Subgroup comparison according to clinical phenotype and serostatus in autoimmune encephalitis: a multicenter retrospective study.


Journal

European journal of neurology
ISSN: 1468-1331
Titre abrégé: Eur J Neurol
Pays: England
ID NLM: 9506311

Informations de publication

Date de publication:
04 2020
Historique:
received: 31 07 2019
accepted: 03 12 2019
pubmed: 10 12 2019
medline: 3 3 2021
entrez: 10 12 2019
Statut: ppublish

Résumé

Autoimmune encephalitides (AE) include a spectrum of neurological disorders whose diagnosis revolves around the detection of neuronal antibodies (Abs). Consensus-based diagnostic criteria (AE-DC) allow clinic-serological subgrouping of AE, with unclear prognostic implications. The impact of AE-DC on patients' management was studied, focusing on the subgroup of Ab-negative-AE. This was a retrospective multicenter study on patients fulfilling AE-DC. All patients underwent Ab testing with commercial cell-based assays (CBAs) and, when available, in-house assays (immunohistochemistry, live/fixed CBAs, neuronal cultures) that contributed to defining final categories. Patients were classified as Ab-positive-AE [N-methyl-d-aspartate-receptor encephalitis (NMDAR-E), Ab-positive limbic encephalitis (LE), definite-AE] or Ab-negative-AE (Ab-negative-LE, probable-AE, possible-AE). Commercial CBAs detected neuronal Abs in 70/118 (59.3%) patients. Testing 37/48 Ab-negative cases, in-house assays identified Abs in 11 patients (29.7%). A hundred and eighteen patients fulfilled the AE-DC, 81 (68.6%) with Ab-positive-AE (Ab-positive-LE, 40; NMDAR-E, 32; definite-AE, nine) and 37 (31.4%) with Ab-negative-AE (Ab-negative-LE, 17; probable/possible-AE, 20). Clinical phenotypes were similar in Ab-positive-LE versus Ab-negative-LE. Twenty-four/118 (20.3%) patients had tumors, and 19/118 (16.1%) relapsed, regardless of being Ab-positive or Ab-negative. Ab-positive-AE patients were treated earlier than Ab-negative-AE patients (P = 0.045), responded more frequently to treatments (92.3% vs. 65.6%, P < 0.001) and received second-line therapies more often (33.3% vs. 10.8%, P = 0.01). Delays in first-line therapy initiation were associated with poor response (P = 0.022; odds ratio 1.02; confidence interval 1.00-1.04). In-house diagnostics improved Ab detection allowing better patient management but was available in a patient subgroup only, implying possible Ab-positive-AE underestimation. Notwithstanding this limitation, our findings suggest that Ab-negative-AE and Ab-positive-AE patients share similar oncological profiles, warranting appropriate tumor screening. Ab-negative-AE patients risk worse responses due to delayed and less aggressive treatments.

Sections du résumé

BACKGROUND AND PURPOSE
Autoimmune encephalitides (AE) include a spectrum of neurological disorders whose diagnosis revolves around the detection of neuronal antibodies (Abs). Consensus-based diagnostic criteria (AE-DC) allow clinic-serological subgrouping of AE, with unclear prognostic implications. The impact of AE-DC on patients' management was studied, focusing on the subgroup of Ab-negative-AE.
METHODS
This was a retrospective multicenter study on patients fulfilling AE-DC. All patients underwent Ab testing with commercial cell-based assays (CBAs) and, when available, in-house assays (immunohistochemistry, live/fixed CBAs, neuronal cultures) that contributed to defining final categories. Patients were classified as Ab-positive-AE [N-methyl-d-aspartate-receptor encephalitis (NMDAR-E), Ab-positive limbic encephalitis (LE), definite-AE] or Ab-negative-AE (Ab-negative-LE, probable-AE, possible-AE).
RESULTS
Commercial CBAs detected neuronal Abs in 70/118 (59.3%) patients. Testing 37/48 Ab-negative cases, in-house assays identified Abs in 11 patients (29.7%). A hundred and eighteen patients fulfilled the AE-DC, 81 (68.6%) with Ab-positive-AE (Ab-positive-LE, 40; NMDAR-E, 32; definite-AE, nine) and 37 (31.4%) with Ab-negative-AE (Ab-negative-LE, 17; probable/possible-AE, 20). Clinical phenotypes were similar in Ab-positive-LE versus Ab-negative-LE. Twenty-four/118 (20.3%) patients had tumors, and 19/118 (16.1%) relapsed, regardless of being Ab-positive or Ab-negative. Ab-positive-AE patients were treated earlier than Ab-negative-AE patients (P = 0.045), responded more frequently to treatments (92.3% vs. 65.6%, P < 0.001) and received second-line therapies more often (33.3% vs. 10.8%, P = 0.01). Delays in first-line therapy initiation were associated with poor response (P = 0.022; odds ratio 1.02; confidence interval 1.00-1.04).
CONCLUSIONS
In-house diagnostics improved Ab detection allowing better patient management but was available in a patient subgroup only, implying possible Ab-positive-AE underestimation. Notwithstanding this limitation, our findings suggest that Ab-negative-AE and Ab-positive-AE patients share similar oncological profiles, warranting appropriate tumor screening. Ab-negative-AE patients risk worse responses due to delayed and less aggressive treatments.

