Received Jan 20, 2026
| Type | Name | Manufacturer | Dose | Lot | Route / Site |
|---|---|---|---|---|---|
| FLUX | INFLUENZA (SEASONAL) (NO BRAND NAME) | UNKNOWN MANUFACTURER | UNK | — | OT |
Leukocytoclastic Vasculitis (LCV) Following Influenza Virus Vaccination; weakness; new-onset mild lower extremity edema; worsening rash of lower extremities; bilateral erythematous palpable purpuric rash with crops of lesions in multiple stages of evolution; bilateral erythematous palpable purpuric rash with crops of lesions in multiple stages of evolution; crops of lesions in multiple stages of evolution/ Lesions were as small as 1-2mm, predominantly clustered on distal extremities with coalescence into larger irregular patches most notably at the ankles; hyponatremic; small pleural effusions; small pericardial effusions; right basal infiltrate; two lung nodules; CASE: An 83-year-old woman presented to the ED with a 6-day history of weakness, new-onset mild lower extremity edema, and worsening rash of lower extremities. Medical history was significant for atrial fibrillation on apixaban, hypertension, hyperlipidemia, osteoporosis, postherpetic neuralgia on gabapentin, and hypothyroidism. A month prior to onset, she recovered from COVID-19. One week prior, she was vaccinated for influenza. One day prior to admission, she presented to urgent care and received cephalexin due to concern of cellulitis. On presentation she was found to have a bilateral erythematous palpable purpuric rash with crops of lesions in multiple stages of evolution. Lesions were as small as 1-2mm, predominantly clustered on distal extremities with coalescence into larger irregular patches most notably at the ankles. Isolated lesions reached up to the inner thighs. Physical exam was otherwise unremarkable. She was found to be hyponatremic and was admitted for sodium management. CBC revealed normal white count and platelets. INR was normal. CMP revealed sodium 121, AST 69, ALT 117. ESR was 61. Blood cultures were sterile; urinalysis was unremarkable. Thoracic x-ray and CT revealed small pericardial and pleural effusions, right basal infiltrate, and two lung nodules. Skin lesion biopsy revealed perivascular inflammation with scattered karyorrhexic dermal neutrophils and mild capillary vessel edema. Immunofluorescence revealed superficial perivascular granular 2+ C3 deposition without IgG, IgA, or IgM. She was diagnosed with LCV. During hospitalization, edema improved and pruritus rapidly self-resolved. The rash continued to evolve and resolved with no intervention within 4 weeks of discharge. IMPACT/DISCUSSION: LCV commonly presents as a burning rash in dependent areas 1-3 weeks after a trigger. Etiologies include autoimmune disease, infection, drugs, and vaccination but LCV is commonly idiopathic. Mild cutaneous LCV has favorable prognosis and is selflimiting, requiring only supportive measures with rest, ice, elevation and management of underlying cause. Pathogenesis involves immune complex deposition, complement activation, neutrophilic karyorrhexis and fibrinoid necrosis on biopsy. Biopsy is most diagnostic when obtained within 24 hours of onset. LCV in our patient was most likely precipitated by influenza vaccination. She had no history of autoimmune disease or recent medication changes, although she did recover from COVID-19 a month prior. Biopsy yield was likely reduced as it was performed a week after rash onset. Further outpatient workup is recommended for autoantibodies and hepatitis serologies. Recurrence is possible but LCV is not a contraindication to vaccination. CONCLUSION: LCV should be considered on the differential when a patient develops a purpuric rash 1 or more weeks after a trigger such as autoimmune disease, illness, or vaccination. LCV is uncommon, prognosis is favorable, and is not a contraindication to vaccination. Initial information received on 12-Jan-2026 via other healthcare professional regarding an unsolicited valid serious case issued from a Conference abstract This case involves an 83 years old female patient who experienced leukocytoclastic vasculitis (LCV) following influenza virus vaccination (latency: 1 day). The patient's past medical treatment(s), vaccination(s) and