Pain and sensory function in HIV-infection : with and without antiretroviral therapy
Author: Martin, Claes
Date: 2000-06-16
Location: Föreläsningssalen, Medicingatan 3, plan 6 (M63), Huddinge sjukhus
Time: 9.00
Department: Institutionen för klinisk neurovetenskap, arbetsterapi och äldrevårdsforskning (NEUROTEC) / Department of Clinical Neuroscience, Occupational Therapy and Elderly Care Research (NEUROTEC)
Abstract
Pain is a common symptom throughout the course of HIV-1 infection, with a
prevalence ranging between 30-80%, varying with study methodology and
patient selection. Neurogenic pain may appear as a consequence of distal
predominantly sensory neuropathy (DSP), a common HIV-1 related
neurological complication of late HIV-1 infection, usually during the
AIDS-stage of the disease. This study set out to analyse pain and sensory
function in HIV-1 infected patients with and without highly active
antiretroviral therapy (HAART).
In study I, a questionnaire was used to assess prevalence of pain and
sensory symptoms in 211 consecutive HIV-1 infected patients without HAART
attending the HIV clinic at Huddinge University Hospital. The mortality
rate was assessed 15 months after completion of the questionnaire. Data
on antiretroviral treatment, mode of HIV-1 transmission and immunological
status were gathered retrospectively from the case files. Pain was found
to be highly prevalent, ranging between 59 and 100%. Pain was more
prevalent among patients with intravenous drug use (IDU) than among
non-IDUs. The presence of pain correlated positively to both
immunological status and mortality, but only in non-IDU patients, as did
sensory Symptoms other than pain in both groups. Forty-four % of the
patients diagnosed with AIDS reported symmetrical sensory symptoms in the
lower extremities, out of which half complained of extremity pain.
In study II, sensory function was analysed in HIV- 1 infected patients
with painful and nonpainful DSP, without HAART, by clinical examination,
quantitative thermal testing (QTT) and nerve conduction studies. Patients
with painful neuropathy had a pronounced impairment of innocuous warm
perception, which in the setting of impaired or absent heat pain
perception, suggests a more generalised loss of function in somatosensory
C-fibre channels, compared to patients with non-painful neuropathy.
In study III, the development of fine calibre nerve channel neurotoxicity
related to antiretroviral agents (didanosine, zalcitabine and stavudine),
commonly included in HAART, was monitored. Interestingly, we found that
virologically successful HAART (also including neurotoxic drugs) had the
capacity to restore function in fine calibre somatosensory nerve
channels, especially in patients with less advanced immunodeficiency
before start of therapy, the latter indicating a shorter duration of the
neurological deficit.
QTT assess function of fine calibre nerve channels from the receptor to
the cerebral cortex. Recent studies suggest that HAART also may improve
HIV-1 related complications of the central nervous system (CNS).
Therefore, it is not unlikely that the observed improvement of thermal
and nociceptive somatosensory functions to some extent could be related
to improved function of central pathways, which may be reflected by the
degree of inflammation and viral load of the CSF In study IV and V, we
analysed viral load and inflammatory changes of the CNS by cerebrospinal
fluid (CSF) in HIV-1 infected patients with and without indinavirbased
HAART. In study IV, approximately 50% of HIV-1 infected patients without
HAART had CSF leucopenia and the number of mononuclear cells (MNC) in CSF
correlated strongly with the blood CD4+ cell count. HIV-1 nucleic acid
(RNA) could be detected in the majority of patients, and a strong
correlation was found between the number of CSF MNC and the CSF HIV-1 RNA
levels, suggesting that most of the virus detected in the CSF emanated
from circulating MNC of systemic origin, not from the brain.
In HIV-1 infected patients of study V, treated with indinavir-based
HAART, only one fifth had detectable CSF HIV-1 RNA at threshold levels,
and inflammatory CSF parameters had normalised (cell content and
IgG-index). The protease inhibitor indinavir could be detected in the CSF
in therapeutic concentrations in all patients, and thus probably
contributing to the observed antiretroviral effect.
List of papers:
I. Martin C, Pehrsson P, Österberg A, Sönnerborg A, Hansson P (1999). "Pain in ambulatory HIV-infected patients with and without intravenous drug use" Eur J Pain 3(2): 157-164
II. Martin C, Solders G, Sönnerborg A, Hansson P (2000). "Painful and non-painful neuropathy in HIV-infected patients: an analysis of sensory nerve function" (Submitted)
III. Martin C, Solders G, Sönnerborg A, Hansson P (2000). "Antiretroviral therapy may improve sensory function in HIV-infected patients: a pilot study" Neurology (In Print)
IV. Martin C, Albert J, Hansson P, Pehrsson P, Link H, Sönnerborg A (1998). "Cerebrospinal fluid mononuclear cell counts influence CSF HIV-1 RNA levels" J Acquir Immune Defic Syndr Hum Retrovirol 17(3): 214-219
Pubmed
V. Martin C, Sönnerborg A, Svensson JO, Ståhle L (1999). "Indinavir-based treatment of HIV-1 infected patients: efficacy in the central nervous system" AIDS 13(10): 1227-1232
Pubmed
I. Martin C, Pehrsson P, Österberg A, Sönnerborg A, Hansson P (1999). "Pain in ambulatory HIV-infected patients with and without intravenous drug use" Eur J Pain 3(2): 157-164
II. Martin C, Solders G, Sönnerborg A, Hansson P (2000). "Painful and non-painful neuropathy in HIV-infected patients: an analysis of sensory nerve function" (Submitted)
III. Martin C, Solders G, Sönnerborg A, Hansson P (2000). "Antiretroviral therapy may improve sensory function in HIV-infected patients: a pilot study" Neurology (In Print)
IV. Martin C, Albert J, Hansson P, Pehrsson P, Link H, Sönnerborg A (1998). "Cerebrospinal fluid mononuclear cell counts influence CSF HIV-1 RNA levels" J Acquir Immune Defic Syndr Hum Retrovirol 17(3): 214-219
Pubmed
V. Martin C, Sönnerborg A, Svensson JO, Ståhle L (1999). "Indinavir-based treatment of HIV-1 infected patients: efficacy in the central nervous system" AIDS 13(10): 1227-1232
Pubmed
Issue date: 2000-05-26
Publication year: 2000
ISBN: 91-628-4238-2
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