Treatment and Prevention Strategies for Herpes Zoster and Postherpetic Neuralgia in Older Adults
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Herpes zoster (HZ) affects millions of older adults annually worldwide and lowers quality of life in a substantial number of older individuals via acute and chronic pain or postherpetic neuralgia (PHN). Herpes zoster is caused by the reactivation of varicella-zoster virus (VZV) in sensory ganglia and is spread in afferent peripheral nerves in the setting of age, disease, and drug-related decline in cellular immunity to VZV. This article reviews treatment strategies and recent research for the prevention and treatment of HZ and PHN. Pharmacotherapeutic strategies to reduce HZ pain include antiviral agents, corticosteroids, and analgesics. In addition, a substantial evidence base has been growing for the pharmacotherapy of PHN. Finally, exciting research findings regarding the zoster vaccine for the prevention of HZ and PHN have been recently published. These combinations of strategies hold promise for reducing the burden of illness that HZ places on older adults.
BACKGROUND
Herpes zoster is a neurocutaneous disease caused by the reactivation of VZV from a latent infection of sensory ganglia. After primary infection, which is usually manifested as varicella, VZV establishes a latent infection for the lifetime of the host, and retains the capacity after many decades to emerge at unpredictable times to cause HZ. During latency, VZV appears to evade the immune system by markedly limiting the number of genes expressed, and by downregulating expression of major histocompatibility complex (MHC) class I antigens on the surface of infected cells.1 During reactivation, VZV escapes immune containment and spreads in the affected ganglia and sensory nerves to the skin. This event is more likely to occur in elderly persons partly because of age-related decline in specific cell-mediated immune responses to VZV. This paper will focus on HZ in the older, immunocompetent host.
Herpes zoster epidemiology studies consistently describe a marked increase in the likelihood of HZ around the age of 60 years that continues an upward course in the decades after 60 years.2,3 The annual incidence of HZ is about 11 per 1000 person-years in individuals older than 65 years of age. Extrapolating from HZ epidemiology studies, experts calculate the lifetime incidence of HZ to be 10-20% in the general population and as high as 50% of a cohort surviving to age 85 years. Investigators estimate an annual incidence of up to 1 million cases of HZ in the United States, most of which occur in elderly and immunosuppressed persons. In one study, patients age 50 years or older had a 14.7-fold higher prevalence (95% CI; 6.8-32.0) of pain 30 days after rash onset, compared to patients younger than 50 years of age.3 Hence, not only is HZ considerably more frequent in the elderly but so too is chronic HZ pain.
The clinical expression of VZV reactivation is rooted in the spread of the virus in the affected sensory ganglion and peripheral sensory nerves, and the cellular immune response that results in neuronal inflammation and destruction. Before the virus reaches the skin, the patient experiences a prodrome of pain or discomfort in the affected dermatome. The prodrome may confuse patients, caregivers, and physicians because it mimics many other painful conditions in the older adults. The prodrome usually lasts a few days, although there are case reports of it lasting weeks to months. Eventually, the virus infects cells in the skin and produces the characteristic rash. The unilateral, dermatomal rash begins as a red, maculopapular eruption that usually develops vesicles. Along with the rash, most patients experience a dermatomal pain syndrome due to acute neuritis. In a patient with the typical dermatomal, vesicular rash and neuralgic pain, a diagnosis of HZ made clinically is sufficient.
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