Urticaria multiforme (UM) is a benign hypersensitivity reaction of early childhood characterized by transient annular urticarial plaques with dusky centers and acral edema. Although self-limited, UM is frequently misdiagnosed as serum sickness-like reaction (SSLR), erythema multiforme (EM), or urticarial vasculitis due to overlapping features such as fever, edema, and inflammatory laboratory abnormalities. Diagnostic uncertainty may therefore lead to extensive investigations, hospitalization, and unnecessary systemic corticosteroid therapy. A three-year-old male with a history of atopic dermatitis presented with decreased oral intake, lethargy, fever, and intermittent erythematous wheals associated with swelling of the feet and extremities. Initial evaluation revealed influenza A (H3) infection, thrombocytosis, and mildly elevated C-reactive protein. Extensive diagnostic evaluation, including multiple imaging studies and laboratory investigations, was largely unremarkable except for preserved complement levels. Due to concern for a serum sickness-like reaction, systemic corticosteroids were initiated. The dermatology consultation subsequently favored urticaria multiforme based on the transient nature of lesions lasting less than 24 hours, absence of mucosal involvement or palpable purpura, preserved complement levels, and progressive clinical improvement. The patient was managed with antihistamines and supportive care, with complete resolution of fever, edema, and urticarial lesions prior to discharge after a hospital course of six days. This case highlights influenza-associated urticaria multiforme presenting with fever and mild inflammatory marker elevation, closely mimicking immune complex-mediated disease. Recognition of lesion duration, morphology, and complement preservation is essential for accurate diagnosis and to prevent unnecessary immunosuppressive therapy.

Immunoglobulin A (IgA) vasculitis is a systemic small-vessel vasculitis with frequent gastrointestinal involvement; however, isolated terminal ileitis mimicking Crohn's disease is rare in adults. We report a case of a previously healthy adult patient who presented with acute abdominal pain and bloody diarrhea, with imaging and endoscopic findings suggestive of Crohn's disease. Colonoscopy revealed isolated terminal ileitis with a distinctive purplish cyanotic appearance. The development of palpable purpura and biopsies demonstrating IgA deposition in the skin and ileal tissue confirmed the diagnosis of IgA vasculitis. Recognition of characteristic endoscopic vascular features is critical to avoid misdiagnosis and inappropriate biological therapy.

The relationship between antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) and solid malignancies is uncommon and poses significant diagnostic challenges, particularly in individuals with underlying immune dysregulation, such as human immunodeficiency virus (HIV) infection. A 61-year-old man with well-controlled HIV infection presented with nephritic syndrome and palpable purpura. Laboratory evaluation revealed active urinary sediment and positive myeloperoxidase (MPO)-ANCA. Alternative causes of vasculitis were reasonably excluded based on clinical, serological, and histopathological evaluation. Skin biopsy demonstrated leukocytoclastic vasculitis, while renal biopsy showed pauci-immune necrotizing glomerulonephritis. During hospitalization, the patient developed hematochezia, for which a colonoscopy was performed, and a mass was identified in the ascending colon. Histopathological analysis confirmed stage IIIA colorectal adenocarcinoma. Treatment included glucocorticoids, plasmapheresis, and azathioprine, followed by right hemicolectomy and adjuvant CAPEOX chemotherapy. Partial improvement in the cutaneous lesions and glomerular filtration rate was observed following vasculitis-directed therapy, the patient achieved complete resolution of both the renal and cutaneous manifestations only after right hemicolectomy and adjuvant CAPEOX chemotherapy. This case is consistent with a possible paraneoplastic link between MPO-AAV and colorectal adenocarcinoma. In patients with HIV infection, distinguishing true vasculitis from incidental autoantibody positivity is challenging. The temporal relationship and improvement with cancer-directed therapy raise the possibility that malignancy may act as a trigger for clinically overt vasculitis. Recognition of this relationship may help guide appropriate management and avoid unnecessary or prolonged immunosuppression.

IgA vasculitis (IgAV), previously known as Henoch-Schönlein purpura, is a small-vessel vasculitis that may involve the skin, joints, gastrointestinal tract, and kidneys. While purpura is a key clinical feature, presentations without rash at onset can occur and may lead to diagnostic uncertainty. We report the case of a two-year-old boy who presented with a three-day history of acute right knee pain, swelling, and reduced weight-bearing ability following a recent febrile respiratory illness. Ultrasound of the knee demonstrated mild periarticular fluid, and a provisional diagnosis of transient synovitis was made. No rash or systemic features were present at initial presentation. Two days later, the child developed a progressive rash over the lower limbs with erythematous lesions and evolving purpuric features, along with right elbow swelling and intermittent abdominal pain. These findings prompted further evaluation and led to a clinicoradiological diagnosis of IgAV. Abdominal ultrasound excluded intussusception and demonstrated mesenteric lymphadenitis. Laboratory investigations showed mild inflammatory changes and reactive thrombocytosis, while renal function and serial urinalysis remained normal. The patient was managed conservatively with close monitoring and safety-netting, without corticosteroid therapy. Symptoms gradually resolved, and no renal involvement was identified during follow-up. This case highlights an atypical presentation of IgAV in which isolated monoarthritis preceded the development of purpura, emphasizing the importance of diagnostic vigilance and serial clinical reassessment.

