Purpose Pyoderma gangrenosum (PG) is a rare, neutrophilic dermatosis characterized by rapidly developing, painful ulcers. This study explores the potential of spesolimab, an anti-IL-36R antibody, as a therapeutic option for refractory PG.
Psoriasis is a chronic inflammatory disease that involves both the innate and adaptive immune systems. Type I interferons (IFNs), the production of which is partially regulated by toll-like receptors (TLRs), play an important role in the pathogenesis of psoriasis, especially psoriasis caused by skin trauma, known as the Koebner phenomenon. IFN regulatory factors (IRFs) function in both innate and adaptive immune responses, and their effect is associated with the regulation of type I IFNs. In this review, we focus on recent advances in understanding the expression of TLRs, IRFs, and type I IFNs in psoriasis. We also highlight the interplay among TLRs, IRFs, and type I IFNs.
The aim of this study was to confirm the association of RHOB and FAM167A-BLK gene polymorphisms with susceptibility to systemic sclerosis (SSc) in a Chinese Han population.A total of 248 SSc patients and 251 healthy controls of Chinese Han ethnicity, which visited the department of dermatology of Peking Union Medical College Hospital, were included in the study. Six selected single nucleotide polymorphisms (SNPs) in the RHOB and FAM167A-BLK regions were selected as markers and were genotyped using a MassARRAY system, which is based on the matrix-assisted laser desorption/ionization time of flight mass spectrometry technique.Three SNPs in the coding regions of the RHOB and FAM167A-BLK genes displayed an association with SSc: (1) rs1062292T, which is a newly discovered SNP in the RHOB gene (P = 0.03, odds ratio [OR] = 1.62, 95% confidence interval (CI) = 1.05-2.50), (2) rs2736340T (P = 0.03, OR = 1.39, 95%CI = 1.03-1.85), and (3) rs13277113A (P = 0.04, OR = 1.34, 95%CI = 1.01-1.76), both in the FAM167A-BLK gene. Our results support previous findings that vaiants in the RHOB and FAM167A-BLK genes may be associated with susceptibility to SSc. However, the loci of the SNPs in RHOB region that displayed an association with SSc are quite different from the loci which were identified in studies of Caucasian populations.Our results confirm that RHOB and FAM167A-BLK polymorphisms exist in Chinese Han SSc patients. Therefore, variants of the RHOB and FAM167A-BLK genes are promising genetic markers for SSc.
Homocysteine is a sulfur-containing amino acid with potential clinical significance. Abnormal homocysteine levels have been found in patients with psoriasis. This review summarizes the possible correlations among homocysteine, cardiovascular risk, and DNA methylation in psoriasis.We retrieved the articles published in English from the PubMed database up to January 2017, using the keywords including "psoriasis," "homocysteine," "cardiovascular risk," "DNA methylation," "methylenetetrahydrofolate reductase," "MTHFR," and "MTHFR C677T."Articles about the roles of homocysteine in the cardiovascular risk and DNA methylation in psoriasis were obtained and reviewed.Observational studies consistently reported that elevated homocysteine is an independent risk factor for cardiovascular diseases. Several studies also consistently reported an association between psoriasis and increased cardiovascular risk. A substantial body of evidence also suggested that an elevated homocysteine level is related to the demethylation of DNA. Data from clinical trials also demonstrated that MTHFR C677T polymorphisms as well as DNA methylation aberrations are associated with psoriasis.This review highlighted the relationships among homocysteine, cardiovascular risk, and DNA methylation, suggesting that homocysteine may be a biological link between cardiovascular risk and DNA methylation in psoriasis.