family history were not provided. The patient presented to the emergency department (ED) with a 6-day history of weakness (asthenia), new-onset mild lower extremity edema (oedema peripheral), and worsening rash of lower extremities (rash). Medical history was significant for atrial fibrillation on apixaban, hypertension, hyperlipidemia, osteoporosis, postherpetic neuralgia on gabapentin, and hypothyroidism. A month prior to onset, she recovered from COVID-19 (corona virus disease). One week prior, she was vaccinated for influenza (strength, form, dose, frequency: unspecified). One day prior to admission, she presented to urgent care and received cephalexin due to concern of cellulitis. On presentation she was found to have a bilateral erythematous palpable purpuric rash with crops of lesions in multiple stages of evolution (Rash pruritic) (Rash erythematous) (Skin lesion). Lesions were as small as 1-2mm, predominantly clustered on distal extremities with coalescence into larger irregular patches most notably at the ankles (Skin lesion). Isolated lesions reached up to the inner thighs. Physical exam was otherwise unremarkable. She was found to be hyponatremic (Hyponatraemia) and was admitted for sodium management. Complete blood count (CBC) revealed normal white count and platelets. INR was normal. Complete metabolic panel (CMP) revealed sodium 121, Aspartate aminotransferase (AST) 69, Alanine Aminotransferase (ALT) 117. Erythrocyte sedimentation rate (ESR) was 61. Blood cultures were sterile; urinalysis was unremarkable. Thoracic x-ray and Computed tomography (CT) revealed small pericardial and pleural effusions (pleural effusion) (pericardial effusion), right basal infiltrate (lung infiltration), and two lung nodules (pulmonary mass). Skin lesion biopsy revealed perivascular inflammation with scattered karyorrhexic dermal neutrophils and mild capillary vessel edema. Immunofluorescence revealed superficial perivascular granular 2+ Complement factor 3 (C3) deposition without Immunoglobulin (Ig)G, IgA, or IgM. She was diagnosed with Leukocytoclastic Vasculitis (LCV). During hospitalization, edema improved and pruritus rapidly self-resolved. The rash continued to evolve and resolved with no intervention within 4 weeks of discharge. LCV commonly presents as a burning rash in dependent areas 1-3 weeks after a trigger. Etiologies include autoimmune disease, infection, drugs, and vaccination but LCV is commonly idiopathic. Mild cutaneous LCV has favorable prognosis and is selflimiting, requiring only supportive measures with rest, ice, elevation and management of underlying cause. Pathogenesis involves immune complex deposition, complement activation, neutrophilic karyorrhexis and fibrinoid necrosis on biopsy. Biopsy is most diagnostic when obtained within 24 hours of onset. LCV in this patient was most likely precipitated by influenza vaccination. She had no history of autoimmune disease or recent medication changes, although she did recover from COVID-19 a month prior. Biopsy yield was likely reduced as it was performed a week after rash onset. Further outpatient workup is recommended for autoantibodies and hepatitis serologies. Recurrence is possible but LCV is not a contraindication to vaccination. LCV should be considered on the differential when a patient develops a purpuric rash 1 or more weeks after a trigger such as autoimmune disease, illness, or vaccination. LCV is uncommon, prognosis is favorable, and is not a contraindication to vaccination. Information regarding batch number and expiration date corresponding to the one at time of event occurrence was requested. Seriousness Criteria: Medically significant Action taken: not applicable Outcome: Recovered Corrective Treatment: Not reported Reporter Causality: Related; Sender's Comments: Sanofi company comment dated 20-Jan-2026: This case involves an 83-year-old female patient who experienced leukocytoclastic vasculitis (LCV) following influenza virus vaccination with a latency of one day, presenting with bilateral erythematous palpable purpuric rash, lower extremity edema, and weakness. Based on the information received, a causal role of the influenza vaccine cannot be excluded due to the