Global burden and future trends in psoriasis epidemiology: insights from the global burden of disease study 2019 and predictions to 2030.

BACKGROUND: Millions of people worldwide are affected by psoriasis, one of the most prevalent skin conditions. Currently, there is a lack of high-quality epidemiological reports on psoriasis. OBJECTIVE: This study aimed to reveal trends in psoriasis epidemiology in 1990-2019. METHODS: Using data from the GBD study 2019, we examined psoriasis epidemiology globally and across regions defined by the social-demographic index (SDI). Trends in incidence, prevalence, and disability-adjusted life year (DALY) rates were assessed using estimated annual percentage changes (EAPC)s. Age-period-cohort analysis examined risk variations, and decomposition analysis identified factors impacting the psoriasis burden. A Bayesian Age-Period-Cohort model predicted future incidence. Frontier analysis associated psoriasis outcomes with socio-demographic development. RESULTS: In 2019, the global psoriasis burden included 4,622,594 incidence, 40,805,386 prevalence, and 3,505,736 DALY cases. Despite variations in SDI regions, the overall trend showed a decline in psoriasis rates from 1990 to 2019 (EAPC = - 0.76). The age-specific analysis indicated that the highest incidence of psoriasis was observed among individuals aged 40-64 years (global, 1,606,429). Epidemiological shifts contributed negatively to global incidence and DALYs by - 80.52% and - 103.06%, respectively. Countries like San Marino and Spain displayed the highest effective differences in the decomposition analysis. By 2030, while incidence cases per 10,000 might rise (487.36, 423.62 to 551.10), age-standardized incidence rates per 100,000 were predicted to decline (53.67, 0.00 to 259.99). CONCLUSION: This research revealed a global decline in psoriasis incidence rate from 1990 to 2019, with predictions suggesting this trend continues through 2030. Geographic disparities underscore the importance of tailored healthcare policies.

Livin is protective in UVB-induced skin photodamage by regulating keratinocyte activation and inflammatory responses.

UVB radiation can lead to skin photodamage, which might arise from keratinocyte (KC) activation. Nuclear factor kappa B (NF-κB) assumes an essential function in the context of UVB-triggered skin photodamage. Initiating the NF-κB cascade leads to the release of inflammatory factors from KCs. Livin can modulate both KC activation and function, yet it remains uncertain whether and how Livin regulates KC activation induced by UVB. To explore the involvement of Livin in UVB-triggered skin photodamage and its impact on skin damage through NF-κB activation. Immunofluorescence staining was used to analyse the expression of Livin in individuals with skin photodamage and in mice treated with UVB radiation. KC-specific Livin knockout (LivinΔKC ) mice and HaCaT cells with Livin knockdown were employed to examine the function of Livin in regulating KC activation induced by UVB radiation. Additionally, the impact of Livin on the NF-κB cascade during KC activation was confirmed via western blot analysis. In patients with skin photodamage, UVB-treated mice and HaCaT cells, Livin expression was reduced in KCs. LivinΔKC mice displayed heightened sensitivity to UVB radiation, resulting in more pronounced skin damage and inflammatory responses compared to the control Livinfl/fl mice. Following UVB exposure, both LivinΔKC mice and Livin-knockdown HaCaT cells released elevated levels of cytokines compared to their respective controls. Moreover, the UVB-induced activation of NF-κB in HaCaT cells was significantly enhanced following Livin knockdown. Our findings propose that Livin within KCs could contribute to reducing UVB-induced skin photodamage by regulating the NF-κB pathway.

Talaromyces marneffei infection with IFNGR1 gene mutation in a patient with negative Anti-Interferon-γ autoantibodies.

