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1.
Rheumatology (Oxford) ; 60(6): 2896-2905, 2021 06 18.
Article in English | MEDLINE | ID: mdl-33274366

ABSTRACT

OBJECTIVE: To build a prediction model for uveitis in children with JIA for use in current clinical practice. METHODS: Data from the international observational Pharmachild registry were used. Adjusted risk factors as well as predictors for JIA-associated uveitis (JIA-U) were determined using multivariable logistic regression models. The prediction model was selected based on the Akaike information criterion. Bootstrap resampling was used to adjust the final prediction model for optimism. RESULTS: JIA-U occurred in 1102 of 5529 JIA patients (19.9%). The majority of patients that developed JIA-U were female (74.1%), ANA positive (66.0%) and had oligoarthritis (59.9%). JIA-U was rarely seen in patients with systemic arthritis (0.5%) and RF positive polyarthritis (0.2%). Independent risk factors for JIA-U were ANA positivity [odds ratio (OR): 1.88 (95% CI: 1.54, 2.30)] and HLA-B27 positivity [OR: 1.48 (95% CI: 1.12, 1.95)] while older age at JIA onset was an independent protective factor [OR: 0.84 (9%% CI: 0.81, 0.87)]. On multivariable analysis, the combination of age at JIA onset [OR: 0.84 (95% CI: 0.82, 0.86)], JIA category and ANA positivity [OR: 2.02 (95% CI: 1.73, 2.36)] had the highest discriminative power among the prediction models considered (optimism-adjusted area under the receiver operating characteristic curve = 0.75). CONCLUSION: We developed an easy to read model for individual patients with JIA to inform patients/parents on the probability of developing uveitis.


Subject(s)
Arthritis, Juvenile/complications , Clinical Decision Rules , Uveitis/diagnosis , Uveitis/etiology , Child , Child, Preschool , Female , Humans , Male , Predictive Value of Tests , Risk Factors
2.
Medicine (Baltimore) ; 94(29): e1183, 2015 Jul.
Article in English | MEDLINE | ID: mdl-26200625

ABSTRACT

This article estimates the frequency of cardiovascular (CV) events that occurred after diagnosis in a large Spanish cohort of patients with systemic lupus erythematosus (SLE) and investigates the main risk factors for atherosclerosis. RELESSER is a nationwide multicenter, hospital-based registry of SLE patients. This is a cross-sectional study. Demographic and clinical variables, the presence of traditional risk factors, and CV events were collected. A CV event was defined as a myocardial infarction, angina, stroke, and/or peripheral artery disease. Multiple logistic regression analysis was performed to investigate the possible risk factors for atherosclerosis. From 2011 to 2012, 3658 SLE patients were enrolled. Of these, 374 (10.9%) patients suffered at least a CV event. In 269 (7.4%) patients, the CV events occurred after SLE diagnosis (86.2% women, median [interquartile range] age 54.9 years [43.2-66.1], and SLE duration of 212.0 months [120.8-289.0]). Strokes (5.7%) were the most frequent CV event, followed by ischemic heart disease (3.8%) and peripheral artery disease (2.2%). Multivariate analysis identified age (odds ratio [95% confidence interval], 1.03 [1.02-1.04]), hypertension (1.71 [1.20-2.44]), smoking (1.48 [1.06-2.07]), diabetes (2.2 [1.32-3.74]), dyslipidemia (2.18 [1.54-3.09]), neurolupus (2.42 [1.56-3.75]), valvulopathy (2.44 [1.34-4.26]), serositis (1.54 [1.09-2.18]), antiphospholipid antibodies (1.57 [1.13-2.17]), low complement (1.81 [1.12-2.93]), and azathioprine (1.47 [1.04-2.07]) as risk factors for CV events. We have confirmed that SLE patients suffer a high prevalence of premature CV disease. Both traditional and nontraditional risk factors contribute to this higher prevalence. Although it needs to be verified with future studies, our study also shows-for the first time-an association between diabetes and CV events in SLE patients.


