Differences in ethanol pharmacokinetics within the menstrual cycle have previously been reported and attributed to variations in body composition, hormonal influences and gastric emptying. To establish the role of the menstrual cycle in ethanol pharmacokinetics associated with changes in body composition, ethanol blood concentrations were measured in nine healthy women during the midfollicular (P1, days 8-10) and midluteal (P2, days 22-24) phases of the menstrual cycle after a postprandial oral ethanol dose (0.3 g kg(-1)). Total body water was assessed by dual-energy x-ray densitometry (DEXA) on both occasions. Median total body water did not vary during either phase of the menstrual cycle (P1 = 54.54%, P2 = 54.66%; P = 0.9296). Median area under the ethanol concentration-time curve (AUC) was lower during P1 (215.33 mg.h dl(-1)) than during P2 (231.33 mg.h dl(-1))(P = 0.8253). No significant differences were found on ethanol pharmacokinetics in either phase of the menstrual cycle.
INVESTIGADORES DE LA FACULTAD DE MEDICINA Y MEDICOS CLINICOS DEL HOSPITAL GENERAL DE MEXICO, ENCABEZADOS POR DAVID KERSHENOBICH, GUILLERMO ROBLES DIAZ Y MAX SCHMULSON, UNIERON ESFUERZOS PARA MEJORAR ESTUDIO Y LA ATENCION DE ENFERMEDADES HEP TICAS Y PANCRE TICAS, JUNTO CON LOS TRASTORNOS FUNCIONALES DEL APARATO DIGESTIVO. EN LAS INSTALACIONES DEL HOSPITAL GENERAL DE MEXICO CREARON UNA UNIDAD DE ESTUDIO Y ATENCION DENOMINADA LABORATORIO HIPAM (HIGADO, P NCREAS Y MOTILIDAD), QUE PERTENECE A LA UNIVERSIDAD. LOS ESPECIALISTAS PRETENDEN ENCONTRAR LA MANERA DE RELACIONAR EFICAZMENTE ESTUDIO DE ESAS ENFERMEDADES CON LOS ASPECTOS M S AVANZADOS DE LA ATENCION A PACIENTES. EN CUANTO A LAS ENFERMEDADES HEP TICAS, PUNTUALIZO KERSHENOBICH, SE BUSCA ENTENDER MEJOR SU FISIOPATOLOGIA PARA DESARROLLAR NUEVOS ESQUEMAS TERAPEUTICOS. PARA ESTE PROPOSITO CONVOCARON A INVESTIGADORES EN MEDICINA B SICA, BIOQUIMICA Y FISIOLOGIA, Y A MEDICOS CLINICOS, TODOS DE ALTO NIVEL Y CON EXPERIENCIA EN FIBROSIS EN GENERAL. AUNQUE LA FIBROSIS AFECTA DIVERSOS ORGANOS, SE HA PUESTO MAYOR INTERES EN ALGUNAS PARTES DEL APARATO DIGESTIVO, EN ESPECIFICO HIGADO, P NCREAS E INTESTINO DELGADO. ALGUNOS ESPECIALISTAS DEL LABORATORIO HIPAM EFECTUAN INVESTIGACIONES ORIGINALES, UNA DE LAS CUALES EST DEDICADA, CON LA RESPONSABILIDAD DE KERSHENOBICH, A LA FIBROSIS HEP TICA Y SE HAN OBTENIDO RESULTADOS ESPERANZADORES. ENTRE OTRAS CAUSAS, UNA PERSONA -EXPLICO INVESTIGADOR- PUEDE ENFERMAR DEL HIGADO POR VIRUS DE LA HEPATITIS B O C, POR CONSUMO EXCESIVO DE BEBIDAS ALCOHOLICAS O POR ACUMULACION DE GRASA EN EL, Y DESARROLLAR FIBROSIS, LA CUAL, A SU VEZ, DA LUGAR A LA CIRROSIS HEP TICA. COMO SE SABE, LA CIRROSIS ES LA ETAPA TERMINAL DE CASI TODAS LAS ENFERMEDADES CRONICAS DEL HIGADO Y, POR ENDE, CONSTITUYE UN PROBLEMA DE SALUD PUBLICA MUY SERIO. AUNQUE ES INUTIL TRATAR UNA CIRROSIS HEP TICA EN SU FASE FINAL, CON HIGADO DANADO SEVERAMENTE, COMENTA, HOY SE SABE QUE LA FIBROSIS PUEDE SER REVERSIBLE, CON POSIBILIDADES DE CURA. A PARTIR DE ESTE HALLAZGO -REALIZADO HACE ANOS POR KERSHENOBICH, EN COLABORACION CON RUY PEREZ TAMAYO Y MARCO RODKIN- SURGEN PREGUNTAS TALES COMO: ¨CU LES SON LOS MECANISMOS QUE DESATAN LA PRODUCCION DE TEJIDO FIBROSO? Y ¨COMO PUEDEN SER BLOQUEADOS? AL OBSERVAR PACIENTES EN CUALESQUIERA DE LAS DISTINTAS ETIOLOGIAS CONDICIONANTES DE LA FIBROSIS, LOS ESPECIALISTAS NOTARON QUE UNAS CELULAS CONOCIDAS COMO ESTELARES