Abstract
Morphea, also known as localized scleroderma (LoS), is a chronic autoimmune disease of the connective tissue. The clinical picture of LoS distinguishes between active and inactive lesions. Sometimes the clinical findings are challenging to identify, and therefore, the need for additional methods is emphasized. Our study aimed to demonstrate the characteristic dermoscopic features in morphea skin lesions, focusing on demonstrating features in active and inactive lesions. In our patients (n = 31) with histopathologically proven LoS, we performed clinical evaluation of lesions (n = 162): active/inactive and according to both disease activity (modified localized scleroderma severity index, mLoSSI) and damage (localized scleroderma skin damage index, LoSDI) parameters. In addition, we took into account compression locations to determine whether skin trauma, a known etiopathogenetic factor in LoS, affects the dermoscopic pattern of the lesions. We performed a dermoscopy of the lesions, categorizing the images according to the severity within the observed field. We showed that within the active lesions (clinically and with high mLoSSI), white clouds and linear branching vessels had the highest severity. These features decreased within the observed field in inactive lesions and with high LoSDI. Brownish structureless areas were most intense in inactive lesions with high LoSDI. Erythematous areas, linear branching vessels, dotted vessels, and crystalline structures were statistically significant for pressure locations. We have shown dermoscopy is a valuable tool to assess the activity or inactivity of lesions, which translates into appropriate therapeutic decisions and the possibility of monitoring the patient during and after therapy for possible relapse.
Highlights
Morphea, known as localized scleroderma (LoS), is a relatively rare autoimmune disease of still not fully understood etiology
We focused on demonstrating features in active and inactive lesions, which would help to facilitate the therapeutic decision, as well as to monitor the patient during treatment and to follow-up for recurrence
Each patient underwent clinical evaluation, and, initially, the investigators determined whether the lesion was active/inactive, used activity/damage indices, namely modified localized scleroderma severity index (mLoSSI) and localized scleroderma skin damage index (LoSDI), for each lesion
Summary
Known as localized scleroderma (LoS), is a relatively rare autoimmune disease of still not fully understood etiology. The disease has a characteristic three-stage course, including consecutive phases: inflammation, fibrosis, and atrophy. The active phases include inflammation and fibrosis of the skin, followed by a phase of nonactive changes, i.e., damage and atrophy [2]. Erythematous lesions are initially observed, sometimes with an edematous component, which is histopathologically observed as a perivascular inflammatory infiltrate combined with lymphocytes, plasma cells, eosinophils, and monocytes within the reticular layer of the dermis and subcutaneous tissue. As the fibrosis, defined as the accumulation of extracellular matrix components progresses, one can observe indurated and sclerotic, porcelain-like lesions, often surrounded by an erythematous or violet margin [3]. The inflammation within the lesions is diminished, and atrophy, sometimes involving deep tissues, is seen. A common finding is the hyperpigmentation of the basal layer of the epidermis, which is manifested as a local discoloration of the skin [1,4]
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.