[Blood groups and disease]. / Grupos sanguíneos y enfermedad.

The erythrocyte membrane was used as general model for the plasma membrane knowledge. Some of their structures are antigens from blood group systems being characterized at molecular and functional level as specific receptors, transporters or enzymes, even receptors for infectious agents. Plasmodium vivax malarial parasites require the Duffy blood group glycoprotein to penetrate into human red blood cells and the main antigen of P system (P1) is also the Parvovirus B19 receptor. Furthermore, these substances have an effect on several tissues, plasma and secretions involving pathogenic relationships. Certain aggressive Escherichia coli strains require the P1 antigen to attach to the urothelial cells, the Lewis(b) antigen is the gastric receptor for H. pylori, the anti-B from O or A individuals might protect them against the sepsis produced by E. coli, the Lewis group determines the CA-19.9 serum levels or the protective effect of breast milk. However, the most important effect could be the plasma hypocoagulability observed among the O blood group population (with lower factor VIII levels) in association with a reduced prevalence of thromboembolic diseases.

Grupos sanguíneos y enfermedad / Blood groups and disease

La membrana eritrocitaria sirvió como modelo general para el conocimiento de la membrana plasmática. Algunas de sus estructuras son antígenos pertenecientes a los sistemas de grupos sanguíneos y están siendo caracterizadas molecular y funcionalmente como receptores, transportadores o enzimas, incluso como puertas de entrada para patógenos. Así, el Plasmodium vivax (causante de la malaria) requiere la glucoproteína Duffy para penetrar en el interior de los hematíes humanos, y el antígeno principal del sistema P (P1) es también el receptor para el acceso del parvovirus B19. Estos antígenos no siempre se limitan a los glóbulos rojos, sino que pueden influir en diversos tejidos, el plasma o las secreciones con importantes relaciones patogénicas. Ciertas cepas agresivas de Eschirichia coli precisan antígeno P1 para anclarse al epitelio urinario, el antígeno Lewis(b) es el receptor de Helicobacter pylori en la mucosa gástrica, el anti-B de los sujetos con los grupos sanguíneos O y A podría ayudarles a combatir las bacteriemias por E. coli, el grupo Lewis condiciona las concentraciones séricas de CA-19.9 y el efecto protector de la leche materna. Sin embargo, la principal influencia sería la hipocoagulabilidad observada en la población de grupo O (valores inferiores de factor VIII) asociada con una prevalencia menor de enfermedades tromboembólicas

The erythrocyte membrane was used as general model for the plasma membrane knowledge. Some of their structures are antigens from blood group systems being characterized at molecular and functional level as specific receptors, transporters or enzymes, even receptors for infectious agents. Plasmodium vivax malarial parasites require the Duffy blood group glycoprotein to penetrate into human red blood cells and the main antigen of P system (P1) is also the Parvovirus B19 receptor. Furthermore, these substances have an effect on several tissues, plasma and secretions involving pathogenic relationships. Certain aggressive Escherichia coli strains require the P1 antigen to attach to the urothelial cells, the Lewis(b) antigen is the gastric receptor for H. pylori, the anti-B from O or A individuals might protect them against the sepsis produced by E. coli, the Lewis group determines the CA-19.9 serum levels or the protective effect of breast milk. However, the most important effect could be the plasma hypocoagulability observed among the O blood group population (with lower factor VIII levels) in association with a reduced prevalence of thromboembolic diseases

Homocisteína y escasa ingestión de folatos: dos formas complementarias de deterioro / Homocysteine and low dietary intake: two complementary forms of improvement

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Prophylaxis with enoxaparin can produce a giant abdominal wall haematoma when associated with low doses of aspirin among elderly patients suffering cough attacks.

