title: [Infections and fingolimod].
abstract: BACKGROUND
  Fingolimod is the first approved drug with oral availability for the treatment of relapsing multiple sclerosis.
  
  
  OBJECTIVE
  To review the mechanism of action of fingolimod and its relationship with the development of infections. To propose preventive measures for those patients who are receiving the drug or will initiate a new treatment. In addition, the role of fingolimod in the development of progressive multifocal leukoencephalopathy on the basis of recent knowledge of its pathophysiology will be discussed.
  
  
  METHODS
  The mechanism of action of fingolimod is based on an antagonic effect on the sphingosine 1-phospate receptors that will generate an inhibition of the egress of naive and central memory lymphocytes into the bloodstream, allowing the free recirculation of memory effectors T lymphocytes. This effect will produce lymphopenia. Fingolimod-associated lymphopenia is a consequence of lymphocyte redistribution, and it is selective and reversible. There is no evidence of higher number of opportunistic and non-opportunistic infections in comparison to placebo or interferon beta-1a in patients receiving fingolimod. However, two patients developed severe herpetic infections under fingolimod.
  
  
  CONCLUSIONS
  Fingolimod induce a selective and reversible lymphopenia that, taking into account the most recent available data, does not seem to be associated with higher risk of opportunistic infections due to a preservation of immuno-surveillance. The risk of herpesvirus infection should be taken into consideration and more studies are warranted to confirm if an association of these infections with the use of fingolimod exists.
authors: Hospital Clinic de Barcelona, 08036 Barcelona, Espana. ccervera@clinic.ub.es
authors: Carlos
authors: C
authors: Cervera
mesh_terms: D017714:Community-Acquired Infections / Q000188:drug therapy / Q000209:etiology / Q000517:prevention & control; D000075202:Contraindications; D019468:Disease Management; D004198:Disease Susceptibility; D004359:Drug Therapy, Combination; D000068876:Fingolimod Hydrochloride; D006084:Graft Rejection / Q000517:prevention & control; D006801:Humans; D016867:Immunocompromised Host; D007156:Immunologic Memory / Q000187:drug effects; D007157:Immunologic Surveillance / Q000187:drug effects*; D007166:Immunosuppressive Agents / Q000008:administration & dosage / Q000009:adverse effects* / Q000494:pharmacology / Q000627:therapeutic use; D016030:Kidney Transplantation; D007968:Leukoencephalopathy, Progressive Multifocal / Q000209:etiology; D008231:Lymphopenia / Q000139:chemically induced* / Q000150:complications; D020529:Multiple Sclerosis, Relapsing-Remitting / Q000150:complications / Q000188:drug therapy; D009894:Opportunistic Infections / Q000188:drug therapy / Q000209:etiology* / Q000517:prevention & control; D011409:Propylene Glycols / Q000008:administration & dosage / Q000009:adverse effects* / Q000494:pharmacology / Q000627:therapeutic use; D049349:Receptors, Lysosphingolipid / Q000037:antagonists & inhibitors; D013110:Sphingosine / Q000008:administration & dosage / Q000009:adverse effects / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D014611:Vaccination
chemical_list: D007166:Immunosuppressive Agents; D011409:Propylene Glycols; D049349:Receptors, Lysosphingolipid; D000068876:Fingolimod Hydrochloride; D013110:Sphingosine