Morphoea is neither associated with features of Borrelia burgdorferi infection, nor is this agent detectable in lesional skin by polymerase chain reaction

Weide, Benjamin; Schittek, Birgit; Klyscz, T.; Schüz, K.; Stark, M.; Rassner, G.; Wilske, Bettina; Garbe, Claus

doi:10.1046/j.1365-2133.2000.03775.x

Cited by 54 publications

(28 citation statements)

References 29 publications

(38 reference statements)

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“…41 Borrelia's role in morphea is further confused by the multitude of studies that have found no evidence of association between the two entities. [42][43][44][45][46][47][48][49][50] Reports of positive borrelia results in patients with morphea almost uniformly come from Europe. European strains of borrelia differ from those in the United States (Borrelia afzelii or B garinii vs B burgdorferi sensu stricto, respectively), and may be an etiologic factor in morphea.…”

Section: Infectionmentioning

confidence: 99%

Update on morphea

Fett

Werth

2011

Journal of the American Academy of Dermatology

334

197

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Section: Infectionmentioning

confidence: 99%

Update on morphea

Fett

Werth

2011

Journal of the American Academy of Dermatology

334

197

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“…autoimmune thyroiditis, alopecia areata, vitiligo, diabetes mellitus type I, and ulcerative enteritis [5][6][7]. The environmental factors such as Borrelia burgdorferi, injuries, radiation and drugs (β-blockers, bleomycin, D-penicillamine, bromocriptine) are also implicated in the etiopathogenesis of LS [2,8,9].…”

Section: Introductionmentioning

confidence: 99%

Evaluation of serum concentrations of the selected cytokines in patients with localized scleroderma

Budzyńska-Włodarczyk

Michalska-Jakubus²,

Kowal³

et al. 2016

pdia

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A b s t r a c t Introduction: Localized scleroderma is an autoimmune disease primarily affecting the skin. The cause of disease remains unexplained although environmental factors are implicated, which are likely to be responsible for activation of the endothelium and subsequent inflammation leading to excessive synthesis of collagen and extracellular matrix components. Aim: To determine concentrations of interleukin (IL)-27, transforming growth factor (TGF)-β1, TGF-β2, IL-6, and sIL-6R in patients with localized scleroderma compared to controls and to assess the relations between their levels and laboratory markers. Material and methods: The study encompassed 17 females with localized scleroderma (aged 25-67). The control group consisted of 30 age-matched healthy women. The blood was sampled from the basilic vein. Serum levels of cytokines were determined using ELISA. Results: The TGF-β2 levels were found to be significantly lower in patients with localized scleroderma compared to controls. Concentrations of TGF-β1 were decreased in scleroderma patients when compared to controls but without statistical significance. There were no significant differences in serum IL-6, sIL-6R and IL-27 levels between patients and the control group; however, we found a significant positive correlation between the level of sIL-6 and ESR among subjects with localized scleroderma. Conclusions: The findings of decreased serum levels of TGF-β1 and TGF-β2 in patients with localized scleroderma demonstrate a possible association of these cytokines with pathogenesis of the disease. The results suggest also that sIL-6R is likely to be involved in inflammation in patients with localized scleroderma.

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“…16,17,18 Borrelia burgdorferi infection could be a driving mechanism in this subset of patients; however; the role of Borrelia burgdorferi in morphea has not been confirmed. 19,20 Data on a possible genetic susceptibility in LoSc area also limited. No studies have identified the association between polymorphisms in several genes correlated with morphea and systemic scleroderma.…”

Section: Pathophysiology Of Localized Sclerodermamentioning

confidence: 98%