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Neurology 2003;60:230-234
© 2003 American Academy of Neurology

Anti-Tr antibodies as markers of paraneoplastic cerebellar degeneration and Hodgkin’s disease

F. Bernal, PhD, S. Shams’ili, MD, I. Rojas, MD, R. Sanchez-Valle, MD, A. Saiz, MD, J. Dalmau, MD PhD, J. Honnorat, MD PhD, P. Sillevis Smitt, MD PhD and F. Graus, MD

From the Service of Neurology and Institut d’Investigació Biomèdica August Pi i Sunyer (IDIBAPS) (Drs. Bernal, Sanchez-Valle, Saiz, and Graus), Hospital Clínic, University of Barcelona, Spain; Department of Neuro-Oncology (Drs. Shams’ili and Sillevis Smitt), Daniel den Hoed Cancer Center, University Hospital of Rotterdam, the Netherlands; Service of Neurology (Dr. Rojas), Ciutat Sanitaria Universitaria de Bellvitge, Hospitalet, Spain; Laboratory of Neuro-Oncology, Arkansas Cancer Research Center (Dr. Dalmau), Little Rock; and Service of Neurology B (Dr. Honnorat), Hôpital Neurologique, Lyon, France.

Address correspondence and reprint requests to Dr. Francesc Graus, Service of Neurology, Hospital Clínic, Villarroel 170, E-08036 Barcelona, Spain; e-mail: graus{at}medicina.ub.es

Background: Preliminary studies suggested that anti-Tr antibodies identify patients with paraneoplastic cerebellar degeneration (PCD) and Hodgkin disease (HD).

Objective: To extend the clinical–immunologic analysis to 28 patients with anti-Tr antibodies.

Methods: Anti-Tr antibodies were detected by immunohistochemistry. A competitive inhibition assay was used to ascertain if anti-Tr antibodies of different sera identify common epitopes. Anti-Tr immunoglobulin G (IgG) subclass distribution was determined by immunohistochemistry using monoclonal antibodies against human IgG isotypes. Tr immunoreactivity was analyzed in tumor sections using biotinylated anti-Tr IgG.

Results: Median age of the 28 patients was 61 years (range 14 to 75 years) and 22 were male. A cerebellar syndrome was present in 27 patients and a possible limbic encephalitis in one. HD was diagnosed in 25 patients. No tumor was found in three patients; the autopsy of one of them disclosed severe loss of Purkinje cells without inflammatory infiltrates. Anti-Tr antibodies spontaneously disappeared in all patients without tumor and in 10/10 patients after successful HD treatment. Anti-Tr antibodies were absent in the serum but positive in the CSF of two patients. All positive anti-Tr sera inhibited the immunoreactivity of biotinylated anti-Tr IgG. The predominant isotypes of anti-Tr were IgG1 and IgG3. Only 1 out of the 15 HD samples studied presented anti-Tr positivity that was localized in some Reed-Sternberg cells.

Conclusions: This study confirms the strong association between anti-Tr antibodies and PCD associated with HD. Anti-Tr antibodies from different patients recognize similar epitopes. Unlike other antineuronal antibodies, anti-Tr antibodies can be detected in the CSF but not in the serum and may spontaneously disappear during the follow-up, and Tr immunoreactivity is usually lacking in the tumor.




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