Comparison of two assays to determine anti-citrullinated peptide antibodies in rheumatoid arthritis in relation to other chronic inflammatory rheumatic diseases: assaying anti-modified citrullinated vimentin antibodies adds value to second-generation anti-citrullinated cyclic peptides testing.

Determination of anti-citrullinated peptide antibodies (ACPA) plays a relevant role in the diagnosis of rheumatoid arthritis (RA). To date, it is still unclear if the use of several tests for these autoantibodies in the same patient offers additional value as compared to performing only one test. Therefore, we evaluated the performance of using two assays for ACPA: second-generation anti-citrullinated cyclic peptides antibodies (anti-CCP2) and anti-mutated citrullinated vimentin (anti-MCV) antibodies for the diagnosis of RA. We compared three groups: RA (n = 142), chronic inflammatory disease (CIRD, n = 86), and clinically healthy subjects (CHS, n = 56) to evaluate sensitivity, specificity, predictive values, and likelihood ratios (LR) of these two assays for the presence of RA. A lower frequency of positivity for anti-CCP2 was found in RA (66.2%) as compared with anti-MCV (81.0%). When comparing RA versus other CIRD, sensitivity increased when both assays were performed. This strategy of testing both assays had high specificity and LR+. We conclude that adding the assay of anti-MCV antibodies to the determination of anti-CCP2 increases the sensitivity for detecting seropositive RA. Therefore, we propose the use of both assays in the initial screening of RA in longitudinal studies, including early onset of undifferentiated arthritis.

Anti-cyclic citrullinated peptide (anti-CCP) and anti-mutated citrullinated vimentin (anti-MCV) relation with extra-articular manifestations in rheumatoid arthritis.

We evaluated the association between anti-cyclic citrullinated peptide antibodies (anti-CCP) and anti-mutated citrullinated vimentin antibodies (anti-MCV) with the presence of extra-articular (ExRA) manifestations in 225 patients with rheumatoid arthritis (RA). Ninety-five patients had ExRA and 130 had no ExRA. There was no association of anti-CCP and anti-MCV levels with the presence of ExRA as total group (P = 0.40 and P = 0.91, resp.). Making an analysis of individual manifestations, rheumatoid nodules were associated with positivity for rheumatoid factor (RF); (P = 0.01), anti-CCP (P = 0.048), and anti-MCV (P = 0.02). Instead, RF, anti-CCP, or anti-MCV were not associated with SS, chronic anemia, or peripheral neuropathy. Levels of anti-CCP correlated with the score of the Health Assessment Questionnaire-Disability Index (HAQ-Di) (r = 0.154, P = 0.03), erythrocyte sedimentation rate (ESR); (r = 0.155, P = 0.03), and RF (P = 0.254, P < 0.001), whereas anti-MCV titres only correlated with RF (r = 0.169, P = 0.02). On adjusted analysis, ExRA was associated with longer age (P = 0.015), longer disease duration (P = 0.007), higher DAS-28 score (P = 0.002), and higher HAQ-DI score (P = 0.007), but serum levels of anti-CCP and anti-MCV were not associated. These findings show the need to strengthen the evaluation of the pathogenic mechanisms implied in each specific ExRA manifestation.

The clinical significance of posttranslational modification of autoantigens.

Posttranslational modifications (PTMs) are defined as covalent modifications occurring in a specific protein amino acid in a time- and signal-dependent manner. Under physiological conditions, proteins are posttranslationally modified to carry out a large number of cellular events from cell signaling to DNA replication. However, an absence, deficiency, or excess in PTMs of a given protein can evolve into a target to trigger autoimmunity, since PTMs arise in the periphery and may not occur in the thymus; hence, proteins with PTMs never tolerize developing thymocytes. Consequently, when PTMs arise during cellular responses, such as inflammation, these modified self-antigens can be taken up and processed by the antigen-presenting cells (APCs). Autoreactive T cells, which recognize peptides presented by APCs, can then infiltrate into host tissue where the modified antigen serves to amplify the autoimmune response, eventually leading to autoimmune pathology. Furthermore, a PTM occurring in an amino acid residue can induce changes in the net charge of the protein, leading to conformational modifications in the tertiary and quaternary structure of the protein, especially interaction with human leukocyte antigen (HLA) molecules. Molecular mimicry (MM) was until now the prevailing hypothesis explaining generation of autoimmunity; nevertheless, experimental animal models need inflammation via infection or other immunogens to ensure autoimmunity; MM alone is not sufficient to develop autoimmunity. PTMs could arise as an additive factor to MM, which is required to start an autoimmune response. PTMs have been found to be present in different pathologic conditions such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), antiphospholipid syndrome, and primary biliary cirrhosis. The aim of the present review is to expose protein posttranslational modifications and the evidence suggesting their role in the generation of autoimmunity.

