Indicaciones de la anticoagulación en pacientes con diabetes / Indications for anticoagulation in patients with diabetes

Las enfermedades cardiovasculares son la causa principal de muerte en lospacientes con diabetes. A los factores clásicos de riesgo aterogénico y aterotrombóticose suman otros específicos de la diabetes, como la disfunción endotelial,la alteración de procesos hemostáticos y la dislipemia diabética. Losresultados de laboratorio indican la existencia de un estado de hipercoagulabilidadcon aumento del funcionalismo plaquetario, alteración de la coagulaciónplasmática y disminución de sus inhibidores naturales. Esta situaciónfavorece la aparición de episodios tromboembólicos, de lo que se desprendela importancia del tratamiento antitrombótico preventivo en estos pacientes. Laindicación de tratamiento anticoagulante será individualizada para cada pacientesegún la etiopatogenia del riesgo tromboembólico absoluto y/o del procedimientointervencionista que se vaya a realizar, si se precisa(AU)

Cardiovascular diseases are the main cause of death in diabetic patients. Besidesthe classic atherogenic and atherothrombotic risk factors, other specificfactors of diabetes should be added as endothelial dysfunction, alteration ofhemostatic processes and diabetic dyslipidemia. Laboratory results indicatethe existence of a hypercoagulable state with increase of the platelet function,alteration of the plasmatic coagulation and decreases in natural inhibitors. Thissituation facilitates the appearance of thrombosis, underlying the importance ofthe preventive antithrombotic therapy in these patients. The indication of anticoagulanttherapy should be individualized for every patient according to theetiopathogenesis of the absolute thromboembolic risk and/or of the interventionalprocedure to be performed, if it is necessary(AU)

[Prevalence of genetic prothrombotic factors (factor V Leiden and II20210 prothrombin mutation) in glomerular nephropathies with or without thrombosis]. / Prevalencia de factores protrombóticos de base genética (factor V Leiden y mutación II20210 de la protrombina) en nefropatías glomerulares con o sin trombosis.

The presence of genetic prothrombotic factors (factor V Leiden and the prothrombin II20210 mutation) was investigated in 38 patients with glomerulonephritis with or without a history of thrombotic events and/or nephrotic syndrome. We found an increased prevalence (36%) of heterozygous factor V Leiden in those patients with a history of thrombotic events. This is ten times the prevalence in the normal Spanish population. Carrier status for this mutation may be a determining factor in the development of thrombotic events along with the acquired disorders of coagulation to which these patients are prone. We found only one patient who was a carrier of the G-A II20210 mutation of the prothrombin gene; this patient had no history of venous thrombosis or embolism. Our findings suggest the need to measure activated protein C resistance and to look for the most frequent genotype causing it, Factor V Leiden, in patients with glomerulonephritis to identify those at risk who may benefit from prophylaxis against thrombosis.

Prevalencia de factores protrombóticos de base genética (factor V Leiden y mutación II20210 de la protrombina) en nefropatías glomerulares con o sin trombosis / Prevalence of genetic protrombotic factors (factor V Leiden and protrombin II20210 mutation) in glomerular nephropathies with or without thrombosis

Se investigó de forma prospectiva en 38 pacientes portadores de nefropatías glomerulares, con o sin antecedentes de síndrome nefrótico y/o manifestaciones tromboembólicas, la presencia de factores protrombóticos de base genética (factor V Leiden y mutación 1120210 de la protrombina), comprobando una elevada prevalencia de factor V Leiden (36 por ciento) en aquellos que tenían antecedentes de manifestaciones trombóticas, 10 veces superior a la de la población normal en nuestra Área de Salud (4 por ciento), y similar a la de pacientes no nefrológicos con enfermedad tromboembólica venosa. La situación de portador de esta mutación podría ser un factor determinante en la aparición de trombosis, en asociación con otros trastornos adquiridos de la coagulación que tienen lugar en estos pacientes. Por lo que respecta a la mutación 11202,0 de la protrombina estuvo presente sólo en un caso aunque en ausencia de manifestaciones de enfermedad tromboembólica venosa. Creemos aconsejable, por tanto, la determinación de la resistencia a la proteína C activada y su genotipo más frecuente, el factor V Leiden, en enfermos con glomerulonefritis con vistas a posibles actuaciones de profilaxis tromboembólica (AU)

Distinct cholesterol and phospholipid incorporation at the platelet plasma membrane of hyperlipidemic subjects: structural order and function.

