Effectiveness and persistence of golimumab as a second biological drug in patients with spondyloarthritis: A retrospective study.

ABSTRACT: This observational, longitudinal retrospective, noncomparative study was designed to assess the persistence and effectiveness of golimumab as a second anti-tumor necrosis factor (TNF) drug in patients with spondyloarthritis requiring discontinuation from a first anti-TNF drug.Data were collected retrospectively for all patients with axial spondyloarthritis or psoriatic arthritis from 20 rheumatology clinics in Spain who started golimumab as a second anti-TNF drug between January 2013 and December 2015. Golimumab persistence was assessed with Kaplan-Meier survival analysis, and associated factors were assessed with Cox regression analysis.210 patients started golimumab as a second anti-TNF drug: 131 with axial spondyloarthritis and 79 with psoriatic arthritis. In axial spondyloarthritis patients, the mean (standard deviation) Bath Ankylosing Spondylitis Disease Activity Index score at baseline was 5.5 (2.1), decreasing to 3.9 (2.0) at month 3 and 3.5 (2.0) at year 1, and remaining stable thereafter. In psoriatic arthritis patients, mean (standard deviation) baseline Disease Activity Score was 4.0 (1.3), reducing to 2.5 (1.2) at month 3 and to 2.2 (1.3) at year 1. Corresponding improvements were recorded from baseline in C-reactive protein levels and erythrocyte sedimentation rates. The probability of persistence of treatment with golimumab was 80% at year 1, 70% at year 2 and 65% at years 3 and year 4, and was similar in those who had stopped the first anti-TNF due to loss of efficacy or other reasons. Cox regression analysis showed that the probability of survival with golimumab was higher in patients with higher erythrocyte sedimentation rate, in patients with axial spondyloarthritis than with psoriatic arthritis, and in those who had discontinued adalimumab as first anti-TNF. Seventy-two patients (34.3%) discontinued golimumab during follow-up, 50 of them due to lack of efficacy.In patients with spondyloarthritis requiring discontinuation from a first anti-TNF drug, treatment with golimumab was effective and showed a high probability of persistence up to 4 years of treatment.

Autoencoded DNA methylation data to predict breast cancer recurrence: Machine learning models and gene-weight significance.

Breast cancer is the most frequent cancer in women and the second most frequent overall after lung cancer. Although the 5-year survival rate of breast cancer is relatively high, recurrence is also common which often involves metastasis with its consequent threat for patients. DNA methylation-derived databases have become an interesting primary source for supervised knowledge extraction regarding breast cancer. Unfortunately, the study of DNA methylation involves the processing of hundreds of thousands of features for every patient. DNA methylation is featured by High Dimension Low Sample Size which has shown well-known issues regarding feature selection and generation. Autoencoders (AEs) appear as a specific technique for conducting nonlinear feature fusion. Our main objective in this work is to design a procedure to summarize DNA methylation by taking advantage of AEs. Our proposal is able to generate new features from the values of CpG sites of patients with and without recurrence. Then, a limited set of relevant genes to characterize breast cancer recurrence is proposed by the application of survival analysis and a pondered ranking of genes according to the distribution of their CpG sites. To test our proposal we have selected a dataset from The Cancer Genome Atlas data portal and an AE with a single-hidden layer. The literature and enrichment analysis (based on genomic context and functional annotation) conducted regarding the genes obtained with our experiment confirmed that all of these genes were related to breast cancer recurrence.

PAI1 is a Marker of Bad Prognosis in Rectal Cancer but Predicts a Better Response to Treatment with PIM Inhibitor AZD1208.

