Demonstration of interleukin 8 in serum samples of patients with localized scleroderma

Ihn, H.

doi:10.1001/archderm.130.10.1327

Cited by 16 publications

(17 citation statements)

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“…Methotrexate's mechanism of action seems to be based on an inhibition of various cytokines (eg, interleukins 2, 4, 6, and 8) that were shown to be increased in LS and parallel with the degree of skin sclerosis. 15,16 Beneficial effects of oral corticosteroids were reported by Joly et al 9 in a follow-up study that included 17 patients with severe LS. 9 Although mean duration of treatment was 18 months (0.5-1 mg/kg of oral prednisone per day, followed by a decrease in dose), 6 patients experienced a relapse after discontinuation of therapy.…”

Section: Commentmentioning

confidence: 90%

Pulsed High-Dose Corticosteroids Combined With Low-Dose Methotrexate in Severe Localized Scleroderma

Kreuter¹,

Gambichler²,

Breuckmann³

et al. 2005

Arch Dermatol

165

115

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Setting: Dermatology department at a university hospital in Bochum, Germany.Patients: Fifteen patients with histologically confirmed severe LS.Interventions: Oral methotrexate (15 mg/wk) combined with pulsed intravenous methylprednisolone (1000 mg for 3 days monthly) for at least 6 months.Main Outcome Measures: Treatment outcome was evaluated by means of a clinical score, 20-MHz ultrasonography, and histopathologic analysis. Safety assess-ment included the monitoring of adverse effects and clinical laboratory parameters.Results: One patient discontinued therapy. In most of the remaining 14 patients, significant elimination of all signs of active disease (inflammation) and remarkable softening of formerly affected sclerotic skin that resulted in a decrease of the mean±SD clinical score from 10.9±5.3 at the beginning to 5.5±2.5 at the end of therapy was observed (PϽ.001). Clinical improvement was confirmed by histologic and ultrasonographic assessments. No serious adverse effects were noted.Conclusions: These data suggest that pulsed high-dose corticosteroids combined with orally administered lowdose methotrexate therapy is beneficial and safe in the treatment of patients with LS. This treatment regimen should especially be considered for severe forms of LS in which conventional treatments have failed.

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Section: Commentmentioning

confidence: 90%

Pulsed High-Dose Corticosteroids Combined With Low-Dose Methotrexate in Severe Localized Scleroderma

Kreuter¹,

Gambichler²,

Breuckmann³

et al. 2005

Arch Dermatol

165

115

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“…Since perivascular lymphocyte infiltration is one of the histologic characteristics of this disorder, upregulated chemokine or endothelial activation by TNF may contribute to the lesional lymphocyte infiltration and subsequent skin sclerosis in this disorder. In agreement with this observation, IL-8, a chemotactic factor for neutrophils and T lymphocytes, has been reported to be elevated in serum from patients with LSc [13]. Serum levels of soluble functional adhesion molecules shed by activated endothelial cells such as intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin are also elevated in patients with LSc [15, 45].…”

Section: Discussionmentioning

confidence: 71%

“…These immunologic abnormalities observed in patients with LSc may be related to enhanced production of some cytokines in these patients. We and other groups have demonstrated that elevated serum interleukin (IL)-2, IL-4, IL-6, IL-8, transforming growth factor β1 (TGF-β1), soluble IL-2 receptor (sIL-2R), and sIL-6R in patients with LSc [13, 14, 15, 16, 17, 18, 19]. Other candidates that may contribute to the pathogenesis of LSc are tumor necrosis factor (TNF; previously TNF-α) and IL-13.…”