Levofloxacin and other fluoroquinolones are widely used antibiotics, though they can cause rare immune-mediated adverse events. We report a man in his late 50 s with long-standing type 2 diabetes mellitus and a new plantar foot wound who was prescribed oral levofloxacin for presumed soft-tissue infection. Within 48-72 h of starting levofloxacin, he developed rapidly progressive palpable purpura that began on the upper extremities and spread to the lower extremities up to the thighs, with intense pruritus, migratory arthralgias, and bullous lesions on the distal lower extremities and right upper extremity. He had no mucosal involvement and no pulmonary or gastrointestinal symptoms. Dermatologic evaluation favored small-vessel vasculitis; systemic corticosteroids were initiated and the patient was transferred for further management. Skin biopsy demonstrated leukocytoclastic vasculitis with leukocytoclasis and fibrinoid necrosis of superficial dermal vessels. Direct immunofluorescence showed perivascular IgG and C3 without IgA deposition. Workup revealed elevated inflammatory markers, elevated serum IgA, positive p-ANCA with negative MPO and PR3, probable mixed cryoglobulins, and mild hematuria and proteinuria without casts; nephrology assessed low likelihood of clinically significant renal vasculitis. Levofloxacin was discontinued and a short corticosteroid taper was completed, with steady improvement of rash and stable renal function. This case highlights the recognition and evaluation of suspected fluoroquinolone-associated cutaneous small-vessel vasculitis and the importance of early biopsy of fresh lesions when IgA vasculitis is considered.

Evans syndrome (ES) is a rare autoimmune disorder characterized by autoimmune hemolytic anemia and immune thrombocytopenic purpura, conferring an increased risk of postoperative bleeding, thrombosis, and infection. Limited guidance for perioperative management is available for patients with ES undergoing free flap reconstruction.

We report the case of an 87-year-old woman whose initial presentation was palpable purpura. Henoch-Schönlein purpura was initially diagnosed, for which she received intravenous methylprednisolone and epinastine, resulting in complete remission of the skin lesions. After discontinuation of corticosteroid therapy, she experienced multiple relapses over the ensuing months with an incomplete response to medical treatment. Metastatic breast cancer was diagnosed 7 months later, which retrospectively suggested a paraneoplastic etiology for the vasculitis. Although the association between cutaneous vasculitis and malignancy-particularly hematologic cancers-is well documented, the underlying mechanisms remain poorly understood. The link with breast cancer is rare, though sporadically reported. Vasculitis in this context may occur before, during, or after cancer diagnosis or treatment. Notably, only two cases of breast cancer-associated vasculitis have been reported in patients aged 80 or older. Paraneoplastic vasculitis typically resolves with treatment of the underlying malignancy. However, given the presence of metastatic disease in this patient, immunosuppressive therapy with azathioprine was needed, resulting in complete resolution of lesions.

Computed coronary tomography angiography (CCTA) is an important diagnostic tool in patients with suspected acute coronary syndromes (ACS). We present a case of vasculitis and coronary involvement, in which CCTA provided critical insights for both diagnosis and management.

Leukocytoclastic vasculitis (LCV) is a rare, immune-mediated small-vessel vasculitis that can be triggered by infections, autoimmune diseases, or medications, including biologic therapies. We present a case of a patient with Crohn's disease who developed biopsy proven LCV during longterm infliximab therapy. After four years of sustained remission on infliximab, she developed cutaneous palpable purpura affecting the lower extremities. Laboratory evaluation excluded systemic vasculitis, infection, and other secondary causes. Histopathology confirmed leukocytoclastic vasculitis. Discontinuation of infliximab, led to complete resolution of skin lesions. This case underscores the importance of clinician awareness of rare biologic-associated adverse effects and highlights the need for timely recognition and management to prevent systemic involvement.

Clozapine is the most effective drug for treatment-resistant schizophrenia (TRS) but is associated with several adverse effects, including rare immune-mediated reactions. Cutaneous small vessel vasculitis (CSVV), also known as leukocytoclastic vasculitis, is an uncommon complication that typically presents as palpable purpura involving dependent areas of the body. We describe a case of a 22-year-old male patient with TRS who developed a painful, non-blanching purpuric, papular rash over both lower limbs two weeks after initiation and dose escalation of clozapine. Laboratory evaluation showed mild leukocytosis with eosinophilia, while renal, hepatic, infectious, and immunological investigations were normal, and there was no evidence of systemic involvement. In view of the clear temporal association with clozapine initiation and absence of alternative causes, a diagnosis of drug-induced CSVV was made. Clozapine was discontinued, and the patient was transitioned to quetiapine for ongoing psychiatric management. The vasculitic lesions were managed with systemic corticosteroids, antihistamines, pentoxifylline, and supportive measures, resulting in marked improvement within two weeks and complete resolution over six weeks without recurrence. Causality assessment using the Naranjo adverse drug reaction probability scale gave a score of 6, suggestive of a probable association with clozapine. Rechallenge was avoided due to the risk of recurrence. This case emphasizes the need for clinicians to recognize rare immune-mediated cutaneous reactions associated with clozapine. Early recognition and prompt discontinuation of the offending agent are essential to prevent progression and ensure favorable outcomes.