Colorectal cancer (CRC) is the third most common cancer worldwide. The standard treatment in locally advanced rectal cancer is preoperative radiation alone or in combination with chemotherapy, followed by adjuvant chemotherapy. Rectal cancer is highly lethal, with only 20% of patients showing a complete remission (by RECIST) after standard treatment, although they commonly show local or systemic relapse likely due to its late detection and high chemotherapy resistance, among other reasons. Here, we explored the role of PAI1 (Serpin E1) in rectal cancer through the analyses of public patient databases, our own cohort of locally advanced rectal cancer patients and a panel of CRC cell lines. We showed that PAI1 expression is upregulated in rectal tumors, which is associated with decreased overall survival and increased metastasis and invasion in advanced rectal tumors. Accordingly, PAI1 expression is correlated with the expression of (Epithelial-to-Mesenchymal Transition) EMT-associated genes and genes encoding drug targets, including the tyrosine kinases PDGFRb, PDGFRa and FYN, the serine/threonine kinase PIM1 and BRAF. In addition, we demonstrate that cells expressing PAI1 protein are more sensitive to the PIM inhibitor AZD1208, suggesting that PAI1 could be used to predict response to treatment with PIM inhibitors and to complement radiotherapy in rectal tumors.

New markers for human ovarian cancer that link platinum resistance to the cancer stem cell phenotype and define new therapeutic combinations and diagnostic tools.

BACKGROUND: Ovarian cancer is the leading cause of gynecologic cancer-related death, due in part to a late diagnosis and a high rate of recurrence. Primary and acquired platinum resistance is related to a low response probability to subsequent lines of treatment and to a poor survival. Therefore, a comprehensive understanding of the mechanisms that drive platinum resistance is urgently needed. METHODS: We used bioinformatics analysis of public databases and RT-qPCR to quantitate the relative gene expression profiles of ovarian tumors. Many of the dysregulated genes were cancer stem cell (CSC) factors, and we analyzed its relation to therapeutic resistance in human primary tumors. We also performed clustering and in vitro analyses of therapy cytotoxicity in tumorspheres. RESULTS: Using bioinformatics analysis, we identified transcriptional targets that are common endpoints of genetic alterations linked to platinum resistance in ovarian tumors. Most of these genes are grouped into 4 main clusters related to the CSC phenotype, including the DNA damage, Notch and C-KIT/MAPK/MEK pathways. The relative expression of these genes, either alone or in combination, is related to prognosis and provide a connection between platinum resistance and the CSC phenotype. However, the expression of the CSC-related markers was heterogeneous in the resistant tumors, most likely because there were different CSC pools. Furthermore, our in vitro results showed that the inhibition of the CSC-related targets lying at the intersection of the DNA damage, Notch and C-KIT/MAPK/MEK pathways sensitize CSC-enriched tumorspheres to platinum therapies, suggesting a new option for the treatment of patients with platinum-resistant ovarian cancer. CONCLUSIONS: The current study presents a new approach to target the physiology of resistant ovarian tumor cells through the identification of core biomarkers. We hypothesize that the identified mutations confer platinum resistance by converging to activate a few pathways and to induce the expression of a few common, measurable and targetable essential genes. These pathways include the DNA damage, Notch and C-KIT/MAPK/MEK pathways. Finally, the combined inhibition of one of these pathways with platinum treatment increases the sensitivity of CSC-enriched tumorspheres to low doses of platinum, suggesting a new treatment for ovarian cancer.

The cargo protein MAP17 (PDZK1IP1) regulates the immune microenvironment.

Inflammation is a complex defensive response activated after various harmful stimuli allowing the clearance of damaged cells and initiating healing and regenerative processes. Chronic, or pathological, inflammation is also one of the causes of neoplastic transformation and cancer development. MAP17 is a cargo protein that transports membrane proteins from the endoplasmic reticulum. Therefore, its overexpression may be linked to an excess of membrane proteins that may be recognized as an unwanted signal, triggering local inflammation. Therefore, we analyzed whether its overexpression is related to an inflammatory phenotype. In this work, we found a correlation between MAP17 expression and inflammatory phenotype in tumors and in other inflammatory diseases such as Crohn's disease, Barrett's esophagus, COPD or psoriasis. MAP17 expression correlated also with the markers of inflammation HLAs, BBS10, HERC2, ADNP and PYCARD. Furthermore, we found that MAP17 expression directly regulates NFAT2 and IL-6 activation, inducing the differentiation of monocytes to dendritic cells and suggesting a causal role of MAP17 in inflammation. Immunohistochemistry confirms local inflammation, mainly CD45+ cells, at the site of expression of MAP17, at least in tumors, Crohn's and psoriasis. Therefore, our data indicates that the overexpression of the protein MAP17 plays important role in diseases involving chronic inflammation.

