Postural changes, dysphagia, and systemic sclerosis

Barrera, P.; Broeder, Alfons A den; Hoogen, F.H.J. van den; Engelen, B.G.M. van; Putte, Leovinus B.A. van de

doi:10.1136/ard.57.6.331

Cited by 11 publications

(12 citation statements)

References 49 publications

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“…The clinical and demographic features of the patients with moderate or severe arthritis at the time of joint biopsies have been published (15,16). All patients had active disease as defined by the inclusion criterion of disease activity scores Ͼ3.2.…”

Section: Resultsmentioning

confidence: 99%

“…All patients met the American College of Rheumatology criteria for RA (35). The disease activity was calculated by using the disease activity score, and, for the current study only, patients with a disease activity score Ͼ3.2 were included (15,16). The therapeutic regimens of all patients were recorded before blood sampling.…”

Section: Methodsmentioning

confidence: 99%

“…Staining for IL-32 was semiquantitatively scored on a five-point scale (range 0-4) at ϫ200 magnification; a score of 0 represented no or minimal staining, a score of 1 indicated 10-20% positive cells, a score of 2 indicated 30-40% positive cells, a score of 3 indicated 50-60% positive cells, and a score of 4 represented staining of Ͼ60% of the cells. Staining for IL-1␤, IL-18, and TNF␣ was performed as described (15,16). PGE2 Production by Human PBMC.…”

Section: Antibodies For Detection Of Il-32 Il-18 Il-1␤ and Tnf␣mentioning

confidence: 99%

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IL-32, a proinflammatory cytokine in rheumatoid arthritis

Joosten¹,

Netea

Kim

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

308

328

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IL-32 is a recently discovered cytokine that induces TNF␣, IL-1␤, IL-6, and chemokines. We investigated whether IL-32 is expressed in the synovia of patients with rheumatoid arthritis (RA) and studied associations with disease severity and the presence of other cytokines. Immunohistochemistry revealed that IL-32 is highly expressed in RA synovial tissue biopsies, whereas IL-32 was not observed in synovial tissues from patients with osteoarthritis. Moreover, in synovial biopsies from 29 RA patients with active disease, the level of IL-32 staining correlated with erythrocyte sedimentation rate, a marker of systemic inflammation (R ‫؍‬ 0.63 and P < 0.0003). Synovial staining of IL-32 also correlated with indices of synovial inflammation (R ‫؍‬ 0.80 and P < 0.0001) as well as synovial presence of TNF␣ (R ‫؍‬ 0.68 and P < 0.004), IL-1␤ (R ‫؍‬ 0.79 and P < 0.0001), and IL-18 (R ‫؍‬ 0.82 and P < 0.001). IL-32 was a potent inducer of prostaglandin E2 release in mouse macrophages and human blood monocytes, an important property for inflammation. After the injection of human IL-32␥ into the knee joints of naïve mice, joint swelling, with pronounced influx of inflammatory cells and cartilage damage, was observed. In TNF␣-deficient mice, IL-32-driven joint swelling was absent and cell influx was markedly reduced, but loss of proteoglycan was unaffected, suggesting that IL-32 activity is, in part, TNF␣-dependent. IL-32, strongly associated with TNF␣, IL-1␤, and IL-18, appears to play a role in human RA and may be a novel target in autoimmune diseases.autoimmune ͉ inflammation ͉ tumor necrosis factor

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Antibodies For Detection Of Il-32 Il-18 Il-1␤ and Tnf␣mentioning

confidence: 99%

See 1 more Smart Citation

IL-32, a proinflammatory cytokine in rheumatoid arthritis

Joosten¹,

Netea

Kim

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

308

328

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“…Radiological progression over a one and two year period was effectively abolished [22]. Blocking TNF-α in RA results in down regulation of IL1β mRNA at the systemic level and in reduction of the endogenous antagonists for IL1 and TNF and of other cytokines related to the acute phase response, such as IL-6 within days [23].…”

Section: Rheumatoid Arthritismentioning

confidence: 97%

Biological Therapies of Autoimmune Diseases

Kourbeti

Boumpas²

2005

CDTIA

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The advances in the understanding of the pathogenesis of the autoimmune diseases have led to new treatment targets. Biological agents enhance or replace conventional immunosuppressive therapies in the treatment of autoimmune diseases. TNF-alpha has been validated as a good treatment target but the potential modalities also include the inhibition of the interaction between LFA-3 (lymphocyte function-associated antigen 3) and CD2, the blockade of the IL-1 receptors, the antibodies against the alpha4 integrins, the antibodies against B-cell CD20 and the inhibition of the activation of T-cells. The new treatments have had a major impact on inflammatory symptoms, the radiological damage and the anemia of chronic disease in rheumatoid arthritis and have substantially controlled the signs and symptoms in the spondylarthropathies group and plaque-type psoriasis. The efficacy of the biologic agents in systemic lupus erythematosus warrants further investigation but there have been some promising results in proliferative lupus nephritis. Several small studies have explored their use in the treatment of Sjogren's syndrome, adult onset Still's disease and several vasculitides but the results are still preliminary and warrant confirmation. The efficacy of the biological agents has been impressive. Susceptibility to infections has always been a major concern; a high level of suspicion is necessary and strategies should be implemented for the prevention, the rapid identification and pre-emptive therapy of such infections.

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“…Dans trois études prospectives récentes, le RGO est plus fréquent et plus sévère en présence d'une OR qu'en son absence, en particulier lors du décubitus [5,6,23]. Il a été également démontré que si chez le sujet sain la position influe peu sur la clairance oesophagienne, chez le patient porteur d'une SS, la gravité joue un rôle important comme en témoignent la diminution de la clairance et l'augmentation de l'exposition acide lors du décubitus [24][25][26][27]. Dans notre série, la prévalence du RGO est significativement plus élevée en présence d'une OR qu'en son absence, et le RGO y est significativement plus sévère aussi bien au décubitus qu'en orthostatisme.…”

Section: Facteurs De Survenueunclassified