Endocrinology Unit, Graves’ Orbitopathy Center, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Milan, Italy
Search for other papers by Ilaria Muller in
Google Scholar
PubMed
Search for other papers by Sara Maioli in
Google Scholar
PubMed
Search for other papers by Mirco Armenti in
Google Scholar
PubMed
Search for other papers by Laura Porcaro in
Google Scholar
PubMed
Ophthalmology Unit, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Milan, Italy
Search for other papers by Nicola Currò in
Google Scholar
PubMed
Search for other papers by Elisabetta Iofrida in
Google Scholar
PubMed
Department of Specialistic Surgical Sciences, Otolaryngology and Head and Neck Surgery, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Milan, Italy
Search for other papers by Lorenzo Pignataro in
Google Scholar
PubMed
Search for other papers by Jacopo Manso in
Google Scholar
PubMed
Search for other papers by Caterina Mian in
Google Scholar
PubMed
National Institute of Molecular Genetics (INGM) “Romeo and Enrica Invernizzi”, Milan, Italy
Search for other papers by Jens Geginat in
Google Scholar
PubMed
Search for other papers by Mario Salvi in
Google Scholar
PubMed
Ours is the first description of the immune cell profiling derived from the consecutive administration of alemtuzumab for multiple sclerosis and rituximab for thyroid eye disease. B-cell depletion induced by rituximab is an effective treatment for
Search for other papers by Ilaria Muller in
Google Scholar
PubMed
Search for other papers by Carla Moran in
Google Scholar
PubMed
Search for other papers by Beatriz Lecumberri in
Google Scholar
PubMed
Search for other papers by Brigitte Decallonne in
Google Scholar
PubMed
Search for other papers by Neil Robertson in
Google Scholar
PubMed
Search for other papers by Joanne Jones in
Google Scholar
PubMed
Search for other papers by Colin M. Dayan in
Google Scholar
PubMed
recovery of immune cell numbers following a depletion phase, which to date has been reported in 3 settings: (1) following alemtuzumab (Lemtrada) treatment for active relapsing remitting multiple sclerosis (MS); (2) after treatment of human immunodeficiency
Search for other papers by Earn H. Gan in
Google Scholar
PubMed
Search for other papers by Anna L. Mitchell in
Google Scholar
PubMed
Search for other papers by Ruth Plummer in
Google Scholar
PubMed
Search for other papers by Simon Pearce in
Google Scholar
PubMed
Search for other papers by Petros Perros in
Google Scholar
PubMed
immunotherapy, such as alemtuzumab, a human anti-CD52 monoclonal antibody therapy, with onset ranging from 6 to 61 months after the first course of treatment [ 29 , 30 ]. One might suggest that our case was an incidental finding of isolated Graves disease
Search for other papers by Alessandro Brancatella in
Google Scholar
PubMed
Search for other papers by Nicola Viola in
Google Scholar
PubMed
Search for other papers by Sandra Brogioni in
Google Scholar
PubMed
Search for other papers by Lucia Montanelli in
Google Scholar
PubMed
Search for other papers by Chiara Sardella in
Google Scholar
PubMed
Search for other papers by Paolo Vitti in
Google Scholar
PubMed
Search for other papers by Claudio Marcocci in
Google Scholar
PubMed
Search for other papers by Isabella Lupi in
Google Scholar
PubMed
Search for other papers by Francesco Latrofa in
Google Scholar
PubMed
autoimmune hyperthyroidism and Graves’ ophthalmopathy. Of note, euthyroid Graves’ ophthalmopathy is very uncommon after other immunotherapy drugs (e.g., interferon and alemtuzumab); in these settings, ophthalmopathy is usually associated with hyperthyroidism
Search for other papers by George J. Kahaly in
Google Scholar
PubMed
Search for other papers by Luigi Bartalena in
Google Scholar
PubMed
Search for other papers by Lazlo Hegedüs in
Google Scholar
PubMed
Search for other papers by Laurence Leenhardt in
Google Scholar
PubMed
Search for other papers by Kris Poppe in
Google Scholar
PubMed
Search for other papers by Simon H. Pearce in
Google Scholar
PubMed
-depleting alemtuzumab (Campath-H1) antibody treatment [ 161 ]. This treatment causes initial lymphopenia, but 12–24 months later 20–30% of patients developed TSH-R-Ab-positive GD, as lymphocyte populations recover. A similar pattern of GD has been observed in patients