Cryoglobulinemic vasculitis is an immune-complex-mediated small-vessel vasculitis characterized by complement activation and endothelial injury. Its clinical manifestations are heterogeneous and may range from limited cutaneous involvement to systemic disease. We report the case of a 65-year-old woman who developed a symmetrical violaceous dermatosis involving the upper and lower extremities, accompanied by arthralgias and distal paresthesias. Laboratory investigations revealed marked hypocomplementemia and positive circulating cryoglobulins. Histopathological examination of a skin biopsy demonstrated leukocytoclastic vasculitis, leading to the diagnosis of idiopathic cryoglobulinemic vasculitis after exclusion of hepatitis C virus infection, autoimmune diseases, and associated hematologic malignancies, with no evidence of major systemic organ involvement. Treatment with corticosteroid- and cyclophosphamide-based immunosuppression achieved sustained disease control, resulting in approximately 90% symptomatic improvement. This case highlights the importance of recognizing cardinal manifestations, such as palpable purpura, arthralgias, and hypocomplementemia, when evaluating patients with suspected cryoglobulinemic vasculitis, even in the absence of identifiable secondary causes. Early recognition, histopathological confirmation, and a multidisciplinary approach are essential for establishing an accurate diagnosis and implementing timely therapeutic intervention aimed at preventing disease progression and irreversible organ damage.

Erythema elevatum diutinum (EED) is a rare and chronic form of cutaneous vasculitis often associated with systemic diseases including such hematologic malignancies as IgA monoclonal gammopathy, multiple myeloma, and non-Hodgkin lymphoma, as well as such autoimmune disorders and infections human immunodeficiency virus (HIV) and streptococcus. Clinically, EED presents as symmetrical red-to-brown papules, plaques, or nodules, primarily on extensor surfaces including the elbows, knees, and hands. These lesions may be asymptomatic or associated with burning, tenderness, or pruritus, and their chronic nature often leads to fibrosis and discoloration over time. Histologically, EED exhibits leukocytoclastic vasculitis associated with neutrophilic infiltration in the upper and mid dermis with sparing of the papillary and periadnexal dermis, fibrin deposition, and progressive dermal changes, including granulation tissue and fibrosis in late-stage lesions. While no cure exists, the first-line treatment is dapsone. Corticosteroids and immunosuppressive agents are employed for resistant cases. Early diagnosis and management are essential, particularly given the condition's potential to signal serious underlying systemic diseases. Although EED lesions may persist for decades, treating theunderlying conditions can influence the disease course, offering a pathway to improved outcomes.

BACKGROUND Over 5000 plant species produce milky latex sap utilized in decoration and various industries. Sap exposure, however, can elicit toxic reactions, including acute keratoconjunctivitis and corneal stromal infiltration. The common ornamental plant Dieffenbachia can cause acute keratoconjunctivitis and the deposition of fine blue crystals within the corneal stroma. This report analyzes 3 cases of Dieffenbachia-induced keratitis and reviews existing literature on plant-induced keratitis. CASE REPORT Three patients presented with ocular irritation, pain, and redness following accidental exposure to Dieffenbachia sap. Clinical examination revealed chemosis and corneal edema in all cases. Slit-lamp microscopy identified fine, needle-like oxalate crystals located within the epithelial and stromal layers of the inferior cornea. The 3 patients received conservative management: ocular irrigation, topical antibiotics, and localized anti-inflammatory agents. The treatment protocol was altered, depending on the clinical ocular response. When symptoms gradual improved, anti-inflammatory medication was decreased by 1 to 2 doses after 1 to 2 weeks, throughout a treatment duration of 4 to 8 weeks. Complete resolution of crystal deposits in the cornea was observed after a 4- to 8-week follow-up period. All patients retained satisfactory visual acuity and exhibited no corneal opacities. CONCLUSIONS Patients with keratitis caused by Dieffenbachia sap typically achieve full recovery without complications, but the potential for crystal deposition in the cornea must be recognized. Safety measures, including protective eyewear, gloves, and long-sleeved clothing during plant maintenance are essential. Comprehensive knowledge of the pathogenesis and clinical trajectory of ocular Dieffenbachia exposure will enable ophthalmologists to optimize treatment strategies.

