Contributions
Abstract: EP1644
Type: Poster Sessions
Abstract Category: Therapy - Long-term treatment monitoring
Alemtuzumab is a humanised monoclonal antibody which targets the surface molecule CD52, resulting in a rapid depletion of innate and adaptive immune cells. The major complications of therapy with alemtuzumab are infectious and autoimmune diseases.
We report a case of 25-year-old Multiple Sclerosis (MS) patient who switched to alemtuzumab due to high disease activity, after having been treated with two different disease modifying therapies.
After twelve weeks from the first five-day cycle of alemtuzumab, he developed Guillain-Barré Syndrome (GBS). The patient reported a flu-like syndrome two weeks earlier. Electrophysiological exam and cerebrospinal tap confirmed the suspect. He was treated with four cycles of plasmapheresis with a complete clinical and instrumental recovery after two months.
No cases of GBS have been described in MS patients, however few cases have been reported during treatment with alemtuzumab in Chronic Lymphocytic Leukemia. In haematologic patients however, alemtuzumab is given at different dose and following different protocols, but symptoms have an onset at CD4+ nadir.
A defined mechanism of the etiology of GBS while in treatment with alemtuzumab is not yet known. Suppression of CD4+ regulatory T cells, that normally have an inhibitory role on autoimmunity may be involved. Although antecedent infection should be considered as a probable risk factor for the development of GBS, a correlation between alemtuzumab and acute polyneuropathy cannot be excluded. Therefore, further studies are necessary to better characterise this mechanism and clinicians should be aware of this possible complication during therapy with alemtuzumab
Disclosure: Nothing to disclose.
Abstract: EP1644
Type: Poster Sessions
Abstract Category: Therapy - Long-term treatment monitoring
Alemtuzumab is a humanised monoclonal antibody which targets the surface molecule CD52, resulting in a rapid depletion of innate and adaptive immune cells. The major complications of therapy with alemtuzumab are infectious and autoimmune diseases.
We report a case of 25-year-old Multiple Sclerosis (MS) patient who switched to alemtuzumab due to high disease activity, after having been treated with two different disease modifying therapies.
After twelve weeks from the first five-day cycle of alemtuzumab, he developed Guillain-Barré Syndrome (GBS). The patient reported a flu-like syndrome two weeks earlier. Electrophysiological exam and cerebrospinal tap confirmed the suspect. He was treated with four cycles of plasmapheresis with a complete clinical and instrumental recovery after two months.
No cases of GBS have been described in MS patients, however few cases have been reported during treatment with alemtuzumab in Chronic Lymphocytic Leukemia. In haematologic patients however, alemtuzumab is given at different dose and following different protocols, but symptoms have an onset at CD4+ nadir.
A defined mechanism of the etiology of GBS while in treatment with alemtuzumab is not yet known. Suppression of CD4+ regulatory T cells, that normally have an inhibitory role on autoimmunity may be involved. Although antecedent infection should be considered as a probable risk factor for the development of GBS, a correlation between alemtuzumab and acute polyneuropathy cannot be excluded. Therefore, further studies are necessary to better characterise this mechanism and clinicians should be aware of this possible complication during therapy with alemtuzumab
Disclosure: Nothing to disclose.