We report three patients aged 75-80 years observed in the Emergency Room with severe anaemia (requiring transfusion) due to a large abdominal wall haematoma while receiving standard prophylaxis against venous thromboembolism (40 mg/day enoxaparin for 6 days on average). All of them concomitantly received 100 mg/day aspirin because of previous ischaemic heart disease and presented similar clinical features: sudden onset of abdominal pain during a severe cough episode due to bronchial infection. A giant haematoma in the rectus abdominis muscle was recognized (by computed tomography) in every case. The cough has been related with this complication in some reports but its association with antiplatelet drugs and low molecular weight heparin could increase the risks in older patients. Sudden abdominal pain must alert the clinician to the rectus muscle sheath haematoma in order to avoid the risks of an exploratory laparotomy.

The concentrations of soluble vascular cell adhesion molecule-1 and lipids are independently associated with venous thromboembolism.

BACKGROUND AND OBJECTIVES: Venous thromboembolism (VTE) involves inflammation and a relation with dyslipidemia which remains controversial. The vascular cell adhesion molecule-1 (VCAM-1) is a ligand expressed by activated endothelium (and recruits leukocytes) whose soluble form (sVCAM-1) increases in atherosclerosis, severe hypertriglyceridemia or deep vein thrombosis (DVT) in acute phase. We analyzed the association between VTE (> 6 months after), sVCAM-1 and lipid concentrations. DESIGN AND METHODS: Case-control study involving 126 consecutive patients (aged 25-80 years, 49% males) and 125 controls of similar age and gender. RESULTS: The patients had a more unfavorable lipid profile than controls [higher triglycerides (p<0.001), LDLc/HDLc ratio (p<0.01) or total cholesterol (TC) (p=0.07)] and higher sVCAM-1 concentration (p<0.01) even adjusting for arterial diseases. VTE was associated with extreme values of TC, LDL-c, triglycerides (>P90) and HDL-c (P90) (OR=4.2)(p<0.0001). The sVCAM-1 values were age-related (r=0.26, p<0.001) but independent of lipid levels. Hazards ratios from five-fold to ten-fold appeared when combining the sVCAM-1 top quartile (>970 ng/mL) with TC >250 mg/dL or HDL-c <45 mg/dL (p<0.01) irrespective of thrombophilic status. Recurrent or severe VTE cases (pulmonary embolism or proximal DVT vs. distal DVT) showed higher sVCAM-1 values (p<0.05). All the associations weakened among females. In stepwise logistic regression, obesity (p<0.001), sVCAM-1 (p<0.001) and LDL-c (p=0.004) in men and sVCAM-1 (p=0.02) and triglycerides (p=0.04) in women retained their independent association. INTERPRETATION AND CONCLUSIONS: Although the exact mechanisms linking abnormal lipid and sVCAM-1 concentrations to VTE await clarification, both seem to be independently associated.

Reducción de concentraciones elevadas de homocisteína con ácido fólico y vitaminas b en pacientes con tromboembolia venosa: relación entre respuesta y genotipo c677t de la metilén tetrahidrofólico reductasa (mthfr) / Lowering high levels of fasting total homocysteine with folic acid and vitamins B in patients with venous thromboembolism: relationship between response and the C677T methylenetetrahydrofolate reductase (MTHFR) genotype

