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: a.gambardella@unicz.it 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:https://www.ncbi.nlm.nih.gov/pubmed/10956013 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 (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.Ferlazzo et al. BMC Neurology 2014, 14:148 http://www.biomedcentral.com/1471-2377/14/Page 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.