Coordinated downregulation of Spinophilin and the catalytic subunits of PP1, PPP1CA/B/C, contributes to a worse prognosis in lung cancer.

The scaffold protein Spinophilin (Spinophilin, PPP1R9B) is one of the regulatory subunits of phosphatase-1 (PP1), directing it to distinct subcellular locations and targets. The loss of Spinophilin reduces PP1 targeting to pRb, thereby maintaining higher levels of phosphorylated pRb. Spinophilin is absent or reduced in approximately 40% of human lung tumors, correlating with the malignant grade. However, little is known about the relevance of the coordinated activity or presence of Spinophilin and its reported catalytic partners in the prognosis of lung cancer. In the present work, we show that the downregulation of Spinophilin, either by protein or mRNA, is related to a worse prognosis in lung tumors. This effect is more relevant in squamous cell carcinoma, SCC, than in adenocarcinoma. Downregulation of Spinophilin is related to a decrease in the levels of its partners PPP1CA/B/C, the catalytic subunits of PP1. A decrease in these subunits is also related to prognosis in SCC and, in combination with a decrease in Spinophilin, are markers of a poor prognosis in these tumors. The analysis of the genes that correlate to Spinophilin in lung tumors showed clear enrichment in ATP biosynthesis and protein degradation GO pathways. The analysis of the response to several common and pathway-related drugs indicates a direct correlation between the Spinophilin/PPP1Cs ratio and the response to oxaliplatin and bortezomib. This finding indicates that this ratio may be a good predictive biomarker for the activity of the drugs in these tumors with a poor prognosis.

Cost per response for abatacept versus adalimumab in rheumatoid arthritis by ACPA subgroups in Germany, Italy, Spain, US and Canada.

Rheumatoid arthritis (RA) is a chronic inflammatory disorder leading to disability and reduced quality of life. Effective treatment with biologic DMARDs poses a significant economic burden. The Abatacept versus Adalimumab Comparison in Biologic-Naïve RA Subjects with Background Methotrexate (AMPLE) trial was a head-to-head, randomized study comparing abatacept in serum anti-citrullinated protein antibody (ACPA)-positive patients, with increasing efficacy across ACPA quartile levels. The aim of this study was to evaluate the cost per response accrued using abatacept versus adalimumab in ACPA-positive and ACPA-negative patients with RA from the health care perspective in Germany, Italy, Spain, the US and Canada. A cost-consequence analysis (CCA) was designed to compare the monthly costs per responding patient/patient in remission. Efficacy, safety and resource use inputs were based on the AMPLE trial. A one-way deterministic sensitivity analysis (OWSA) was also performed to assess the impact of model inputs on the results for total incremental costs. Cost per response in ACPA-positive patients favoured abatacept compared with adalimumab (ACR20, ACR90 and HAQ-DI). Subgroup analysis favoured abatacept with increasing stringency of response criteria and serum ACPA levels. Cost per remission (DAS28-CRP) favoured abatacept in ACPA-negative patients, while cost per CDAI and SDAI favoured abatacept in ACPA-positive patients. Abatacept was consistently favoured in ACPA-Q4 patients across all outcomes and countries. Cost savings were greater with abatacept when more stringent response criteria were applied and also with increasing ACPA levels, which could lead to a lower overall health care budget impact with abatacept compared with adalimumab.

