Systemic lupus erythematosus mimicking leprosy: A challenge to early diagnosis.

We describe a case of a male patient with systemic lupus erythematosus (SLE) and lupus nephritis. A patient who was initially diagnosed with multibacillary leprosy, an infectious disease, with clinical symptoms for two years. However, after hospitalization and investigation, his diagnosis was revoked and replaced with SLE. The aim of this study is to emphasize the importance of knowing the most important and significant clinical changes in SLE and thus allowing an accurate diagnosis, preventing disease progression with target organ involvement, and allowing better clinical management.

Decreased SIRT1 protein may promote HMGB1 translocation in the keratinocytes of patients with cutaneous lupus erythematosus.

Background Ultraviolet radiation causes DNA damage in keratinocytes, aggravating cutaneous lupus erythematosus (CLE). High mobility group box 1 (HMGB1) participates in nucleotide excision and may transfer from the nucleus to the cytoplasm in immune active cells and the translocation of HMGB1 may result in DNA repair defects. HMGB1 was observed to transfer from the nucleus to the cytoplasm in the keratinocytes of CLE patients. As a class III histone deacetylases (HDACs), sirtuin-1 (SIRT1) can induce HMGB1 deacetylation. Epigenetic modification of HMGB1 may lead to HMGB1 translocation. Aims We aimed to evaluate the expressions of SIRT1 and HMGB1 in the epidermis of CLE patients and whether decreased SIRT1 leads to HMGB1 translocation through HMGB1 acetylation in keratinocytes. Methods We measured the messenger RNA (mRNA) and protein expressions of SIRT1 and HMGB1 in CLE patients using real-time reverse transcription polymerase chain reaction (RT-qPCR) and western blotting. Keratinocytes were treated with SIRT1 activator resveratrol (Res) and irradiated with ultraviolet B (UVB). We detected the localization expression of HMGB1 by immunofluorescence. The apoptosis level and the cell cycle proportions were measured by flow cytometry. The acetyl-HMGB1 level was detected by immunoprecipitation. Results Compared to healthy controls, the mRNA and protein expressions of SIRT1 in the epidermis of CLE patients were significantly decreased and there was translocation of HMGB1 from the nucleus to the cytoplasm. In keratinocytes, UVB irradiation led to HMGB1 translocation from the nucleus to the cytoplasm. Res treatment inhibited HMGB1 translocation, attenuated the cell apoptosis induced by UVB and decreased the acetyl-HMGB1 level. Limitations We only treated keratinocytes with the SIRT1 activator but did not perform the relevant experiments in keratinocytes with SIRT1 knockdown or overexpression. In addition, the lysine residue site of action of SIRT1 deacetylation of HMGB1 is unclear. The specific mechanism of action of SIRT1 deacetylation of HMGB1 needs to be further investigated. Conclusion SIRT1 may inhibit HMGB1 translocation by HMGB1 deacetylation which inhibited the apoptosis of keratinocytes induced by UVB. Decreased SIRT1 may promote HMGB1 translocation in the keratinocytes of patients with CLE.

Pigmented linear discoid lupus erythematosus following the lines of Blaschko: A retrospective study of a Chinese series.

BACKGROUND: Linear cutaneous lupus erythematosus is a rare subtype of lupus erythematosus (LE) that develops linear lesions following the lines of Blaschko. Linear cutaneous lupus erythematosus may present as various subtypes of LE, including linear discoid lupus erythematosus. There are few reports about pigmentedlinear discoid lupus erythematosus in the literature. AIMS: We aimed to summarize the clinical and pathological features of patients with pigmented linear discoid lupus erythematosus following the lines of Blaschko. METHODS: Eighteen patients with pigmented linear discoid lupus erythematosus attending the outpatient department of the Dermatology, Peking Union Medical College Hospital, China, were enrolled in the study. We recorded clinical data including sex, age at onset, disease duration, location and distribution of the lesions, symptoms, trigger factors, antinuclear antibody (ANA) testing, therapy, and therapeutic responses. Histopathological features were also summarized. RESULTS: All 18 patients presented with well-defined brownish pigmented linear or segmental macules or plaques, following the lines of Blaschko. All the lesions were located on the head or neck. Unilaterally distributed lesions were found in 94.4% of patients. Two patients showed low titers of ANA in a speckled pattern. No systemic involvement or progression to systemic LE was noted. The patients were clinically diagnosed as pigmented lichen planus (55.6%), pigmented linear discoid lupus erythematosus (33.3%), and linear morphea (11.1%) before histopathological examination. LIMITATIONS: The study was retrospective and direct immunofluorescence was not performed. Not all patients' information was available and 4 patients were lost to follow-up because their contact information was changed. CONCLUSION: Pigmented linear discoid lupus erythematosus mostly occurs on the head and neck. It manifests as brownish macules along the lines of Blaschko. Differentiation between pigmented linear discoid lupus erythematosus and other dermatoses that have a linear distribution can be difficult both clinically and pathologically, but histological details can help distinguish them.