Abstract: The application of biologics such as anti-tumor necrosis factor (TNF) has shown great efficacy in livedoid vasculopathy (LV). However, new biological options need to be identified for those with a high tuberculosis reactivation risk. In this study, we evaluated the efficacy of anti-17A biologics for LV therapy. Two patients with LV who were irresponsive to traditional anticoagulation therapy were studied at the outpatient dermatology clinic of Peking Union Medical College Hospital. All patients received anti-17A biological therapy for at least two–four weeks. Both patients reported an exacerbation of the skin lesions, which might indicate that the IL-17 pathway plays a critical role in LV pathogenesis. Keywords: livedoid vasculopathy, biologic therapy, TNF-alpha, IL-17, atrophied blanched
Abstract Background Palmoplantar pustulosis (PPP) is a chronic inflammatory disease of ill‐defined etiopathology. Recent studies have proposed complete blood count‐based hematological parameters, such as neutrophil/lymphocyte ratio (NLR) and platelet/lymphocyte ratio (PLR), as biomarkers to monitor disease status in many inflammatory diseases. This study aimed to analyze for the first time the clinical significance of hematological parameters, including NLR, monocyte/lymphocyte ratio (MLR), PLR, mean platelet volume (MPV), plateletcrit (PCT), and pan‐immune‐inflammation value (PIV) in PPP patients. Methods We retrospectively investigated the clinical and laboratory data of 237 patients with PPP and 250 sex‐age‐matched healthy controls (HCs). Hematological parameters were compared between patients with PPP and HCs. The correlations between these parameters and disease severity, as well as treatment response, were analyzed. Results NLR, MLR, MPV, PCT, and PIV values were significantly higher in PPP patients than in HCs. But in receiver‐operating characteristic analyses, only monocyte count (Youden Index = 0.53), PCT (Youden Index = 0.65), and PIV (Youden Index = 0.52) performed relatively accurate distinguishment between moderate‐to‐severe cases and mild cases. PCT and PIV values were significantly correlated with disease severity. After treatment, both PIV and PCT values decreased significantly in the responder group but not in the non‐responder group. Conclusions Hematological parameters altered significantly in PPP patients. PCT and PIV can be used as simple and inexpensive biomarkers for systemic inflammation in PPP patients.
Background: Livedoid vasculopathy is an uncommon cutaneous ulcerative dermatosis that is challenging to diagnose.Diagnostic delay brought both pain and uncurable atrophied scar to patients.Purpose: We conducted this study to identify the factors responsible for the initial misdiagnosis of livedoid vasculopathy and to identify possible methods to increase the diagnostic accuracy of livedoid vasculopathy.Patients and Methods: We conducted a retrospective medical record review to confirm the diagnosis of livedoid vasculopathy in patients who visited the Department of Peking Union Medical College Hospital for the first time.We used the Diagnosis Error Evaluation and Research taxonomy to evaluate missed cases.Results: Twenty-three patients (85.18%) had an alternate diagnosis, including 10 (43.4%) with two or more diagnoses.The average time from disease onset to the final diagnosis of livedoid vasculopathy was 4.61 ± 0.69 years.The major diagnostic errors were clinician assessment failures and failures in the timely follow-up and rechecking of patients.Allergic vasculitis was the most common misdiagnosis.Other alternate diagnoses include Henoch-Schoenlein purpura, pigmented purpuric dermatosis, eczema, erythema nodosum, and reactive perforating collagenases.Twenty-three patients (65.21%) received systemic corticosteroid therapy before the final diagnosis of livedoid vasculopathy. Conclusion:It is critical to raise the awareness of clinicians about livedoid vasculopathy, especially when patient present with extensive livedo racemosa or long-lasting purpuric lesions on the lower limbs.Long-term follow-up is necessary, especially for younger patients.Skin biopsy is recommended before systematic therapy.
'/%3e%3cuse xlink:href='%23a' transform='rotate(23.036 .093 25.536)'/%3e%3cuse xlink:href='%23a' transform='rotate(45.87 1.273 16.18)'/%3e%3cuse xlink:href='%23a' transform='rotate(69.945 .996 12.078)'/%3e%3cuse xlink:href='%23a' transform='rotate(20.66 -19.689 31.932)'/%3e%3c/svg%3e)