Potential uses, limitations, and basic procedures of micronuclei and nuclear abnormalities in buccal cells.

The use of biomarkers as tools to evaluate genotoxicity is increasing recently. Methods that have been used previously to evaluate genomic instability are frequently expensive, complicated, and invasive. The micronuclei (MN) and nuclear abnormalities (NA) technique in buccal cells offers a great opportunity to evaluate in a clear and precise way the appearance of genetic damage whether it is present as a consequence of occupational or environmental risk. This technique is reliable, fast, relatively simple, cheap, and minimally invasive and causes no pain. So, it is well accepted by patients; it can also be used to assess the genotoxic effect derived from drug use or as a result of having a chronic disease. Furthermore the beneficial effects derived from changes in life style or taking additional supplements can also be evaluated. In the present paper, we aim to focus on the explanation of MN test and its usefulness as a biomarker; we further give details about procedures to perform and interpret the results of the test and review some factors that could have an influence on the results of the technique.

PADI4 haplotypes in association with RA Mexican patients, a new prospect for antigen modulation.

Peptidyl arginine deiminase IV (PAD 4) is the responsible enzyme for a posttranslational modification called citrullination, originating the antigenic determinant recognized by anti-cyclic citrullinated peptide antibodies (ACPA). Four SNPs (single nucleotide polymorphisms) have been described in PADI4 gene to form a susceptibility haplotype for rheumatoid arthritis (RA); nevertheless, results in association studies appear contradictory in different populations. The aim of the study was to analyze if the presence of three SNPs in PADI4 gene susceptibility haplotype (GTG) is associated with ACPA positivity in patients with RA. This was a cross-sectional study that included 86 RA patients and 98 healthy controls. Polymorphisms PADI4_89, PADI4_90, and PADI4_92 in the PADI4 gene were genotyped. The susceptibility haplotype (GTG) was more frequent in RA patients; interestingly, we found a new haplotype associated with RA with a higher frequency (GTC). There were no associations between polymorphisms and high scores in Spanish HAQ-DI and DAS-28, but we did find an association between RARBIS index and PADI4_89, PADI4_90 polymorphisms. We could not confirm an association between susceptibility haplotype presence and ACPA positivity. Further evidence about proteomic expression of this gene will determine its participation in antigenic generation and autoimmunity.

The clinical significance of coagulation and the inflammatory response in autoimmunity.

Maintenance of normal blood flow requires equilibrium between procoagulant and anticoagulant factors; occasionally, procoagulant activity predominates, leading to clot formation; frequently, tissue damage is the triggering factor. Hereditary factors, primary or acquired, play a role in the development of thrombosis. Primary thrombophilia is associated with hereditary factors, which promote hypercoagulability because natural anticoagulants are not exerting their activity. On the other hand, acquired thrombophilia may occur associated to autoimmune diseases, cancer, surgical procedures, pregnancy, postpartum period, and obesity. Activation of the coagulation system is characterized by the co-participation of inflammatory response components, factors related to the subjacent disease, and other procoagulant factors. The study of patients with thrombosis should include both inflammatory and autoimmune response markers.

Anti-cyclic citrullinated peptide antibodies and rheumatoid factor sera titers in leprosy patients from Mexico.

