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Izquierdo-ramírez, Yojhan Edilberto - One of the best experts on this subject based on the ideXlab platform.
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Cambios radiográficos del penacho de la falange distal de las manos en pacientes con psoriasis, artritis psoriásica, eSclerosis sistémica, artritis reumatoide y osteoartrosis. Meta-análisis y revisión sistemática
2018Co-Authors: Izquierdo-ramírez, Yojhan EdilbertoAbstract:Introducción: el penacho de la falange distal de las manos (PFDM) es una estructura ósea que presenta cambios sutiles en enfermedades musculo-esqueléticas. Hasta el momento se desconoce el tipo y la frecuencia de las lesiones del PFDM en psoriasis, artritis psoriásica (APs), eSclerosis sistémica (ES), artritis reumatoide (AR) y osteoartrosis (OA). Objetivo: determinar en radiografía simple las anormalidades del PFDM en adultos con psoriasis, APs, ES, AR y OA. Materiales y métodos: se realizó una revisión sistemática sobre los cambios radiográficos del PFDM siguiendo las recomendaciones de las guías PRISMA. La prevalencia de los hallazgos fue sintetizada usando un modelo de efectos fijos. Las asociaciones se expresaron como odds ratio (OR) con intervalos de confianza (IC) y valores p. Resultados: se incluyeron 43 estudios observacionales. La resorción del PFDM fue la alteración más frecuente en sujetos con ES y APs con una prevalencia del 28.3% y 16% respectivamente. En AR la prevalencia de eSclerosis del PFDM fue del 28.3%. En sujetos con onicopatía psoriásica el compromiso del PFDM fue mayor en comparación a individuos sin lesión ungueal (OR=2.91; IC95%: 1.04–8.13; p=0.04), siendo las erosiones y la eSclerosis los hallazgos más importantes. No se encontró información suficiente acerca del compromiso del PFDM en OA. Conclusión: la evidencia actual acerca del compromiso del PFDM en APs, psoriasis, ES, AR y OA es limitada. La resorción del PFDM es el hallazgo radiográfico característico en pacientes con ES y APs. La eSclerosis es la alteración radiográfica más frecuente en el PFDM de sujetos con AR, sin embargo, no constituye un hallazgo patognomónico. Por último, existe relación entre las alteraciones del PFDM y la patología ungueal en individuos con psoriasis.Abstract: Introduction: the distal phalanx tuft of the hand (DPTH) is a bone structure that undergoes subtle changes in various musculoskeletal diseases. To date, the type and frequency of DPTH injuries involved in psoriasis and psoriatic arthritis (PsA), systemic Sclerosis (SS), rheumatoid arthritis (RA) and osteoarthrosis (OA) are unknow. Objective: to determine the abnormal findings related to DPTH through plain X-rays in adult subjects with psoriasis, PsA, SS, RA and OA. Materials and methods: A systematic review of radiographic alterations of the DPTH detected in plain hand radiographs was performed following the PRISMA guidelines. The prevalence of findings were summarized using a fixed effects model. Statistical associations were expressed as odds ratio (OR) with confidence intervals (CI) and p values. Results: 43 observational studies were included. The resorption of the DPTH was the most frequent alteration in subjects with SS and PsA with a prevalence of 28.3% and 16% respectively. In RA the prevalence of Sclerosis of the DPTH was 28.3%. The involvement of DPTH in subjects with psoriatic onicopathy was higher than in subjects without ungueal affectation (OR=2.91, 95%CI: 1.04-8.13; p=0.04), being erosions and Sclerosis the most important findings. The evidence about the DPTH compromise in OA is insufficient. Conclusion: the current evidence about the involvement of the DPTH in PsA, psoriasis, SS, RA and OA is limited. The resorption of the DPTH is the characteristic radiographic finding in patients with PsA and SS. In RA the Sclerosis of the DPTH is the most frequent radiographic change in this structure, however, it is not a pathognomonic finding. Finally, there is a relationship between DPTH alterations and nail disease in subjects with psoriasis
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Cambios radiográficos en el penacho de la falange distal de las manos en pacientes con psoriasis o artritis psoriásica. Revisión sistemática
