Biomedical subjects

E Curiel

Publications and source records attributed to E Curiel.

3 recordsLinked to original sources

PubMed2006

[MARS (Molecular Absorbent Recirculating System) as hepatic extracorporeal care in serious acute liver failure of alcoholic etiology].

Acute liver failure with criteria of seriousness and alcoholic etiology is a picture of worldwide distribution, with an elevated mortality, of approximately 50%, that requires admission to the ICU. Acute serious alcoholic hepatitis is defined by a Maddrey score value > 32 and/or spontaneous encephalopathy. Together with the classical treatment with corticosteroids and nutritional supplements, alcoholic abstinence and others such as anti-TNF therapy, we introduce MARS (Molecular Adsorbent recirculating System) as a extracorporeal liver assistance system with detoxification function, that is presented as a support measure that makes it possible to maintain the patient in good conditions until an organ becomes available or until the functional recovery of the native liver. In our case, MARS has shown some spectacular results and above all, results maintained over time, associated to the rest of the therapeutic measures characteristic of this disease.

Adult↗

PubMed2001

[Creatine kinase increases after coronary interventions].

INTRODUCTION AND OBJECTIVES: Percutaneous revascularization has led to an important change in the treatment of patients with symptomatic ischemic heart disease in recent years. There is controversy concerning the incidence and prognostic significance of postprocedural increases in creatine kinase. The aim of this study was to assess the incidence of these elevations and the related factors and to observe the prognosis of patients with and without creatin kinase elevations. METHODS: We reviewed 447 patients in whom an angioplasty was done in our department from January 1997 to June 1998, excluding 138 patients with myocardial infarction in the previous four days or unsuccessful angioplasty. Creatine kinase was measured in all patients at 0, 4, 8 and 24 hours after angioplasty. We analyzed the incidence of elevated levels of creatine kinase following coronary surgery and the characteristics of the patients in comparison with a control group made up of patients who, at a similar time had undergone a similar angioplasty procedure including, a similar vessel and type of lesion, and equivalent left ventricular function but without elevated serum levels of creatine kinase. Major adverse coronary events were defined as: cardiac death, nonfatal myocardial infarction, new revascularization and unstable angina in which hospitalization was required. RESULTS: Out of 309 patients studied, an elevation in creatine kinase was observed in 24 patients (7.7%). Complications related to the procedure were found in 50% of these elevations, most of which involved side branch occlusion. There were no differences with respect to the demographical or anatomical characteristics of the lesions in the groups studied. During the follow-up of 9.5 months, complications were observed in 37.5% of the group of patients with elevated creatine kinase levels and in 20% of the control group, but this difference did not achieve statistical significance. CONCLUSIONS: Creatine kinase elevations are produced in 7.7% of the patients after coronary angioplasty. Complications related to the procedure were observed in 50% of the cases, most being side branch occlusion and no complications were seen in the remaining patients. Continuous measurement of creatine kinase after angioplasty shows a low sensitivity for detecting complications during follow-up. New, more sensitive and specific cardiac markers, such as troponin, could define this group of patients.

Angioplasty, Balloon, Coronary↗

PubMed1989

Alpha 1-antitrypsin deficiency caused by the alpha 1-antitrypsin Nullmattawa gene. An insertion mutation rendering the alpha 1-antitrypsin gene incapable of producing alpha 1-antitrypsin.

alpha 1-Antitrypsin (alpha 1AT) deficiency is a hereditary disorder associated with reduced serum alpha 1AT levels and the development of pulmonary emphysema. An alpha 1AT gene is defined as "Null" when no alpha 1AT in serum is attributed to that alpha 1AT gene. Although all alpha 1AT Null genes have identical phenotypic consequences (i.e. no detectable alpha 1AT in the serum), different genotypic mechanisms can cause the Null state. This study defines the molecular basis for the alpha 1AT gene Nullmattawa, identified and cloned from genomic DNA of an individual with the Null-Null phenotype and emphysema resulting from the heterozygous inheritance of the Nullmattawa and Nullbellingham genes. Sequencing of exons Ic-V and all exon-intron junctions of the Nullmattawa gene demonstrated it was identical to the common normal M1(Val213) alpha 1AT gene except for the insertion of a single nucleotide within the coding region of exon V, causing a 3' frameshift with generation of a premature stop signal. Family analysis using oligonucleotide probes specific for the Nullmattawa sequence demonstrated the gene was inherited in an autosomal fashion. Examination of blood monocytes demonstrated that a normal-sized, 1.8-kb alpha 1AT mRNA transcript is associated with the Nullmattawa gene and in vitro translation of mRNA with the Nullmattawa mutation showed it translated at a normal rate but produced a truncated alpha 1AT protein. Additionally, retroviral transfer of the alpha 1AT Nullmattawa cDNA to murine fibroblasts demonstrated no detectable intracellular or secreted alpha 1AT, despite the presence of alpha 1AT Nullmattawa mRNA transcripts. These findings are consistent with the concept that the molecular pathophysiology of Nullmattawa is likely manifested at a posttranslational level. The identification of the Nullmattawa gene supports the concept that Null alpha 1AT alleles represent a heterogenous group in which very different mechanisms cause the identical phenotypic state.

Adult↗