Hongmei Wang

The co-morbidity of psoriasis (PsO) and metabolic syndrome (MetS) is prevalent. While the mechanisms causing PsO in MetS remain unknown, it is understood that gut microbiota plays a critical role in maintaining immune and metabolic balance. However, the specific mechanisms and whether biomarkers are involved in the pathophysiological process of PSO in MetS patients have yet to be elucidated. This study involved 29 patients with PSO and MetS (PM) and 29 with MetS (M). It analyzed their clinical parameters, microbial composition, function, diagnostic, and predictive performance. The results unveiled significant differences between the two groups concerning microbial diversity and community composition. Most of the differential microbiota in the PM group exhibited a negative correlation with high-density lipoprotein (HDL) and a positive correlation with serum uric acid (SUA). In contrast, the opposite was observed in the M group. Sixteen MetaCyc pathways showed significance in the PM group, encompassing peptidoglycan biosynthesis II (staphylococci), the super pathway of L-arginine and L-ornithine degradation, teichoic acid (poly-glycerol) biosynthesis, and palmitic biosynthesis II (bacteria and plants). Six KEGG pathways were enriched in the M group, such as flavone, flavonol biosynthesis, and carotenoid biosynthesis. Most importantly, we determined that eight biomarkers, represented by Akkermansia, demonstrated robust diagnostic predictive power. This study elucidates the potential mechanism through which metabolic disorders impact the onset and progression of psoriasis via intestinal microbiota. Furthermore, it offers novel strategies for preventing, diagnosing, and treating PsO in MetS.

We report the case of a patient with chronic lymphoedema who presented with extensive red papules and plaques on the left arm for 3 months. This patient achieved good therapeutic effects from monotherapy with clarithromycin.

The main objective is to evaluate clinical efficacy and safety of using calcipotriol–betamethasone compounding agent for psoriasis treatment through a systematic review and meta-analysis. We searched MEDLINE, Embase, The Cochrane Library, China National Knowledge Infrastructure (CNKI), China Biomedical Literature Database (CBM), and WanFang Data from inception till July 31, 2020. Efficacy was evaluated based on primary outcome indicators including skin lesion improvement and overall adverse reaction rate. Secondary outcome indicators included degree of life quality improvement, clinical effectiveness rate, and specific adverse reaction rates. RevMan5.3 was used to perform the meta-analysis. 22 studies finally met our inclusion criteria for the meta-analysis. The results indicated that for short-term treatment, a sequential therapy that uses calcipotriol betamethasone compounding agent and calcipotriol improves PASI score (MD = −0.94, 95% CI − 1.38 ~ − 0.49, P < 0.0001, I² = 49%), comparing with using only calcipotriol. From a drug safety perspective, the difference in overall adverse reaction rate is not significant between the calcipotriol group and the sequential treatment group (RR = 0.50, 95% CI 0.22 ~ 1.14, P = 0.10, I² = 33%). Calcipotriol betamethasone compounding agent may be more effective in plaque psoriasis treatment compared to use only calcipotriol, with no significant difference in adverse reaction rate between the two groups. Although the data were collected from 13 comparison groups, each group may not have sufficient data for a thorough and comprehensive analysis. Further research may be necessary for a more detailed evaluation of effectiveness of using calcipotriol betamethasone compounding agent for plaque psoriasis treatment.

Background: Psoriasis vulgaris (PV) is a chronic autoimmune inflammatory disease with epidermal hyperkeratosis and parakeratosis. Methods: The study was to elucidate the pathogenesis of PV by quantitative proteomic analysis of skin lesion biopsies of PV and healthy tissues with tandem mass tags (TMTs) coupled with liquid chromatography–mass spectrometry (LC–MS)/MS. Results: A total of 4562 differentially expressed proteins (DEPs) between PV lesional tissues (n = 11) and healthy tissues (n = 11) were identified, of which 299 were upregulated and 206 were downregulated using |fold change| > 1.3 as the cutoff threshold. The Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis revealed that the DEPs were mainly enriched in the activation of immune cells (drug metabolism pathway, NOD-like pathway, and IL-17 pathway), cell proliferation (ribosomal pathway, DNA replication pathway, and base replication pathway), metabolism-related pathways (fatty acid biosynthesis and metabolism, PPAR pathway, glycerophospholipid metabolism, and cortisol synthesis and breakdown), and glandular secretion (saliva secretion, gastric acid secretion, and pancreatic fluid secretion). Thirteen DEPs that were relatively highly expressed in the drug metabolism pathway were validated with parallel reaction monitoring (PRM), of which MPO, TYMP, IMPDH2, GSTM4, and ALDH3A1 were highly expressed in PV, whereas CES1, MAOB, MGST1, and GSTT1 were less expressed in PV. Conclusions: These findings confirmed that these proteins participate in the drug metabolism-other enzyme pathways and play crucial roles in the activation and proliferation of immune cells in the pathogenesis of PV.