Universidad Nacional de Colombia - Sede Bogotá - Facultad de Medicina, 2017Co-Authors: Izquierdo-ramírez, Yojhan Edilberto, Calvo-páramo Enrique, Castañeda-castillo, Luisa María, Gómez-correa, Sandra Viviana, Zambrano, Fernán SantiagoAbstract:Introducción. El penacho de la falange distal de las manos (PFDM) es una estructura ósea que sufre cambios sutiles en diversas enfermedades musculoesqueléticas. Hasta el momento, se desconoce el tipo y frecuencia de las lesiones del PFDM en psoriasis y artritis psoriásica (APs).Objetivo. Determinar en radiografía simple las anormalidades del PFDM en adultos con psoriasis y APs.Materiales y métodos. Se realizó una revisión sistemática buscando alteraciones radiográficas del PFDM en adultos con psoriasis y APs. La prevalencia de los hallazgos fue sintetizada usando un modelo de efectos fijos. Las asociaciones se expresaron como odds ratio (OR) con intervalos de confianza (IC) y valores p.Resultados. Se incluyeron 11 estudios observacionales. La alteración de mayor frecuencia en APs fue la resorción del PFDM con una prevalencia del 16%. El compromiso del PFDM en sujetos con onicopatía psoriásica fue mayor que en sujetos sin compromiso ungueal (OR=2.91; IC95%: 1.04–8.13; p=0.04), siendo las erosiones y la eSclerosis los hallazgos de mayor importancia.Conclusión. La evidencia actual acerca del compromiso del PFDM en APs y psoriasis es limitada. Existe relación entre las alteraciones del PFDM y la patología ungueal en donde las erosiones y la eSclerosis son las anormalidades más significativas.Introduction: The distal phalanx tuft of the hand (DPTH) is a bone structure that undergoes subtle changes in various musculoskeletal diseases. To date, the type and frequency of DPTH injuries involved in psoriasis and psoriatic arthritis (PsA) are unknown.Objective: To determine the abnormal findings related to DPTH through plain X-rays in adult subjects with psoriasis and psoriatic arthritis (PsA).Materials and methods: A systematic review of radiographic alterations of the DPTH detected in plain hand radiographs was performed following the PRISMA guidelines. The prevalence of findings was summarized using a fixed effects model. Statistical associations were expressed as odds ratio (OR) with confidence intervals (CI) and p values.Results: Eleven observational studies were included. The most frequent alteration in PsA was DPTH resorption with a prevalence of 16%. The involvement of DPTH in subjects with psoriatic onicopathy was higher than in subjects without ungueal affectation (OR=2.91, 95%CI: 1.04-8.13; p=0.04), being erosions and Sclerosis the most important findings.Conclusion: Current evidence regarding DPTH involvement in PsA and psoriasis is limited. However, an apparent correlation between DPTH findings and ungual abnormalities could exist, where erosions and Sclerosis are the most significant abnormalities
Pietro Fratta - One of the best experts on this subject based on the ideXlab platform.
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Is SOD1 loss of function involved in amyotrophic lateral Sclerosis
Brain, 2013Co-Authors: Rachele A. Saccon, Rosie K. A. Bunton-stasyshyn, Elizabeth M. C. Fisher, Pietro FrattaAbstract:Mutations in the gene superoxide dismutase 1 (SOD1) are causative for familial forms of the neurodegenerative disease amyotrophic lateral Sclerosis. When the first SOD1 mutations were identified they were postulated to give rise to amyotrophic lateral Sclerosis through a loss of function mechanism, but experimental data soon showed that the disease arises from a—still unknown—toxic gain of function, and the possibility that loss of function plays a role in amyotrophic lateral Sclerosis pathogenesis was abandoned. Although loss of function is not causative for amyotrophic lateral Sclerosis, here we re-examine two decades of evidence regarding whether loss of function may play a modifying role in SOD1–amyotrophic lateral Sclerosis. From analysing published data from patients with SOD1–amyotrophic lateral Sclerosis, we find a marked loss of SOD1 enzyme activity arising from almost all mutations. We continue to examine functional data from all Sod1 knockout mice and we find obvious detrimental effects within the nervous system with, interestingly, some specificity for the motor system. Here, we bring together historical and recent experimental findings to conclude that there is a possibility that SOD1 loss of function may play a modifying role in amyotrophic lateral Sclerosis. This likelihood has implications for some current therapies aimed at knocking down the level of mutant protein in patients with SOD1–amyotrophic lateral Sclerosis. Finally, the wide-ranging phenotypes that result from loss of function indicate that SOD1 gene sequences should be screened in diseases other than amyotrophic lateral Sclerosis.
Albert C Ludolph - One of the best experts on this subject based on the ideXlab platform.
