1,721,044 research outputs found
Efficacy and safety of duloxetine in fibromyalgia
No full textFibromyalgia is a chronic disorder of uncertain aetiology, more common in women than in man, characterized by widespread pain, muscle tenderness and decreased pain threshold to pressure and other stimuli. The pathophysiology of fibromyalgia is still unknown, but some evidences suggest that abnormalities in central monoaminergic transmission might play an important role. These abnormalities include dysfunction in both serotonin (5-HT) and norepinephrine (NE) systems. In addition, fibromyalgia frequently presents in comorbidity with depression and anxiety disorders. On these basis antidepressants are the most widely studied drugs and, probably the most effective therapy of fibromyalgia. Until now amitriptyline, a tricyclic antidepressant, was considered the most effective, with some evidence of efficacy for other antidepressant such as the SSRI fluoxetine and sertraline. Here we review the efficacy and safety of duloxetine, a SNRI antidepressant, in the management of fibromyalgia
Infliximab and insulin resistance
No full textInsulin resistance is the most important pathophysiologic feature of obesity, type 2 diabetes mellitus and prediabetic states. TNF-α, a proinflammatory cytokine, plays a pivotal role in the pathogenesis of inflammation-associated insulin resistance during the course of rheumatic diseases. Therapies aimed at neutralizing TNF-α, such as the monoclonal antibody infliximab, represent a novel approach for the treatment of rheumatic diseases and allow to obtain significant results in terms of control of the inflammatory process. In this article we reviewed the scientific evidence published in the literature about a potential role of TNF-α blockade in improving insulin resistance in non-diabetic rheumatic patients. © 2009 Elsevier B.V. All rights reserved.Insulin resistance is the most important pathophysiologic feature of obesity, type 2 diabetes mellitus and prediabetic states. TNF-alpha, a proinflammatory cytokine, plays a pivotal role in the pathogenesis of inflammation-associated insulin resistance during the course of rheumatic diseases. Therapies aimed at neutralizing TNF-alpha, such as the monoclonal antibody infliximab, represent a novel approach for the treatment of rheumatic diseases and allow to obtain significant results in terms of control of the inflammatory process. In this article we reviewed the scientific evidence published in the literature about a potential role of TNF-alpha blockade in improving insulin resistance in non-diabetic rheumatic patients. (C) 2010 Elsevier B.V. All rights reserved
Serum complement C3 correlates with insulin resistance in never treated psoriatic arthritis patients
No full textThe objective of this cross-sectional study is to investigate the relationship between inflammatory markers (C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), white blood cell (WBC) count, and complement C3) and insulin resistance (estimated with the surrogate measure homeostasis model assessment of insulin resistance (HOMA-IR)) in Psoriatic arthritis (PsA) patients. Sixty-seven patients with PsA and 138 age- and sex-matched controls were recruited from the Rheumatology Outpatient Clinic of the University of Catanzaro, Catanzaro (Italy). Plasma glucose, insulin, triglycerides, total cholesterol, LDL cholesterol, and high-density lipoprotein (HDL) cholesterol were measured after at least 12-h fasting. CRP was measured by a high-sensitivity turbidimetric immunoassay. ESR was measured by capillary photometry. Serum C3 and C4 were measured by nephelometry. Insulin resistance was estimated using the original HOMA as reported by Matthews et al. (Diabetologia 28(7):412–419, 1985) from overnight fasting insulin and glucose values, with the following formula: HOMA-IR = glucose (in milligrams per deciliter) × insulin (in micro units per milliliter)/405. Patients and controls had similar body mass index (BMI), blood pressure, and fasting glucose, but fasting serum insulin was higher in PsA patients (median (interquartile range (IQR)) 12.96 (6.35–24.65) for PsA and 10.37 (6.97–15.11) for controls; p = 0.005). Consequently, also the surrogate measure of insulin resistance HOMA-IR was significantly higher in patients (median (IQR) 3.77 (1.58–5.18) for PsA and 2.33 (1.67–3.62) for controls; p = 0.008). In univariate analysis, ln(HOMA-IR) correlated positively with BMI, systolic blood pressure (sBP), dBP, ln(TG), WBC, ln(ESR), ln(CRP) and C3, while correlated negatively with total and HDL cholesterol. In multiple linear regression analysis including age, sex and BMI, serum C3 reached the higher standardized β coefficient, while among other variables only ln(ESR) maintained a weak correlation with ln(HOMA-IR) when sBP was added to the model. When all variables were inserted in a single model, only C3 was independently correlated with ln(HOMA-IR). In a stepwise multiple regression model, serum C3 was selected as the strongest single contributing variable. The model explained 61 % of the variance in ln(HOMA-IR) (R2 = 0.61). Insulin resistance, estimated with the surrogate measure HOMA-IR, is higher in PsA patients compared to