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including pain had no impact on HIV‐1 RNA levels in patients with stable suppression of
viremia (Nettles et al, 2005 Level IV).
Disease‐specific therapy, psychosocial interventions and physical modalities should
accompany standard analgesic treatment (Jacox et al, 1994; Glare, 2001). Disease‐specific
therapy may need to be ceased prematurely if pain is a side effect (eg peripheral neuropathy
caused by some antiretrovirals, in particular nucleoside reverse transcriptase inhibitors).
Treatment of HIV/AIDS-related pain
A significant reduction in pain intensity was achievable with CR opioids in a variety of painful
conditions with limited or manageable side effects, supporting the usefulness of opioid
analgesia for HIV‐related severe pain (Kaplan et al, 1996; Kaplan et al, 2000 Level IV).
Approximately 15% to 20% of patients need parenteral opioids in the terminal phase (Dixon &
Higginson, 1991 Level IV; Kimball & McCormick, 1996 Level IV; Frich & Borgbjerg, 2000 Level IV).
Transdermal fentanyl provided better pain relief and improvement in daily functioning in
patients with severe AIDS‐related pain who were previously taking oral opioids (Newshan &
Lefkowitz, 2001 Level IV).
Painful peripheral neuropathy associated with HIV infection has been the subject of a number
of treatment trials. Lamotrigine (Simpson et al, 2000 Level II) and gabapentin (La Spina et al, 2001
Level IV) were better than placebo. A single application of a high‐concentration capsaicin patch
was safe and provided at least 12 weeks of pain reduction in patients with HIV‐associated
distal sensory polyneuropathy, suggesting that such patches could have a role in the analgesic
regimens of people with painful HIV neuropathy (Simpson et al, 2008 Level II).
Smoking cannabis was significantly more effective in reducing HIV‐related neuropathic pain
than smoking placebo cigarettes (Abrams et al, 2007 Level II); the rate of responders (30%
reduction in pain) in one trial was 46% with cannabis and 18% with placebo (Ellis et al, 2009
Level II).
The use of nucleoside reverse transcriptase inhibitors (NRTIs) can lead to a toxic neuropathy
with neuropathic pain. Acetyl‐L‐carnitine (ALCAR) can provide neurotrophic support of sensory
neurones and therefore its use in the setting of NRTI therapy may encourage nerve
regeneration and analgesia. IM or oral ALCAR use was safe and well‐tolerated and resulted in a
reduction of pain intensity compared to placebo (Youle & Osio, 2007 Level II).
TCAs (Kieburtz et al, 1998 Level II; Shlay et al, 1998 Level II), antiarrythymics (Kemper et al, 1998
Level II; Kieburtz et al, 1998 Level II), Peptide T (Simpson et al, 1996 Level II), vibratory CHAPTER 9
counterstimulation (Paice et al, 2000 Level III‐1) and acupuncture (Shlay et al, 1998 Level II) have
not been shown to be effective.
Several complex drug interactions may occur between opioids and other medications taken by
patients with HIV/AIDS; however the clinical relevance of most of these interactions is still
unclear.
The HIV‐1 protease inhibitor ritonavir inhibits the metabolism of methadone and
buprenorphine (Iribarne et al, 1998) but this has no relevant clinical effect (McCance‐Katz et al,
2003 Level III‐2). However, ritonavir results in a clinically relevant inhibition of fentanyl
metabolism (Olkkola et al, 1999 Level II) and leads to increased concentrations of the toxic
metabolite norpethidine (normeperidine) if used in combination with pethidine (Piscitelli et al,
2000 Level III‐2). Lopinavir induces metabolism of methadone leading to withdrawal symptoms
in patients on maintenance doses (McCance‐Katz et al, 2003 Level III‐2). Rifampicin and rifabutin
may increase opioid metabolism (particularly methadone) (Finch et al, 2002) and fluconazole
may potentiate adverse effects of methadone (Tarumi et al, 2002). Zidovudine metabolism is

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