scholarly journals The role of TNF-α and TNF-β gene polymorphism in the pathogenesis of Rheumatoid Arthritis

2013 ◽  
Vol 4 (1) ◽  
pp. 29-53
Author(s):  
Hannan Al- Rayes ◽  
Misbahul Arfin ◽  
Mohammad Tariq ◽  
Abdulrahman Al-Asmari

Rheumatoid arthritis (RA) is a chronic systemic inflammatory disorder of unknown etiology that affects the synovial membrane of multiple joints. The clinical presentation of RA may vary from mild to severe with excessive erosions of periarticular bone leading to the loss of functional capacity. Both genetic and environmental factors are important in the development of this disorder. The genetic contribution to susceptibility for RA is underlined by a three-to four-fold higher concordance percentage for clinically expressed disease in monozygotic twins compared to dizygotic twins. The severity and long term outcome of RA have also been related to various genetic factors. Tumor necrosis factor (TNF), a pro-inflammatory cytokine, is involved in the pathogenesis of a variety of autoimmune disorders, including RA. A large number of studies have been undertaken to determine the role of TNF-α promoter polymorphisms in the pathogenesis of RA. On the other hand few attempts have been made to identify the association between TNF-α (lymphotoxin-alfa) polymorphism and RA. In this narrative review of published literature, an attempt has been made to determine the association between TNF-α promoter polymorphisms at positions –308, –238, –489, –857, –863 and TNF-β at +252 with respect to susceptibility to and severity of RA, as well as response to drug therapy. In spite of intra-and inter-ethnic variations, analysis of data suggests a significant role of TNF-α/TNF-β polymorphisms in determining the susceptibility/severity of RA and responsiveness to anti-TNF drug therapy. The TNF gene polymorphisms may be an interesting target for novel strategies to prevent RA and/or in its early treatment. Further studies using larger samples are needed to pinpoint the regulatory polymorphisms or haplotypes and their effects on the development of certain manifestations in RA.

2013 ◽  
Vol 4 (1) ◽  
pp. 29
Author(s):  
Hannan Al- Rayes ◽  
Misbahul Arfin ◽  
Mohammad Tariq ◽  
Abdulrahman Al-Asmari

Rheumatoid arthritis (RA) is a chronic systemic inflammatory disorder of unknown etiology that affects the synovial membrane of multiple joints. The clinical presentation of RA may vary from mild to severe with excessive erosions of periarticular bone leading to the loss of functional capacity. Both genetic and environmental factors are important in the development of this disorder. The genetic contribution to susceptibility for RA is underlined by a three-to four-fold higher concordance percentage for clinically expressed disease in monozygotic twins compared to dizygotic twins. The severity and long term outcome of RA have also been related to various genetic factors. Tumor necrosis factor (TNF), a pro-inflammatory cytokine, is involved in the pathogenesis of a variety of autoimmune disorders, including RA. A large number of studies have been undertaken to determine the role of TNF-α promoter polymorphisms in the pathogenesis of RA. On the other hand few attempts have been made to identify the association between TNF-α (lymphotoxin-alfa) polymorphism and RA. In this narrative review of published literature, an attempt has been made to determine the association between TNF-α promoter polymorphisms at positions –308, –238, –489, –857, –863 and TNF-β at +252 with respect to susceptibility to and severity of RA, as well as response to drug therapy. In spite of intra-and inter-ethnic variations, analysis of data suggests a significant role of TNF-α/TNF-β polymorphisms in determining the susceptibility/severity of RA and responsiveness to anti-TNF drug therapy. The TNF gene polymorphisms may be an interesting target for novel strategies to prevent RA and/or in its early treatment. Further studies using larger samples are needed to pinpoint the regulatory polymorphisms or haplotypes and their effects on the development of certain manifestations in RA.


The Lancet ◽  
1987 ◽  
Vol 329 (8542) ◽  
pp. 1108-1111 ◽  
Author(s):  
D.L. Scott ◽  
B.L. Coulton ◽  
D.P.M. Symmons ◽  
A.J. Popert

1985 ◽  
Vol 66 (4) ◽  
pp. 318-318
Author(s):  
L. V. Chernetsova ◽  
A. G. Ibragimova

The comparative analysis of treatment of 76 patients with rheumatoid arthritis using electromagnetic waves of the decimeter range and lithium electrophoresis, depending on the activity of the process and the type of drug therapy.