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diffusion tensor imaging analysis of sequential spreading of disease in amyotrophic lateral Sclerosis confirms patterns of tdp 43 pathology
Brain, 2014Co-Authors: Jan Kassubek, Hanspeter Muller, Kelly Del Tredici, Johannes Brettschneider, Elmar H Pinkhardt, Dorothee Lule, Sarah Bohm, Heiko Braak, Albert C LudolphAbstract:Diffusion tensor imaging can identify amyotrophic lateral Sclerosis-associated patterns of brain alterations at the group level. Recently, a neuropathological staging system for amyotrophic lateral Sclerosis has shown that amyotrophic lateral Sclerosis may disseminate in a sequential regional pattern during four disease stages. The objective of the present study was to apply a new methodological diffusion tensor imaging-based approach to automatically analyse in vivo the fibre tracts that are prone to be involved at each neuropathological stage of amyotrophic lateral Sclerosis. Two data samples, consisting of 130 diffusion tensor imaging data sets acquired at 1.5 T from 78 patients with amyotrophic lateral Sclerosis and 52 control subjects; and 55 diffusion-tensor imaging data sets at 3.0 T from 33 patients with amyotrophic lateral Sclerosis and 22 control subjects, were analysed by a tract of interest-based fibre tracking approach to analyse five tracts that become involved during the course of amyotrophic lateral Sclerosis: the corticospinal tract (stage 1); the corticorubral and the corticopontine tracts (stage 2); the corticostriatal pathway (stage 3); the proximal portion of the perforant path (stage 4); and two reference pathways. The statistical analyses of tracts of interest showed differences between patients with amyotrophic lateral Sclerosis and control subjects for all tracts. The significance level of the comparisons at the group level was lower, the higher the disease stage with corresponding involved fibre tracts. Both the clinical phenotype as assessed by the amyotrophic lateral Sclerosis functional rating scale-revised and disease duration correlated significantly with the resulting staging scheme. In summary, the tract of interest-based technique allowed for individual analysis of predefined tract structures, thus making it possible to image in vivo the disease stages in amyotrophic lateral Sclerosis. This approach can be used not only for individual clinical work-up purposes, but enlarges the spectrum of potential non-invasive surrogate markers as a neuroimaging-based read-out for amyotrophic lateral Sclerosis studies within a clinical context.
Corrado Cordova - One of the best experts on this subject based on the ideXlab platform.
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Signal-averaged electrocardiography and echocardiography in the evaluation of myocardial involvement in progressive systemic Sclerosis
International Journal of Cardiology, 1996Co-Authors: Maria Paradiso, Gabrielli F, L. Coppotelli, Giancarlo Aguglia, Mario Pergolini, Massimo Leonardo, Enrico Alcini, Carmelo Masala, Stefania Basili, Corrado CordovaAbstract:To assess the myocardial involvement in progressive systemic Sclerosis we evaluated the presence of late potentials by signal-averaged electrocardiography (signal-averaged ECG) and the left ventricular function by M-mode, two dimensional and Doppler echocardiography. Fifteen outpatients, 7 with diffuse progressive systemic Sclerosis and 8 with CREST syndrome variant, without clinical or electrocardiographic evidence of cardiac disease were studied and compared with 18 normal subjects. Late potentials occurred in 5 out of 15 progressive systemic Sclerosis patients (33%) with a significant difference versus controls (P < 0.05) and were present only in the patients with diffuse progressive systemic Sclerosis (P ≤ 0.001 vs. controls). All progressive systemic Sclerosis patients showed a normal left ventricular systolic function. Abnormal left ventricular filling was found in 9 progressive systemic Sclerosis patients (5 with diffuse progressive systemic Sclerosis and 4 with CREST). A more severe impairment of the mean values of diastolic function indexes was found in diffuse progressive systemic Sclerosis than in CREST. In all diffuse progressive systemic Sclerosis patients at least one method showed altered results, whereas half the CREST patients showed no pathological findings with both techniques. These results confirm a lower myocardial involvement in the CREST syndrome than in diffuse progressive systemic Sclerosis and consequently this is probably related to a better prognosis.
Hans Lassmann - One of the best experts on this subject based on the ideXlab platform.
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Multiple scler...