BACKGROUND: Talaromyces Marneffei (TM) is a rare opportunistic pathogen that mostly infects patients with low immunity compared to those with normal immunity. It may be related to immune deficiency or genetic factors. OBJECTIVE: To evaluate the gene mutation of a patient infected with TM in an endemic area with negative anti-interferon-γ autoantibodies, and negative human immunodeficiency virus (HIV) infection. METHODS: Extract deoxyribonucleic acid (DNA) samples from the patient's peripheral blood, detect the mutation gene by whole exome sequencing (WES), and carry out Sanger sequencing verification for the detected mutation gene. RESULTS: The authors detected a mutation in the IFNGR1 gene (NM_001363526.1) and validated the detected gene mutation using Sanger sequencing. The results showed a heterozygous mutation c.4C>T (p.L2F) located in the IFNGR1 gene (NM_001363526.1). STUDY LIMITATIONS: The mechanism of the IFNGR1 gene has not been further investigated in this study. CONCLUSIONS: The IFNGR1 gene mutation may be a potential risk factor for TM infection, and the presence of anti-interferon-γ autoantibodies can aggravate disease symptoms.

Talaromyces marneffei infection with IFNGR1 gene mutation in a patient with negative Anti-Interferon-γ autoantibodies

Abstract Background Talaromyces Marneffei (TM) is a rare opportunistic pathogen that mostly infects patients with low immunity compared to those with normal immunity. It may be related to immune deficiency or genetic factors. Objective To evaluate the gene mutation of a patient infected with TM in an endemic area with negative anti-interferon-γ autoantibodies, and negative human immunodeficiency virus (HIV) infection. Methods Extract deoxyribonucleic acid (DNA) samples from the patient's peripheral blood, detect the mutation gene by whole exome sequencing (WES), and carry out Sanger sequencing verification for the detected mutation gene. Results The authors detected a mutation in the IFNGR1 gene (NM_001363526.1) and validated the detected gene mutation using Sanger sequencing. The results showed a heterozygous mutation c.4C>T (p.L2F) located in the IFNGR1 gene (NM_001363526.1). Study limitations The mechanism of the IFNGR1 gene has not been further investigated in this study. Conclusions The IFNGR1 gene mutation may be a potential risk factor for TM infection, and the presence of anti-interferon-γ autoantibodies can aggravate disease symptoms.

Analysis of circRNA profiles and clinical value in Stevens-Johnson syndrome and toxic epidermal necrolysis.

Severe cutaneous adverse drug reactions, including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN), are challenging to be early diagnosed and evaluate their prognoses. This investigation aimed to analyse the expression profiles of SJS/TEN in peripheral blood mononuclear cells (PBMC) and assess the correlation between circular RNA (circRNA) and disease severity. Sixteen SJS/TEN patients and sixteen controls were enrolled and serum samples of both groups were obtained. CircRNA expression profiles in three SJS/TEN patients and three controls were detected by RNA sequencing and bioinformatic analyses were then performed. The differentially expressed circRNAs were verified by quantitative polymerase chain reaction (qPCR). Then, analysing the correlation of circRNAs with the toxic epidermal necrolysis-specific severity of illness score (SCORTEN) and the epidermal detachment area. A total of 134 circRNAs were differentially expressed in the PBMCs of SJS/TEN individuals, according to our results. The qPCR showed that three circRNAs (hsa_circ_0000711, hsa_circ_0083619 and hsa_circ_0005615) were down-regulated, and one circRNA (hsa_circ_0003028) was up-regulated, which were compatible with the sequencing findings. The concentration of hsa_circ_0083619 was closely associated with the SCORTEN scale (r = -0.581, p = 0.037) and the epidermal detachment area (r = -0.576, p = 0.039). The circRNA-miRNA-mRNA prediction network was used to construct the hsa_circ_0083619/miR-18a-5p/BCL2L10 axis. The hsa_circ_0083619 could serve as a disease severity indicator for SJS/TEN. Through bioinformatics analysis, we speculated that hsa_circ_0083619/miR-18a-5p/BCL2L10 axis might play a role in SJS/TEN pathogenesis.

Comparative Efficacy Between Intense Pulsed Light Narrow Spectrum and Broad Spectrum in the Treatment of Post-Acne Erythema (PAE).

