Prevalence of battering among 1780 outpatients at an internal medicine institution in Mexico

Violence against women has recently drawn attention in the medical community as a leading cause of preventable morbidity and mortality. Specific algorithms designed to identify women at risk can be applied to create an opportunity for screening, diagnosis and treatment during medical care initiated for common conditions. This study investigated the incidence and history of battering among women seeking general medical care, and looked for potential risk factors and associations with presenting symptoms. We used a self-administered, anonymous survey to question 1780 adult female outpatients visiting a tertiary care internal medicine teaching hospital in Mexico City. We calculated current abuse (physical and/or sexual abuse by a partner within the past year), abuse during pregnancy, childhood abuse, and lifetime abuse. We found levels of violence against women in Mexico comparable to those reported from other countries. 152 women (9%) reported current physical and/or sexual abuse. An identical number also reported abuse during pregnancy. Lifetime prevalence was 41%. Women currently or previously abused reported more physical symptoms in the last six months than did non-abused participants. Pelvic pain, depression, headache and substance abuse were frequent among abused women. Currently abused women also scored higher (pMexico Domestic violence Family violence Sexual abuse Battering syndrome

Frontiers of SLE: review of the 5th International Congress of Systemic Lupus Erythematosus, Cancun, Mexico, April 20-25, 1998.

Objective: To review the recent advances in clinical and experimental research in systemic lupus erythematosus (SLE). Methods: Review of the 5th International Congress of SLE that took place in Cancun, Mexico, on April 20-25, 1998. Results: The main topics presented at the conference are summarized. These include new findings about the genetics of SLE due to fine mapping of the patients' genes and lupus mouse models, the nucleosome as a major autoantigen in SLE, serving as an immunogen for pathogenic T helper and B cells and contributing to the development of lupus nephritis, abnormalities of apoptosis as a cause of SLE, and apoptotic mechanisms as a cause of autoimmunization. Other topics included the pathophysiologic role of anti-endothelial cell antibodies in lupus with central nervous system involvement, vasculitis, the thrombotic diathesis associated with the antiphospholipid syndrome, induction of endothelial cell apoptosis and its regulation by the idiotypic network, the penetration of antinuclear antibodies to the cytoplasm and nucleus and the subsequent interaction with cellular organelles, and new aspects in the antiphospholipid syndrome, including animal models of the disease and the importance of antibodies to beta-2-glycoprotein-I and prothrombin. Advances in the clinical aspects of SLE included clinical manifestations, diagnosis, pregnancy and neonatal SLE, infections, hormones, and treatment. Additionally, four "Lectures of A Lifetime," entitled (1) What causes lupus? (2) From natural autoimmunity to autoimmune disease; (3) The idiotypic network and SLE; and (4) Late-stage morbidity and mortality in SLE-the role of accelerated atherosclerosis were presented. Conclusions: Recent advances provide new insights into the pathogenesis of SLE, as well as hope for novel therapeutic modalities and diagnostic measures. These offer the possibility of improving life quality and decreasing mortality from the disease and its complications. Semin Arthritis Rheum 29:112-130. Copyright (C) 1999 by W.B. Saunders Company

HLA Class I and Class II Alleles and Haplotypes in Mexican Mestizos Established from Serological Typing of 50 Families

We describe new information on the frequency and association of class II antigens (HLA-DR and HLA-DQ) of the major histocompatibility complex (MHC) in Mexicans. The study includes HLA-B typing and its association with the HLA-DR antigens determined in 50 families, which included 100 individuals. This family study allowed the establishment of the precise composition of the 200 HLA haplotypes, which cannot be obtained from unrelated individuals. The predominant antigens in decreasing order of frequency were B35, B39, and B61 at the B locus; DR4, DR5, and DR8 at the DR locus; and DQ3 at the DQ locus. The most common HLA-B,HLA-DR haplotype (considering broad specificities) was B16,DR4, with a frequency of 8.0%. Five HLA-B,HLA-DR haplotypes showed significant delta values (observed vs. expected frequencies) after correcting for the number of comparisons. On the other hand, the most common HLA-DR,HLA-DQ haplotypes were DR4,DQ3 and DR5,DQ3 with a frequency higher than 10%. Ten of the 17 HLADR, HLA-DQ haplotypes had significant postcorrection delta values

A regulatory polymorphism in PDCD1 is associated with susceptibility to systemic lupus erythematosus in humans.

To access publisher full text version of this article. Please click on the hyperlink in Additional Links fieldSystemic lupus erythematosus (SLE, OMIM 152700) is a complex autoimmune disease that affects 0.05% of the Western population, predominantly women. A number of susceptibility loci for SLE have been suggested in different populations, but the nature of the susceptibility genes and mutations is yet to be identified. We previously reported a susceptibility locus (SLEB2) for Nordic multi-case families. Within this locus, the programmed cell death 1 gene (PDCD1, also called PD-1) was considered the strongest candidate for association with the disease. Here, we analyzed 2,510 individuals, including members of five independent sets of families as well as unrelated individuals affected with SLE, for single-nucleotide polymorphisms (SNPs) that we identified in PDCD1. We show that one intronic SNP in PDCD1 is associated with development of SLE in Europeans (found in 12% of affected individuals versus 5% of controls; P = 0.00001, r.r. (relative risk) = 2.6) and Mexicans (found in 7% of affected individuals versus 2% of controls; P = 0.0009, r.r. = 3.5). The associated allele of this SNP alters a binding site for the runt-related transcription factor 1 (RUNX1, also called AML1) located in an intronic enhancer, suggesting a mechanism through which it can contribute to the development of SLE in humans