Background Morphoea (scleroderma) is a chronic disorder characterized by circumscribed sclerotic plaques with the hallmark of increased fibroblast activation and fibrosis. Through its effect on connective tissue cells and immune cells, insulin-like growth factor (IGF)-I has been found to play a role in some autoimmune connective tissue diseases and has been implicated in the pathogenesis of several fibrotic disorders.
Objectives To evaluate the role of IGF-I in the pathogenesis of morphoea.
Methods The study was carried out on 15 patients with morphoea and nine healthy controls. Two 5-mm punch skin biopsies were taken from every patient (one from lesional and one from non-lesional skin) and a single biopsy was taken from the normal skin of each control. A 10-mL blood sample was also taken from each patient and control. Quantitative detection of tissue and serum levels of IGF-I was done using an enzyme-linked immunosorbent assay technique.
Results IGF-I in lesional skin was significantly higher than in non-lesional and control skin (P = 0·001 and P = 0·021, respectively). Moreover, a significantly higher level of IGF-I was detected in patient serum when compared with control serum (P < 0·001). A direct significant correlation existed between lesional and non-lesional skin level (r = 0·618, P = 0·014), and between lesional skin level and Rodnan score (r = 0·538, P = 0·039).
Conclusions Despite the small sample size, this study suggests that IGF-I plays an important role in the pathogenesis of fibrosis, characteristic of morphoea. Studies on a larger number of patients with morphoea as well as on patients with systemic sclerosis are recommended. Furthermore, therapeutic trials using IGF-I antagonist (octreotide) are highly recommended in patients with morphoea.