). CONCLUSIONS: The mini chop technique reduced permanent endothelial cell damage in comparison with the phaco chop method and might be more effective in decreasing corneal swelling during the early postoperative period than the phaco chop method.