Numb-like (NumbL) downregulation increases tumorigenicity, cancer stem cell-like properties and resistance to chemotherapy.

NumbL, or Numb-like, is a close homologue of Numb, and is part of an evolutionary conserved protein family implicated in some important cellular processes. Numb is a protein involved in cell development, in cell adhesion and migration, in asymmetric cell division, and in targeting proteins for endocytosis and ubiquitination. NumbL exhibits some overlapping functions with Numb, but its role in tumorigenesis is not fully known. Here we showed that the downregulation of NumbL alone is sufficient to increase NICD nuclear translocation and induce Notch pathway activation. Furthermore, NumbL downregulation increases epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC)-related gene transcripts and CSC-like phenotypes, including an increase in the CSC-like pool. These data suggest that NumbL can act independently as a tumor suppressor gene. Furthermore, an absence of NumbL induces chemoresistance in tumor cells. An analysis of human tumors indicates that NumbL is downregulated in a variable percentage of human tumors, with lower levels of this gene correlated with worse prognosis in colon, breast and lung tumors. Therefore, NumbL can act as an independent tumor suppressor inhibiting the Notch pathway and regulating the cancer stem cell pool.

Decoding Warburg's hypothesis: tumor-related mutations in the mitochondrial respiratory chain.

Otto Warburg observed that cancer cells derived their energy from aerobic glycolysis by converting glucose to lactate. This mechanism is in opposition to the higher energy requirements of cancer cells because oxidative phosphorylation (OxPhos) produces more ATP from glucose. Warburg hypothesized that this phenomenon occurs due to the malfunction of mitochondria in cancer cells. The rediscovery of Warburg's hypothesis coincided with the discovery of mitochondrial tumor suppressor genes that may conform to Warburg's hypothesis along with the demonstrated negative impact of HIF-1 on PDH activity and the activation of HIF-1 by oncogenic signals such as activated AKT. This work summarizes the alterations in mitochondrial respiratory chain proteins that have been identified and their involvement in cancer. Also discussed is the fact that most of the mitochondrial mutations have been found in homoplasmy, indicating a positive selection during tumor evolution, thereby supporting their causal role.

Recent methodological advances in the analysis of protein tyrosine nitration.

Tyrosine nitration is a common post-translational modification affecting protein structure and function. It is based on the addition of a -NO2 group at the ortho position of the phenolic hydroxyl group of tyrosine to yield 3-nitrotyrosine (3-NTyr). Understanding how tyrosine nitration affects the structure and functionality of proteins is of considerable interest, as it is associated with pathogenesis in diseases related to oxidative stress in all living organisms. There are several methods to nitrate tyrosine residues in native proteins. Among them, nitration by the chemical agent peroxynitrite stands out for its biological relevance. Recently, a genetically evolved suppressor tRNA has been developed to provide in vivo incorporation of 3-NTyr into proteins. In this minireview, we discuss the advantages and limitations of these chemical and biological methods and propose a non-damaging method to analyze the configuration and dynamics of nitrotyrosine residues in native proteins by NMR spectroscopy.

Perturbation of the redox site structure of cytochrome c variants upon tyrosine nitration.

Post-translational nitration of tyrosine is considered to be an important step in controlling the multiple functions of cytochrome c (Cyt-c). However, the underlying structural basis and mechanism are not yet understood. In this work, human Cyt-c variants in which all but one tyrosine has been substituted by phenylalanine have been studied by resonance Raman and electrochemical methods to probe the consequences of tyrosine nitration on the heme pocket structure and the redox potential. The mutagenic modifications of the protein cause only subtle conformational changes of the protein and small negative shifts of the redox potentials which can be rationalized in terms of long-range electrostatic effects on the heme. The data indicate that the contributions of the individual tyrosines for maintaining the relatively high redox potential of Cyt-c are additive. Nitration of individual tyrosines leads to a destabilization of the axial Fe-Met80 bond which causes the substitution of the native Met ligand by a water molecule or a lysine residue for a fraction of the proteins. Electrostatic immobilization of the protein variants on electrodes coated by self-assembled monolayers (SAMs) of mercaptounadecanoic acid destabilizes the heme pocket structure of both the nitrated and non-nitrated variants. Here, the involvement of surface lysines in binding to the SAM surface prevents the replacement of the Met80 ligand by a lysine but instead a His-His coordinated species is formed. The results indicate that structural perturbations of the heme pocket of Cyt-c due to tyrosine nitration and to local electric fields are independent of each other and occur via different molecular mechanisms. The present results are consistent with the view that either tyrosine nitration or electrostatic binding to the inner mitochondrial membrane, or both events together, are responsible for the switch from the redox to the peroxidase function.