2013Co-Authors: Don Mahad, Hans Lassmann, Iryna Ziabreva, Douglas TurnbullAbstract:Multiple Sclerosis is a chronic inflammatory disease, which leads to focal plaques of demyelination and tissue injury in the CNS. The structural and immunopathological patterns of demyelination suggest that different immune mechanisms may be involved in tissue damage. In a subtype of lesions, which are mainly found in patients with acute fulminant multiple Sclerosis with Balo’s type concentric Sclerosis and in a subset of early relapsing remitting multiple Sclerosis, the initial myelin changes closely resemble those seen in white matter stroke (WMS), suggesting a hypoxia-like tissue injury. Since mitochondrial injury may be involved in the pathogenesis of such lesions, we analysed a number of mitochondrial respiratory chain proteins in active lesions from acute multiple Sclerosis and from WMS using immunohistochemistry. Functionally important defects of mitochondrial respiratory chain complex IV [cytochrome c oxidase (COX)] including its catalytic component (COX-I) are present in Pattern III but not in Pattern II multiple Sclerosis lesions.The lack of immunohistochemically detected COX-I is apparent in oligodendrocytes, hypertrophied astrocytes and axons, but not in microglia. The profile of immunohistochemically detected mitochondrial respiratory chain complex subunits differs between multiple Sclerosis and WMS. The findings suggest that hypoxia-like tissue injury in Pattern III multiple Sclerosis lesions may be due to mitochondrial impairment
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the relation between inflammation and neurodegeneration in multiple Sclerosis brains
Brain, 2009Co-Authors: Josa M Frischer, Per Soelberg Sørensen, Stephan Bramow, Assunta Dalbianco, Claudia F Lucchinetti, Helmut Rauschka, Manfred Schmidbauer, Henning Laursen, Hans LassmannAbstract:Some recent studies suggest that in progressive multiple Sclerosis, neurodegeneration may occur independently from inflammation. The aim of our study was to analyse the interdependence of inflammation, neurodegeneration and disease progression in various multiple Sclerosis stages in relation to lesional activity and clinical course, with a particular focus on progressive multiple Sclerosis. The study is based on detailed quantification of different inflammatory cells in relation to axonal injury in 67 multiple Sclerosis autopsies from different disease stages and 28 controls without neurological disease or brain lesions. We found that pronounced inflammation in the brain is not only present in acute and relapsing multiple Sclerosis but also in the secondary and primary progressive disease. T- and B-cell infiltrates correlated with the activity of demyelinating lesions, while plasma cell infiltrates were most pronounced in patients with secondary progressive multiple Sclerosis (SPMS) and primary progressive multiple Sclerosis (PPMS) and even persisted, when T- and B-cell infiltrates declined to levels seen in age matched controls. A highly significant association between inflammation and axonal injury was seen in the global multiple Sclerosis population as well as in progressive multiple Sclerosis alone. In older patients (median 76 years) with long-disease duration (median 372 months), inflammatory infiltrates declined to levels similar to those found in age-matched controls and the extent of axonal injury, too, was comparable with that in age-matched controls. Ongoing neurodegeneration in these patients, which exceeded the extent found in normal controls, could be attributed to confounding pathologies such as Alzheimer's or vascular disease. Our study suggests a close association between inflammation and neurodegeneration in all lesions and disease stages of multiple Sclerosis. It further indicates that the disease processes of multiple Sclerosis may die out in aged patients with long-standing disease.
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patterns of oligodendroglia pathology in multiple Sclerosis
Brain, 1994Co-Authors: K Ozawa, Gerda Suchanek, Helene Breitschopf, Wolfgang Bruck, Herbert Budka, K Jellinger, Hans LassmannAbstract:Patterns of inflammation, demyelination and oligodendrocyte pathology were studied in acute multiple Sclerosis and during early and late exacerbations of chronic multiple Sclerosis. Cells within lesions were identified by immunocytochemistry with markers for T lymphocytes, macrophages, oligodendro-cytes and astrocytes. In addition, in situ hybridization for proteolipid protein mRNA was used to identify myelinating and myelin supporting oligodendrocytes. Degenerating cells in the lesions were detected by DNA fragmentation in cell nuclei. The inflammatory reaction in all three types of multiple Sclerosis lesions was shown to be dominated by T lymphocytes and macrophages. In late chronic multiple Sclerosis lesions, a significant increase in the number of immunoglobulin producing plasma cells was found in infiltrates as compared with acute and early multiple Sclerosis lesions. In all three types of multiple Sclerosis, confluent plaques of demyelination were found to be present. In acute multiple Sclerosis, demyelination was found to be associated with extensive destruction of other tissue elements, including oligodendrocytes, astro-Acytes and axons, but even in these destructive lesions a considerable number of oligodendrocytes was preserved and at disposal therefore, for rapid remyelination. During early exacerbations of chronic multiple Sclerosis, selective demyelination was associated with almost complete preservation of oligodendrocytes in the majority of cases. Correspondingly, a high number of remyelinating lesions was present at that stage of disease. In lesions developing late after onset of multiple Sclerosis, demyelination generally accompanied extensive destruction and loss of oligodendrocytes. In these lesions, remyelination was sparse and restricted to lesional borders. The observed patterns of cell death suggest that in some cases oligodendrocytes, in others myelin sheaths are the primary target of the destructive process. Our data indicate that the type and amount of inflammation, de- and remyelination, and of tissue damage vary between different forms of multiple Sclerosis and between different stages of the disease, possibly reflecting different pathogenic mechanisms in a disease spectrum.