Leprosy offers a broad spectrum of altered immunological sceneries, ranging from strong cell-mediated immune responses seen in tuberculoid leprosy (TT), through borderline leprosy (BB), to the virtual absence of T cell responses characteristic in lepromatous leprosy (LL). The exact mechanism of autoantibodies production remains unknown in leprosy and other chronic inflammatory diseases and also the contribution of these antibodies to the pathogenesis of the disease. The aim of this study is to evaluate the frequency and profiles of serum anti-cyclic citrullinated peptide antibodies (a-CCP), rheumatoid factor (RF) and its relationship with leprosy spectrum. Serum samples from 67 leprosy patients (54 LL, 5 TT and 8 BB) and 46 clinically healthy subjects (CHS) from the same endemic region were investigated. The clinical chart and questionnaire were used to obtain clinical information. Anti-cyclic citrullinated peptide antibodies (a-CCP) were measured by enzyme-linked immunosorbent assay, whereas the rheumatoid factor (RF) levels were measured by nephelometric method. The mean age of patients was 51.5 ± 13 years. Sera levels of a-CCP where higher in leprosy patients than in CHS (5.9 ± 11.6 vs. 0.3 ± 0.29) (P < 0.0001); the same pattern was found for RF sera titers without reaching statistical significance (16.8 ± 22.5 vs. 9.9 ± 3) (P = NS). We did not find a correlation between a-CCP and RF Rho =0.02786 (IC 95%) P = 0.8229. However, LL patients had higher a-CCP and RF levels than TT patients. Although an absence in correlation was observed, the serum levels of a-CCP antibodies and RF appeared to be useful in distinguishing LL from TT patients with a limited significance in detecting reactional leprosy patients.

Influence of prevalent vertebral fractures on the quality of life of patients with systemic lupus erythematosus.

BACKGROUND: The prevalence of vertebral fractures in systemic lupus erythematosus (SLE) ranges between 20% and 21.4%, and patients with these fractures have impaired walking and activities of daily living. Moreover, clinical and radiological vertebral fractures have been associated with increased mortality. OBJECTIVES: To compare the quality of life of patients with SLE with and without vertebral fractures. METHODS: The study group comprised 140 women with SLE undergoing screening for vertebral fractures using a standardized method. SLE disease activity and organ damage were measured by the Mexican Systemic Lupus Erythematosus Disease Activity Index (MEX-SLEDAI) and the Systemic International Collaborating Clinics/American College of Rheumatology damage index (SLICC), respectively. The QUALEFFO and Center for Epidemiologic Studies Depression Scale were used to measure health-related quality of life and depression, respectively. RESULTS: The median age of the 140 patients was 43 years (range 18-76); disease duration was 72 months (range 6-432); 49.7% were menopausal. Thirty-four patients (24.8%) had vertebral fractures (> or = 1), mostly in the thoracic spine. Patients with vertebral fractures had a higher mean age (49.5 +/- 13.4 vs. 41 - 13.2 years, P= 0.001) and disease damage (57.1% vs. 34.4%, P = 0.001). The global QUALEFFO score was not different between the vertebral fractures group and the non-vertebral group. The only significant difference in the QUALEFFO items was in physical function (P = 0.04). A significant correlation was found between the severity of vertebral fractures and the QUALEFFO pain (r = 0.27, P = 0.001) and physical function (r = 0.37, P = 0.02) scores. The number of vertebral fractures correlated only with physical function (r = 0.01). CONCLUSIONS: The HRQOL of women with SLE is low, regardless of whether they have vertebral fractures or not, but patients with vertebral fractures have worse physical function compared to those without. Strategies to improve the HRQOL of patients with SLE with or without vertebral fractures are necessary.

Torsion of the omentum. A rare cause of acute abdomen.

OBJECTIVE: To describe the clinical aspects, treatment and evolution of acute abdomen caused by torsion of the greater omentum. METHODS: Retrospective analysis study consisted of a group of eleven patients with acute abdomen caused by torsion of the greater omentum. The variables included were age, sex, body mass index (BMI), clinical picture, evolution time, laboratory tests, radiology and treatment. Descriptive statistical analysis was employed. RESULTS: Seven (63.6%) women and four (36.36%) men; mean age 33 (20 to 58) years; BMI > 25.0 in nine (81.81%); average evolution 6.54, SD 3.47 days. All presented abdominal pain, six (54.5%) abdominal distension, four (36.3%) walking difficulty, three (27.27%) general malaise, ten (90.9%) slight leucocytosis, five (45.4%) previous surgery. In all cases diagnosis was made by laparotomy, treatment was resection of the affected segment, and no complications were seen. CONCLUSIONS: Segmental torsion of the greater omentum is a rare cause of acute abdomen. Pain is the most frequent symptom, and the condition resembles acute appendicitis. It is often discovered during surgery and is treated by the removal of the affected omentum segment.

