Gastrointestinal basidiobolomycosis (GIB) is a rare invasive fungal infection of immunocompetent hosts that is endemic to Saudi Arabia and the wider Gulf region. Its presentation overlaps with inflammatory bowel disease (IBD), intestinal tuberculosis and malignancy, and many patients reach a definitive diagnosis only after surgery. We report a 39-year-old Saudi woman who presented with a 7-day history of right lower quadrant pain and non-bloody watery diarrhea. Initial bloods showed an elevated C-reactive protein of 21.5 mg/L, an erythrocyte sedimentation rate of 44 mm/hour and an absolute eosinophil count of 0.54 × 10[3]/µL. Contrast-enhanced computed tomography (CT) demonstrated segmental wall thickening of the terminal ileum, cecum and proximal transverse colon, with a 3×5 cm intramural cecal collection. Colonoscopy revealed ulcerated congested mucosa and an ileocecal stricture; targeted biopsies showed an eosinophil-rich granulomatous inflammation with broad, sparsely septate fungal hyphae demonstrating the Splendore-Hoeppli phenomenon, positive on Grocott methenamine silver and periodic acid-Schiff stains; and tissue culture grew Basidiobolus spp. Interventional radiology and surgical drainage were considered but were technically not feasible because of the intramural location, so the patient was managed medically with oral itraconazole at 200 mg every 8 hours for 3 days followed by 200 mg once daily, with monthly liver enzyme monitoring. Surgery was avoided. A repeat CT scan at 2 months showed near complete resolution of wall thickening, and follow-up colonoscopy at 5 months was normal. The patient self-discontinued itraconazole at 9 months because of symptom resolution and remained asymptomatic at follow-up 2 months later. Clinicians working in endemic regions should consider GIB in any patient with an ileocecal mass or abscess, eosinophilia and an IBD-like presentation, because early biopsy with fungal stains and prompt azole therapy can avert surgery.

Eosinophilic fasciitis (EF) is a rare autoimmune disease characterized by fascial inflammation, skin induration, eosinophilia, and progressive functional impairment. Although glucocorticosteroids (GCs) remain the first-line therapy, some patients develop refractory or steroid-dependent disease, highlighting the need for alternative treatment strategies. This case-based review summarizes current evidence on biologic and targeted therapies in severe EF and presents a case of successful treatment with tocilizumab (TCZ). A systematic review of PubMed, Scopus, and Web of Science databases identified 35 eligible articles published between 2008 and 2026. Qualitative synthesis included 49 patients treated with biologic or targeted agents, most commonly rituximab (n = 14), tocilizumab (n = 9), infliximab (n = 7), and mepolizumab (n = 5). Partial or complete response was achieved in 47 of 49 (96%) patients across all treatment groups. Biologic therapy was associated with a pronounced steroid-sparing effect, enabling GCs dose reduction or complete withdrawal in the majority of refractory patients. Furthermore, we describe a 28-year-old man with progressive, treatment-resistant EF who failed to respond adequately to GCs and methotrexate. Following initiation of weekly subcutaneous TCZ, the patient showed marked clinical, laboratory, and radiological improvement, with normalization of inflammatory markers, regression of fascial edema on MRI, and substantial functional recovery. Available case-based evidence suggests that biologic and targeted therapies, including IL-6 inhibition, may be promising options in selected patients with severe, refractory, or GC-dependent EF. However, considering the high risk of publication bias and reliance on case reports, prospective multicenter studies are required to establish standardized treatment recommendations.

Kimura disease typically presents with painless head and neck swelling in young adults of Asian descent, accompanied by peripheral eosinophilia and elevated serum IgE. We report a case of Kimura disease in a woman in her early 30s presenting with a slowly enlarging epitrochlear mass, diffuse encasement of the median and medial brachial cutaneous nerves, and a concurrent prurigo nodularis-like papular rash affecting all 4 extremities. The diagnosis required over 1 year of investigation and 5 tissue specimens, including 2 nondiagnostic core-needle biopsies, before near total excision was performed. The excision revealed characteristic histopathologic features, including hyperplastic reactive secondary lymphoid follicles with preserved architecture, a marked eosinophilic infiltrate with eosinophilic microabscesses, postcapillary venule proliferation, and patternless stromal fibrosis. Immunohistochemistry demonstrated a raised IgG4:IgG plasma cell ratio of approximately 1:1, with 150-200 IgG4-positive plasma cells per high-power field, raising the differential of IgG4-related disease; however, the absence of storiform fibrosis and obliterative phlebitis, combined with the clinical and serologic profile, favored Kimura disease. This case is notable for its rare epitrochlear location, extensive neural involvement, concurrent diffuse cutaneous eruption, and histopathologic overlap with IgG4-related disease, highlighting the diagnostic challenges posed by atypical presentations of Kimura disease.