2016 ◽  
Vol 51 (4) ◽  
pp. 305-314
Author(s):  
Beata Polińska ◽  
Joanna Matowicka-Karna ◽  
Halina Kemona

Rheumatoid arthritis (RA) is a chronic, autoimmune connective tissue disease of unknown etiology. RA affects about 1% of the human population, women suffer three times more often than men, with the peak incidence between the age of 40 to 50. The up-to-date criteria from 2010 for the diagnosis of RA include: occurrence and duration of clinical signs, indicators of inflammation and serological tests. Neopterin, a protein released by macrophages, is a sensitive indicator of inflammation and the severity of RA. Regarding the serological tests, anti-cyclic citrullinated peptide antibodies represent a well-known marker with the specificity for RA of about 98%. The antibodies may be present in the serum of patients even a few years before the first clinical signs of the disease, heralding erosive changes in the joints and more severe course of RA. The literature also contains reports about autoantibodies anti-CarP and anti-Sa/ anti-MCV, which may occur in people with pain and swelling of joints and precede full-blown development of RA as well as reflect disease activity. Serological diagnosis of RA may be supported by some genetic tests based on PCR for detecting mutations e.g. C1858T in the PNPN22 gene. In turn, the quantitative analysis of different classes of miRNAs seems justified in order to better classify patients showing symptoms of RA. Further studies are needed that take into account the role of different markers in the development of RA, and confirm the high sensitivity and specificity of these markers in the diagnosis of the disease.


2002 ◽  
Vol 10 (4) ◽  
pp. 385-388 ◽  
Author(s):  
Richard Keuneman ◽  
Rajiv Weerasundera ◽  
David Castle

Objective: To review the place of electroconvulsive therapy (ECT) in the treatment of schizophrenia. Conclusions: ECT is as effective, if not more so, than the antipsychotic drugs in certain clinical settings. It can be rapidly effective in acute episodes. When used alone, antipsychotics have comparable or superior efficacy to ECT alone in the short term. However, ECT possibly confers better long-term outcome. Combination treatment with antipsychotic medications and ECT is superior to either treatment alone, and is safe and effective, notably in medication resistant schizophrenia. Benefits of acute courses of ECT may be short-lived unless maintenance ECT is instituted, although there are limited data on the subject. Clinically, patients with acute onset, shorter episodes are more likely to respond to ECT. Catatonia, preoccupation with delusions and hallucinations, and a relative absence of premorbid schizoid and paranoid personality traits, are other clinical factors less strongly predictive of positive response. The presence of affective symptoms is often thought to be predictive of clinical response. However, there is little research evidence for this. While medications remain the mainstay of treatment in schizophrenia, ECT does have a clear and increasingly recognised role which requires further evaluation.


2013 ◽  
Vol 04 (10) ◽  
pp. 937-940 ◽  
Author(s):  
Ramanjaneya V. R. Mula ◽  
Rangaiah Shashidharamurthy
Keyword(s):  

2008 ◽  
Vol 75 (2) ◽  
pp. 163-166 ◽  
Author(s):  
Klemmens Trieb ◽  
Maximillian Schmid ◽  
Thomas Stulnig ◽  
Wolfgang Huber ◽  
Axel Wanivenhaus

2015 ◽  
Vol 122 (5) ◽  
pp. 1087-1095 ◽  
Author(s):  
Raman Mohan Sharma ◽  
Nupur Pruthi ◽  
Arivazhagan Arimappamagan ◽  
Sampath Somanna ◽  
Bhagavathula Indira Devi ◽  
...  

OBJECT Hydrocephalus is one of the commonest complications of tubercular meningitis (TBM), and its incidence is increasing with the HIV epidemic. Literature evaluating the role of ventriculoperitoneal shunts in HIV-positive patients with TBM and their long-term prognosis is scarce. METHODS Between June 2002 and October 2012, 30 HIV-positive patients with TBM and hydrocephalus underwent ventriculoperitoneal shunt placement. Thirty age-, sex-, and grade-matched HIV-negative patients with TBM and hydrocephalus were randomly selected as the control group. Outcome was analyzed at discharge (short-term outcome) and at follow-up (long-term outcome). Univariate and multivariate analyses were performed to look for predictors of outcome; p < 0.05 was considered significant. RESULTS There were no differences in the clinical, radiological, or biochemical parameters between the 2 groups. Short-term outcome was better in the HIV-negative group (76.7% improvement) than in the HIV-positive group (70%). However, the long-term outcome in HIV-positive patients was very poor (66.7% mortality and 76.2% poor outcome) compared with HIV-negative patients (30.8% mortality and 34.6% poor outcome). Seropositivity for HIV is an independent predictor of poor outcome both in univariate and multivariate analyses (p = 0.038). However, in contrast to previous reports, of 5 patients with TBM in good Palur grades among the HIV-positive patients, 4 (80%) had good outcome following shunt placement. CONCLUSIONS The authors recommend that shunt treatment should not be performed in HIV-positive patients in poor Palur grade with hydrocephalus. A trial of external ventricular drainage should be undertaken in such patients, and shunt treatment should be performed only if there is any improvement. However, HIV-positive patients in good Palur grades should undergo VP shunt placement, as these patients have better outcomes than previously reported.


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