Cutaneous squamous cell carcinoma (cSCC) is the most common malignancy in immunesuppressed organ transplant recipients (OTRs). Whilst rates of other malignancies (both cutaneous and non-cutaneous) are elevated in this population, the increase is far less striking. This suggests that cSCC must be a highly immunogenic tumor. The tumor immune microenvironment is altered in cSCC from OTRs. It has reduced anti-tumor properties and instead provides an environment that facilitates tumor growth and survival. Understanding the composition and function of the tumor immune microenvironment in cSCC from OTRs is useful for prognostication and therapeutic decisions.

Giant cellulitis-like Sweet syndrome (GCS) is the most recently defined variant of Sweet syndrome (SS) which could clinically mimic wide-spreading cellulitis. Although there has been only paucity of reports in the literature, it mostly appears at lower half of the body and histologically shows dense infiltration of neutrophils with occasional histiocytoid mononuclear cells. Although its exact etiology has not been clarified, abnormal conditions (e.g., infection, malignancy and drugs) could be related triggering factors and trauma itself can be one of the causative elements as a ‘pathergy phenomenon’. GCS could be confusing manifestation especially when appeared in postoperative condition. A 69-year-old female presented with an erythematous edematous papules and plaques on the right thigh after varicose vein surgery. Skin biopsy revealed diffuse neutrophilic infiltrates that was consistent with SS. To our knowledge, there has been no report of GCS as a postoperative complication after varicose vein surgery. Physicians should be aware of this uncommon reactive neutrophilic dermatoses mimicking infectious cutaneous disease.

Cowden syndrome is caused by mutations in the phosphatase and tensin homolog (PTEN) gene and is part of the PTEN hamartoma tumor syndrome. Skin lesions including trichilemmomas, acral keratosis, mucocunateous neuromas and oral paillomas are the most prevalent feature found in patients with Cowden syndrome. It also possesses an increased risk of developing malignancies including breast, thyroid, endometrial, and colorectal cancers.Due to the increased risk of cancer, early diagnosis and regular surveillance are important for Cowden syndrome patients. Herein, we report a case of Cowden syndrome with diverse cutaneous manifestations and thyroid cancer.

Drug-induced hypersensitivity syndrome (DiHS), also referred to as drug reaction with eosinophilia and systemic symptoms (DRESS), is a rare but potentially life-threatening condition induced by drug hypersensitivity that leads to significant morbidity and mortality and often occurs in patients undergoing combination antibiotic therapy. Due to a recent increase in the incidence of methicillin-resistant Staphylococcus aureus infections, the occurrence of vancomycin-induced DiHS/DRESS has increased rapidly. However, because of insufficient pharmacogenetic data on vancomycin-induced drug eruptions in Asians coupled with the risk of re-eliciting the symptoms by provocation tests, confirmation of the culprit drug in vancomycin-induced DiHS/DRESS is often challenging. Here, we report a case of vancomycin-induced DiHS/DRESS, where the causal relationship was confirmed using a lymphocyte transformation test (LTT). A 51-year-old woman was treated with combination antibiotics, including vancomycin, for infective pericarditis. The patient subsequently developed fever, facial edema, generalized rash followed by multiple internal organ involvement, including the kidney, lung, liver, and heart. Thus, based on the International Registry of Severe Cutaneous Adverse Reaction (RegiSCAR) criteria, the case was diagnosed as ‘definite’ DiHS/ DRESS, although the culprit drug was obscured by combination antibiotic therapy. The LTT confirmed that vancomycin, but not other glycopeptide antibiotics, specifically induced Tcell proliferation in this case. Collectively, our case suggests that clinicians can utilize LTT to identify the causative medication of DiHS/DRESS when the clinical information is limited to defining the culprit drug.

Background: Psoriasis is a complex and heterogeneous disease that widely affects a patient’s life. Biological therapy is usually prescribed in patients with severe psoriasis that do not respond to conventional treatment. However, data on the specific patient characteristics receiving biologics are still unavailable. Objective: To classify patients with psoriasis into subgroups with distinct phenotypes through cluster analysis, and to evaluate the differences between the clusters to predict disease prognosis by examining the response to biological therapy. Methods: The clinical characteristics of the patients with psoriasis were investigated and categorized using hierarchical cluster analysis. After clustering, the clinical characteristics of the patients were compared and the initiation of treatment with biologics according to the clusters were evaluated. Results: A total of 361 patients with psoriasis were classified into two clusters using 16 distinct clinical phenotypes. Group 1 (n=202) consisted of male smokers and alcohol users with higher psoriasis area and severity index (PASI), older age of onset, higher body mass index, and comorbidities including psoriatic arthritis, hypertension, and diabetes when compared to group 2 (n=159). Group 1 had a significantly higher probability of biological treatment initiation than group 2 (p=0.039). The measured risk factors for the initiation of biologics compared were PASI (p<0.001) and nail involvement (p=0.022). Conclusion Cluster analysis classified patients with psoriasis into two subgroups according to their clinical characteristics. Predicting the disease prognosis using a combination of specific clinical parameters may aid in the management of the disease.