Antithrombotic agents are among the most frequently prescribed medications in elderly patients and are essential for the prevention and treatment of cardiovascular and cerebrovascular diseases. Although cutaneous adverse reactions associated with anticoagulants and antiplatelet agents are generally considered uncommon, dermatologists frequently encounter these medications when evaluating patients presenting with pruritic eruptions. This apparent discrepancy may be explained by differences in patient populations. While cardiologists and neurosurgeons manage all patients receiving antithrombotic therapy, dermatologists evaluate a selected population enriched for cutaneous symptoms. This review summarizes the spectrum of cutaneous adverse reactions associated with major antithrombotic agents, including warfarin, heparins, aspirin, ticlopidine, clopidogrel, cilostazol, prasugrel, and direct oral anticoagulants (DOACs). Reported reactions range from common hemorrhagic manifestations to delayed-type hypersensitivity reactions; severe cutaneous adverse reactions, such as drug reaction with eosinophilia and systemic symptoms (DRESS/DIHS), Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), vasculitis, and skin necrosis. Particular emphasis is placed on drug-specific dermatologic phenotypes and diagnostic approaches, including drug-induced lymphocyte stimulation testing, patch testing, and clinicopathological correlation. In addition, Japanese case reports published between 1980 and 2024 are reviewed and integrated with the international literature. These data suggest that antithrombotic agents should not be regarded as a homogeneous dermatologic risk category. Instead, each drug class exhibits characteristic cutaneous reaction patterns that may assist in the differential diagnosis of these reactions in clinical practice. Recognition of these drug-specific phenotypes may facilitate earlier diagnosis, improve interdisciplinary communication, and optimize the management of suspected antithrombotic drug eruptions.

Paragonimiasis is a parasitic disease that involves the lungs but can manifest in extrapulmonary sites, including the peritoneum or subcutaneous tissue. Diagnosis is limited by nonspecific clinical manifestations and overlapping features with other diseases, such as tuberculosis (TB). A 55-year-old Korean male presented with acute abdominal pain and a recurrent subcutaneous mass in the left thigh. Although TB peritonitis was initially suspected, further diagnostic tests were performed. To confirm the diagnosis, multiplex real-time polymerase chain reaction (PCR) targeting the 28S rRNA gene and conventional PCR targeting the ITS2 region were performed on the ascitic fluid. Sequence analysis and phylogenetic clustering confirmed Paragonimus westermani. The patient was treated with praziquantel and showed clinical improvement. This case highlights the importance of considering paragonimiasis in patients with unexplained eosinophilia and peritoneal symptoms, even in the absence of pulmonary involvement. Molecular diagnostic tools can help confirm extrapulmonary infections and prevent misdiagnosis, particularly in endemic regions.

Erythroblastic sarcoma is a rare and aggressive hematologic malignancy presenting as a mass-forming extramedullary proliferation of immature erythroid cells. Myeloid/lymphoid neoplasms with JAK2 rearrangement, most often PCM1::JAK2, may show eosinophilia, myelofibrosis, and expansion of immature erythroid precursors. NUTM1 rearrangements, initially recognized as defining alterations of NUT carcinoma, have subsequently been identified in selected hematologic malignancies but remain exceptionally rare in myeloid neoplasms. Here, we report an adult erythroblastic sarcoma harbouring concurrent PCM1::JAK2 and a novel NOP10::NUTM1 fusion, accompanied by partial chromosome 8p deletion and complicated by secondary hemophagocytic lymphohistiocytosis. To our knowledge, this is the first reported adult erythroblastic sarcoma with concurrent PCM1::JAK2 and NOP10::NUTM1 fusions. This case extends the molecular spectrum of erythroblastic sarcoma and underscores the value of integrated morphologic, immunophenotypic, cytogenetic, and genomic assessment in diagnostically challenging erythroid neoplasms.