Vasculitic skin lesions have been reported in association with both SARS-CoV-2 infection and vaccination. Whether viral proteins persist in lesional vessels beyond the acute phase remains unclear. The aim of this study was to investigate the presence of SARS-CoV-2 spike protein in persistent or delayed-onset cutaneous vasculitis temporally associated with COVID-19 infection or vaccination. This retrospective case-control study includes 9 patients with persistent or delayed-onset vasculitic skin lesions following COVID-19 infection (n=4) or mRNA vaccination (n=5). Skin biopsies were analysed using immunofluorescence for SARS-CoV-2 spike protein. Prepandemic leukocytoclastic vasculitis (n=3) and healthy postinfection/postvaccination skin (n=3) served as controls. Spike protein was detected in vascular endothelial cells of all 9 patients with COVID-19- or vaccine-associated vasculitis. Staining was absent in all prepandemic vasculitis and healthy control samples. Histopathology showed typical features of leukocytoclastic vasculitis without evidence of viral cytopathic changes. We found that SARS-CoV-2 spike protein can persist in endothelial cells of vasculitic skin lesions weeks to months after COVID-19 infection or mRNA vaccination. These findings suggest that retained viral proteins may contribute to prolonged or delayed-onset vasculitic skin manifestations. Further studies are needed to clarify the mechanisms underlying spike persistence and its clinical significance.

Neutrophilic dermatoses are a group of rare heterogenous inflammatory disorders that share the presence of a sterile neutrophilic infiltrate on histopathology due to an underlying systemic illness, which can be a malignancy. This group of disorders can have diverse clinical presentations, including papules, plaques, nodules, vesiculopustular lesions, or ulcerations. We review the clinical and histopathologic features of several neutrophilic dermatoses that can be cutaneous manifestations of an underlying malignancy, including Sweet syndrome (acute febrile neutrophilic dermatosis), pyoderma gangrenosum, neutrophilic eccrine hidradenitis, subcorneal pustular dermatosis, erythema elevatum diutinum, Behçet's disease, Bazex syndrome, and VEXAS syndrome, We also discuss current treatment options. Cutaneous vasculitis, Schnitzler syndrome, and eosinophilic paraneoplastic dermatoses are also discussed in the context of cutaneous presentations of malignancy. These dermatologic conditions that may precede underlying malignancy.

Eosinophilic gastrointestinal diseases (EGID) are characterized by abnormal and prominent eosinophilic inflammation of the gastrointestinal mucosa, associated with symptoms related to the segment involved, in the absence of secondary causes of eosinophilia. EGID may affect different parts of the gastrointestinal tract, causing eosinophilic oesophagitis (EoE), eosinophilic gastritis, eosinophilic enteritis and eosinophilic colitis either individually or in combination. Secondary causes of eosinophilic infiltration of the gastrointestinal tract include parasitic infections, the use of certain medications, vasculitis, allergic syndromes, haematological conditions and other inflammatory diseases. The incidence of EGID is increasing globally. EoE is the most reported form, with a prevalence of ~1 in 700 individuals. Several pathogenetic mechanisms are being investigated, in particular, the crosstalk between aeroallergens and mucosal inflammatory cell activation, which leads to a T helper 2 cell inflammatory response and disruption of epithelial barrier integrity. EGID is frequently associated with other T helper 2 cell-driven disorders, such as atopic dermatitis, allergic rhinitis and asthma. EGID is diagnosed through histological assessment, with biopsy samples of affected areas typically showing increased eosinophils, after excluding secondary causes of eosinophilia. For EoE, new treatments, including biologic therapies, are now available, whereas therapeutic options for non-EoE EGID remain limited. Patients' quality of life may be impaired owing to social and functional limitations from symptoms, such as dysphagia and food impaction in EoE, or diarrhoea and abdominal pain in eosinophilic colitis.

Cutaneous vasculitis is frequently encountered in dermatology practice and is often limited to the skin. However, a subset of patients may have associated systemic involvement affecting the renal, gastrointestinal, pulmonary, or neurologic systems. Distinguishing self-limited cutaneous disease from potentially serious systemic vasculitis can be clinically challenging, particularly in the absence of formal diagnostic guidelines. This brief report reviews factors associated with systemic involvement, including constitutional symptoms, gastrointestinal complaints, hematuria, and ulcerative or necrotic lesions. The role of laboratory evaluation, histopathology, and direct immunofluorescence in guiding risk stratification and targeted workup escalation is also discussed. A focused, evidence-based approach may help dermatology clinicians reduce diagnostic uncertainty while avoiding unnecessary testing.

Acute hemorrhagic edema of infancy (AHEI) is a rare leukocytoclastic vasculitis of young children characterized by cockade-like purpura and edema, usually with a preserved general condition. Because of its dramatic presentation, it may mimic life-threatening disorders such as meningococcemia with purpura fulminans, leading to extensive investigations and unnecessary treatment. We report two cases of AHEI in boys aged 18 and 22 months. The first presented with widespread purpura after a recent fever, prompting a full sepsis workup and empirical ceftriaxone before AHEI was recognized. The second had typical cockade purpura with acral edema and no fever, allowing immediate diagnosis and simple clinical monitoring. Both children recovered spontaneously, with complete resolution within 10-14 days. Early recognition of AHEI is essential to avoid misdiagnosis and to adjust management appropriately in infants presenting with purpura.

