Results of a recent study indicate that, despite improved antiretroviral treatment, nerve damage is still a common complication in people with HIV. The study also found that older age, use of certain antiretroviral drugs, and a history of diabetes are prominent risk factors associated with nerve damage.
“[Nerve damage] is still a prevalent disease in HIV-infected patients, despite virologic control and improved immune function associated with initiation of combination antiretroviral therapies,” said Scott Evans, a senior research scientist at the Harvard School of Public Health and lead author of the study.
Based on these findings, Evans suggested that people with HIV avoid antiretrovirals that are known to cause nerve damage, particularly didanosine (Videx) and stavudine (Zerit). “If using [didanosine or stavudine], avoid simultaneous use of protease inhibitor antiretroviral therapies,” he said.
In addition, Evans recommended that people with HIV maintain strong immune function and avoid illnesses such as diabetes.
HIV-associated nerve damage, or neuropathy, is a condition that causes pain, numbness, burning, or tingling in the extremities. Signs of mild neuropathy can include absent or reduced reflexes in the ankles relative to reflexes in the knees, absent or reduced vibration sensation in the toes, or decreased temperature sensation.
Neuropathy can be caused both by the virus itself and by some HIV treatments, particularly older antiretroviral drugs such as the nucleoside reverse transcriptase inhibitors didanosine or stavudine.
Although there are currently no remedies available for neuropathy, there are some treatments to help manage the symptoms. A review published last year found that high-dose topical capsaicin, smoking marijuana, and a small protein called nerve growth factor may be effective for treating symptoms of peripheral neuropathy (see related AIDS Beacon news). Only capsaicin is currently approved by the U.S. Food and Drug Administration for the management of neuropathy symptoms.
Results from studies before the advent of antiretroviral therapy indicate that high viral loads (amount of HIV in the blood) and low CD4 (white blood cell) counts are risk factors for neuropathy.
After the advent of antiretrovirals, risk factors associated with neuropathy in people with HIV have included prolonged exposure to certain antiretrovirals, particularly protease inhibitors; the use of statins, such as Lipitor (atorvastatin) or simvastatin (Zocor); a history of diabetes; high levels of triglycerides; and taller height.
In this study, researchers investigated the rates of neuropathy in people with HIV at the initiation of antiretroviral therapy; risk factors for neuropathy while using antiretrovirals, including the use of antiretroviral drugs that are known to cause neuropathy; and predictors for recovery from neuropathy after discontinuing antiretroviral drugs that can cause nerve damage.
The study included 2,141 HIV-positive adults who had not previously been treated for HIV. The researchers screened participants for signs and symptoms of neuropathy every 48 weeks after starting antiretroviral therapy.
Participants’ median CD4 count at treatment initiation was 206 cells per microliter of blood, and the median viral load was approximately 80,000 copies per milliliter of blood.
Results showed that prior to starting antiretroviral therapy, almost 23 percent of patients had peripheral neuropathy (mild loss of sensation in the great toes or absent or reduced ankle reflexes relative to the knees), and about 4 percent of patients had symptomatic peripheral neuropathy (associated with symptoms such as numbness, burning sensation, and pain in the limbs or extremities).
Results also showed that neuropathy persisted after treatment initiation despite lowered viral loads and improved immune function. Rates of peripheral neuropathy increased over time despite a decline in the use of antiretroviral drugs that are known to cause neuropathy, with rates of 32 percent and nearly 9 percent for peripheral neuropathy and symptomatic peripheral neuropathy, respectively, after three years.
Most participants diagnosed with peripheral neuropathy did not have any symptoms. In 80 percent of patient visits in which researchers found signs of peripheral neuropathy, patients reported a pain level of 0; in 79 percent of visits, patients reported a complete absence of numbness.
Analysis showed that older age, initial or current CD4 counts of 200 cells per microliter or less, and current use of antiretrovirals that are known to cause neuropathy increased the risk of peripheral neuropathy in people with HIV. Taller height and African-American race were also risk factors for peripheral neuropathy.
Risk factors for symptomatic peripheral neuropathy were similar but also included higher initial viral loads, history of diabetes, and use of statins. Fewer years of antiretroviral therapy was associated with a lower risk.
Approximately 54 percent of participants with peripheral neuropathy who were taking antiretrovirals that are known to cause nerve damage continued to have signs of neuropathy throughout the study period, even after discontinuing the drugs. Eighteen percent of participants completely recovered from peripheral neuropathy after discontinuing nerve-damaging antiretrovirals.
About 37 percent of patients who had symptomatic peripheral neuropathy and were taking antiretrovirals known to cause nerve damage still had symptomatic neuropathy after discontinuation and throughout the remainder of the study period. However, 44 percent of patients completely recovered after discontinuing the drugs.
Older age was associated with lowered odds for recovery from peripheral neuropathy or symptomatic peripheral neuropathy.
For more information, please see the study in the journal AIDS (abstract).
Source: aidsbeacon.com/news/2011
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