EMPIEZAN A PRODUCIR TEJIDO FIBROSO EN LA MEDIDA EN QUE SE ACTIVAN. ASI, LUEGO DE IDENTIFICAR LAS CELULAS ESTELARES Y DESCUBRIR QUE SURGIMIENTO DE LAS BANDAS DE TEJIDO FIBROSO EN DISTINTAS PARTES DEL HIGADO DEPENDE DEL AGENTE RESPONSABLE (VIRUS, ALCOHOL, GRASA U OTRO), HA SIDO POSIBLE DESARROLLAR ESTRATEGIAS PARA INTENTAR IMPEDIR QUE LA FIBROSIS HEP TICA PROGRESE O PARA QUE PUEDA DEGRADARSE, AUN ESTABLECIDA. ANTES SE PARTIA DEL HECHO DE QUE NO HABIA NADA QUE HACER, YA QUE TODOS LOS ENFERMOS EVENTUALMENTE FALLECIAN, NUESTRO GRUPO DEMOSTRO QUE LA FIBROSIS HEP TICA PUEDE SER REVERSIBLE. CABE ACLARAR, SIN EMBARGO, QUE LA FIBROSIS Y LA SI BIEN FORMAN PARTE DE UN MISMO PROCESO, NO SON LO MISMO. ES DISTINTO MODIFICAR LA FIBROSIS QUE ATENDER UNA CIRROSIS, INDICO ESPECIALISTA. ADEM S DE LA INFLAMACION Y LA PERDIDA DE ARQUITECTURA HEP TICA, CON LA CIRROSIS SE PRESENTA EN HIGADO UN PROCESO DE REGENERACION ACELERADO (DESPUES DE LA PLACENTA, AQUEL ES ORGANO CON MAYOR CAPACIDAD DE REGENERACION). NO OBSTANTE, AFIRMO ESPECIALISTA, ESTA RESPUESTA DEL HIGADO CIRROTICO PARA TRATAR DE MANTENER SU FUNCION, PUEDE SALIRSE DE CONTROL Y EVOLUCIONAR HACIA UN CARCINOMA. AHORA BIEN, AUNQUE TODAVIA NO SE DETERMINA CON EXACTITUD POR QUE UNA CIRROSIS PUEDE ACABAR EN C NCER, SI SE SABE QUE NO ES POR CULPA DE LA FIBROSIS. UNA DE LAS VENTAJAS DEL TRABAJO CONJUNTO QUE SE REALIZA ES PERMANENTE INTERCAMBIO DE CONOCIMIENTOS QUE PUEDEN ESTABLECER. AQUI, EN LABORATORIO HIPAM -SENALO KERSHENOBICH-, QUEREMOS QUE LOS MEDICOS CLINICOS, EN CIERNES, SE ENTUSIASMEN Y HAGAN INVESTIGACION, PORQUE ASI SU ASPECTO FORMATIVO SE ENRIQUECER Y LA CALIDAD DE SU ATENCION AL PACIENTE MEJORAR SIGNIFICATIVAMENTE EN LO QUE SE REFIERE AL DIAGNOSTICO NO SOLO DEL QUE, SINO TAMBIEN DEL POR QUE. OTRA VENTAJA DE DICHA RELACION, ANADIO, ES QUE, EN LA MEDIDA EN QUE SE ENTIENDEN LAS MANIFESTACIONES CLINICAS DE UN PADECIMIENTO, LOS INVESTIGADORES CONCENTRADOS EN ASPECTO CELULAR PUEDEN PLANTEARSE SU HIPOTESIS DE INVESTIGACION CON M S PRECISION. POR EJEMPLO, SI UNO INVESTIGA LA PERO NO SABE CU LES SON SUS MANIFESTACIONES CLINICAS (SANGRADOS, RETENCION DE LIQUIDOS, CANSANCIO, ETCETERA), TENDR DIFICULTADES PARA AJUSTAR SUS PROTOCOLOS DE INVESTIGACION. EL OBJETIVO NO SOLO ES QUE LOS INVESTIGADORES B SICOS Y LOS MEDICOS CLINICOS INTERACTUEMOS, SINO TAMBIEN QUE LOS JOVENES EN FORMACION PUEDAN AMPLIAR SU HORIZONTE CIENTIFICO. SE HA VISTO QUE LA INTERRELACION INVESTIGACION-PR CTICA MEDICA PERMITE GRANDES LOGROS EN LOS PAISES AVANZADOS EN MEDICINA, A
Summary The hepatitis C virus ( HCV ) epidemic was forecasted through 2030 for 15 countries, and the relative impact of two scenarios was considered: (i) increased treatment efficacy while holding the treated population constant and (ii) increased treatment efficacy and increased annual treated population. Increasing levels of diagnosis and treatment, in combination with improved treatment efficacy, were critical for achieving substantial reductions in disease burden. In most countries, the annual treated population had to increase several fold to achieve the largest reductions in HCV ‐related morbidity and mortality. This suggests that increased capacity for screening and treatment will be critical in many countries. Birth cohort screening is a helpful tool for maximizing resources. In most of the studied countries, the majority of patients were born between 1945 and 1985.
