Childhood skin rashes are frequently evaluated by primary care physicians and are often diagnosed by recognition of distinguishing features. Atopic dermatitis affects 15% to 20% of children, usually with onset before the age of 2 years. Treatment is based on severity and begins with emollients and topical steroids. Erythema infectiosum presents with the slapped cheek rash that progresses to reticular lesions on the trunk and extremities. Hand-foot-and-mouth disease presents with painful oral ulcers and vesicular eruption of the hands, feet, buttocks, and genitals. Nonbullous impetigo is characterized by lesions with honey-colored crusting, whereas bullous impetigo presents with flaccid bullae; both are treated with antibiotics. Molluscum contagiosum is characterized by dome-shaped umbilicated papules that spontaneously resolve over months to years without intervention but may be treated with cryotherapy, curettage, or topical agents. Pityriasis rosea usually presents with a large herald patch on the trunk followed by the eruption of numerous smaller lesions aligned with Langer lines. Scarlet fever is a group A beta-hemolytic streptococcal infection with a sandpaper-like rash and should be treated with antibiotics to prevent rheumatic fever. Tinea capitis requires treatment with systemic antifungals, whereas tinea corporis is usually treatable with topical agents.

A case of an immunocompetent male patient in his 50s, an oil field worker from the northeastern part of India who presented with fever, weight loss over 4 months, and multiple umbilicated papulonodular lesions on his face and nodular lesions over the hard palate, is reported. The initial suspicion was talaromycosis, which is endemic in that part of the country. Periodic acid-Schiff and Grocott-Gomori's methenamine silver staining of the skin biopsy specimen from the forehead revealed numerous yeast-like bodies morphologically resembling Histoplasma within the histiocytes. A culture of the skin biopsy grew Histoplasma capsulatum. The patient received liposomal amphotericin B (3 mg/kg/day) but later was shifted to oral itraconazole because of acute kidney injury. The patient exhibited improvement, with flattening of skin lesions and no development of new lesions during treatment. This case highlights histoplasmosis mimicking talaromycosis and the importance of tissue diagnosis for accurate identification.

Eczema molluscatum refers to widespread molluscum contagiosum (MC) infection occurring in patients with atopic dermatitis (AD), a setting in which impaired skin barrier function and immune dysregulation both promote viral spread. We report the case of a 29-year-old man with longstanding, treatment-refractory AD who was well controlled on upadacitinib, a selective Janus kinase 1 (JAK1) inhibitor, and methotrexate when he developed multiple pink, dome-shaped papules with central umbilication across the cheeks and forehead over a six-month period. The lesions were unresponsive to topical clindamycin-benzoyl peroxide gel. The differential diagnosis included eczema coxsackium, eczema herpeticum, eruptive syringomas, and a refractory JAK inhibitor-associated acneiform eruption, but the absence of pain, systemic symptoms, vesiculation, and follicular morphology supported a diagnosis of eczema molluscatum. The patient was treated with cryotherapy for each lesion, with marked improvement at one-month follow-up. AD itself is a recognized risk factor for MC, reflecting the disease's inherent Th2-skewed, barrier-disrupted immune environment. However, this case raises the possibility that systemic immunosuppression with JAK1 inhibitors, particularly in combination with methotrexate, may further impair type I interferon-mediated antiviral defense and compound susceptibility to MC in patients with AD. Nonetheless, clinicians should maintain a high index of suspicion for eczema molluscatum in patients with AD on JAK inhibitor therapy who develop new facial papules, as these lesions are readily mistaken for a JAK inhibitor-associated acneiform eruption, potentially delaying appropriate treatment.

