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Systemic sclerosis (SSc) is an autoimmune disease characterized by vasculopathy, aberrant immune activation, and extensive tissue fibrosis of the skin and internal organs. Because of the complicated nature of its pathogenesis, the underlying mechanisms of SSc remain incompletely understood. Angiogenic factor with a G‐patch domain and a Forkhead‐associated domain 1 (AGGF1) is a critical factor in angiogenesis expressed on vascular endothelial cells, associated with inflammatory and fibrotic responses. To elucidate the possible implication of AGGF1 in SSc pathogenesis, we investigated the association between serum AGGF1 levels and clinical manifestations in SSc patients. We conducted a cross‐sectional analysis of AGGF1 levels in sera from 60 SSc patients and 19 healthy controls with enzyme‐linked immunosorbent assay. Serum AGGF1 levels in SSc patients were significantly higher than those in healthy individuals. In particular, diffuse cutaneous SSc patients with shorter disease duration had higher levels compared to those with longer disease duration and limited cutaneous SSc patients. Patients with higher serum AGGF1 levels had a higher incidence of digital ulcers, higher modified Rodnan Skin Scores (mRSS), elevated serum Krebs von den Lungen‐6 (KL‐6) levels, C‐reactive protein levels, and right ventricular systolic pressures (RVSP) on the echocardiogram, whereas they had reduced percentage of vital capacity (%VC) and percentage of diffusing capacity of the lungs for carbon monoxide (%DLCO) in pulmonary functional tests. In line, serum AGGF1 levels were significantly correlated with mRSS, serum KL‐6 and surfactant protein D levels, RVSP, and %DLCO. These results uncovered notable correlations between serum AGGF1 levels and key cutaneous and vascular involvements in SSc, suggesting potential roles of AGGF1 in SSc pathogenesis. [ABSTRACT FROM AUTHOR]

Palmoplantar pustulosis (PPP) is a chronic skin inflammatory disease characterized by sterile pustules on the palms and soles. Pustulotic arthro‐osteitis (PAO) is a major comorbidity of PPP, frequently affecting the anterior chest wall. PPP and PAO are thought to be closely associated with focal infection. We report a female in her 40s who developed pustules on her palms and soles with tenderness of both sternoclavicular and left sacroiliac joints, which were not improved with non‐steroidal anti‐inflammatory drugs. Of note, she showed a great response to amoxicillin, resulting in the almost complete resolution of her skin lesions and arthralgia. We also reviewed previous reports to learn more about the potential therapeutic options of antibiotics for PAO. [ABSTRACT FROM AUTHOR]

Objectives: Graft‐versus‐host disease (GVHD) is an important complication of bone marrow transplantation. Recent reports suggest the significance of T‐cell subsets (Th1, Th17, and cytotoxic CD8+ T cells) as well as CD163+ macrophages in the development of cutaneous GVHD. CD163+ macrophages produce various chemokines to establish the immunological microenvironment following stimulation by stromal factors in lesional skin. Thus, the purpose of this study is to determine the main source of IFN‐inducible chemokines in the lesional skin of GVHD. Methods: We employed immunohistochemical (IHC) staining for CD163 as well as interferon (IFN)‐inducible chemokines (CXCL9, CXCL10, CXCL11) to determine if the main source of IFN‐inducible chemokines in the lesional skin of GVHD was CD163+ macrophages. Moreover, we investigated the possible cytokine profiles of lesional skin in GVHD by evaluating phospho‐signal transducer and activator of transcription (pSTAT) expression in epidermal keratinocytes. Results: Immunohistochemical staining of serial sections for CD163 revealed that CXCL9‐expressing cells, CXCL10‐expressing cells, and CXCL11‐expressing cells were detected in adjacent to CD163+ TAMs in the dermis. In contrast, there were no CCL17‐expressing cells or CCL22‐expressing cells in the dermis. The nuclei of epidermal keratinocytes in GVHD expressed pSTAT1, pSTAT3, and pSTAT5B. Conclusions: The chemokine expression patterns on CD163+ macrophages matched the expected phosphorylation pattern of epidermal STATs. Our present study suggested that CD163 + macrophages may be a therapeutic target in GVHD. The significance of T‐cell subsets (Th1, Th17, and cytotoxic CD8+ T cells) as well as CD163+ macrophages in the development of cutaneous GVHD. ·IHC staining revealed that CXCL9‐expressing cells, CXCL10‐expressing cells, and CXCL11‐expressing cells were detected in adjacent to CD163+ TAMs in the dermis. ·The chemokine expression patterns on CD163+ macrophages matched the expected phosphorylation pattern of epidermal STATs. [ABSTRACT FROM AUTHOR]

A few reports have described cutaneous allergic reactions to peritoneal dialysis catheters during continuous ambulatory peritoneal dialysis (CAPD).[[1]] Here, we report a rare case of subcutaneous granulomatous reaction with eosinophil infiltration caused by a peritoneal dialysis catheter, and confirmed by skin tests. To the best of our knowledge, no similar case of subcutaneous granulomatous reaction with eosinophil infiltration caused by a peritoneal dialysis catheter has been reported, which was histologically confirmed by eosinophilic infiltration in skin tests. Because a catheter infection clinically resembles a subcutaneous allergic reaction, it is important to suspect CAPD catheter-related reactions if patients do not respond to antibiotics. [Extracted from the article]

Introduction: Basal cell carcinoma (BCC) is a common skin cancer that rarely metastasizes but can deeply infiltrate local tissues. The small number of unresectable BCC cases makes it difficult to conduct clinical trials, resulting in delays in the development of effective drugs for BCC. Cancer gene panel testing has led to an increasing number of new treatment proposals for patients with solid tumors for whom no standard treatment is available. Case Presentation: We described a case of unresectable BRCA1 L63*-mutated BCC invading the parietal bone, which was successfully treated with cisplatin and fluorouracil. Conclusion: Our present case suggests that comprehensive mutation analysis by gene panel testing is important in advanced BCC because genes other than those involved in the hedgehog signaling pathway can be driver genes. [ABSTRACT FROM AUTHOR]