The fact is that the research world-wide, is small-scale and inconclusive and frankly, not really good enough. More evidence of the lack of commerciality of our disease - no effective cure, means no money to be made. The most important sentence in this article may the last one, where the idea of removing the components of the medication which are likely cause nerve damage, will prevent neuropathy in the first place...hmmm is that not just too obvious!
Debilitating HIV-associated sensory neuropathy remains commonhttp://eatg.org/eatg/Global-HIV-News/Treatment/Debilitating-HIV-associated-sensory-neuropathy-remains-common
By Dave Levitan, 20/05/2010
Debilitating sensory neuropathy remains prevalent in HIV-infected patients, despite a general decline of neurological complications with use of combination antiretroviral therapy.
This finding is from a study in which the researchers tested 1,539 HIV-infected individuals for clinical signs of neuropathy and neuropathic pain.
"We were surprised by the high prevalence," lead author Dr. Ronald Ellis of the University of California, San Diego, told Reuters Health by e-mail.
"Painful neuropathy frequently persists and requires ongoing management," even when antiretroviral therapy has reduced viral load and restored immune function, he said.
In the May Archives of Neurology, Dr. Ellis and colleagues report that 881 patients (57.2%) had HIV-associated sensory neuropathy, and 335 of those 881 (38.0%) had neuropathic pain.
"Neuropathic pain was significantly associated with disability in daily activities, unemployment, and reduced quality of life," the investigators say.
Patients currently taking combination antiretroviral therapy had an adjusted odds ratio of 1.60 for clinical signs of sensory neuropathy, compared to past users or never users of antiretroviral combinations.
Age (aOR 2.13), past use of stavudine, didanosine, or zalcitabine (aOR 1.95), and lower CD4 nadir (aOR 1.16) were also associated with sensory neuropathy.
Paradoxically, neuropathic pain was associated with a higher CD4 nadir, as well as with past use of stavudine, didanosine, or zalcitabine.
In an editorial, Drs. Dennis Kolson and Francisco Gonzalez-Scarano, both of the University of Pennsylvania in Philadelphia, said the "association between neuropathic pain and a higher CD4 nadir suggests that a functional immune system may contribute to the induction of pain." They also suggest considering the risk of neuropathy - and the disability that results -- when deciding whether to start antiretroviral therapy.
Regarding potential for peripheral nerve regeneration and recovery, Dr. Ellis told Reuters Health, "It may be that treatments can be designed to enhance regeneration. Alternatively, we may find that earlier HAART therapy using agents without neurotoxicity can protect individuals from developing neuropathy in the first place."
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