Purpose: Post-acne erythema (PAE) is one of the most common physical sequelae of acne regression, PAE can resolve spontaneously, but in some patients it may last for years. This study aimed to evaluate the efficacy and safety of narrow and broad spectrum filters of intense pulsed light (IPL) for the treatment of PAE. Patients and Methods: This prospective study evaluated 60 patients with PAE for at least 6 months, assigned equally to three groups: 1st group received narrow-spectrum with vascular filter (530-650 nm and 900-1200 nm), 2nd group received broad-spectrum with (560/590-1200 nm) filters, the appropriate adjustments were made according to patient's skin colour. Every patient received four sessions one month apart. 3rd group is blank control group did not receive any treatment. CAT (CEA (Clinical Erythema Assessment), Area, and Telangiectasia) used to grade clearance of PAE before and after treatment, Investigators Global Assessment (IGA) used to assess the improvement score after the treatment, and Cardiff Acne Disability Index (CADI) used to evaluate the impact of PAE on patients' Quality of Life (QoL). Self-satisfaction scale completed at the follow-up. Adverse events and acne relapse were recorded. Results: A significant decrease of CAT score in vascular group (P<0.05). IGA scale showed significant improvement after vascular treatment. A significant decrease in CADI (P<0.05) after vascular treatment. Patient satisfaction was higher in vascular group than control and blank control groups. Acne relapse observed in control and blank control groups (40% and 15%, respectively).10% of patients showed pigmentation, 15% had blisters after 590 nm treatment. Conclusion: IPL vascular filter (530-650 nm and 900-1200 nm) have efficacy in the treatment of PAE. CADI score, patient satisfaction, and acne relapse were significantly better after vascular narrow spectrum treatment than broad-spectrum treatment.

Functional Involvement of ADRA1D in Cutaneous Melanoma Progression and Angiogenesis.

Cutaneous melanoma is a highly aggressive and malignant skin cancer, and its high recurrence rate and drug resistance increase the difficulty of treating advanced-stage patients. Studies have revealed that treatment via stimulation of alpha-1 adrenergic receptor (ADRA1) subtypes inhibits melanoma growth in mice. However, the associations between alpha-1D adrenergic receptor (ADRA1D) and cutaneous melanoma are poorly understood. Tissue specimens from 16 pairs of patients with a pigmented nevus and cutaneous melanoma were analyzed for ADRA1D expression using immunohistochemical staining. Western blotting and RT-qPCR were carried out in order to detect ADRA1D expression levels in melanoma cells and human epidermal melanocytes (HEMs), hypoxia-inducible factor-1α (HIF-1α), and vascular endothelial growth factor (VEGF) levels in HUVECS. A375 cells were transfected with a lentivirus overexpressing ADRA1D. Wound-healing, Transwell, and cell proliferation assays were utilized to identify the ADRA1D effect on the migration, invasion, and proliferation of the two groups of A375 cells in vitro. In order to evaluate the function of ADRA1D in vivo, a melanoma xenograft model was developed in immunodeficient mice. ADRA1D was low expressed in cutaneous melanoma tissues. Overexpression of ADRA1D inhibited the tubulation and migration of HUVECs in vitro. Overexpression of ADRA1D significantly decreased the HIF-1α and VEGF expression. Overexpression of ADRA1D inhibited the invasion and proliferation of A375 melanoma cells in vitro and reduced its angiogenesis in vivo. ADRA1D inhibits cutaneous melanoma growth and angiogenesis. It attenuates melanoma cell proliferation and invasion. Meanwhile, its anti-angiogenic effect is achieved by negatively regulating the HIF-1α/VEGF axis in melanoma tissue, thereby attenuating the growth of cutaneous melanoma and reducing the potential of metastasis.

Clinical efficacy of LED golden light combined with acyclovir in the treatment of herpes zoster: a single-center prospective study.

