IntroductionCongenital melanocytic nevi (CMN) denote benign melanocytic proliferations, affecting approximately 1 to 2% of newborns, with a higher prevalence observed among Asian and Black children1,2. Manifesting either at birth or within subsequent weeks, these nevi typically manifest as light brown to black patches or plaques, varying in size and distribution across the body. Classification commonly stratifies CMN into small (< 1.5 cm), medium-sized (1.5 to 19.9 cm), and large or giant (20 cm or greater) lesions 3,4. Described as ’garment or bathing trunk’ nevi, large lesions are infrequent, with an incidence ranging from 1:200,000 to 500,000 births and a notable female predilection3. They are often deeply pigmented, accompanied by moderate hair growth, and frequently associated with scattered satellite lesions. While the hairy component, present in 95% of cases, tends to become more prominent in late childhood, the nevus itself typically pales at this stage 1.Giant nevi may exhibit associations with several comorbidities, including neurocutaneous melanosis, diffuse lipomatosis, structural brain malformations, skull bone hypertrophy, limb atrophy, skeletal asymmetry involving soft tissue hyper- and hypoplasia, von Recklinghausen’s disease, and vitiligo 5. The likelihood of neoplastic transformation is directly proportional to CMN size, with an estimated incidence ranging from 6% to 12% over one’s lifetime 6. The emergence of firm nodules warrants vigilant attention, with differential diagnoses encompassing proliferative nodules and malignant melanoma 4. Malignant transformation within giant CMN predominantly occurs in axial locations, with extremity lesions presenting lower risk, and satellite nevi exhibiting negligible risk 6.The cornerstone of treatment for large congenital melanocytic nevi remains surgical excision, often employing staged excision and subsequent resurfacing via skin grafts, tissue expanders, or flaps for giant lesions 5. In this report, we document a case involving a male adolescent presenting with a giant congenital nevus accompanied by lipomatosis localized to the right flank.

IntroductionHerpes simplex virus (HSV), is a member of an enveloped, double-stranded DNA virus family named Herpesviridae, this virus causes latent infection of neural ganglia(1). It has a worldwide distribution and a wide range of clinical presentations depending on the host’s immune status and the infection site. In immunocompetent individuals, the most common presentation includes painful vesicles and erosions on an erythematous base, which can evolve into pustules and/or ulcerations (2, 3). In immunocompromised individuals such as solid organ or bone marrow transplant recipients, patients with hematologic malignancies, and acquired immunodeficiency syndrome (AIDS), HSV infection can have atypical manifestations, including chronic non-healing ulcers, verrucous plaques, and large protruding tumors. In the case of immunosuppressed patients, the lesions may disseminate and occur at multiple sites, including atypical locations such as the buttocks, abdomen, and lower back. Depending on the level of immunosuppression, HSV infection can have a variable duration, severity, and outcome. It can affect multiple or atypical sites, such as the abdominal, and thoracic regions, or even become disseminated(4, 5). In this article, we report a case of cutaneous perianal infection that presented as warty skin-colored papules and plaques underline the challenges in the morphologic and clinical diagnosis of this entity, and review the literature on verrucous HSV lesions in non-HIV patients.

IntroductionTinea capitis is a common infection of the scalp and hair caused by dermatophyte fungi that principally affects children1. It is an uncommon infection in adults and generally occurs in postmenopausal women and immunocompromised patients. Adult tinea capitis may have atypical clinical presentations2 34. The causative pathogens in children and adults belong to two genera: Trichophyton andMicrosporum 5. The clinical manifestations characterized by an erythematous and scaly plaques, itching, suppurative swelling with purulent discharge, areas of alopecia and regional lymphadenopathy. It is often misdiagnosed as a bacterial infection, leading to unnecessary antibiotic prescription or surgical intervention. Treatment delay may result in permanent hair loss6 7. The diagnosis of tinea capitis is made by fungal culture (gold standard), microscopy, wood’s lamp and trichoscopy5 8.