A non-damaging method to analyze the configuration and dynamics of nitrotyrosines in proteins.

Often, deregulation of protein activity and turnover by tyrosine nitration drives cells toward pathogenesis. Hence, understanding how the nitration of a protein affects both its function and stability is of outstanding interest. Nowadays, most of the in vitro analyses of nitrated proteins rely on chemical treatment of native proteins with an excess of a chemical reagent. One such reagent, peroxynitrite, stands out for its biological relevance. However, given the excess of the nitrating reagent, the resulting in vitro modification could differ from the physiological nitration. Here, we determine unequivocally the configuration of distinct nitrated-tyrosine rings in single-tyrosine mutants of cytochrome c. We aimed to confirm the nitration position by a non-destructive method. Thus, we have resorted to (1)H-(15)N heteronuclear single quantum coherence(HSQC) spectra to identify the (3)J(NH) correlation between a (15)N-tagged nitro group and the adjacent aromatic proton. Once the chemical shift of this proton was determined, we compared the (1)H-(13)C HSQC spectra of untreated and nitrated samples. All tyrosines were nitrated at ε positions, in agreement to previous analysis by indirect techniques. Notably, the various nitrotyrosine residues show a different dynamic behaviour that is consistent with molecular dynamics computations.

Specific nitration of tyrosines 46 and 48 makes cytochrome c assemble a non-functional apoptosome.

Under nitroxidative stress, a minor fraction of cytochrome c can be modified by tyrosine nitration. Here we analyze the specific effect of nitration of tyrosines 46 and 48 on the dual role of cytochrome c in cell survival and cell death. Our findings reveal that nitration of these two solvent-exposed residues has a negligible effect on the rate of electron transfer from cytochrome c to cytochrome c oxidase, but impairs the ability of the heme protein to activate caspase-9 by assembling a non-functional apoptosome. It seems that cytochrome c nitration under cellular stress counteracts apoptosis in light of the small amount of modified protein. We conclude that other changes such as increased peroxidase activity prevail and allow the execution of apoptosis.

Cytochrome c signalosome in mitochondria.

Cytochrome c delicately tilts the balance between cell life (respiration) and cell death (apoptosis). Whereas cell life is governed by transient electron transfer interactions of cytochrome c inside the mitochondria, the cytoplasmic adducts of cytochrome c that lead to cell death are amazingly stable. Interestingly, the contacts of cytochrome c with its counterparts shift from the area surrounding the heme crevice for the redox complexes to the opposite molecule side when the electron flow is not necessary. The cytochrome c signalosome shows a higher level of regulation by post-translational modifications-nitration and phosphorylation-of the hemeprotein. Understanding protein interfaces, as well as protein modifications, would puzzle the mitochondrial cytochrome c-controlled pathways out and enable the design of novel drugs to silence the action of pro-survival and pro-apoptotic partners of cytochrome c.

Nitration of tyrosines 46 and 48 induces the specific degradation of cytochrome c upon change of the heme iron state to high-spin.