Identifiants

pubmed: 31814224
doi: 10.1111/ene.14139
doi:

Substances chimiques

Receptors, N-Methyl-D-Aspartate 0

Types de publication

Journal Article Multicenter Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

633-643

Subventions

Organisme : Ministero della Salute
ID : RC1812C
Pays : International

Informations de copyright

© 2019 European Academy of Neurology.

Références

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Auteurs

M Gastaldi (M)

Neuroimmunology Laboratory, IRCCS Mondino Foundation, Pavia, Italy.

S Mariotto (S)

Neurology Unit, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy.

M P Giannoccaro (MP)

Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
UOC Clinica Neurologica, IRCCS Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy.

R Iorio (R)

Istituto di Neurologia, Fondazione Policlinico Universitario 'Agostino Gemelli' IRCCS, Rome, Italy.
Universita' Cattolica del Sacro Cuore, Rome, Italy.

M Zoccarato (M)

Ospedale S. Antonio, AULSS Euganea, Padua, Italy.
Neuroimmunology Group, Paediatric Research Institute "Città della Speranza", Padua, Italy.

M Nosadini (M)

Neuroimmunology Group, Paediatric Research Institute "Città della Speranza", Padua, Italy.
Paediatric Neurology and Neurophysiology Unit, Department of Women's and Children's Health, University Hospital of Padua, Padua, Italy.

L Benedetti (L)

IRCCS Ospedale Policlinico S. Martino, Genoa, Italy.

S Casagrande (S)

Neurosciences Department, Florence University, Italy.
Careggi University Hospital, Florence, Italy.

M Di Filippo (M)

Neurology Clinic, S. Maria della Misericordia Hospital, Perugia University, Perugia, Italy.

M Valeriani (M)

Neurology Unit, Bambino Gesù Children Hospital, Rome, Italy.

S Ricci (S)

Ospedale 'Città-di-Castello-e-Branca', Italy.

S Bova (S)

Pediatric Neurology Unit, ASST Fatebenefratelli Sacco, Children Hospital Vittore Buzzi, Milan, Italy.

C Arbasino (C)

Ospedale Civile, Voghera, Italy.

M Mauri (M)

Neurology and Stroke Unit, Insubria University, Varese, Italy.

M Versino (M)

Neurology and Stroke Unit, Insubria University, Varese, Italy.

F Vigevano (F)

Neurology Unit, Bambino Gesù Children Hospital, Rome, Italy.

L Papetti (L)

Neurology Unit, Bambino Gesù Children Hospital, Rome, Italy.

M Romoli (M)

Neurology Clinic, S. Maria della Misericordia Hospital, Perugia University, Perugia, Italy.
Neurology Unit, Rimini "Infermi" Hospital - AUSL Romagna, Rimini, Italy.

C Lapucci (C)

IRCCS Ospedale Policlinico S. Martino, Genoa, Italy.

F Massa (F)

IRCCS Ospedale Policlinico S. Martino, Genoa, Italy.

S Sartori (S)

Neuroimmunology Group, Paediatric Research Institute "Città della Speranza", Padua, Italy.
Paediatric Neurology and Neurophysiology Unit, Department of Women's and Children's Health, University Hospital of Padua, Padua, Italy.

L Zuliani (L)

Neuroimmunology Group, Paediatric Research Institute "Città della Speranza", Padua, Italy.
Neurology Department, Ospedale S. Bortolo, Vicenza, Italy.

A Barilaro (A)

Careggi University Hospital, Florence, Italy.

P De Gaspari (P)

Neuroimmunology Group, Paediatric Research Institute "Città della Speranza", Padua, Italy.

G Spagni (G)

Universita' Cattolica del Sacro Cuore, Rome, Italy.

A Evoli (A)

Istituto di Neurologia, Fondazione Policlinico Universitario 'Agostino Gemelli' IRCCS, Rome, Italy.
Universita' Cattolica del Sacro Cuore, Rome, Italy.

R Liguori (R)

Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
UOC Clinica Neurologica, IRCCS Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy.

S Ferrari (S)

Neurology Unit, Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, Verona, Italy.

E Marchioni (E)

Neuroncology Unit, IRCCS Mondino Foundation, Pavia, Italy.

B Giometto (B)

APSS Ospedale S. Chiara, Trento, Italy.

L Massacesi (L)

Neurosciences Department, Florence University, Italy.
Careggi University Hospital, Florence, Italy.

D Franciotta (D)

Neuroimmunology Laboratory, IRCCS Mondino Foundation, Pavia, Italy.

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