IgA vasculitis (IgAV) and IgA nephropathy (IgAN) are increasingly recognized as part of a disease spectrum sharing common pathogenic mechanisms involving galactose-deficient IgA1. While IgAN represents kidney-limited disease, IgAV is the systemic manifestation. The development of systemic IgA vasculitis in patients with established end-stage renal disease (ESRD) secondary to IgA nephropathy is rarely reported and presents unique diagnostic challenges. We present a case of a 51-year-old woman with ESRD secondary to IgA nephropathy on maintenance hemodialysis who presented with acute anemia, abdominal pain, arthralgias, and gastrointestinal bleeding. On hospital day three, she developed palpable purpura on the bilateral lower extremities. Skin biopsy demonstrated leukocytoclastic vasculitis with perivascular IgA, IgM, and C3 deposition on direct immunofluorescence, confirming IgA vasculitis. Treatment with high-dose systemic corticosteroids resulted in the resolution of cutaneous and systemic manifestations. This case highlights the diagnostic complexity of adult IgA vasculitis in ESRD patients with underlying IgA nephropathy, where symptoms may mimic common dialysis-related complications. Recognition of the shared pathophysiology between IgAN and IgAV is essential for appropriate diagnosis and management.

Background and Clinical Significance: Left atrial myxoma is the most common benign primary cardiac tumor and is associated with embolic and hemodynamic complications. Complete surgical excision is the treatment of choice, while postoperative cardiovascular rehabilitation is essential for functional recovery. Case Presentation: We report the case of a 75-year-old woman with arterial hypertension, dyslipidemia, and chronic venous insufficiency (Clinical-Etiological-Anatomical-Pathophysiological (CEAP) class 2), and chronic hepatitis B virus (HBV) infection who underwent surgical excision of a left atrial myxoma and was subsequently admitted three weeks postoperatively for phase II cardiovascular rehabilitation. The postoperative course was complicated by transient atrial fibrillation, peripheral edema, pleural effusion, and progressive purpuric lesions of the lower limbs. Laboratory and immunological evaluation revealed positive cryoglobulins, markedly elevated rheumatoid factor (1058 UI/mL) and IgM levels (715 mg/dL), reduced complement levels (C3, C4), normocytic normochromic anemia, microscopic hematuria, and elevated ALT (156 U/L), AST (142 U/L), total bilirubin (1.4 mg/dL), and INR (1.6), suggestive of hepatic inflammatory activity. HBV status was scheduled for evaluation through Gastroenterology referral (HBV DNA viral load, serological markers: HBsAg, HBeAg, anti-HBe), as our Cardiology Rehabilitation Clinic lacks the possibility of evaluation. After systematic exclusion of alternative etiologies, secondary cryoglobulinemic vasculitis in the context of chronic HBV infection with biochemical evidence of hepatic activity was considered the most plausible diagnosis. Conclusions: This case highlights the complexity of managing elderly patients after cardiac tumor surgery, particularly in the presence of systemic comorbidities. Early recognition of extracardiac complications and an individualized, multidisciplinary strategy are essential to optimize outcomes.

Immunoglobulin A vasculitis (IgAV), formerly Henoch-Schönlein purpura, is the most common systemic vasculitis of childhood and is typically self-limited. Renal risk stratification frequently relies on the presence of hematuria or proteinuria; however, early disease severity may not be detected by urinalysis alone. We present a previously healthy seven-year-old boy with palpable purpura and joint pain. The diagnosis was made clinically based on the presence of nonthrombocytopenic palpable purpura in the setting of arthralgia. He was diagnosed with IgAV after initially reassuring laboratory findings, including normal renal function and repeatedly negative urinalysis. Despite this, his clinical course rapidly progressed to persistent vomiting, abdominal pain, gastrointestinal bleeding, scrotal edema, and sustained hypertension requiring hospitalization and pharmacologic management. Repeated urinalyses during the acute illness remained negative for hematuria and proteinuria despite the development of hypertension and severe systemic involvement. This case highlights a clinical pitfall: although IgAV is primarily a clinical diagnosis based on characteristic findings such as palpable purpura and systemic symptoms, early laboratory studies, including urinalysis, may appear reassuring despite evolving systemic involvement. Close follow-up with serial blood pressure monitoring and urinalysis is essential during the disease course, whether initial laboratory findings are reassuring or abnormal.