Background and Clinical Significance: Eczema herpeticum (EH), or Kaposi's varicelliform eruption, is a dermatologic emergency characterized by the abrupt onset of painful monomorphic vesiculopustules with potential for rapid dissemination. Atopic dermatitis (AD) is the main predisposing condition due to skin barrier dysfunction and impaired antiviral immunity. Early recognition is essential because delayed treatment may result in avoidable complications, including ocular involvement and systemic disease. Current recommendations emphasize immediate systemic acyclovir based on clinical suspicion, without awaiting laboratory confirmation. Case Presentation: A 4-year-old boy with moderate AD presented with a 6-day history of fever, malaise, and a rapidly progressive vesiculopustular eruption involving both eczematous and previously unaffected skin. The patient had a recent AD flare, molluscum contagiosum, and had initially received oral amoxicillin-clavulanate for presumed bacterial superinfection without improvement. Physical examination revealed widespread painful monomorphic umbilicated vesiculopustules with hemorrhagic crusts and mild bilateral conjunctival injection. Oral acyclovir was initiated within one hour of evaluation. Laboratory investigations showed mild inflammatory abnormalities without renal or hepatic involvement. Because lesional PCR was unavailable, complementary blood-based investigations were performed; HSV-1 IgM serology and blood PCR provided additional retrospective findings compatible with HSV-1 infection, while Gram stain and bacterial cultures were negative. Fever resolved within 24 h, no new lesions developed after day 3, and complete re-epithelialization was achieved after a 10-day course of acyclovir. Conclusions: This case highlights the importance of bedside recognition of eczema herpeticum in children with atopic dermatitis, particularly when painful monomorphic vesiculopustules are accompanied by fever and rapid dissemination. Early initiation of systemic acyclovir based on clinical suspicion remains the cornerstone of management. While PCR from vesicular lesions is the preferred diagnostic test when available, laboratory confirmation should not delay treatment. This report also illustrates common real-world challenges, including initial misdiagnosis as bacterial infection and limited access to optimal virological testing.

Gastric ectopic pancreas is an uncommon congenital anomaly that is usually asymptomatic but can mimic gastric malignancy when inflamed. We report the case of a 33-year-old previously healthy woman who presented with acute severe epigastric pain and inability to tolerate oral intake. Endoscopy demonstrated annular thickening of the gastric antrum, congested and friable mucosa, and poor gastric distensibility. Contrast-enhanced computed tomography demonstrated irregular circumferential antral wall thickening with an enhancing endoluminal mass, perigastric lymphadenopathy, and minimal free intraperitoneal fluid, raising a strong suspicion for gastric malignancy. Fibroblast activation protein inhibitor positron emission tomography demonstrated a tracer-avid gastric antral lesion. Endoscopic ultrasound showed a large hypoechoic mural lesion with loss of normal wall-layer architecture and perigastric lymph nodes. Conventional biopsy showed Helicobacter pylori-associated chronic gastritis without malignancy, while endoscopic ultrasound-guided sampling revealed spindle cells with eosinophilic inflammatory infiltrate and only mild cytological atypia. Immunohistochemistry helped exclude gastrointestinal stromal tumour, schwannoma, carcinoma, and inflammatory myofibroblastic tumour. Following H. pylori eradication therapy and conservative management, symptoms resolved completely. Repeat endoscopy at three months demonstrated resolution of antral thickening and a residual centrally umbilicated subepithelial lesion, supporting the presumed inflamed gastric ectopic pancreas. This case highlights that fibroblast activation protein inhibitor avidity should be interpreted as a marker of fibroblast activation rather than proof of malignancy and that interval reassessment can prevent unnecessary radical surgery in clinically stable patients with discordant imaging and histology.

Acquired reactive perforating collagenosis (ARPC) is a rare perforating dermatosis that is frequently misdiagnosed, particularly before the development of overt transepidermal elimination. Although early lesions have been sporadically mentioned in previous reports, direct clinicopathological evidence supporting a recognizable pre-perforating stage remains limited. We report the case of a 64-year-old woman with a 3-year history of progressive, generalized pruritic papules and nodules, initially misdiagnosed as eczema and refractory to conventional treatments. The patient had long-standing type 2 diabetes mellitus and other metabolic comorbidities. Dermoscopy of early erythematous papules revealed subtle but reproducible features distinct from those of fully developed lesions. Notably, even in early lesions showing focal epidermal disruption, classic dermoscopic signs of perforation were absent. Targeted biopsy of these early lesions exhibited abnormal aggregation and disorganization of dermal collagen in the superficial dermis, closely apposed to the epidermis but without transepidermal elimination. In contrast, biopsies of mature umbilicated plaques revealed typical collagen extrusion with overlying keratotic plugs. Sequential Masson's trichrome and elastic fiber staining further supported a stepwise evolution from superficial collagen remodeling to overt perforation. By correlating dermoscopic findings with sequential histopathological changes in the same patient, this case report provides direct evidence that ARPC progresses through a definable pre-perforating stage, in which epidermal disruption alone is insufficient to induce collagen elimination. Recognition of this early stage has important implications for timely diagnosis, appropriate biopsy selection, and avoidance of prolonged misdiagnosis.

