Contributions
Abstract: P607
Type: Poster Sessions
Abstract Category: Therapy - Risk management for disease modifying treatments
Introduction: Fingolimod,the first oral immunomodulatory treatment for relapsing multiple sclerosis(MS),acts by blocking lymph-node egress of T cells expressing the CCR7-receptor,resulting lymphopenia by selective lymphocyte redistribution with preservation of immunological memory.
Objectives: To report a visceral Leishmaniasis in a patient treated with fingolimod for 62 months.
Case report: This 55-year-old Caucasian, Spanish woman presented with an evening fever of 37-39°C,night sweats,fatigue and mild pain in the left hypochondriac region for 2 weeks.Physical examination revealed hepatosplenomegaly.During fingolimod treatment regular blood tests had showed acceptable lymphopenia(over 500 /µl).Blood tests revealed normocytic,normochromic anaemia,leukocytopenia (1.980/µl), neutropenia, lymphocytopenia (200/µL), thrombocytopenia, elevated CRP(212.73mg/dl) and ESR(91 mm), increased GGT, liver function tests and serum gammaglobulins.Abdominal ultrasound and computerized tomography revealed marked hepatosplenomegaly.Bone marrow biopsy revealed no evidence of haematologic disease and scattered infiltration by Leishmania between cells and some within macrophages,later confirmed by serum PCR(Leishmania infantum).The patient was treated with intravenous liposomal amphotericin B and made full recovery with normalization of blood tests.
Discussion: Visceral leishmaniasis,a disseminated disease, caused by Leishmania spp., transmitted between vertebrate hosts by the bite of phlebotomine sandflies.In Spain there are about 110 annual cases of human leishmaniasis(18 declared in the Madrid community).In individuals with impaired cellular immunity, visceral leishmaniasis is characterized by increased humoral immune responses. More importantly,there is evidence that both CD4+ and CD8+ T central memory(CM) cells provide immunity to Leishmania spp acting as a reservoir of effector memory T-cells(TEM cells)upon secondary infection.In extended periods of antigen presentation the TEM cells decline and the integrity of TCM cells is a prerequisite for the replenishment of the TEM cells reservoir and the successful immune response.Th1 cells and TCM,mainly affected by fingolimod,are integral parts of an effective immune response to leishmaniasis infection.In patients with MS living in regions where leishmaniasis is endemic the administration of fingolimod should be done with caution,and in a patient with pancytopenia,fever,hepatosplenomegaly we should suspect visceral leishmaniasis.
Disclosure: No disclosures to report
Abstract: P607
Type: Poster Sessions
Abstract Category: Therapy - Risk management for disease modifying treatments
Introduction: Fingolimod,the first oral immunomodulatory treatment for relapsing multiple sclerosis(MS),acts by blocking lymph-node egress of T cells expressing the CCR7-receptor,resulting lymphopenia by selective lymphocyte redistribution with preservation of immunological memory.
Objectives: To report a visceral Leishmaniasis in a patient treated with fingolimod for 62 months.
Case report: This 55-year-old Caucasian, Spanish woman presented with an evening fever of 37-39°C,night sweats,fatigue and mild pain in the left hypochondriac region for 2 weeks.Physical examination revealed hepatosplenomegaly.During fingolimod treatment regular blood tests had showed acceptable lymphopenia(over 500 /µl).Blood tests revealed normocytic,normochromic anaemia,leukocytopenia (1.980/µl), neutropenia, lymphocytopenia (200/µL), thrombocytopenia, elevated CRP(212.73mg/dl) and ESR(91 mm), increased GGT, liver function tests and serum gammaglobulins.Abdominal ultrasound and computerized tomography revealed marked hepatosplenomegaly.Bone marrow biopsy revealed no evidence of haematologic disease and scattered infiltration by Leishmania between cells and some within macrophages,later confirmed by serum PCR(Leishmania infantum).The patient was treated with intravenous liposomal amphotericin B and made full recovery with normalization of blood tests.
Discussion: Visceral leishmaniasis,a disseminated disease, caused by Leishmania spp., transmitted between vertebrate hosts by the bite of phlebotomine sandflies.In Spain there are about 110 annual cases of human leishmaniasis(18 declared in the Madrid community).In individuals with impaired cellular immunity, visceral leishmaniasis is characterized by increased humoral immune responses. More importantly,there is evidence that both CD4+ and CD8+ T central memory(CM) cells provide immunity to Leishmania spp acting as a reservoir of effector memory T-cells(TEM cells)upon secondary infection.In extended periods of antigen presentation the TEM cells decline and the integrity of TCM cells is a prerequisite for the replenishment of the TEM cells reservoir and the successful immune response.Th1 cells and TCM,mainly affected by fingolimod,are integral parts of an effective immune response to leishmaniasis infection.In patients with MS living in regions where leishmaniasis is endemic the administration of fingolimod should be done with caution,and in a patient with pancytopenia,fever,hepatosplenomegaly we should suspect visceral leishmaniasis.
Disclosure: No disclosures to report