Fundamento: Las concentraciones plasmáticas elevadas de homocisteína total (tHcy) se asocian con enfermedad trombótica arterial o venosa. Dependen principalmente del estado nutricional para el ácido fólico y vitaminas B12 o B6 pero también de la actividad enzimática desarrollada por la metilén tetrahidrofólico reductasa (MTHFR). Evaluamos el grado de respuesta de la hiperhomocisteinemia (HHcy) a un sencillo esquema de suplementación vitamínica respecto al genotipo de MTHFR. Pacientes y métodos: Se seleccionaron 227 pacientes, diagnosticados de tromboembolia venosa (TEV) y que fueron analizados para tHcy (ayunas) y para el polimorfismo genético MTHFR-C677T. Cuando la tHcy excedió el límite normal (varones = 16 y mujeres = 15 µmol/l), los pacientes recibieron el equivalente a 1 mg de ácido fólico, 0,2 mg de vitamina B12 y 100 mg de vitamina B6, diariamente durante 6 semanas. Posteriormente fueron reanalizados y la reducción fue comparada por genotipos MTHFR, buscando cualquier diferencia en el grado de respuesta. Resultados: La tHcy media fue de 12,3 µmol/l (DE = 8). Los 51 pacientes hiperhomocisteinémicos (22 por ciento) tenían edad superior (65,1 años) a los no-HHcy (55,0 años) (p = 0,0001). La cumplimentación del tratamiento fue apropiada en 46 pacientes (90 por ciento). La tHcy media pretratamiento fue de 23,2 µmol/l (DE = 10,5), y se redujo a 13,0 (DE = 5,9), el 42,1 por ciento (p = 0,0001). Por genotipos, los pacientes C/C de 21,0 a 13,2 µmol/l (37 por ciento) (n = 18), los C/T de 25,0 a 12,6 µmol/l (46 por ciento) (n = 24), y los homozigotos anormales T/T de 22,7 a 14,5 µmol/l (39 por ciento) (n = 4), aunque sin evidenciarse diferencias estadísticamente significativas. La respuesta fue completa (normalizándose la tHcy) en el 80 por ciento de los casos (37/46). Se observó una correlación negativa (r = -0.471) (p = 0,005) entre edad y respuesta. Conclusiones: El tratamiento con AF/B6/B12 reduce en forma sencilla, rápida y eficaz (> 40 por ciento en 6 semanas) los valores patológicos de tHcy sin ninguna influencia del genotipo MTHFR. Dado que la HHcy parece relacionarse con las recidivas de trombosis venosa, parece prudente determinar la tHcy sistemáticamente en pacientes con TEV, para intentar su reducción en casos seleccionados (AU)

Background: High levels of plasma total homocysteine (tHcy) are involved in arterial or venous occlusive diseases. It esentially depends on the nutritional status of folic acid (FA) and vitamins B12 or B6, but also on the methylenetetrahydrofolate reductase (MTHFR) enzymatic activity. We aim to evaluate the response of the hyperhomocysteinemia (HHcy) to a standard schedule of vitamin supplementation, according with the MTHFR genotype. Patients and methods: 227 patients, diagnosed with venous thromboembolism (VTE) were analysed for tHcy (in fasting conditions), and for the MTHFR-C677T gene polymorphism. When the tHcy exceeded the cut-off point (men = 16, women = 15 µmol/l), the patients were supplemented with a dose equivalent to 1 mg FA, 0.2 mg B12 and 100 mg of B6, daily by 6 weeks. Afterwards they were reanalysed and the reduction was stratified by MTHFR genotype, looking for any difference in the response. Results: The mean fasting tHcy was 12.3 µmol/l (SD = 8). The 51 hyperhomocysteinemic patients (22%) were older (65.1 y) than the normal ones (55.0 y) (p = 0.0001). The treatment was carried out properly in 46 patients (90%). The pre-treatment mean Hcy was 23.2 (SD = 10.5) µmol/l, and it was reduced to 13.0 (SD = 5.9) (p = 0.0001) (mean reduction = 42.1%). By genotype, the C/C reduced from 21.0 to 13.2 µmol/l (37%) (n = 18), the C/T from 25.0 to 12.6 µmol/l (46%) (n = 24), and the abnormal homozygotes T/T from 22.7 to 14.5 µmol/l (39%) (n = 4), although no statistical significant differences were found. In 80% of cases (37/46), tHcy values normalised. A negative correlation (r = ­0.471) (p = 0.005) was observed between age and response. Conclu sions: The FA/B6/B12 based therapy reduces in a simple, quick and effective way (> 40% in 6 weeks) the pathologic tHcy levels on a VTE population and this is not influenced by the MTHFR genotype. As HHcy seems related with recurrences of venous thrombosis, we could speculate if it would be useful to analyse routinely the tHcy, attempting reduction in selected cases (AU)