Patogenia de las miopatías inflamatorias idiopáticas / Pathogenesis of the idiopathic inflammatory myopathies

Las miopatías inflamatorias idiopáticas (MII) son un grupo de enfermedades adquiridas, caracterizadas por un infiltrado inflamatorio del músculo esquelético. Con base en características clínicas e inmunopatológicas, pueden ser identificadas tres enfermedades: dermatomiositis (DM), polimiositis (PM) y miositis por cuerpos de inclusión (MCI). Los mecanismos inmunopatogénicos son cruciales para discriminar entre los tres subtipos de miopatías inflamatorias. En la DM está presente una microangiopatía mediada por complemento que afecta piel y músculo. La PM y la MCI son enfermedades en donde predomina la citotoxicidad mediada por linfocitos T, principalmente linfocitos T citotóxicos de CD8+ que invaden las fibras de músculo que sobreexpresan antígenos clase i del complejo principal de histocompatibilidad. Este artículo resume los principales mecanismos y marcadores immunopatogénicos. El impacto de este conocimiento debe ser definido en su potencial blanco terapéutico en las MII (AU)

The inflammatory myopathies, commonly described as idiopathic, are a group of acquired diseases characterized by an inflammatory infiltrate of the skeletal muscle. On the basis of clinical and immuno-pathological features, three major diseases can be identified: dermatomiositis (DM), polymyositis (PM) and inclusion body myositis (IBM). Immunopathogenesis mechanisms are crucial for discriminating between the three different subsets of inflammatory myopathies. DM is a complement-mediated microangiopathy affecting skin and muscle. PM and IBM are T cell-mediated disorders, where CD8-positive cytotoxic T cells invade muscle fibres expressing MHC class I antigens. This article summarizes the main immunopathological markers. The impact of this new knowledge must be defined in relation to potential therapeutic targets for idiopathic inflammatory myopathies (AU)

Abordaje en el diagnóstico diferencial de las miopatías inflamatorias / Approach to the differential diagnosis of inflammatory myopathies

Las miopatías inflamatorias son un grupo de enfermedades idiopáticas que se caracterizan por un infiltrado inflamatorio en el músculo esquelético e incluyen a la polimiositis, la dermatomiositis y la miositis por cuerpos de inclusión; tienen diferentes características histopatológicas, inmunológicas y patogénicas. La sospecha diagnóstica de las miopatías inflamatorias se basa en las características clínicas, y el diagnóstico es confirmado por las pruebas de laboratorio, la concentración sérica de enzimas musculares, la presencia de autoanticuerpos, la electromiografía y recientemente se han incluido los estudios de resonancia magnética y ultrasonido musculares. El procedimiento diagnóstico definitivo es la biopsia muscular realizada antes del inicio del tratamiento y debe obtenerse de músculo que no muestre atrofia severa. En la evaluación de estos pacientes es trascendental lograr un diagnóstico preciso del tipo de miopatía inflamatoria, ya que ello proporcionará información sobre la respuesta probable al tratamiento, influyendo en el pronóstico (AU)

Inflammatory myopathies are a group of idiopathic diseases characterized by an inflammatory infiltrate of the skeletal muscles that includes Polymyositis, Dermatomyositis, and Inclusion Body Myositis, each one displaying distinctive histopathological, immunological, and pathogenic features. The diagnosis of Inflammatory Myopathies is suspected on the basis of clinical features and supported by evidence obtained from laboratory tests, plasma levels of muscle enzymes, detection of autoantibodies, electromyography and, recently, magnetic resonance and ultrasonographic image studies have been included into the diagnostic arsenal. A definitive diagnosis relies on the findings in the muscle biopsy, performed before treatment and preferably before severe muscle atrophy has developed. Precision in diagnosis plays a fundamental role in the evaluation of these patients, allowing conclusions to be drawn regarding the response to treatment and prognosis (AU)

[Anesthesiologist's aptitude for peri-operative detection and treatment of latex allergy]. / Aptitud del anestesiólogo para la detección y tratamiento perioperatorios de la alergia al látex.

BACKGROUND: Latex allergy is the second cause of perioperative anaphylaxis. Anesthesiologists play a key role in opportune identification of risk factors, as well as clinical diagnosis and therapeutic management. OBJECTIVE: To evaluate the anesthesiologists aptitude to identify and treat latex allergy. PARTICIPANTS AND METHODS: Sixty-six anesthesiologists from five general hospitals located at Guadalajara, Jalisco, Mexico, were evaluated. Aptitude was determined by applying a validated structured instrument. Aptitude levels were measured by using an ordinal scale. Comparisons were performed using Mann Whitney U test. RESULTS: Anesthesiologist's global aptitude ranged from -2 to 27 with a median of 8 (from a maximum value in the scale of 40); frequencies by each category of the scale were: Random 48 (72.7%), Very bad 11 (16.7%), Bad 4 (6.1%) and Medium only 3 (4.5%). Both Good and Very good categories registered no anesthesiologist. The relationship of this indicator with other variables did not reach statistical significance (KW 6.478; p = 0.16617). CONCLUSIONS: A suboptimal aptitude was identified among anesthesiologists regarding identification of latex allergy. A need to establish new strategies for educative intervention in order to improve this issue was identified.