The Reactive Nitrogen and Oxygen Species (the so-called RNOS), which are well-known radicals formed in the mitochondria under nitro-oxidative cell stress, are responsible for nitration of tyrosines in a wide variety of proteins and, in particular, in cytochrome c (Cc). Only three out of the five tyrosine residues of human Cc, namely those at positions 67, 74 and 97, have been detected in vivo as nitrotyrosines. However, nitration of the two other tyrosines, namely those at positions 46 and 48, has never been detected in vivo despite they are both well-exposed to solvent. Here we investigate the changes in heme coordination and alkaline transition, along with the peroxidase activity and in cell degradation of Cc mutants in which all their tyrosine residues - with the only exception of that at position 46 or 48 - are replaced by phenylalanines. In Jurkat cell extracts devoid of proteases inhibitors, only the high-spin iron nitrated forms of these monotyrosine mutants are degraded. Altogether the resulting data suggest that nitration of tyrosines 46 and 48 makes Cc easily degradable upon turning the heme iron state to high-spin.

[Analysis of the body composition of Spanish women with fibromyalgia]. / Análisis de la composición corporal en mujeres con fibromialgia.

OBJECTIVES: To describe the anthropometric profile and body composition of women from Southern Spain diagnosed with fibromyalgia (FM) and to compare the observed values with values from other studies conducted on FM patients and with national reference values. MATERIALS AND METHODS: The body composition of 104 women diagnosed with FM was assessed using an eight-electrode impedance meter. The reliability of the body composition measurement was tested in a randomly selected sub-sample (n=28). The reliability study showed a test-retest systematic error close to zero in most of the parameters studied. RESULTS: The women with FM who were studied had a mean weight of 71.3±13.4 kg, height of 158±6 cm, body mass index of 28.6±5.1 kg/m(2), body fat mass of 38.6±7.6%, total body water of 31.6±3.8 l and muscle mass of 23.4±3.0 kg. In general, there were no substantial differences in weight and body mass index between women with FM and those analyzed in other Spanish and European studies involving FM patients, nor when they were compared with regional or national reference values. However, the prevalence of obesity in the women with FM under study was 33.7%, a higher figure than that from the national reference data for obesity in similarly aged women (i.e. 26,4%). CONCLUSIONS: The results suggest that obesity is a common condition in women diagnosed with FM, its prevalence in this population being higher than the national reference values. This study provides detailed information about the body composition characteristics of women with FM.

Tyrosine phosphorylation turns alkaline transition into a biologically relevant process and makes human cytochrome c behave as an anti-apoptotic switch.

Cytochrome c (Cc) is a key protein in cell life (respiration) and cell death (apoptosis). On the one hand, it serves as a mitochondrial redox carrier, transferring electrons between the membrane-embedded complexes III and IV. On the other hand, it acts as a cytoplasmic apoptosis-triggering agent, forming the apoptosome with apoptosis protease-activating factor-1 (Apaf-1) and activating the caspase cascade. The two functions of cytochrome c are finely tuned by the phosphorylation of tyrosines and, in particular, those located at positions 48 and 97. However, the specific cytochrome c-phosphorylating kinase is still unknown. To study the structural and functional changes induced by tyrosine phosphorylation in cytochrome c, we studied the two phosphomimetic mutants Y48E and Y97E, in which each tyrosine residue is replaced by glutamate. Such substitutions alter both the physicochemical features and the function of each mutant compared with the native protein. Y97E is significantly less stable than the WT species, whereas Y48E not only exhibits lower values for the alkaline transition pK (a) and the midpoint redox potential, but it also impairs Apaf-1-mediated caspase activation. Altogether, these findings suggest that the specific phosphorylation of Tyr48 makes cytochrome c act as an anti-apoptotic switch.

Interrater reliability and time measurement validity of speed-agility field tests in adolescents.

