Introduction: The fundamental component in the pathogenesis of systemic scleroderma, as well as localized scleroderma, is immunologically determined fibrosis. INF-γ is considered to be a strong, natural fibrosis inhibitor. Low level of this cytokine was observed in other skin diseases with the course of fibrosis.
Aim: The aim of the study was to measure INF-γ level in serum collected from patients with localized scleroderma.
Material and methods: The group of localized scleroderma patients comprised 18 patients with en plaque type of localized scleroderma (M), 18 patients with atrophoderma Pasini-Pierini (APP) and 5 patients with both types of skin lesions (M + APP). Control group serum was taken from 18 healthy volunteers. INF-γ level was assessed with the ELISA method.
Results: INF-γ serum level was lower in all patients with localized scleroderma in comparison with the control group. INF-γ serum level in patients with M + APP was also lower, whereas in patients with APP it was higher than in the control group. No statistical significance was observed. INF-γ serum level was significantly (p=0.04) lower in patients with the active stage of M compared with patients with the inactive one. Moreover, it was lower – but not significantly – in the active stage of M + APP and the whole group of patients with localized scleroderma than in inactive ones. INF-γ serum level was higher only in the active stage of APP. INF-γ serum level correlated with the number and area of skin lesions in all LS patients. The higher the number of skin lesions present, the lower was the INF-γ serum level observed. The lowest INF-γ serum level was observed in patients with greater than 30 cm² area of skin affected by lesions (p=0.003).
Conclusions: INF-γ serum level was lower in all patients with localized scleroderma in comparison with the control group. Moreover, INF-γ serum level was lower in the active stage of diseases in comparison with the inactive one. Serum level of INF-γ might be a useful factor in predicting the intensity of skin fibrosis in localized scleroderma.