Multiple organ failure and death if not early diagnosed [1]. AAV may

Multiple organ failure and death if not early diagnosed [1]. AAV may Camptothecin involve different organs especially upper and lower respiratory tracts, kidneys, skin. Neurological manifestations are observed in about 20 of patients, in particular peripheral neuropathy [1]. Seizures, headache and stroke have rarely been reported in AAV [2-7]. We herein report 3 patients presenting SE of unclear origin, whose sera were positive for p-ANCA.Cases presentationPatient* Correspondence: 1 Department of Medical and Surgical Sciences, Magna Graecia University, Catanzaro, Italy 3 Institute of Neurology, University Magna Graecia – Catanzaro, Italy Full list of author information is available at the end of the articleA 48-year-old man was diagnosed AAV with extracapillary necrotizing glomerulonephritis confirmed by laboratory analyses and kidney biopsy. He was treated with a single iv bolus of cyclophosphamide 5 mg and iv methylprednisolone 250 mg/day for 3 days, followed by oral prednisone 1 mg/kg/day. Two months later he was admitted because of generalized convulsive SE treated with iv bolus of lorazepam 4 mg. Post-ictal neurological examination showed no deficits. Neither skin lesions nor involvement of joints were evident. Brain MRI (Figure 1A) showed small-sized hyperintense T2- and FLAIR-weighted lesions in periventricular and subcortical white matter without contrast enhancement. A vast haematological screening was normal and included haemachrome, liver function, electrolytes, coagulation, angiotensin-converting enzyme, microbiological tests for hepatitis, toxoplasma, rubella, CMV, HSV 1 and 2, syphilis, ferritin, immunoglobulin dosage, antinuclear antibodies (ANA), extractable nuclear antibody (ENA) including anti-dsDNA, anti-Ro/ SSA, anti-La/SSB, PubMed ID: anti-histone, anti-nRNP, anti-Jo-1, anti-Scl70, anti-Sm, c-ANCA, rheumatoid factor, C3, C4, lupus anticoagulant (LAC), anti-thyroid antibodies, alphafetoprotein, carcino-embryonic antigen, neuronal-specific enolase, prostatic-specific antigen, CA19-9. Abnormal results were serum creatinine 7.82 mg/dl (not worsened as?2014 Ferlazzo et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.Ferlazzo et al. BMC Neurology 2014, 14:148 2 ofFigure 1 Brain MRI in our series. A (patient 1, at entry): hyperintense spots in axial FLAIR sequence involving periventicular and subcortical white matter. B, C (patient 1, one month later): axial FLAIR sequence showing multiple cortico-subcortical hyperintense lesions, some of which enhanced after gadolinium administration (axial T1: C). No meningeal enhancement is observed. D, E (patient 2, at entry): multiple nodular cortico-subcortical FLAIR hyperintense lesions involving fronto-temporal and insular regions. F (patient 2, three years later): axial FLAIR sequence revealing no abnormality. G (patient 3, three years after disease onset): axial FLAIR sequence showing a vast hyperintense cortico-subcortical temporo-occipital lesion. H, I (patient 3, two years after treatment onset.

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