We evaluated the causal effects of blood lipid levels on systemic lupus erythematosus with a two-sample Mendelian randomization analysis. Independent single-nucleotide polymorphisms related to blood lipids levels (p < 5 × 10⁻⁸) were selected as instrumental variables (IVs) from a published genome-wide association study (GWAS). SLE GWAS analysis that included 4036 cases and 6959 controls of European ancestry provided the related roles between instrumental variables and result (SLE). The causal effects were evaluated with two-sample Mendelian randomization (MR) analyses. According to the inverse-variance weighted approaches, genes predictive of increased LDL cholesterol (OR: 1.131; 95% CI: 0.838, 1.528; p = 0.420), HDL cholesterol (OR: 1.093; 95% CI: 0.884, 1.352; p = 0.412), triglycerides (OR: 0.903; 95% CI: 0.716, 1.137; p = 0.384), Apolipoprotein A-I (OR: 0.854; 95% CI: 0.680, 1.074; p = 0.177), and Apolipoprotein B (OR: 0.933; 95% CI: 0.719, 1.211; p = 0.605) were not causally related to the risk of SLE, consistent with multivariate Mendelian randomization analysis. The reverse-MR analyses showed no massive causal roles between SLE and LDL cholesterol (OR: 0.998; 95% CI: 0.994, 1.001; p = 0.166) as well as Apolipoprotein B (OR: 0.998; 95% CI: 0.994, 1.001; p = 0.229). Nevertheless, a causal role of SLE in decreasing HDL cholesterol (OR: 0.993; 95% CI: 0.988, 0.997; p = 0.002), triglycerides (OR: 0.996; 95% CI: 0.993, 0.999; p = 0.010), and Apolipoprotein A-I (OR: 0.995; 95% CI: 0.990, 0.999; p = 0.026) was validated to some extent. Our study found no causal association between abnormal blood lipids and SLE nor a causal effect between SLE and LDL cholesterol as well as Apolipoprotein B. Nevertheless, some evidence showed that SLE exerted a causal effect on lowering HDL cholesterol, Apolipoprotein A-I, and triglyceride levels.

Objective: This study aimed to investigate the infection rate, types of human papillomavirus (HPV), and the relationship between HPV types and host factors in Zhejiang and lay a foundation for developing a prophylactic HPV vaccine. Methods: A retrospective analysis of the genotyping results of 27 hPV types using exfoliated cells from the cervix, vulva, perianal region, or oral mucosa of 28206 females, and exfoliated cells from the penis, perianal region or oral mucosa of 2923 male patients undergoing treatment between January 2016 and December 2021 at Zhejiang Provincial People’s Hospital was performed. Results: In females, the overall positive rate was 30.26%. The top five HPV types were HPV52, 58, 16, 6, and 53. In males, the overall positive rate was 31.85%. The top five HPV types were HPV6, 11, 16, 52, and 43. About 90.48% of patients with CINII+ were HR-HPV+. HPV33, 16 were the top two HPV types that increased CINII+ risks. Conclusion: Currently, the bivalent (HPV16, 18), quadrivalent (HPV6, 11, 16, 18), and 9-valent (HPV6, 11, 16, 18, 31, 33, 45, 52, 58) HPV vaccines are marketed. Of these, the 9-valent HPV vaccines are more suitable for people in the Zhejiang province; however, it is still insufficient. Therefore, the 11-, 14-, and 15-valent vaccines being developed and marketed include more genotypes, and their outcomes are worth anticipating.

Atopic dermatitis (AD) is a common chronic inflammatory cutaneous disease. Upadacitinib, a selective JAK-1 inhibitor, has been approved as a systemic medication for moderate-to-severe AD in patients aged ≥ 12 years. Although previous studies have examined the safety profile of upadacitinib, this is the first report to describe a potential association between amenorrhea and upadacitinib or other JAK inhibitors. Herein, we report a rare adverse event of amenorrhea in an adolescent female patient who was treated with upadacitinib for AD. This case report expands the range of adverse events potentially associated with upadacitinib therapy.

Purpose: To investigate the expression of Plasmacytoid Dendritic Cells (pDCs) and TLR7/9-MyD88-IRAKs pathway in chronic eczema lesions. Patients and Methods: Lesional tissues and the surrounding healthy tissues were collected from 25 individuals with chronic eczema, and immunohistochemistry was used to detect and comparatively analyze the expression profile of CD123, CD2AP, toll-like receptor 7 (TLR7), toll-like receptor 9 (TLR9) along with interleukin-1 receptor-associated kinase 1 (IRAK1) and interferon regulatory factor 7 (IRF7) in signaling pathways. Results: The positive rates of CD2AP + pDC and CD123 + pDC in lesional tissues were significantly elevated compared to the surrounding healthy tissues (P < 0.05). They were distributed in both the epidermal and dermal layers of the lesional tissue, but the majority were in the dermal layer. The TLR7, TLR9, IRAK1 and IRF7 were more expressed in dermal layers of the lesional tissue with higher positive rates of expression compared to the surrounding healthy tissues (P < 0.05). IRAK1 and IRF7 were expressed in a small amount in the epidermal layer with higher positive rates of expression than in the surrounding healthy tissues (P < 0.05), while the positive rates of TLR7 and TLR9 expression in the epidermal layer were not statistically different from those in the surrounding healthy tissues (P > 0.05). Conclusion: PDC and TLR7/9-MyD88-IRAKs pathways are actively expressed in chronic eczema lesions and may be involved in pathogenesis and disease progression.