Subject(s)
Cardiovascular Diseases/complications , Lupus Erythematosus, Systemic/complications , Registries/statistics & numerical data , Adult , Age Factors , Aged , Atherosclerosis/complications , Comorbidity , Cross-Sectional Studies , Female , Humans , Male , Middle Aged , Risk Factors , Sex Factors , Smoking/epidemiology , Socioeconomic Factors , Spain , White People
3.
Reumatol. clín. (Barc.) ; 8(5): 263-269, sept.-oct. 2012.
Article in Spanish | IBECS | ID: ibc-103727

ABSTRACT

Glucocorticoides, aspirina, antipalúdicos e inmunosupresores convencionales constituyen la base del tratamiento del lupus eritematoso sistémico (LES). Hasta recientemente, los 3 primeros eran los únicos agentes aprobados para su tratamiento. El mejor conocimiento de la fisiopatología del sistema inmunitario ha permitido identificar nuevas dianas terapéuticas. De hecho, belimumab, un anticuerpo monoclonal humano inhibidor de BLyS, se ha convertido hace pocos meses en el primer fármaco aprobado para el tratamiento del LES desde 1957, lo que subraya las dificultades de todo tipo, incluyendo las económicas y organizativas, inherentes a los ensayos clínicos sobre esta enfermedad. Otras muchas moléculas se encuentran en distintas fases de desarrollo y en poco tiempo dispondremos de resultados concretos. En esta revisión repasamos el mecanismo de acción y los datos clínicos más relevantes de estas moléculas (AU)


Glucocorticoids, aspirin, conventional antimalarials and immunosuppressants are the mainstay of treatment of Systemic Lupus Erythematosus (SLE). Until recently, the first three were the only agents approved for treatment. A better understanding of the pathophysiology of the immune system has identified new therapeutic targets. In fact, belimumab, a human monoclonal antibody to BLyS inhibitor has become, in recent months, the first drug approved for the treatment of SLE since 1957, underscoring difficulties of all kinds, including economic and organizational ones inherent to clinical trials on this disease. Many other molecules are in various stages of development and soon will have concrete results. In this review, we examined the mechanism of action and most relevant clinical data for these molecules (AU)


Subject(s)
Humans , Male , Female , Lupus Erythematosus, Systemic/therapy , Biological Therapy/instrumentation , Biological Therapy/methods , Glucocorticoids/therapeutic use , Antimalarials/therapeutic use , Immunosuppressive Agents/therapeutic use , CD28 Antigens , CD28 Antigens/physiology , T-Lymphocytes/enzymology , Lupus Erythematosus, Systemic/epidemiology , Lupus Erythematosus, Systemic/prevention & control , Biological Therapy/trends , Biological Therapy , Cell Adhesion Molecules , Cell Adhesion Molecules
4.
Reumatol. clín. (Barc.) ; 8(4): 201-207, jul.-ago. 2012. ilus
Article in Spanish | IBECS | ID: ibc-100769

ABSTRACT

Glucocorticoides, aspirina, antipalúdicos e inmunosupresores convencionales constituyen la base del tratamiento del lupus eritematoso sistémico (LES). Hasta recientemente, los 3 primeros eran los únicos agentes aprobados para su tratamiento. El mejor conocimiento de la fisiopatología del sistema inmunitario ha permitido identificar nuevas dianas terapéuticas. De hecho, belimumab, un anticuerpo monoclonal humano inhibidor de BLyS, se ha convertido hace pocos meses en el primer fármaco aprobado para el tratamiento del LES desde 1957, lo que subraya las dificultades de todo tipo, incluyendo las económicas y organizativas, inherentes a los ensayos clínicos sobre esta enfermedad. Otras muchas moléculas se encuentran en distintas fases de desarrollo y en poco tiempo dispondremos de resultados concretos. En esta revisión repasamos el mecanismo de acción y los datos clínicos más relevantes de estas moléculas (AU)


Glucocorticoids, aspirin, antimalarials and conventional immunosuppressants are the mainstay of treatment of Systemic Lupus Erythematosus (SLE). Until recently, the first three were the only agents approved for treatment. A better understanding of the pathophysiology of the immune system has identified new therapeutic targets. In fact, belimumab, a human monoclonal antibody to BLyS inhibitor has become, in recent months, the first drug approved for the treatment of SLE since 1957, underscoring difficulties of all kinds, including economic and organizational ones inherent to clinical trials on this disease. Many other molecules are in various stages of development and soon will have concrete results. In this review, we examined the mechanism of action and most relevant clinical data for these molecules (AU)


