JC virus leukoencephalopathy complicating Wegener’s granulomatosis

Pagnoux, Christian; Hayem, Gilles; Roux, Fabienne; Rouidi, Sid Ahmed; Palazzo, E.; Hénin, Dominique; Meyer, Olivier

doi:10.1016/s1297-319x(03)00062-9

Cited by 21 publications

(6 citation statements)

References 13 publications

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“…Because of the frequently grim prognosis and lethal outcomes, it is of paramount importance to consider the diagnosis of medication-associated PML at an early stage during treatment with immunosuppressive drugs. The clinical phenotype in the articles reviewed, however, was not seldom initially misinterpreted as an exacerbation or the cerebral manifestations of the underlying disease, i.e., an MS relapse, neuropsychiatric lupus, or central nervous system vasculitis [ 23 , 28 , 50 , 67 , 78 , 101 , 103 , 117 , 122 , 149 , 158 , 185 , 201 , 213 , 223 , 224 , 226 , 233 , 235 , 236 ]. It was only after further clinical and radiological worsening upon high doses of immunosuppressive therapies that the possibility of PML was considered in these cases.…”

Section: Discussionmentioning

confidence: 99%

Drug-associated progressive multifocal leukoencephalopathy: a clinical, radiological, and cerebrospinal fluid analysis of 326 cases

et al. 2016

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The implementation of a variety of immunosuppressive therapies has made drug-associated progressive multifocal leukoencephalopathy (PML) an increasingly prevalent clinical entity. The purpose of this study was to investigate its diagnostic characteristics and to determine whether differences herein exist between the multiple sclerosis (MS), neoplasm, post-transplantation, and autoimmune disease subgroups. Reports of possible, probable, and definite PML according to the current diagnostic criteria were obtained by a systematic search of PubMed and the Dutch pharmacovigilance database. Demographic, epidemiologic, clinical, radiological, cerebrospinal fluid (CSF), and histopathological features were extracted from each report and differences were compared between the disease categories. In the 326 identified reports, PML onset occurred on average 29.5 months after drug introduction, varying from 14.2 to 37.8 months in the neoplasm and MS subgroups, respectively. The most common overall symptoms were motor weakness (48.6 %), cognitive deficits (43.2 %), dysarthria (26.3 %), and ataxia (24.1 %). The former two also constituted the most prevalent manifestations in each subgroup. Lesions were more often localized supratentorially (87.7 %) than infratentorially (27.4 %), especially in the frontal (64.1 %) and parietal lobes (46.6 %), and revealed enhancement in 27.6 % of cases, particularly in the MS (42.9 %) subgroup. Positive JC virus results in the first CSF sample were obtained in 63.5 %, while conversion after one or more negative outcomes occurred in 13.7 % of cases. 52.2 % of patients died, ranging from 12.0 to 83.3 % in the MS and neoplasm subgroups, respectively. In conclusion, despite the heterogeneous nature of the underlying diseases, motor weakness and cognitive changes were the two most common manifestations of drug-associated PML in all subgroups. The frontal and parietal lobes invariably constituted the predilection sites of drug-related PML lesions.

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Section: Discussionmentioning

confidence: 99%

Drug-associated progressive multifocal leukoencephalopathy: a clinical, radiological, and cerebrospinal fluid analysis of 326 cases

et al. 2016

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“…PML has been described mainly in patients infected with the human immunodeficiency virus (HIV). However, other immunosuppressed patient populations, including those with malignancies, organ transplants, and systemic lupus erythematosus (SLE) (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) and other rheumatic diseases (22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32), are at risk of developing this complication.…”

Section: Introductionmentioning

confidence: 99%

Progressive multifocal leukoencephalopathy in rheumatic diseases: Evolving clinical and pathologic patterns of disease

Calabrese¹,

Molloy²,

Huang³

et al. 2007

Arthritis & Rheumatism

168

102

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“…Although two case reports in the literature described patients with PML that showed an association with azathioprine (16,17), both cases received steroids along with azathioprine for myasthenia gravis and Wegener's granulomatosis. Steroids are well known to increase the risk of opportunistic infection.…”

Section: Discussionmentioning

confidence: 99%

Progressive Multifocal Leukoencephalopathy in Myelodysplastic Syndrome Involving Pure Red Cell Aplasia

et al. 2010

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Progressive multifocal leukoencephalopathy (PML) is a rare and fatal demyelinating disease of the central nervous system caused by JC polyomavirus (JCV) reactivation in an immunocompromized host. We describe a case of PML in a 76-year-old woman with myelodysplastic syndrome, who had been treated with azathioprine for a pure red cell aplasia-like condition. PML was diagnosed based on the neurologic symptoms, the magnetic resonance imaging patterns and the detection of JCV DNA in the cerebrospinal fluid. She died ten months after the diagnosis. An autopsy confirmed the diagnosis, and JCV DNA was detected in the cerebrum. Azathioprine might have triggered PML.

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JC virus leukoencephalopathy complicating Wegener’s granulomatosis

Cited by 21 publications

References 13 publications

Drug-associated progressive multifocal leukoencephalopathy: a clinical, radiological, and cerebrospinal fluid analysis of 326 cases

Drug-associated progressive multifocal leukoencephalopathy: a clinical, radiological, and cerebrospinal fluid analysis of 326 cases

Progressive multifocal leukoencephalopathy in rheumatic diseases: Evolving clinical and pathologic patterns of disease

Progressive Multifocal Leukoencephalopathy in Myelodysplastic Syndrome Involving Pure Red Cell Aplasia

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