RESUMEN
Transforming growth factor-beta-1 [TGF-beta-1] exerts a broad spectrum of biologic activities through both autocrine and paracrine pathways. It is supposed to be the mediator of fibrosis in liver cirrhosis. It also strongly promotes local tumor progression. The aim of the present study was to assess the clinical relevance of urinary TGF- beta-1 in chronic liver disease [CLD] and hepatocellulary carcinoma [HCC]. The study also tried to evaluate the clinical utility of TGF-beta-1 in detecting HCC. The study was conducted on 40 patients with CLD [20 patients with chronic active hepatitis [CAH] and 20 patients with cirrhosis], 40 patients with HCC and 40 age and sex matched healthy controls. In conclusion, this study showed that urinary TGF-beta-1 is a good indicator of the severity of liver disease and has a prognostic value in patients with cirrhosis. Furthermore, elevated urinary TGF-beta-1 level can be considered as a novel tumor marker for HCC. Parallel assay of TGF- beta-1 and AFP provide significant improvement in the detection of HCC, particularly in cases with low AFP production
Asunto(s)
Humanos , Masculino , Femenino , Hepatopatías , Diagnóstico , Cirrosis Hepática , Carcinoma Hepatocelular , Pruebas de Función Hepática , alfa-Fetoproteínas , Enfermedad CrónicaRESUMEN
This study was conducted on 40 patients; 18 with acute coronary syndrome [ACS] [group 1] and 22 with chronic coronary heart disease [CHD] [group 2]. Fifteen healthy age- and sex-matched subjects were taken as controls. CPn [Chlamydia pneumoniae] DNA was detected by a highly sensitive polymerase chain reaction [PCR] technique using primers derived from outer membrane protein gene [ompl]. The serological assay of CPn-IgG antibodies was determined by an indirect immunofluorescence technique. Serum homocysteine was also measured by an enzyme conversion immunoassay method. In conclusion, patients with CHD, particularly ACS, have a high prevalence of CPn infection than the healthy controls. Besides, CPn DNA detection is more sensitive than the serological tests in identifying subjects with current infection. The contribution of CPn infection in the pathogenesis of atherosclerosis is independent of the other conventional atherogenic risk factors
Asunto(s)
Humanos , Masculino , Femenino , /aislamiento & purificación , Pruebas Serológicas , Prevalencia , Arteriosclerosis , Reacción en Cadena de la Polimerasa , Homocisteína/sangre , Lipoproteínas LDL , Lipoproteínas HDL , Enfermedad Aguda , Hospitales Universitarios , Enfermedad Crónica , ADNRESUMEN
This study was conducted on 72 patients with febrile convulsions. They were 45 males and 27 females. Their ages ranged between 6 and 48 months with a mean of 24.7 +/- 8.78 months. They were recruited from the patients attending the Emergency Department, Children's Hospital, Ain Shams University. A cohort of 40 healthy siblings of the patients was chosen as a control group. All cases and controls were subjected to detailed medical history taking, clinical examination and laboratory investigations including complete hemogram, total iron binding capacity as well as serum levels of iron, ferritin and lead. In addition, hemoglobin and iron indices of the cases were reassessed 6 months after institution of iron therapy. The study showed that iron deficiency anemia was more prevalent in febrile convulsive children compared to their controls. However the lead status was not different among the studied groups. The frequency of febrile convulsions correlated significantly negative with serum levels of iron and ferritin and positively with TIBC. However, neither the iron indices nor the frequency of febrile convulsions showed any correlation with the frequency of febrile illnesses. Responders to iron therapy demonstrated lower seizure frequency compared to non-responders, although they were not different regarding the frequency of febrile illnesses. So it can be concluded that iron deficiency anemia is a direct risk factor for the development and recurrence of febrile convulsions. This risk is primarily due to iron deficiency per se rather than due to increased risk of febrile illnesses. So we recommend iron therapy in iron deficient febrile convulsive children to minimize the risk of recurrent fits