Acute Guillain–Barré syndrome during the chronic phase of HIV infection and dramatic improvement under highly active antiretroviral therapy

In HIV-infected patients, Guillain–Barré syndrome is usually concomitant with HIV seroconversion, and has a benign course with spontaneous resolution [1]. During the chronic phase of HIV infection, partial or complete regression of Guillain–Barré syndrome has been reported in individuals treated by either plasmapheresis or high-dose intravenous immunoglobulin [2,3]. We report here the first case, to the best of our knowledge, of the complete resolution of Guillain–Barré syndrome in a patient with chronic HIV infection receiving highly active antiretroviral therapy (HAART). A 35-year-old African man, HIV infected since 1995, CDC stage A, presented in July 2001 with a 2 week history of a progressive ascending tetraplegia. He had no medical history and was not receiving antiretroviral therapy. He was afebrile. The power in his legs was Medical Research Council grade 2/5 and in his arms grade 3/5. A left Bell's palsy was noted. There were no sensory or sphincter symptoms. Reflexes were absent and plantar responses were flexor. The CD4 T cell count and plasma HIV-RNA viral level were 149 cells/mm3 and 745 400 copies/ml, respectively. Cerebrospinal fluid (CSF) examination showed 14 leukocytes/mm3, a protein level of 0.74 g/l, and a glucose level of 3.4 mmol/l. Cultures for bacteria, fungi, mycobacteria and herpesvirus (including cytomegalovirus) were negative, as were tests for cryptococcal antigen, a Treponema pallidum haemagglutination assay/Venereal Disease Research Laboratory test, and polymerase chain reactions for herpes simplex virus, cytomegalovirus and enterovirus. The CSF HIV-RNA viral level was 141 600 copies/ml. The detection of antibodies against Campylobacter, lyme, Bartonella and hepatitis C was negative, as was stool culture for the detection of Campylobacter. Computed tomodensitometry of the brain was normal. Electrophysiological examination showed a slowing of nerve-conduction velocities, an important prolongation of F-wave latencies, and conduction blocks on different nerves, all abnormalities consistent with the diagnosis of an acute Guillain–Barré syndrome. Antiretroviral therapy with zidovudine 600 mg/day, lamivudine 300 mg/day, ritonavir 200 mg/day and indinavir 1200 mg/day was started, and followed by a progressive improvement in muscle power. Three weeks later, the patient was able to walk. Two months later, the power in his legs and arms was normal, Bell's palsy had disappeared and normal tendon reflexes were present. The CD4 T cell count was 330 cells/mm3 and the plasma HIV-RNA viral load had dropped to undetectable levels (< 50 copies/ml). We present a case of Guillain–Barré syndrome with complete resolution under HAART. Although the pathogenesis of Guillain–Barré syndrome in HIV infection is unknown, the dramatic improvement seen in our patient under HAART argues in favour of a direct role of HIV as it has been postulated during primary HIV infection [1,4]. Indeed, during primary HIV infection, neurological symptoms correlate with high levels of HIV RNA in the CSF [4]. These symptoms often disappeared spontaneously with the decrease in HIV-RNA levels of up to 2–3 log over a few weeks [1,4]. In our patient, the high level of HIV RNA in the blood and CSF was similar to that seen during primary HIV infection. Futhermore, all three drugs, zidovudine, lamivudine and indinavir, used in the patient have good penetration in the CSF [5]. HAART, with high levels of penetration in the CSF, should be considered as a potential treatment for Guillain–Barré syndrome related to HIV, before plasmapheresis or high-dose intravenous immunoglobulin. Firouzé Bani-Sadra Ségolène Neuvillea Isabelle Crassardb Amélie Guihota Jean Michel Molinaa