LETTER TO EDITOR
|Year : 2003 | Volume
| Issue : 4 | Page : 560-
Guillain-Barre syndrome presenting in the anti-HIV seroconversion period
S Kumar, M Alexander, V Markandeyulu, C Gnanamuthu
eurology Unit, Department of Neurological Sciences, Christian Medical College Hospital, Vellore - 632004, India
eurology Unit, Department of Neurological Sciences, Christian Medical College Hospital, Vellore - 632004
|How to cite this article:|
Kumar S, Alexander M, Markandeyulu V, Gnanamuthu C. Guillain-Barre syndrome presenting in the anti-HIV seroconversion period.Neurol India 2003;51:560-560
|How to cite this URL:|
Kumar S, Alexander M, Markandeyulu V, Gnanamuthu C. Guillain-Barre syndrome presenting in the anti-HIV seroconversion period. Neurol India [serial online] 2003 [cited 2021 Oct 28 ];51:560-560
Available from: https://www.neurologyindia.com/text.asp?2003/51/4/560/5045
Guillain-Barre syndrome (GBS) has been reported in HIV infection.,,, The long-term outcome of these patients is not well known. We describe a case of GBS occurring in the acute anti-HIV seroconversion period.
A 21-year-old man presented with 3-day history of weakness of all four limbs, 1-day history of dysphagia, dysarthria and breathlessness and paresthesia of hands and feet. Power was Grade 2/5 and 0/5 in the upper and lower limbs respectively. All reflexes were absent. Nerve conduction studies showed features of demyelinating polyradiculoneuropathy. Cerebrospinal fluid (CSF) analysis showed a total WBC count of 30/cu.mm with 55% lymphocytes. CSF protein was 98 mg% and sugar was 108 mg%. A diagnosis of GBS was made.
Serum HIV testing results were as follows: Rapid test and ELISA I were negative. ELISA II showed a weak reactivity. Immunoblot showed reactivity to gp41 and p24 antigens. Repeat testing 6 days later showed reactivity to both ELISA I and ELISA II and immnuoblot positive for HIV-1. These results were suggestive of acute anti-HIV seroconversion state and it was concluded that the GBS in this patient was related to this.
He was treated with plasmapheresis. He started improving within a week and was weaned off the ventilator 3 weeks later. He was functionally independent at 3-month follow up. At the last follow-up 4 years after the initial diagnosis, he had no deficits.
The 2 larger studies, on the association of GBS and HIV infection are from Africa. A high prevalence of HIV infection (among those with GBS) was found- 55% in Zimbabwe and 30.5% in the Tanzania study. GBS was the presenting illness in all of them as seen in our case too. The duration between the onset to the peak of illness varied from 24 days in the Zimbabwe study to only 2.5 days in the Tanzania study. Our patient reached the peak of illness on the third day. Nerve conduction studies do not differ significantly between HIV-positive and HIV-negative groups. CSF analysis shows a greater degree of pleocytosis in the HIV-positive group. CD4 count is normal as GBS usually occurs early in the illness. Both plasmapheresis and intravenous immunoglobulins (IVIG) have been used to treat GBS in HIV-seropositive individuals. The reported results have ranged from ineffective and mild benefit to good response. Our patient had an excellent response. Outcomes after ICU care were found to be similar in HIV-positive and HIV-negative patients with GBS. This is encouraging evidence for all who care for HIV-positive GBS patients.
There is insufficient data on the long-term outcome in HIV-positive GBS patients. A retrospective study of 10 patients has reported a recurrence of GBS in 3 (30% of cases) in a period between 9 weeks to 4 years. However, a 4-year follow up of our case has shown a good long-term outcome without any recurrence.
In conclusion, GBS in an HIV-positive patient should be aggressively treated and ICU care with mechanical ventilation provided, if required, as the outcome is satisfactory.
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