A Case of Vitiligo Combined with Systemic Lupus Erythematosus Treated with Tofacitinib.

Vitiligo is a skin depigmentation disease resulting from melanocyte destruction and often co-occurring with autoimmune disorders like hyperthyroidism, alopecia areata, pernicious anemia, and systemic lupus erythematosus (SLE). Although various traditional treatments exist for vitiligo, their effectiveness varies considerably. This report presents a unique case of a vitiligo patient with concomitant systemic lupus erythematosus. Remarkably, after a 30-day course of treatment with tofacitinib, complete repigmentation of the white macular rash was achieved, and there were no adverse drug reactions. These findings provide compelling evidence for the efficacy and safety of oral JAK inhibitors, such as tofacitinib, in vitiligo treatment. Additionally, JAK inhibitors can yet be regarded as a promising new treatment option for vitiligo patients with concurrent autoimmune diseases.

The hsa_circ_0082152 maintains NF-κB mRNA stability by binding to MTDH to promote anti-tuberculosis drug-induced liver injury.

Anti-tuberculosis drug-induced liver injury (ADLI) is a common adverse reaction during anti-tuberculosis treatment and often leads to treatment interruptions. Circular RNAs (circRNAs) have been identified as key modulators in liver diseases. CircRNAs is a special class of noncoding RNAs that have been found to have significant impacts on the progression of inflammation via various mechanisms. In the serum of ADLI patients, upregulation of the circular RNA hsa_circ_0082152 (derived from the host gene snd1) was observed, along with increased ALT and AST levels, as well as alterations in the levels of inflammation-related factors such as NF-κB, IL-1ß and TNF-α. To elucidate the underlying mechanisms, we established an HL-7702-ADLI cell model and confirmed similar upregulation of hsa_circ_0082152. Downregulation of hsa_circ_0082152 significantly inhibited inflammatory injury in ADLI cells, while upregulation had the opposite effect. RNA immunoprecipitation showed that hsa_circ_0082152 functions by interacting with metadherin (MTDH). Our study further verified that the interaction of hsa_circ_0082152 with the MTDH protein binding to NF-κB mRNA to maintain NF-κB mRNA stability, which increases the expression of NF-κB and its targets IL-1ß and TNF-α. Conversely, depletion of MTDH rescued the promotive effect of hsa_circ_0082152 overexpression on ADLI inflammation. Therefore, hsa_circ_0082152 overexpression promotes ADLI progression via the MTDH/NF-κB axis.