Treatment of alcoholic liver disease is for the most part based on the stage of the disease and the pathogenic event that is being targeted. The primary treatment modalities that are considered in the treatment of alcoholic liver disease include abstinence, agents that suppress inflammation, anticytokine therapy, nutritional support, modifiers of alcohol metabolism, anti-oxidants, and inhibitors of hepatic fibrosis. Future therapeutic options include exploration of new pathways such as the patatin-like phospholipase domain containing 3 protein (PNPLA-3).
Aim: To investigate the accuracy of non-invasive tests for assessing residual cirrhosis in HCV patients after an SVR. Methods: All HCV patients with a pre-treatment histological diagnosis of cirrhosis and available post-SVR liver biopsies had residual liver fibrosis assessed through the following non-invasive methods: APRI, CDS, Fib4, FibroQ, Forns score, Guci Index, King score, Lok Index, PLF. Liver fibrosis staged according to the METAVIR score was the reference standard. The performances of non-invasive tests to diagnose residual cirrhosis were calculated using receiver operating characteristic (ROC) curves analysis. Results: 20 out of 33 patients (61%) included in the study had cirrhosis regression after 61 (48–104) months from an SVR. The overall diagnostic accuracy of all the non invasive serum panels analyzed was suboptimal as indicated by the AUROC values and the operative characteristics of the tests. None of these tests is useful in identifying patients with residual cirrhosis when using both the cut-off indicated by the literature (bold) and the cut off with the best sensitivity and specificity derived from the ROC curves (Table 1).
Abstract: Background/Aim: Pro‐inflammatory cytokines and chemokines, such as interleukin (IL) 8, are important mediators of hepatic injury and repair following an insult. The purpose of this work was to study the regulation of IL‐8 by IL‐10 and IL‐4 in HepG2 cells treated with acetaldehyde (Ac). Methods: HepG2 cells were pretreated with IL‐10 or IL‐4 before exposure to Ac, examining IL‐8 expression by reverse transcription polymerase chain reaction and Western blot. Results: Ac treatment produced an increment in IL‐8 induction and secretion that was prevented by IL‐4 pretreatment, while IL‐10 pretreatment failed to decrease Ac‐induced IL‐8 production. Consistent with these findings Ac increased NF‐κB and AP‐1 activation that were prevented by IL‐4 but not by IL‐10, findings accompanied by greater IκB‐α levels in IL‐4 but not IL‐10 pretreated cells. In contrast to the pro‐inflammatory role of IL‐10 in HepG2, IL‐10 did not show any change in the activation of NF‐κB by Ac in WRL‐68 cells, a human fetal hepatic cell line. Moreover, IL‐10 did not induce the degradation of IκB‐α in cellular extract from rat primary cultured cells. Conclusions: While the present findings demonstrate the anti‐inflammatory role of IL‐4 in preventing the expression of IL‐8 by Ac, the regulation of chemokines by anti‐inflammatory cytokines is complex and depends on the cellular lineage.
This article analyzes the Mexican regulation on palliative care and its relationship with the public debate on assisted death or suicide. This paper focuses on the rights that people with incurable diseases have, given the current contents of the General Health Statute and other applicable rules. Its main purpose is to activate the public debate on these matters.
To determine the prevalence of diabetic retinopathy (DR) and diabetic macular oedema (DME) and their associated risk factors in patients recently diagnosed with type 2 diabetes.We carried out a cross-sectional study from April 2014 to August 2017. We included patients aged ≥18 years. Diabetes was defined as fasting plasma glucose of >7.8 mmol/L or 2-hour postload plasma glucose of >11.1 mmol/L. Non-mydriatic fundus examination with a digital-fundus camera was performed. Three images centred in the macula, optic disc and temporal to the macula were obtained and graded according to the Scottish Scale Classification of Diabetic Retinopathy.1232 patients (mean age 51.5 years) with a diabetes duration of 0-5 years were examined. Age-adjusted and sex-adjusted prevalence of DR and DME was 17.4% (95% CI 15.3% to 19.6%) and 6.6% (95% CI 5.4% to 8.2%), respectively. DR was associated with diabetes duration (OR per year=1.20, p<0.001), haemoglobin A1c (HbA1c) from 7.0 to 8.9 (OR=2.19, p<0.001), HbA1c≥9 (OR=2.98, p<0.001) and systolic blood pressure (SBP) (OR=1.16 per 5 mm Hg, p<0.001). DME was associated with diabetes duration (OR per year=1.26, p<0.01), HbA1c from 7.0 to 8.9 (OR=2.26, p<0.05), HbA1c≥9 (OR=2.38, p<0.01), SBP (OR per mm Hg=1.15, p<0.001) and albuminuria (OR=2.45, p<0.01).Our study contributes to the evidence of progressive increase in DR and DME risk in early stages of diabetes, supporting the urgent need for early screening.