Ear, nose and throat (ENT) involvement is a frequent and early manifestation of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). This study aimed to comprehensively evaluate and compare ENT features in patients with granulomatosis with polyangiitis (GPA) and eosinophilic granulomatosis with polyangiitis (EGPA). In this cross-sectional study, 50 consecutive patients with GPA (n = 35) and EGPA (n = 15) were recruited from Rheumatology and ENT clinics at King Saud University Medical City, Riyadh, Saudi Arabia. Patients underwent clinical, audiological, imaging, and laboratory assessments. ENT evaluation included otologic, sinonasal, and laryngeal examinations, supplemented with standardized questionnaires and audiometry. Upper airway involvement was highly prevalent (90%) in both groups. Pulmonary involvement was more frequent in EGPA, whereas renal involvement did not differ significantly between the groups. Hearing loss, including subclinical sensorineural forms, occurred in 50% of patients and was associated with older age at diagnosis (≥ 34 years) and longer disease duration (median 8 vs. 1.5 years, p = 0.01). Otologic involvement did not differ between GPA and EGPA. Sinonasal manifestations varied: nasal edema, allergic rhinitis, and polyposis were more frequent in EGPA, whereas destructive lesions, including saddle-nose deformity, occurred only in GPA. Laryngeal involvement was present in 46%; subglottic stenosis occurred only in GPA (14%) and was absent in EGPA. ENT involvement is common in both GPA and EGPA, with distinct sinonasal and laryngeal patterns. Hearing loss is frequent and often subclinical, highlighting the importance of audiometric and tailored ENT assessments. Further prospective studies are needed to determine the value of routine audiometric screening.

Sweet's syndrome (acute febrile neutrophilic dermatosis) is an inflammatory condition characterized by the abrupt onset of erythematous, oedematous plaques or nodules and a dense neutrophilic dermal infiltrate. Although usually associated with fever and tender lesions on the face and upper extremities, its clinical spectrum is broad, and atypical presentations may pose diagnostic challenges. We report the case of a 50-year-old female patient who presented with an acute eruption of widespread, annular, erythematous, and oedematous plaques predominantly involving the trunk and extremities, accompanied by severe pruritus. The patient denied fever or other systemic symptoms. Laboratory investigations demonstrated marked leukocytosis with neutrophilia and elevated inflammatory markers. An extensive infectious, immunological, and malignancy workup was unremarkable. Histopathological examination revealed a dense neutrophilic dermal infiltrate with leukocytoclasia in the absence of true vasculitis, consistent with Sweet's syndrome. Direct immunofluorescence was negative. The patient reported a history of similar episodic eruptions over two decades, often temporally associated with respiratory infections. Systemic glucocorticoid therapy led to rapid clinical improvement and normalization of inflammatory parameters, with complete resolution at follow-up. This case highlights the clinical heterogeneity of Sweet's syndrome, demonstrating that prominent pruritus, truncal predominance, and afebrile presentation may occur. Recognition of atypical manifestations is essential to avoid misdiagnosis, particularly with urticarial or allergic disorders. Thorough evaluation for associated systemic disease and careful documentation of recurrent patterns remain crucial. Early histopathological confirmation and prompt initiation of appropriate therapy enable rapid disease control and favourable outcomes.

Mendelian susceptibility to mycobacterial disease (MSMD), caused by IL12RB1 or IL12B mutations, typically presents with intra-cellular infections such as BCG-adenitis or Salmonella. Rarely, patients with IL12RB1/IL12B defects can exhibit cutaneous manifestations such as Henoch-Schonlein purpura (HSP). This study aimed to evaluate such vasculitic manifestations in genetically confirmed cases with MSMD in India and review the literature for similar associations. We included nine patients with genetically proven MSMD presenting with features of HSP-like small vessel vasculitis from pediatric immunology clinics across three tertiary care centers in India. Clinical, laboratory, histopathological, and genetic data were recorded using a structured proforma. Skin biopsy findings, IgA levels, renal involvement, and infection history were analyzed. Additionally, a literature review was performed using PubMed, Scopus, and Google Scholar databases to identify similar reported cases. In our cohort, eight patients had IL12RB1 defect, and one had IL12B defect. All had maculopapular purpuric rash in lower limbs, predominantly in the anterior aspect of legs and posterior thighs resembling the rash of HSP. Leukocytoclastic vasculitis was observed in 77.7% patients (n = 7), with two out of five had IgA deposits in dermo-epidermal junction. Concurrent infections due to Salmonella sp. and Pandorea apista were documented in 44.4% (n = 4) and 22.2% (n = 2), respectively. Treatment focused on antimicrobial therapy led to clinical improvement. The HSP-like vasculitic rash usually occurred in setting of underlying bacterial infections in patients with particularly IL12RB1/IL12B defects. These skin lesions can also be considered as one of the potential clinical clues for underlying IL12RB/IL12B defects.