[Assessment of serum IgG activity correlation against cyclic citrullinated peptide antibodies, topoisomerase I and centromere proteins in Mexican patients with progressive systemic sclerosis]. / Evaluación de la correlación de la actividad de IgG sérica contra péptido citrulinado cíclico, topoisomerasa I y proteínas de centrómero en pacientes mexicanos con esclerosis sistémica progresiva.

OBJECTIVE: To evaluate sera titers for antibodies anti-cyclic citrullinated peptide and their correlation against sera levels of anti-topoisomerase I and anti-centromere antibodies in Mexican patients with systemic sclerosis. PATIENTS AND METHODS: Consecutive outpatients with systemic sclerosis who attending to rheumatology clinic at a second level hospital facility. The antibodies anti-cyclic citrullinated peptide, anti-topoisomerase I and anti-centromere were determined by enzymatic immunoassay (ELISA). STATISTICAL ANALYSIS: Spearman for correlation between numerical variables with nonparametric distribution. Fisher exact test or chi2 to compare proportions and Student t test for dimensional variables. RESULTS: Thirty female patients were included; aged 53 +/- 13, the disease duration at the time of the study was 10 +/- 9. Twenty-three patients (77%) exhibited diffuse disease. Anti-centromere, anti-topoisomerase I, and anti-cyclic citrullinated peptide were detected in nine, nine and three patients respectively. The correlation analysis showed the independence of autoantibodies anti-centromere and anti-topoisomerase I with respect to the levels of anti-cyclic citrullinated peptide. CONCLUSIONS: This study confirms the low frequency of anti-cyclic citrullinated peptide antibodies in patients with systemic sclerosis. A lack of correlation between autoantibodies considered as "mutually excluded" anti-topoisomerase I and anti-centromere, indicating that the analysis of the relevance for anti-cyclic citrullinated peptide in systemic sclerosis must include other clinical and serological variables.

Management of patients with rheumatoid arthritis in Latin America: a consensus position paper from Pan-American League of Associations of Rheumatology and Grupo Latino Americano De Estudio De Artritis Reumatoide.

OBJECTIVE: A consensus meeting of representatives of 18 Latin-American and Caribbean countries gathered in Reñaca, Chile, for 2 days to identify problems and provide recommendations for the care of patients with rheumatoid arthritis (RA) in Latin America, a region where poverty and other health priorities make the efforts to provide effective and high quality care difficult. This report includes recommendations for health professionals, patients, and health authorities in Latin America, with an emphasis on education and therapeutic issues. METHODS: Fifty-one rheumatologists (list available only online on the JCR website) from 18 Latin-American and Caribbean countries with a special interest in RA participated in the consensus meeting. Participants were experts identified and appointed by the National Societies of Rheumatology affiliated with the Pan-American League of Associations for Rheumatology (PANLAR) and by the Grupo Latino Americano De Estudio de Artritis Reumatoide (GLADAR)-an independent group of Latin American rheumatologist researchers were also invited to the meeting. Eight topics were identified as priorities: patient, community and allied health professional education, health policy and decision making, programs for early detection and appropriate treatment of RA, role of classic disease modifying antirheumatic drugs (DMARDs), role of biologic therapy, and drug safety surveillance. To reach consensus, a survey with questions relevant to the topic of interest was sent to all participants before the meeting. During a 2 day meeting, the answers of the survey were reviewed and discussed by each group, with final recommendations on action items. RESULTS: The specific topic of the survey was answered by 86% of the participants and 68% of them answered the entire survey. It was agreed that RA and rheumatic diseases which are currently not but should be public health priorities in Latin America, because of their prevalence and impact on quality of life. CONCLUSIONS: Strategic areas identified as priorities for our region included: early diagnosis and access to care by multidisciplinary teams, creation of databases to identify infections with the use of biologic agents in RA which are relevant to Latin America, and overall efforts to improve the care of RA patients in accordance with international standards. Implementation of educational programs aimed to improve self-management for patients with RA was also considered crucial.

