Hashimoto encephalopathy in the 21st century

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Citações na Scopus
74
Tipo de produção
article
Data de publicação
2020
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
LIPPINCOTT WILLIAMS & WILKINS
Autores
MATTOZZI, Simone
SABATER, Lidia
ESCUDERO, Domingo
ARINO, Helena
ARMANGUE, Thais
IIZUKA, Takahiro
HARA, Makoto
SAIZ, Albert
SOTGIU, Stefano
Citação
NEUROLOGY, v.94, n.2, p.E217-E224, 2020
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
ObjectiveTo report the presenting syndromes and to determine whether pretreatment criteria of Hashimoto encephalopathy (HE) predict response to steroids.MethodsWe assessed symptoms and steroid responsiveness in 24 patients with pretreatment criteria of HE, including (1) subacute onset of cognitive impairment, psychiatric symptoms, or seizures; (2) euthyroid status or mild hypothyroidism; (3) serum thyroid peroxidase antibodies (TPOAb) >200 IU/mL; (4) absent neuronal antibodies in serum/CSF; and (5) no other etiologies. Additional studies included determination of TPOAb (>200 IU/mL) in 74 patients with criteria of possible autoimmune encephalitis (AE) without neuronal antibodies and 205 patients with different neuroimmunologic diseases, psychosis, or new-onset refractory status epilepticus (NORSE). Serum antibodies to the amino (Nu Eta 2)-terminal of alpha -enolase (NH2-alpha -enolaseAb) were examined in the indicated 24 patients and 13 controls.ResultsThe 24 patients (14 women) with suspected HE had a median age of 48 years (range 8-79 years). Four syndromes were identified: psychiatric (7, 29%), encephalopathy (7, 29%), NORSE-like (6, 25%), and limbic encephalitis (4, 17%). Only 6 of 19 (31.6%) patients completely responded to steroids. The frequency of TPOAb in the 74 patients with possible AE (6 of 74, 8.1%) was similar to that of the 205 controls (17 of 205, 8.2%; p = 0.84). NH2-alpha -enolaseAb were identified in 1 of 24 suspected HE cases and 1 of 13 controls.ConclusionCurrent pretreatment criteria of HE do not predict steroid responsiveness. The detection of TPOAb across all control groups reveals their poor disease-specificity. NH2-alpha -enolaseAb did not help in the diagnosis of HE. These findings imply a redefinition of HE that requires a systematic exclusion of antibody-mediated encephalitis.
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URI
https://observatorio.fm.usp.br/handle/OPI/36201
Referências
  1. Afshari M, 2012, NEUROLOGY, V78, pE134, DOI 10.1212/WNL.0b013e3182582fd4
  2. Ances BM, 2005, NEUROLOGY, V64, pA51
  3. Armangue T, 2016, JAMA NEUROL, V73, P417, DOI 10.1001/jamaneurol.2015.4607
  4. BUCHHALTER JR, 1991, BRAIN RES BULL, V26, P333, DOI 10.1016/0361-9230(91)90003-3
  5. Castillo P, 2006, ARCH NEUROL-CHICAGO, V63, P197, DOI 10.1001/archneur.63.2.197
  6. Chong JY, 2003, ARCH NEUROL-CHICAGO, V60, P164, DOI 10.1001/archneur.60.2.164
  7. Dalmau J, 2007, ANN NEUROL, V61, P25, DOI 10.1002/ana.21050
  8. Dalmau J, 2018, NEW ENGL J MED, V378, P840, DOI 10.1056/NEJMra1708712
  9. Dubey D, 2017, EPILEPSIA, V58, P1181, DOI 10.1111/epi.13797
  10. Feo S, 2000, FEBS LETT, V473, P47, DOI 10.1016/S0014-5793(00)01494-0
  11. Fujii A, 2005, J NEUROIMMUNOL, V162, P130, DOI 10.1016/j.jneuroim.2005.02.004
  12. Graus F, 2018, EUR J NEUROL, V25, P1011, DOI 10.1111/ene.13661
  13. Graus F, 1997, J NEUROIMMUNOL, V74, P55, DOI 10.1016/S0165-5728(96)00205-6
  14. Graus F, 2016, LANCET NEUROL, V15, P391, DOI 10.1016/S1474-4422(15)00401-9
  15. Hacohen Y, 2014, J CHILD NEUROL, V29, P769, DOI 10.1177/0883073813480392
  16. Hayashi Y, 2017, PRION, V11, P454, DOI 10.1080/19336896.2017.1377876
  17. Hollowell JG, 2002, J CLIN ENDOCR METAB, V87, P489, DOI 10.1210/jc.87.2.489
  18. Jones AL, 2015, JAMA NEUROL, V72, P1304, DOI 10.1001/jamaneurol.2015.2378
  19. Kayser MS, 2013, JAMA NEUROL, V70, P1133, DOI 10.1001/jamaneurol.2013.3216
  20. Kishitani T, 2017, MEDICINE, V96, DOI 10.1097/MD.0000000000006181
  21. KothbauerMargreiter I, 1996, J NEUROL, V243, P585, DOI 10.1007/BF00900946
  22. Lancaster E, 2010, LANCET NEUROL, V9, P67, DOI 10.1016/S1474-4422(09)70324-2
  23. Laurent C, 2016, AUTOIMMUN REV, V15, P1129, DOI 10.1016/j.autrev.2016.09.008
  24. Litmeier S, 2016, ACTA NEUROL SCAND, V134, P452, DOI 10.1111/ane.12556
  25. Mahmud FH, 2003, PEDIATRICS, V112, P686, DOI 10.1542/peds.112.3.686
  26. Martinez-Hernandez E, 2016, JAMA NEUROL, V73, P714, DOI 10.1001/jamaneurol.2016.0133
  27. Matsunaga A, 2013, EUR NEUROL, V69, P14, DOI 10.1159/000342217
  28. Montagna G, 2016, AUTOIMMUN REV, V15, P466, DOI 10.1016/j.autrev.2016.01.014
  29. Schiess N, 2008, ANN NY ACAD SCI, V1142, P254, DOI 10.1196/annals.1444.018
  30. TIEN RD, 1995, RADIOLOGY, V194, P249, DOI 10.1148/radiology.194.1.7997562
  31. Yoneda M, 2007, J NEUROIMMUNOL, V185, P195, DOI 10.1016/j.jneuroim.2007.01.018

Coleções
Artigos e Materiais de Revistas Científicas - HC/ICHC