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Objective:To evaluate the usefulness of serum lipid peroxide (LPO) for hypoxic ischemic encephalopathy (HIE) in full-term neonates.Study Design:Diagnostic test evaluation forming three groups: (1) healthy full-term neonates (n=59), (2) at-risk full-term neonates without HIE (n=57) and (3) at-risk full-term neonates with HIE (n=57). HIE diagnosis was made using the Finer clinical classification at 48 h after birth. Serum LPO was taken at 4 h after birth and determined by spectrophotometry.Result:One hundred seventy-three full-term neonates were studied. Fifty-one of the at-risk full-term neonates with HIE (51/57) had high serum LPO and two of the at-risk full-term neonates without HIE (2/57) (P<0.001). Serum LPO level had 89% sensitivity, 96% specificity, 96% positive predictive value, 90% negative predictive value, 24 positive probability ratio, 0.11 negative probability ratio and 92% diagnostic usefulness.Conclusion:Serum LPO level could be a useful test for early diagnosis of HIE in full-term neonates. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) is the prototype of the rheumatic diseases worldwide. Methotrexate (MTX) is the drug of first choice in the treatment of this disease due to its immunosuppressant effect. However, side events are present in 30% of the patients. The C677T and A1298C polymorphisms of the methylenetetrahydrofolate reductase (MTHFR) gene are involved in the metabolism of MTX. Earlier studies reported an association between these polymorphisms and elevation of hepatic enzymes. We analyzed the frequencies of both polymorphisms and the presence of transaminasemia in 70 Mexican patients with rheumatic arthritis treated with MTX. The 19% (13/70) of patients had an increase in the serum level of transaminases. The A1298C polymorphism was associated with elevation of transaminases (P=0.024). The identification of MTHFR genotypes for C677T and A1298C polymorphisms could lead clinicians to identify patients in risk of elevation of transaminases, and give them an individualized treatment, as is a goal of pharmacogenetics. [ABSTRACT FROM AUTHOR]

Tumor necrosis factor-α (TNF-α) plays a central role in inflammation, and it has been directly implicated in the pathogenesis of rheumatoid arthritis (RA). TNF-α activity is mediated through TNFRI and TNFRII cell surface receptors, which act as physiological attenuators of TNF-α activity. We recruited 190 RA patients and 190 healthy subjects (HS) in order to associate the −383A>C TNFRI polymorphism with sTNFRI levels and DAS28 score in RA. In results, sTNFRI levels were higher in RA patients than HS ( P = 0.04). The −383A>C TNFRI polymorphism did not show significant differences in both studied groups. However, in the RA group the sTNFRI levels were significantly elevated ( P = 0.004) in A/A genotype carriers. In addition, the A/A genotype carriers had the higher DAS28 score than A/C genotype ( P = 0.02). These data suggest that −383A>C TNFRI polymorphism is not a susceptibility marker in RA, whereas the increased levels of sTNFRI could reflect the clinical activity in RA patients. [ABSTRACT FROM AUTHOR]