Clinical competence for autoimmune and non-autoimmune rheumatic disorders in primary care.

OBJECTIVE: To evaluate the competence of the primary care physicians for the evaluation of rheumatic disorders. PARTICIPANTS AND METHODS: In a cross-sectional survey we included primary care physicians working at the official Mexican Social Security Institute that provides nation-wide health-care for salaried workers. Four hospitals from 23 potentially eligible primary-care hospitals in Guadalajara, Jalisco, Mexico, were randomly selected. From these hospitals the physicians who agree to participate were asked to answer a questionnaire for clinical competence. Using a Delphi modified approach; this questionnaire was elaborated by a group of rheumatologists and researchers working in continuous medical education. A Kuder-Richardson reliability index was computed in 0.94. The diseases included in the questionnaire were: (1) rheumatoid arthritis, (2) Sjogren syndrome, 3) gout, 4) osteoarthritis and 5) systemic lupus erythematosus and questions regarding to these were made using the technique of "representative patients". Domains included in the questionnaire were: assessment of risk factors, strategies for diagnosis, and treatment. According to the scores obtained in the questionnaire the ranges for clinical competence were: very high level 93-110 points, high level 75-92, moderate 57-74, low 39-56, very low 21-38 and <20 points was considered obtained by chance. RESULTS: One-hundred and four primary care physicians were interviewed. From the total, 60 (58%) physicians had the speciality of family physician. Only 11% (95% CI 5-17) of the interviewed had a high level of competence according to the instrument. Moderate competence was achieved by 20% (95% CI 13-27), whereas suboptimal levels had 51%: being low 31% (95% CI 22-40), very low 20% (95% CI 13-27). An additional 18% had scores obtained by chance (95% CI 11-25). There was no statistical difference in the scores between physicians with or without the specialty in family medicine. CONCLUSIONS: These results pointed-out a sub-optimal competence in a significant proportion of the primary care-physicians attending rheumatic disorders. Higher efforts need to be made to increase the levels of competence and improve the effectiveness of continuous medical education for these physicians.

Clinical Characteristics of Torsion of the Omentum.

BACKGROUND: The aim of this paper is to describe clinical aspects of the torsion of the omentum. METHODS: In this observational, retrospective study, the study group consisted of patients surgically managed for torsion of the omentum, between 1998 and 2008, in a second level medical facility in Mexico. Variables in the study included age, sex, signs and symptoms, body mass index (BMI), treatment and evolution time. Descriptive statistical analysis was employed. RESULTS: Eleven patients were confirmed torsion of omentum, 7 (63.63%) women and 4 (36.36%) men, median age 33 (20 to 58) years, BMI > 25.0 in 9 (81.81%), average evolution 6.54, SD 3.47 days. All presented with abdominal pain, 6 (54.54%) with abdominal distension, 4 (36.36%) with ambulatory difficulty, 3 (27.27%) with malaise, and 5 (45.45%) with previous surgery. In all cases diagnosis was made by means of laparotomy, treatment was the resection of the affected segment, and there were no further complications. CONCLUSIONS: Torsion of the omentum resembles acute appendicitis; abdominal pain and abdominal distension are the most common symptoms. It is often discovered during surgery and it is treated surgically by removal of the affected segment of the omentum.

[Pathogenesis of the idiopathic inflammatory myopathies]. / Patogenia de las miopatías inflamatorias idiopáticas.

The inflammatory myopathies, commonly described as idiopathic, are a group of acquired diseases characterized by an inflammatory infiltrate of the skeletal muscle. On the basis of clinical and immuno-pathological features, three major diseases can be identified: dermatomiositis (DM), polymyositis (PM) and inclusion body myositis (IBM). Immunopathogenesis mechanisms are crucial for discriminating between the three different subsets of inflammatory myopathies. DM is a complement-mediated microangiopathy affecting skin and muscle. PM and IBM are T cell-mediated disorders, where CD8-positive cytotoxic T cells invade muscle fibres expressing MHC class I antigens. This article summarizes the main immunopathological markers. The impact of this new knowledge must be defined in relation to potential therapeutic targets for idiopathic inflammatory myopathies.

[Approach to the differential diagnosis of inflammatory myopathies]. / Abordaje en el diagnóstico diferencial de las miopatías inflamatorias.

