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Repeated courses of granulocyte colony‐stimulating factor in amyotrophic lateral sclerosis: Clinical and biological results from a prospective multicenter study
Author(s) -
Chiò Adriano,
Mora Gabriele,
Bella Vincenzo La,
Caponnetto Claudia,
Mancardi Gianluigi,
Sabatelli Mario,
Siciliano Gabriele,
Silani Vincenzo,
Corbo Massimo,
Moglia Cristina,
Calvo Andrea,
Mutani Roberto,
Rutella Sergio,
Gualandi Francesca,
Melazzini Mario,
Scimè Rosanna,
Petrini Mario,
Bondesan Paola,
Garbelli Silvia,
Mantovani Stefania,
Bendotti Caterina,
Tarella Corrado
Publication year - 2011
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.21851
Subject(s) - granulocyte colony stimulating factor , medicine , amyotrophic lateral sclerosis , cerebrospinal fluid , proinflammatory cytokine , chemokine , bone marrow , gastroenterology , immunology , chemotherapy , inflammation , disease
Granulocyte colony‐stimulating factor (G‐CSF) induces a transient mobilization of hematopoietic progenitor cells from bone marrow to peripheral blood. Our aim was to evaluate safety of repeated courses of G‐CSF in patients with amyotrophic lateral sclerosis (ALS), assessing disease progression and changes in chemokine and cytokine levels in serum and cerebrospinal fluid (CSF). Twenty‐four ALS patients entered an open‐label, multicenter trial in which four courses of G‐CSF and mannitol were administered at 3‐month intervals. Levels of G‐CSF were increased after treatment in the serum and CSF. Few and transitory adverse events were observed. No significant reduction of the mean monthly decrease in ALSFRS‐R score and forced vital capacity was observed. A significant reduction in CSF levels of monocyte chemoattractant protein‐1 (MCP‐1) and interleukin‐17 (IL‐17) was observed. G‐CSF treatment was safe and feasible in a multicenter series of ALS patients. A decrease in the CSF levels of proinflammatory cytokines MCP‐1 and IL‐17 was found, indicating a G‐CSF–induced central anti‐inflammatory response. Muscle Nerve 43: 189–195, 2011