Development of a clinical scale to assess the severity of striae distensae.

BACKGROUND AND OBJECTIVE: There is no validated instrument to assess the clinical severity of striae distensae. Here, we aimed to develop a striae distensae severity scale. MATERIAL AND METHODS: After a Delphi-based consensus, 15 items related to striae severity were assessed in 110 areas (breasts, abdomen, and buttocks) from 45 participants. The items were analyzed through a partial least squares model to select the most important variables. To assess the reliability of the scale, 43 areas were retested. RESULTS: Of the 110 areas evaluated, 34 were breasts, 24 abdomens, and 52 buttocks. Striae were considered mild in 30% of the evaluations, moderate in 33%, severe in 21%, and extremely severe in 16%. The final model was composed by: width of the widest striae, width of the striae with the most frequent pattern, atrophy, number of affected quadrants, distribution (multiple or isolated), hypo or hyperchromia and topography. The scores of the scale demonstrated a high correlation with the clinical classification (rho = 0.77). There was a high agreement in the scores from the reassessed areas (intraclass correlation coefficient = 0.90). CONCLUSION: An objective and reliable scale to assess the clinical severity of striae distensae on the breasts, abdomen, and buttocks was developed.

Human endogenous retrovirus expression is inversely related with the up-regulation of interferon-inducible genes in the skin of patients with lichen planus.

Lichen planus (LP) is a common inflammatory skin disease of unknown etiology. Reports of a common transactivation of quiescent human endogenous retroviruses (HERVs) support the connection of viruses to the disease. HERVs are ancient retroviral sequences in the human genome and their transcription is often deregulated in cancer and autoimmune diseases. We explored the transcriptional activity of HERV sequences as well as the antiviral restriction factor and interferon-inducible genes in the skin from LP patients and healthy control (HC) donors. The study included 13 skin biopsies from patients with LP and 12 controls. Real-time PCR assay identified significant decrease in the HERV-K gag and env mRNA expression levels in LP subjects, when compared to control group. The expressions of HERV-K18 and HERV-W env were also inhibited in the skin of LP patients. We observed a strong correlation between HERV-K gag with other HERV sequences, regardless the down-modulation of transcripts levels in LP group. In contrast, a significant up-regulation of the cytidine deaminase APOBEC 3G (apolipoprotein B mRNA-editing), and the GTPase MxA (Myxovirus resistance A) mRNA expression level was identified in the LP skin specimens. Other transcript expressions, such as the master regulator of type I interferon-dependent immune responses, STING (stimulator of interferon genes) and IRF-7 (interferon regulatory factor 7), IFN-ß and the inflammassome NALP3, had increased levels in LP, when compared to HC group. Our study suggests that interferon-inducible factors, in addition to their role in innate immunity against exogenous pathogens, contribute to the immune control of HERVs. Evaluation of the balance between HERV and interferon-inducible factor expression could possibly contribute to surveillance of inflammatory/malignant status of skin diseases.