Update upon efficacy and safety of TNF-α inhibitors

Murdaca, Giuseppe; Colombo, Barbara Maria; Cagnati, Paola; Gulli, Rossella; Spanò, Francesca; Puppo, Francesco

doi:10.1517/14740338.2012.630388

Cited by 61 publications

(54 citation statements)

References 25 publications

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“…TNF-a inhibitors have demonstrated efficacy in large, randomized controlled clinical trials either as monotherapy or in combination with DMARDs in the treatment of chronic immune-mediated or inflammatory diseases (Taylor, 2003;Chang and Girgis, 2007) and are effective in improving skin and joint inflammation and in retarding joint erosion in PsA patients (Chang and Girgis, 2007;Murdaca et al, 2009;Murdaca et al, 2011, Murdaca et al, 2012. As far as the potential influence of TNF-a gene polymorphisms in the therapeutic response to TNF-a inhibitors in PsA patients is concerned, Seitz et al (2007) reported an association with the SNP À 308 G/G genotype.…”

Section: Discussionmentioning

confidence: 99%

TNF-α Gene Polymorphisms: Association with Disease Susceptibility and Response to Anti-TNF-α Treatment in Psoriatic Arthritis

Murdaca

Gulli

Spanò

et al. 2014

Journal of Investigative Dermatology

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The tumor necrosis factor-α (TNF-α) gene has been proposed as a major candidate gene in psoriatic arthritis (PsA). TNF-α is a therapeutic target for patients responding poorly to conventional treatments. We investigated the role of single-nucleotide polymorphisms (SNPs) at positions -238, -308, and +489 of the TNF-α gene in the genetic susceptibility to PsA, in the severity of the disease, and, finally, in the response to TNF-α inhibitors (adalimumab, etanercept, or infliximab). Fifty-seven Caucasian PsA patients and 155 healthy matched controls were studied. The SNP +489 variant allele A was significantly associated with PsA susceptibility (P=0.0136) and severity of clinical (Psoriasis Area and Severity Index score, American College of Rheumatology criteria, Disease Activity Score 28, and Disability Index Health Assessment Questionnaire) and laboratory (C-reactive protein and erythrocyte sedimentation rate) parameters (P-values ranging from 0.016 to 2.908 × 10(-12)). The difference in severity was accounted for by the differences between the AA and GA genotypes with respect to the GG genotype. The SNP +489A allele shows a trend of association with the response to PsA treatment with etanercept. These findings suggest a role of the SNP +489A allele in the susceptibility and severity of PsA.

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Section: Discussionmentioning

confidence: 99%

TNF-α Gene Polymorphisms: Association with Disease Susceptibility and Response to Anti-TNF-α Treatment in Psoriatic Arthritis

Murdaca

Gulli

Spanò

et al. 2014

Journal of Investigative Dermatology

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“…There are now five TNF inhibitors available for the treatment of various immune-mediated and inflammatory diseases [9][10][11][12][13] : Infliximab (IFX), Adalimumab, and Golimumab are full-length monoclonal antibodies; Etanercept is a fusion protein of two TNFR2 receptor extracellular domains and the Fc fragment of human immunoglobulin 1 (IgG1); and Certolizumab is a humanized Fab fragment conjugated to polyethylene glycol. 14,15 While these drugs appear to have a similar efficacy, 14,16 the choice of one or another TNF inhibitor is personalized for each psoriatic patient. 17 It is important to note that TNF-α also acts as a potent inducer of ROS generation through impairment of mitochondrial biogenesis and activation of NADPH oxidase.…”

Section: Introductionmentioning

confidence: 99%

Altered redox status in the blood of psoriatic patients: involvement of NADPH oxidase and role of anti-TNF-α therapy

et al. 2013

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Background: Psoriasis is a chronic hyperproliferative inflammatory skin disease, characterized by a generalized redox imbalance. Anti-tumor necrosis factor (TNF)-α therapy is widely used for the treatment of this disease, but its effect on blood redox status hasn't been explored. Objective: To investigate the effects of anti-TNF-α therapy on blood redox status in psoriatic patients. Methods: Twenty-nine psoriatic patients (PSO) were divided into two groups: one remained untreated (NRT) and to another the anti-TNF-α therapy was prescribed (TR). The levels of main oxidative stress markers and total antioxidant capacity (TAC) in plasma, levels of total reactive oxygen species (ROS) production, lipoperoxidation, TAC, glutathione content, and activity of NADPH oxidase in white blood cells (WBC) were evaluated in PSO, in NTR and TR after 6 months of the study. Results: Plasma levels of malondialdehyde (MDA) and protein carbonyl content (PCO), ROS production, lipoperoxidation, and glutathione content in WBC were increased, while TAC in both plasma and WBC was decreased in PSO with respect to controls. In the plasma of TR, levels of MDA and PCO were significantly lower with respect to PSO and NTR. The activity of NADPH oxidase was significantly increased in WBC of PSO and NTR but not in TR versus controls. Discussion: Our results represent novel data about the redox status of WBC in psoriatic patients. A significant redox-balancing effect of anti-TNF-α therapy, probably associated with the normalization of NADPH oxidase activity in WBC, was demonstrated.

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“…After treatment with intravenous cyclophosphamide and concomitant oral prednisone, AVPc antibodies disappeared, CDI improved and vasopressin replacement therapy was completely withdrawn. Finally, TNF-α inhibitors appeared efficient in the treatment of chronic immune-mediated or inflammatory diseases, such as rheumatoid arthritis, ankylosing spondylitis, psoriasis and/or psoriatic arthritis (25)(26)(27)(28)(29)(30)(31). Which may be their potential effectiveness in treating autoimmune CDI, is a question that remains unanswered so far.…”

Section: Treatment Of Central Diabetes Insipidusmentioning

confidence: 99%

Autoimmune central diabetes insipidus in a patient with ureaplasma urealyticum infection and review on new triggers of immune response

Murdaca

Russo

Spanò

et al. 2015

Arch. Endocrinol. Metab.

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SUMMARYDiabetes insipidus is a disease in which large volumes of dilute urine (polyuria) are excreted due to vasopressin (AVP) deficiency [central diabetes insipidus (CDI)] or to AVP resistance (nephrogenic diabetes insipidus). In the majority of patients, the occurrence of CDI is related to the destruction or degeneration of neurons of the hypothalamic supraoptic and paraventricular nuclei. The most common and well recognized causes include local inflammatory or autoimmune diseases, vascular disorders, Langerhans cell histiocytosis (LCH), sarcoidosis, tumors such as germinoma/craniopharyngioma or metastases, traumatic brain injuries, intracranial surgery, and midline cerebral and cranial malformations. Here we have the opportunity to describe an unusual case of female patient who developed autoimmune CDI following ureaplasma urealyticum infection and to review the literature on this uncommon feature. Moreover, we also discussed the potential mechanisms by which ureaplasma urealyticum might favor the development of autoimmune CDI. Arch Endocrinol Metab. 2015;59(6):554-8

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Update upon efficacy and safety of TNF-α inhibitors

Cited by 61 publications

References 25 publications

TNF-α Gene Polymorphisms: Association with Disease Susceptibility and Response to Anti-TNF-α Treatment in Psoriatic Arthritis

TNF-α Gene Polymorphisms: Association with Disease Susceptibility and Response to Anti-TNF-α Treatment in Psoriatic Arthritis

Altered redox status in the blood of psoriatic patients: involvement of NADPH oxidase and role of anti-TNF-α therapy

Autoimmune central diabetes insipidus in a patient with ureaplasma urealyticum infection and review on new triggers of immune response

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