The aim of this study was to examine the interrater reliability (trained vs. untrained raters) and criterion-related validity (manual vs. automatic timing) of the 4 × 10-m shuttle run and 30-m running speed tests (times measured). The study comprised 85 adolescents (38 girls) aged 13.0-16.9 years from the Healthy Lifestyle in Europe by Nutrition in Adolescence study. The time required to complete the 4 × 10-m shuttle run and 30-m running tests was simultaneously measured (a) manually with a stopwatch by both trained and untrained raters (for interrater reliability analysis), and (b) by using photoelectric cells (for validity analysis). Systematic error, random error, and heteroscedasticity were studied with repeated-measured analysis of variance and Bland-Altman plots. The systematic error for untrained vs. trained raters and the untrained raters vs. photoelectric cells were in all cases ∼0.1 seconds (p < 0.01), that is, untrained raters recorded higher times. No systematic error was found between trained raters and photoelectric cells (p > 0.05). No heteroscedasticity was shown in any case (p > 0.05). The findings indicate that manual measurements by a trained rater, using a stopwatch, seem to be a valid method to assess speed and agility fitness testing in adolescents. Researchers must be trained to minimize the measurement error.

Análisis de la composición corporal en mujeres con fibromialgia / Analysis of the body composition of Spanish women with fibromyalgia

Objetivos. Caracterizar el perfil antropométrico y de composición corporal de mujeres con fibromialgia (FM) del sur de España y compararlo con otros estudios nacionales e internacionales de similares características, así como con valores normativos de mujeres españolas. Materiales y métodos. Se ha analizado la composición corporal de 104 mujeres diagnosticadas de FM mediante un bioimpedianciómetro de 8 electrodos. La fiabilidad de la medida fue estudiada en una submuestra seleccionada aleatoriamente (n=28). El estudio de fiabilidad mostró un error sistemático test vs re-test cercano a cero en la mayoría de los parámetros estudiados. Resultados. Las mujeres con FM estudiadas tuvieron un peso promedio de 71,3±13,4kg, 158,1±6cm de altura, 28,6±5,1kg/m2 de índice de masa corporal, 38,6±7,6% de porcentaje graso, 31,6±3,8l de agua corporal total y 23,4±3,0kg de masa muscular. En general, no se observan diferencias importantes en peso e índice de masa corporal, tanto entre las mujeres con FM estudiadas y enfermas procedentes de otros estudios nacionales o europeos, como en comparación con los valores de referencia andaluces o nacionales. Sin embargo, la prevalencia de obesidad en el grupo de mujeres con FM fue del 33,7%, un valor superior a la prevalencia de obesidad nacional en mujeres de igual rango de edad (i.e. 26,4%). Conclusiones. Los resultados sugieren que la obesidad es una condición frecuente entre mujeres con FM, siendo su prevalencia sustancialmente superior a los valores normativos nacionales. Este estudio presenta información detallada sobre la composición corporal de mujeres con FM (AU)

Objectives. To describe the anthropometric profile and body composition of women from Southern Spain diagnosed with fibromyalgia (FM) and to compare the observed values with values from other studies conducted on FM patients and with national reference values. Materials and methods. The body composition of 104 women diagnosed with FM was assessed using an eight-electrode impedance meter. The reliability of the body composition measurement was tested in a randomly selected sub-sample (n=28). The reliability study showed a test-retest systematic error close to zero in most of the parameters studied. Results. The women with FM who were studied had a mean weight of 71.3±13.4 kg, height of 158±6 cm, body mass index of 28.6±5.1 kg/m2, body fat mass of 38.6±7.6%, total body water of 31.6±3.8 l and muscle mass of 23.4±3.0 kg. In general, there were no substantial differences in weight and body mass index between women with FM and those analyzed in other Spanish and European studies involving FM patients, nor when they were compared with regional or national reference values. However, the prevalence of obesity in the women with FM under study was 33.7%, a higher figure than that from the national reference data for obesity in similarly aged women (i.e. 26,4%). Conclusions. The results suggest that obesity is a common condition in women diagnosed with FM, its prevalence in this population being higher than the national reference values. This study provides detailed information about the body composition characteristics of women with FM (AU)