Plasma lipid composition, platelet aggregation, cholesterol (Ch)/glycoprotein IIb-IIIa (GP) and phospholipid (Ph)/GP molar ratios, fatty acid composition and structural order (1, 6-diphenyl-1, 3, 5-hexatriene (DPH) fluorescence anisotropy at 35 degrees C (r(DPH,35)) of human platelet plasma membranes (HPPM) were measured in four DPH,35 groups of hyperlipidemic patients (II: plasma Ch < 250 mg/dl and TG (triglycerides) <220 mg/dl, n = 21; III: Ch > 250 mg/dl and TG < 220 mg/dl, n = 23; IV: Ch < 250 mg/dl and TG > 220 mg/dl, n = 18; and V: Ch > 250 mg/dl and TG > 220 mg/dl, n = 12) and compared with those of the control group (I). Our results were: (i) in groups III, IV and V the HPPM (Ch + Ph)/GP molar ratio increased 7.0+/-7.7% (mean SD); (ii) the Ph/GP molar ratio increased significantly in groups III, IV and V, but most in IV and V, while the Ch/GP molar ratio increased only in groups III and V; (iii) the mean relative increase of Ch with respect to Ph in the HPPM of groups III, IV and V was 140% 21% and 54%, respectively; (iv) the Ch/GP molar ratio was correlated with LDL-Ch (0.41+/-0.16, P < 0.002, n = 55, for all the subjects and 0.60+/-0.11, P < 2.10(-4), n = 33, for subjects with TG < 220 mg/dl), however, it was totally uncorrelated with HDL-Ch; (v) the HPPM Ch/Ph molar ratio was positively correlated with plasma Ch (r = 0.51+/-0.08, P < 1.10(-6), n = 83) and with (LDL + HDL) Ch (r = 0.64+/-0.07, P < 1.10(-6), n = 73), the former correlation increased significantly ( r = 0.67+/-0.07, P < 1.10(-6), n = 53) when done only for subjects with TG < 220 mg/dl; (vi) the Ch/Ph molar ratio was only increased in group III (0.70+/-0.03, P < 3.10(-5), n = 23) and decreased in group IV (0.62+/-0.02, P < 0.001, n = 18); (vii) the fatty acid/GP molar ratio was significantly increased in groups IV and V, however, a significant absolute and relative increase of C16:0 and C18:1 was observed only in severe hypertriglyceridemia (> 500 mg/dl), together with a relative decrease of C18:0 and C20:4 ( n - 6); (viii) the HPPM structural order, as probed by r(DPH,35), was negatively correlated with DPH,35 plasma TG (r =- 0.61+/-0.10, P < 4.10(-5), n = 39), the Ph/GP molar ratio (r =-0.58+/-0.10, P < 2.10(-4), n = 39) and the the (C18:1 + C18:2))/GP molar ratio (r =- 0.80+/-0.05, P < 1.10(-6), n = 39), however, it was independent of plasma and HPPM Ch; (ix) the higher HPPM Ch/Ph molar ratio in group III was associated (r = 0.58+/-0.12, P < 0.005, n = 22) with a moderately higher platelet reactivity to collagen. We conclude that Ch and Ph were distinctly incorporated to HPPM in the different groups of hyperlipidemia and, therefore, that the absolute increase of Ch and Ph was more informative to understand the structural and functional modifications of the HPPM in hyperlipidemias, than the Ch/Ph molar ratio. On the other hand, the r was sensitive to the DPH,35 increase in the content of HPPM Ph and C18:1 + C18:2 and it was insensitive to the increase in the Ch content.

Coagulation abnormalities in patients with eosinophilia.

Haematological variables in patients with eosinophilia and in healthy control subjects were studied in order to determine whether there were abnormalities in the coagulation system in patients. We found significantly elevated levels of fibrinogen, fibrin degradation products, platelet number and beta-thromboglobulin in patients. The abnormalities were not related to the causes of eosinophilia nor to its severity. This lack of correlation could be due to the heterogeneity of human peripheral blood eosinophils.