This study aimed to explore the safety and clinical efficacy of light emitting diode (LED) golden light combined with acyclovir in treating herpes zoster (HZ). According to the random number table, 54 inpatients with HZ were divided into control group, golden-light group, and red-light group, with 18 cases in each group. The control group received acyclovir intravenous drip, while the patients in the red-light group received acyclovir intravenous drip and red-light LED phototherapy, and the golden-light group received acyclovir intravenous drip and golden-light LED phototherapy. Primary assessments included herpes stopping time, incrustation time, decrustation time, pain visual analog scale scores (VAS), and incidence of postherpetic neuralgia (PHN) on the 30th and 90th days. Golden-light group and red-light group showed a shorter herpes stopping time, incrustation time, and decrustation time (P < 0.05) compared to the control group (P < 0.05), while the golden-light group showed a shorter incrustation time and decrustation time than the red light group (all P < 0.05). After treatment VAS scores, the golden-light group showed a significant improvement compared to the control group. The golden-light group showed a better PHN incidence than the control group at 30 days follow-up. Compared with the comprehensive curative effect, the total effective rates of the golden-light group, red-light group, and control group were 88.89%, 77.78%, and 72.22%, respectively, and the efficacy of the golden-light group was better than that of the control group and red-light group. Golden light combined with acyclovir can shorten the course of HZ, relieve pain, and reduce the occurrence of PHN, and the effect is better than that of the red-light group and the control group.

Analysis of clinical features and inflammatory-related molecules with the disease in acute infectious urticaria.

Acute infectious urticaria, a subset of acute urticaria, with severe persistence wheals and systemic symptoms, response well to corticosteroids treatment in combination with antibiotics. The exact pathogenic mechanisms are not fully understood. In this study, we aim to analyze the different clinical features, compare the level of neutrophil activation, and investigate the expression of inflammatory related cytokine in patients with acute urticaria and acute infectious urticaria. Eighteen patients with acute infectious urticaria and eighteen patients with acute urticaria were included in this study. We analyzed the difference between the clinical features and the serum expressions of pro-inflammatory factors in the two groups, then examined the levels of inflammation-associated cytokines before and after treatment of acute infectious urticaria. Hematoxylin & eosin (HE) staining and immunohistochemistry (IHC) were used to further study the relationship between neutrophil and neutrophil-derived Myeloperoxidase (MPO) of lesions in the two groups. The expression levels of C-reactive protein (CRP), D-dimer, interleukin 6 (IL-6), IL-8 and chemokine ligand 8 (CCL8) in serum were significantly higher in acute infectious urticaria than acute urticaria. In acute infectious urticaria, the serum expression levels of CCL8 were significantly decreased after the treatment, a significant correlation observed between CRP levels and IL-6, both CCL8 and CRP were positively correlated with neutrophil granulocytes. Neutrophils infiltration were not observed by HE stains in two groups, but in IHC stains we found a positive expression of MPO in acute infectious urticaria lesions. Elevated neutrophil in the serum, which is associated with the levels of IL-8 & CCL8, and positively expressed MPO in lesions, may be involved in the pathogenic mechanism of acute infectious urticaria.

Classic Eosinophilic Pustular Folliculitis in an Immunocompetent Patient with Syphilis: Are They Related?

Eosinophilic pustular folliculitis (EPF) is a rare, chronic, non-infectious inflammatory skin disease. Although the pathogenesis of EPF is unknown, eosinophilic pustular folliculitis may be associated with human immunodeficiency virus (HIV) infection, malignancies or syphilis. Here, we report the first case of EPF associated with syphilis, indicating that syphilis and EPF are correlated with T-helper type 2 immune responses. A 48-year-old man gradually developed erythema and pustules on the face, neck. Physical examination revealed multiple infiltrative red patches and plaques on the face, neck with tiny pustules. Skin biopsy results revealed that the dermal follicular sebaceous gland unit was infiltrated by a large number of neutrophils and eosinophils, forming eosinophilic microabscesses. Therefore, the patient was diagnosed with EPF associated with syphilis and received drug treatment. After the treatment, the pustules markedly decreased, leaving behind pigmentation. Furthermore, the patient is still being followed up.