Background: Adiponectin is an adipose-derived hormone that plays a role in various metabolic diseases. We previously demonstrated that adiponectin inhibits melanin synthesis through adenosine monophosphate-activated protein kinase (AMPK) activation in melanocytes. However, melanocytes can be affected by neighboring keratinocytes, and the effect of adiponectin on these functional units has not been investigated. Objective: We investigated the effect of adiponectin on melanogenesis in co-cultured models of normal human melanocytes (NHMs), normal human keratinocytes (NHKs), and human dermal fibroblasts (HDFs), and the effect of adiponectin on melanin content in human skin tissues. Methods: Quantitative real-time polymerase chain reaction (qPCR) was performed for tyrosinase and microphthalmia-associated transcription factor (MITF). The degree of phosphorylation of AMPK, cAMP response element binding protein (CREB), and AKT was evaluated by western blot assay, and Fontana-Masson staining was performed on cultured human skin tissues. Results: Adiponectin decreased the melanin content in the co-culture models of NHMs with NHKs, NHMs with HDFs, and NHMs with both NHKs and HDFs. qPCR revealed that both tyrosinase and MITF were decreased after adiponectin treatment in the co-culture system. Following adiponectin treatment, AMPK was activated in all cell groups; however, the phosphorylation of CREB was decreased in HDFs and NHKs. The phosphorylation of AKT was decreased in only NHMs. In the experiment with human skin tissues cultured ex vivo, the densitometric analysis of Fontana-Masson staining revealed that adiponectin treatment reduced the melanin level of ultraviolet-irradiated human skin tissues. Conclusion Adiponectin inhibited melanogenesis in both co-culture models and human skin tissues ex vivo.

Acne fulminans shows severe inflammatory changes in acne lesions and is accompanied by systemic symptoms, such as fever and myalgia. Acne fulminans can leave scars, which can profoundly affect patients’ quality of life and require proper treatment. Herein, we present a case of acne fulminans that occurred after COVID-19 vaccination in a 15-year-old male patient. Considering no signs of infection, new drug administration, and immunological factors that can cause acne fulminans other than COVID-19 vaccination and the short time interval between the time of vaccination and the acne fulminans outbreak, acne fulminans is thought to have been caused by COVID-19 vaccination. Oral steroid and isotretinoin treatment was initiated, and 3 months after the treatment, acne lesions recovered to pre-COVID-19 vaccination status, with no exacerbated episode until 6 months follow-up.

A capillary hemangioma is a vascular tumor with small capillary sized vascular channel. Multiple capillary hemangioma in relation with drugs have been rarely reported. Here in, we report a case of multiple capillary hemangioma in patient diagnosed with chronic myeloid leukemia who received tyrosine kinase inhibitors (TKIs). Histopathological findings have shown capillary proliferation in the upper dermis, which is consistent with capillary hemangioma. Since TKIs can paradoxically activate the MEK/ERK pathway which is required for angiogenesis, we presumed that the lesions as the cutaneous side effects of TKIs.

A capillary hemangioma is a vascular tumor with small capillary sized vascular channel. Multiple capillary hemangioma in relation with drugs have been rarely reported. Here in, we report a case of multiple capillary hemangioma in patient diagnosed with chronic myeloid leukemia who received tyrosine kinase inhibitors (TKIs). Histopathological findings have shown capillary proliferation in the upper dermis, which is consistent with capillary hemangioma. Since TKIs can paradoxically activate the MEK/ERK pathway which is required for angiogenesis, we presumed that the lesions as the cutaneous side effects of TKIs.

Keratoacanthomas (KAs) are epithelial skin tumors characterized by rapid growth and spontaneous regression, with histopathologic features similar to those of cutaneous squamous cell carcinoma (SCC). KA arising after the use of anti-programmed cell death protein 1 (PD1) and anti-transforming growth factor beta (TGF-β) antibody have been reported. The patient in the present case was administered a new anti-cancer drug under clinical trial, which comprised anti-PD-ligand 1 (PD-L1) and anti-TGF-β antibodies. Nine months after the drug was used, a hyperkeratotic nodular lesion appeared on the patient's left arm. As a result of histopathologic examination by excision of the corresponding lesion, it was diagnosed as KA.