age- and sex-matched controls. Serum C3 could represent a simple marker of insulin resistance in psoriatic arthritis patients. © 2013, Clinical Rheumatology.The objective of this cross-sectional study is to investigate the relationship between inflammatory markers (C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), white blood cell (WBC) count, and complement C3) and insulin resistance (estimated with the surrogate measure homeostasis model assessment of insulin resistance (HOMA-IR)) in Psoriatic arthritis (PsA) patients. Sixty-seven patients with PsA and 138 age- and sex-matched controls were recruited from the Rheumatology Outpatient Clinic of the University of Catanzaro, Catanzaro (Italy). Plasma glucose, insulin, triglycerides, total cholesterol, LDL cholesterol, and high-density lipoprotein (HDL) cholesterol were measured after at least 12-h fasting. CRP was measured by a high-sensitivity turbidimetric immunoassay. ESR was measured by capillary photometry. Serum C3 and C4 were measured by nephelometry. Insulin resistance was estimated using the original HOMA as reported by Matthews et al. (Diabetologia 28(7):412–419, 1985) from overnight fasting insulin and glucose values, with the following formula: HOMA-IR = glucose (in milligrams per deciliter) × insulin (in micro units per milliliter)/405. Patients and controls had similar body mass index (BMI), blood pressure, and fasting glucose, but fasting serum insulin was higher in PsA patients (median (interquartile range (IQR)) 12.96 (6.35–24.65) for PsA and 10.37 (6.97–15.11) for controls; p = 0.005). Consequently, also the surrogate measure of insulin resistance HOMA-IR was significantly higher in patients (median (IQR) 3.77 (1.58–5.18) for PsA and 2.33 (1.67–3.62) for controls; p = 0.008). In univariate analysis, ln(HOMA-IR) correlated positively with BMI, systolic blood pressure (sBP), dBP, ln(TG), WBC, ln(ESR), ln(CRP) and C3, while correlated negatively with total and HDL cholesterol. In multiple linear regression analysis including age, sex and BMI, serum C3 reached the higher standardized β coefficient, while among other variables only ln(ESR) maintained a weak correlation with ln(HOMA-IR) when sBP was added to the model. When all variables were inserted in a single model, only C3 was independently correlated with ln(HOMA-IR). In a stepwise multiple regression model, serum C3 was selected as the strongest single contributing variable. The model explained 61 % of the variance in ln(HOMA-IR) (R2 = 0.61). Insulin resistance, estimated with the surrogate measure HOMA-IR, is higher in PsA patients compared to age- and sex-matched controls. Serum C3 could represent a simple marker of insulin resistance in psoriatic arthritis patients
Fibromyalgia and obesity: the hidden link
No full textFibromyalgia is a chronic disorder of uncertain etiology, characterized by widespread pain, muscle tenderness, and decreased pain threshold to pressure and other stimuli. Obesity is a well-known aggravating factor for certain rheumatologic conditions, such as knee osteoarthritis. Emerging evidences are exploring the link between obesity and other rheumatic diseases, such as fibromyalgia. Epidemiological data show that fibromyalgia patients have higher prevalence of obesity (40%) and overweight (30%) in multiple studies compared with healthy patients. Several mechanisms have been proposed to explain "the hidden link", but at this time is not possible to ascertain whether obesity is cause or consequence of fibromyalgia. Among mechanisms proposed, there are the following: impaired physical activity, cognitive and sleep disturbances, psychiatric comorbidity and depression, dysfunction of thyroid gland, dysfunction of the GH/IGF-1 axis, impairment of the endogenous opioid system. In this article, we review the scientific evidence supporting a possible link between obesity and fibromyalgia, how obesity influences fibromyalgia symptoms and how fibromyalgia severity can be improved by weight loss. In addition, we analyze the possible mechanisms by which fibromyalgia and obesity interrelate. © 2011 Springer-Verlag.Fibromyalgia is a chronic disorder of uncertain etiology, characterized by widespread pain, muscle tenderness, and decreased pain threshold to pressure and other stimuli. Obesity is a well-known aggravating factor for certain rheumatologic conditions, such as knee osteoarthritis. Emerging evidences are exploring the link between obesity and other rheumatic diseases, such as fibromyalgia. Epidemiological data show that fibromyalgia patients have higher prevalence of obesity (40%) and overweight (30%) in multiple studies compared with healthy patients. Several mechanisms have been proposed to explain "the hidden link", but at this time is not possible to ascertain whether obesity is cause or consequence of fibromyalgia. Among mechanisms proposed, there are the following: impaired physical activity, cognitive and sleep disturbances, psychiatric comorbidity and depression, dysfunction of thyroid gland, dysfunction of the GH/IGF-1 axis, impairment of the endogenous opioid system. In this article, we review the scientific evidence supporting a possible link between obesity and fibromyalgia, how obesity influences fibromyalgia symptoms and how fibromyalgia severity can be improved by weight loss. In addition, we analyze the possible mechanisms by which fibromyalgia and obesity interrelate