Inflammatory myopathies are a group of idiopathic diseases characterized by an inflammatory infiltrate of the skeletal muscles that includes Polymyositis, Dermatomyositis, and Inclusion Body Myositis, each one displaying distinctive histopathological, immunological, and pathogenic features. The diagnosis of Inflammatory Myopathies is suspected on the basis of clinical features and supported by evidence obtained from laboratory tests, plasma levels of muscle enzymes, detection of autoantibodies, electromyography and, recently, magnetic resonance and ultrasonographic image studies have been included into the diagnostic arsenal. A definitive diagnosis relies on the findings in the muscle biopsy, performed before treatment and preferably before severe muscle atrophy has developed. Precision in diagnosis plays a fundamental role in the evaluation of these patients, allowing conclusions to be drawn regarding the response to treatment and prognosis.

[Serum levels of antistreptolysin O in teenagers from Mexican urban and rural areas]. / Titulos séricos de antiestreptolisina O en adolescentes del area urbana y rural en México.

BACKGROUND: Antistreptolysin O (ASLO) may be an isolated evidence of recent infection by group A Streptococcus, especially in patients suspected of having a nonsuppurative sequel to this infection. We evaluated ASLO titers in students from urban and rural areas, age and geographic characteristics of study population among several other variables, could be factors that may influence in the ASLO levels in children. OBJECTIVE: To determine sera titers ofASLO in healthy adolescents from rural and urban areas in Mexico. MATERIAL AND METHODS: ASLO were detected by nephelometry, including 218 sera from asymptomatic high school students, two schools belong to government, one was at urban area (group 1; n = 68) and other was located at country side (rural) area (group 2; n = 75). The remaining school belong to private system and was located at urban area (group 3; n = 75). RESULTS: We included 218 sera, 58% were from females. Age (years) was expressed as median (maximum-minimum values) for groups 1, 2, and 3; 13 (12-18), 14 (12-18) and 14 (12-16) respectively. Weight (kg), height (cm) and body mass index (BMI) was expressed by mean +/- SD values for groups 1, 2, and 3; weight 48.8 +/- 8.8, 50.8 +/- 7.8, 57.2 +/- 11 respectively; height 154 +/- 6.9, 156 +/- 6.8, 161 +/- 8.2 and BMI 20.2 +/- 3.0, 20.9 +/- 2.9, and 21.9 +/- 3.6 respectively; when comparison among groups was performed, we found statistical differences in all variables. Titers for ASLO (UI/mL) expressed as median (maximum-minimum values) for groups 1, 2, and 3 were: 147 (20-828), 129 (25-1390) and 84 (25-848). Statistical differences between groups 1 vs 3, and 2 vs 3 were found. DISCUSSION: We confirm the variability of serum ASLO values among high school students. Thus, group 1 exhibited the highest levels of ASLO, and lowest values of weight, height, and BMI. When comparing against group 2 differences were non-significant. When comparing ASLO titers, Group 3 displayed lowest levels, which significantly differed from those of both groups 1 and 2. These findings discard influence of geographic location in ASLO titers, and indicate that better socioeconomic conditions may play a role.

[Thrombophilia, autoimmunity, and perioperative thromboprophylaxis]. / Trombofilia, autoinmunidad y tromboprofilaxis perioperatoria.

Thrombosis is observed in several areas of medicine. Equilibrium between pro- and anticoagulant factors is required for maintaining blood flow. Tissue injury from multiple causes may induce coagulum formation mediated by coagulation pathway activation. Tissue factor (F III) + F VIIa interacts with both platelet and endothelial cell receptors. This coagulation model displays four stages: a) initiation, b) amplification, c) propagation and d) stabilization. Development of thrombosis is associated with either primary or hereditary and acquired factors. Primary thrombophilia is determined genetically by a hypercoagulative state shown by loss of natural anticoagulant activity, such as antithrombin III, C, S protein or procoagulant activity gaining resistance to activated C protein: factor V (Leiden), prothrombin and methylenetetrahydrofolate reductase mutations. Acquired thrombophilia mainly relates to an autoimmune condition such as the presence of anticardiolipin antibodies or lupus anticoagulant. Surgical procedures enhance mechanisms that predispose to thrombosis, e.g., acidosis, hypothermia, plasma expanders, extracorporeal circulation, duration of surgical procedure, and tissue manipulation. Adequate classification of the patient's thrombosis risk and adequate use of primary and secondary prophylactic recommendations in these groups of patients is necessary.