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CP-070 Interleukin-2 treatment of two patients with multifocal progressive leukoencephalopathy associated with hiv infection
  1. A Ferrada Gascó1,
  2. JE Megías Vericat1,
  3. MJ Company Albir1,
  4. AA García Robles1,
  5. C Favieres Puigcerver1,
  6. O Ballesta López1,
  7. MJ Fernández Megía1,
  8. FC Pérez Miralles2,
  9. JL Poveda Andrés1,
  10. B Casanova Estruch2
  1. 1Hospital Universitari y Politecnic La Fe, Servicio de farmacia-area del medicamento, Valencia, Spain
  2. 2Hospital Universitari y Politecnic La Fe, Unidad Mixta de Esclerosis Múltiple y Neurorregeneración- IIS Hospital La Fe, Valencia, Spain

Abstract

Background Progressive multifocal leukoencephalopathy(PML) is caused by JC virus (JCV) and has severe consequences for the central nervous system. PML is an opportunistic infection, affecting HIV positive patients. There is no curative treatment, and the current approach is focused on immune reconstitution and antiviral therapy.1

Purpose This is a case report of two patients with PML associated with HIV infection treated with aldesleukin/interleukin-2 (IL-2).

Material and methods We report two cases, both men, aged 48 years (patient A) and 57 years (patient B), HIV diagnosed in 1992 and 1993, who developed LMP opportunistic JCV infection. Antiretrovirals were the only therapy previously employed. Patient A developed progressive neurological impairment, slow psychic reactions and right upper limb strength loss. Symptoms in patient B were progressive cognitive impairment, memory loss, lack of coordination, dysarthria, strength loss and right facial paralysis. Both patients showed hypodensity of white matter in the semi-oval centre on cranial CT.

Results IL-2 was administered intravenously to both patients at 0.5 MU/m²/day for 4 weeks. Patient-A: IL-2 treatment (from 8 February 2010 to 7 March 2010) was well tolerated, although a self-limited fever and eosinophilia were reported without clinical correlations. The patient showed improvements in image tests (disappearance of signal hyperintensity and cytotoxic oedema on CT and MRI) and clinical outcomes (improvement of neurological symptoms), although progressive spasticity and dysarthria were maintained. JCV load was undetectable in February 2011. Patient A was treated for 1 year with mefloquine 250 mg/24 hours with good tolerance and stabilisation of PML, but without resolution. The patient died in December 2012 following intraparenchymal cerebral haemorrhage. Patient-B: therapy with IL-2 and mirtazapine (from 8 September 2016 to 5 October 2016) was well tolerated, but the infusion was discontinued once by a fever episode. Cranial CT showed no significant changes. The patient´s neurological impairment, hemiparesis and dysarthria persisted, but a slight improvement was observed. JCV load declined from >100 million to 12 million copies/mL, HIV from 645 to 147 copies/mL and CD4 T lymphocytes increased.

Conclusion IL-2 could be an effective and well tolerated therapy in LMP, without severe adverse events. Patient A showed improvements in neurological and image tests, and undetectable viral load, whereas the response in patient B was only partial, with a decline in JCV and HIV, but maintaining neurological deterioration.

References and/or acknowledgements 1. Pavlovic D, et al. Ther Adv Neurol Disord2015;8:255–73.

No conflict of interest

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