Section: Introductionmentioning

confidence: 99%

Serum Levels of Tumor Necrosis Factor and Interleukin-13 Are Elevated in Patients with Localized Scleroderma

et al. 2003

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Background: The enhanced production of some cytokines may be related to the pathogenesis of localized scleroderma (LSc). Objective: To determine whether serum levels of tumor necrosis factor (TNF) and interleukin (IL)-13 are elevated, and whether they correlated with clinical or serological features in patients with LSc. Methods: Serum levels of TNF and IL-13 were examined by ELISA in 45 patients with LSc and in 20 healthy controls. Results: The frequency of serum TNF detection was significantly higher in patients with LSc (24%) compared with that in healthy controls (0%). The frequency of serum IL-13 detection was also significantly higher in patients with LSc (29%) compared with that in controls (0%). In patients with LSc, elevated TNF levels significantly correlated with the presence of IgM antihistone antibodies, anti-single-stranded DNA antibodies, elevated serum IL-6 levels, the number of linear lesions, and muscle involvement. Elevated IL-13 levels were significantly associated with the number of plaque lesions and the total number of lesions. Conclusions: These results suggest that TNF and IL-13 may be associated with the development of LSc.

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“…The stimulated endothelial cells, cells of inflammatory infiltrate, and finally activated fibroblasts provide the source of several cytokines and growth factors which may participate in pathogenesis of the disease. This include profibrotic factors [transforming growth factor β -TGF-β, connective tissue growth factor (CTGF), interleukin 4 (IL-4), IL-13], angiogenic factors [IL-8, vascular endothelial growth factor (VEGF)], and proinflammatory factors [IL-1, tumor necrosis factor α (TNF-α)] [27][28][29]. In parallel, a lowered production is postulated of cytokines manifesting antifibrotic properties, such as interferon γ (INF-γ) [30,31].…”

Section: Pathogenesis Of Sclerodermamentioning

confidence: 99%

“…However, attempts to introduce the latter to morphea treatment did not show favourable results. Additionally, soma cases of induced type SSc in multiple sclerosis patients treated with INF-γ were found [28,31]. Moreover, intensified deposition of extracellular matrix components, including collagen I and III, fibronectin, glycosaminoglycans depends on their intensified production and, on diminished decomposition by matrix metalloproteinases [14,[32][33][34][35].…”

Section: Pathogenesis Of Sclerodermamentioning

confidence: 99%

Role of UVA1 phototherapy in treatment of scleroderma and scleroderma-like disorders”

Osmola‐Mańkowska¹,

Dańczak‐Pazdrowska²,

Olek‐Hrab³

et al. 2012

cejoi

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Treatment of scleroderma and scleroderma-like diseases poses a serious challenge to contemporary dermatology due to the complexity of its pathogenesis, low incidence of the diseases and their heterogenous clinical expression. the manifestation of this autoimmune disease includes an increased production and deposition of collagen fibres types I and III in the skin and connective tissue as well as vascular alterations. Ultraviolet A1 (UVA1) phototherapy affects various stages of a morbid process in scleroderma: it inhibits inflammation and affects the consequences of it, fibrosis. Currently, UVA1 is proposed as a potential treatment and is believed to have a multifold mechanism of action. This includes, inducing apoptosis in T and B lymphocytes, inhibition of proinflammatory cytokine production and ability to induce collagenase production by fibroblasts. UVA1 irradiation may also interact with endothelial cells, promoting angiogenesis. Efficacy of high, moderate, and low doses of UVA1 was documented. Advantages of UVA1 phototherapy include the evident avoidance of systemic side effects of psoralens such as nausea and vomiting or photokeratitis as well as lower risk of phototoxic reactions with deeper penetration of radiation. Its disadvantages include high cost of equipment, thus reducing the accessibility of the treatment to specialized centres. Due to its unique mechanism of action, attempts to useUVA1 phototherapy seem justified in other rare diseases, developing with skin induration.

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Demonstration of interleukin 8 in serum samples of patients with localized scleroderma

Cited by 16 publications

References 0 publications

Pulsed High-Dose Corticosteroids Combined With Low-Dose Methotrexate in Severe Localized Scleroderma

Pulsed High-Dose Corticosteroids Combined With Low-Dose Methotrexate in Severe Localized Scleroderma

Serum Levels of Tumor Necrosis Factor and Interleukin-13 Are Elevated in Patients with Localized Scleroderma

Role of UVA1 phototherapy in treatment of scleroderma and scleroderma-like disorders”

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