Subject(s)
Humans , Male , Female , Lupus Erythematosus, Systemic/therapy , Biological Therapy , Lupus Erythematosus, Systemic/pathology , Drug Delivery Systems/methods , Drug Delivery Systems , Antibodies, Monoclonal/therapeutic use , Biological Therapy/methods , Biological Therapy/trends , Immune System/physiopathology , Interferons/therapeutic use , Receptors, Interferon/therapeutic use
5.
Reumatol Clin ; 8(4): 201-7, 2012.
Article in English, Spanish | MEDLINE | ID: mdl-22483661

ABSTRACT

Glucocorticoids, aspirin, antimalarials and conventional immunosuppressants are the mainstay of treatment of Systemic Lupus Erythematosus (SLE). Until recently, the first three were the only agents approved for treatment. A better understanding of the pathophysiology of the immune system has identified new therapeutic targets. In fact, belimumab, a human monoclonal antibody to BLyS inhibitor has become, in recent months, the first drug approved for the treatment of SLE since 1957, underscoring difficulties of all kinds, including economic and organizational ones inherent to clinical trials on this disease. Many other molecules are in various stages of development and soon will have concrete results. In this review, we examined the mechanism of action and most relevant clinical data for these molecules.


Subject(s)
Lupus Erythematosus, Systemic/drug therapy , Molecular Targeted Therapy , Antibodies, Monoclonal/pharmacology , Antibodies, Monoclonal/therapeutic use , Apoptosis/immunology , Autoimmunity , Clinical Trials as Topic , Complement Inactivating Agents/therapeutic use , Drugs, Investigational/therapeutic use , Humans , Immune Tolerance/drug effects , Inflammation , Interferons/antagonists & inhibitors , Lupus Erythematosus, Systemic/immunology , Lupus Erythematosus, Systemic/physiopathology , Lymphocyte Depletion , Protein Kinase Inhibitors/pharmacology , Protein Kinase Inhibitors/therapeutic use , Recombinant Fusion Proteins/pharmacology , Recombinant Fusion Proteins/therapeutic use , Signal Transduction/drug effects , Therapies, Investigational , Toll-Like Receptors/antagonists & inhibitors
6.
Reumatol Clin ; 8(5): 263-9, 2012.
Article in English | MEDLINE | ID: mdl-22483664

ABSTRACT

Glucocorticoids, aspirin, conventional antimalarials and immunosuppressants are the mainstay of treatment of Systemic Lupus Erythematosus (SLE). Until recently, the first three were the only agents approved for treatment. A better understanding of the pathophysiology of the immune system has identified new therapeutic targets. In fact, belimumab, a human monoclonal antibody to BLyS inhibitor has become, in recent months, the first drug approved for the treatment of SLE since 1957, underscoring difficulties of all kinds, including economic and organizational ones inherent to clinical trials on this disease. Many other molecules are in various stages of development and soon will have concrete results. In this review, we examined the mechanism of action and most relevant clinical data for these molecules.


Subject(s)
Antibodies, Monoclonal/therapeutic use , Immunosuppressive Agents/therapeutic use , Lupus Erythematosus, Systemic/drug therapy , Molecular Targeted Therapy , Recombinant Fusion Proteins/therapeutic use , Antibodies, Monoclonal/pharmacology , Antibody Formation/drug effects , Apoptosis/drug effects , B-Cell Activating Factor/antagonists & inhibitors , B-Cell Activating Factor/immunology , B-Lymphocytes/drug effects , B-Lymphocytes/pathology , Cell Adhesion Molecules/antagonists & inhibitors , Clinical Trials as Topic , Cytokines/antagonists & inhibitors , Humans , Immunosuppressive Agents/pharmacology , Intracellular Signaling Peptides and Proteins/antagonists & inhibitors , Lupus Erythematosus, Systemic/immunology , Lupus Erythematosus, Systemic/metabolism , Lymphocyte Activation/drug effects , Lymphocyte Cooperation/drug effects , Lymphopoiesis/drug effects , Protease Inhibitors/pharmacology , Protease Inhibitors/therapeutic use , Proteasome Endopeptidase Complex/drug effects , Receptors, Immunologic/antagonists & inhibitors , Recombinant Fusion Proteins/pharmacology , T-Lymphocytes/immunology , Transcription Factors/antagonists & inhibitors , Tumor Necrosis Factor Ligand Superfamily Member 13/antagonists & inhibitors , Tumor Necrosis Factor Ligand Superfamily Member 13/immunology
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