Improvement in insulin resistance after short-term treatment with abatacept: Case report and short review
No full textInsulin resistance, a key feature of type 2 diabetes, is an independent risk factor for developing cardiovascular diseases (CVD), and represents the core of metabolic syndrome (MetS). Actually, an intriguing correlation between MetS and inflammation associated with rheumatoid arthritis (RA) is largely accepted but not yet completely clarified in detail. Recently, the therapeutic arsenal against RA has been enriched of abatacept, a fusion protein (CTLA4 immunoglobulin) designed to modulate the T cell co-stimulatory signal mediated through the CD28-CD80/86 pathway. Here, we report a case of dramatic improvement in insulin resistance, estimated with the surrogate measure HOMA-IR, after treatment with abatacept. Lastly, we shortly review the preclinical evidences supporting a possible role of T lymphocytes in rheumatoid arthritis-associated insulin resistance and how abatacept could improve glucose metabolism by suppressing adipose tissue infiltrating cells. © Clinical Rheumatology 2012.Insulin resistance, a key feature of type 2 diabetes, is an independent risk factor for developing cardiovascular diseases (CVD), and represents the core of metabolic syndrome (MetS). Actually, an intriguing correlation between MetS and inflammation associated with rheumatoid arthritis (RA) is largely accepted but not yet completely clarified in detail. Recently, the therapeutic arsenal against RA has been enriched of abatacept, a fusion protein (CTLA4 immunoglobulin) designed to modulate the T cell co-stimulatory signal mediated through the CD28-CD80/86 pathway. Here, we report a case of dramatic improvement in insulin resistance, estimated with the surrogate measure HOMA-IR, after treatment with abatacept. Lastly, we shortly review the preclinical evidences supporting a possible role of T lymphocytes in rheumatoid arthritis-associated insulin resistance and how abatacept could improve glucose metabolism by suppressing adipose tissue infiltrating cells
Sudden progression from impaired glucose tolerance to type 2 diabetes after discontinuation of administration of anti-tumor necrosis factor-alpha antibody infliximab
No full textWe present the case of a 45-year-old man with psoriasis and psoriatic arthritis and concomitant impaired fasting glucose (IFG) and impaired glucose tolerance (IGT). In this patient, refractory to DMARD's, infliximab was started to control the arthritis. After achieving clinical remission of the disease, infliximab was discontinued and a 75 g- oral glucose tolerance test (OGTT) was performed. After the test, we observed a conversion from IFG/IGT glucose tolerance status to type 2 diabetes. No diet, lifestyle or therapy modifications were made during the observation period. Autoimmune diabetes was ruled out by serum antibodies determination and body weight remained constant, sustaining a protective role of infliximab in the worsening of glucose tolerance. Copyright © by BIOLIFE, s.a.s
To supplement or not to supplement? The rationale of vitamin D supplementation in systemic lupus erythematosus
No full textBackground: Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease characterised by abnormal activation of the immune system, chronic inflammation and organ damage. Lupus patients are more prone to be vitamin D deficient. However, current evidence is not conclusive with regards to the role played by vitamin D in SLE development, progression, and clinical manifestations. Objective: Here, we will summarise the current knowledge about vitamin D deficiency prevalence, risk factors, molecular effects, and potential pathogenic role in SLE. We will focus on the link between vitamin D deficiency and lupus clinical manifestations, and on the clinical trials assessing the effects of vitamin D supplementation in SLE. Method: A detailed literature search was performed exploiting the available databases, using “vitamin D and lupus/SLE” as keywords. The relevant interventional trials published over the last decade have been considered and the results are reported here. Conclusion: Several immune cells express vitamin D receptors. Thus, an immunomodulatory role for vitamin D in lupus is plausible. Numerous observational studies have investigated the relationship between vitamin D levels and clinical/serological manifestations of SLE with contrasting results. Negative correlations between vitamin D levels and disease activity, fatigue, renal and cardiovascular disease, and anti-dsDNA titres have been described but not conclusively accepted. In experimental models of lupus, vitamin D supplementation can improve the disease. Interventional trials have assessed the potential therapeutic value of vitamin D in SLE, but further larger studies are needed
Kaposi's sarcoma in a psoriatic arthritis patient treated with infliximab
No full textKaposi's sarcoma in a psoriatic arthritis patient treated with inflixima
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