BackgroundGenital mpox has been scarcely described in Central and West Africa where the disease is endemic. This study aimed to describe the clinical manifestations of genital mpox acquired through sexual contact in heterosexual African couples.MethodsThis was a case series of patients presenting with genital lesions associated or without febrile pustular or vesicular eruptions and confirmed with a positive PCR. Medical records of patients were scrutinized between March 2022 and December 2025 in three dermatology centres located either in Cameroon or Benin. Sociodemographic characteristics, clinical features, laboratory results, treatment, and outcomes were systematically documented.ResultsIn total, nine cases of genital mpox from six heterosexual couples were documented. Patients' median age was 35 years (IQR 31-42 years; range: 28-45 years). Two heterosexual partners were living with HIV with undetectable plasma viral loads. Sexual contact preceding genital lesions' onset was reported in seven of 9 cases (78%). The incubation period ranged from 3 to 10 days. Clinical manifestations included vesicles, pustules, erosions, ulcerations, genital edema, umbilicated necrotic papules, and inguinal lymphadenopathy. The morphology of lesions varied from rounded/oval to arcuate and linear patterns. The recovery time ranged from 2 to 8 weeks, though longer for ulcerations. People living with HIV experienced severe presentations and prolonged recovery.ConclusionGenital manifestations of mpox on black skin are polymorphic and can present with atypical features. Mpox should be considered as a differential diagnosis of genital lesions following condomless sexual intercourse, particularly in endemic areas.

Juvenile xanthogranuloma (XGJ) is a generally benign non-Langerhans cell histiocytosis (non-LCH) that primarily affects infants and children. It typically presents as a single skin lesion. Disseminated and profuse forms remain rare and can pose diagnostic or therapeutic challenges. The classification of histiocytoses has recently evolved, incorporating disseminated XGJ into group "C" of non-LCH cutaneous histiocytoses. While the prognosis for isolated cutaneous forms is excellent, vigilance regarding potential associations (type 1 neurofibromatosis and juvenile myelomonocytic leukemia) and systemic complications remains essential. We report the case of a four-month-old infant presenting with a purely cutaneous disseminated form of XGJ, confirmed by histopathology and immunohistochemistry, which required systemic corticosteroid therapy due to the rapid spread of the lesions. This study involves a four-month-old infant with no significant family history who has been presenting with gradually progressive papular skin lesions for one month. Clinical examination revealed multiple umbilicated, yellowish-brown papulonodules scattered across the face, trunk, limbs, skin folds, genital mucosa, and scalp; a café-au-lait spot was detected on one limb. Dermoscopy revealed a characteristic "sunset" pattern. Histopathological and immunohistochemical analysis (CD68+, CD163+, CD1a-, CD34-, S100-) confirmed the diagnosis. The staging evaluation revealed no abnormalities. After three months of simple monitoring, the extensive spread of the lesions prompted the initiation of oral corticosteroid therapy (1 mg/kg/day), resulting in partial regression at six weeks. Disseminated XGJ in infants remains a rare condition. Although the course is most often self-limiting, justifying an initial conservative approach, certain extensive forms may require systemic treatment. The dermatologist plays a central role in diagnosis, based on a combination of clinical, dermoscopic, histopathological, and immunohistochemical findings, and in the multidisciplinary decision-making regarding treatment.