temporal relationship, with symptoms developing one day post-vaccination, which falls within the recognized timeframe for vaccine-associated LCV (typically 1-3 weeks post-trigger, though earlier onset has been reported). The skin biopsy findings demonstrating perivascular inflammation with karyorrhexic dermal neutrophils, capillary vessel edema, and granular C3 deposition without immunoglobulin deposition are consistent with LCV pathophysiology involving immune complex formation and complement activation. The self-limiting nature of the rash with complete resolution within four weeks without specific intervention is characteristic of mild cutaneous LCV with favorable prognosis. However, multiple significant confounding factors complicate the causality assessment, including the patient's recent recovery from COVID-19 infection one month prior to LCV onset, which itself is a recognized trigger for vasculitis and immune-mediated complications, the concurrent initiation of cephalexin one day prior to admission for suspected cellulitis, as antibiotics are well-documented causes of drug-induced LCV, and the presence of multiple comorbidities including atrial fibrillation on apixaban, hypertension, hyperlipidemia, and hypothyroidism with associated chronic medications. The reporter acknowledged that COVID-19 recovery could have contributed to the presentation, and the diagnostic yield was likely reduced as the biopsy was performed one week after rash onset rather than within the optimal 24-hour window. The lack of information regarding the influenza vaccine's specific strength, formulation, dosage, batch number, expiration date, past vaccination history, previous adverse reactions to vaccines, complete medication list with dosing details, results of recommended outpatient workup for autoantibodies and hepatitis serologies, the clinical significance of incidental findings including pleural and pericardial effusions, right basal infiltrate, lung nodules, elevated liver enzymes (AST 69, ALT 117), and hyponatremia (sodium 121) precludes a comprehensive assessment of this case. Furthermore, the complex clinical picture involving recent viral infection with known immunological sequelae, concurrent antibiotic exposure within the critical timeframe, multiple chronic conditions requiring polypharmacy, and the inherently multifactorial and often idiopathic nature of LCV makes it challenging to definitively attribute the leukocytoclastic vasculitis solely to influenza vaccination without considering the substantial contribution of recent COVID-19 infection and cephalexin exposure as equally plausible alternative or contributory triggers.
Atrial fibrillation; Hyperlipidemia; Hypertension; Hypothyroidism; Osteoporosis; Post herpetic neuralgia
Medical History/Concurrent Conditions: COVID-19
APIXABAN; GABAPENTIN; CEPHALEXIN [CEFALEXIN]
Test Name: ALT; Test Result: 117 {DF}; Result Unstructured Data: 117; Test Name: AST; Test Result: 69 {DF}; Result Unstructured Data: 69; Test Name: Skin lesion biopsy; Result Unstructured Data: revealed perivascular inflammation with scattered karyorrhexic dermal neutrophils and mild capillary vessel edema; Test Name: blood cultures; Result Unstructured Data: were sterile; Test Name: Sodium; Test Result: 121 {DF}; Result Unstructured Data: 121; Test Name: Thoracic x-ray; Result Unstructured Data: revealed small pericardial and pleural effusions, right basal infiltrate, and two lung nodules.; Test Name: chest CT; Result Unstructured Data: revealed small pericardial and pleural effusions, right basal infiltrate, and two lung nodules.; Test Name: Immunofluorescence; Result Unstructured Data: revealed superficial perivascular granular 2+ C3 deposition without IgG, IgA, or IgM; Test Name: INR; Result Unstructured Data: normal; Test Name: physical exam; Result Unstructured Data: Physical exam was otherwise unremarkable. She was found to be hyponatremic and was admitted for sodium management.; Test Name: Platelets; Result Unstructured Data: normal; Test Name: ESR; Test Result: 61 {DF}; Result Unstructured Data: 61; Test Name: urinalysis; Result Unstructured Data: was unremarkable; Test Name: white blood cell count; Result Unstructured Data: normal