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11.06.2015

Zoster treatment up to date, md anderson alternative medicine - .

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Despite the relatively recent advent of multiple vaccines for both chickenpox and shingles, the overall incidence of herpes zoster is on the rise. This article will review the ocular complications associated with varicella zoster virus (VZV) in both children and adults, as well as discuss potential treatment options for shingles and postherpetic neuralgia. Primary VZV infection causes varicella (chickenpox), and virus reactivation from cranial nerve ganglia or dorsal root ganglia produces zoster (shingles). Oral antivirals to treat VZV infection or reactivation (varicella or zoster, respectively) include acyclovir, valacyclovir, and famciclovir; acyclovir is also licensed for intravenous treatment of VZV infections (Table 1). In healthy children under the age of 12, varicella is usually self-limited, and treatment is usually limited to antihistamines and acetaminophen for relief of pruritus and fever, respectively. Prophylaxis is recommended for pregnant women who have been exposed to varicella or zoster.
With advancing age or immunosuppression, cell-mediated immunity to VZV declines and virus reactivates to cause herpes zoster (shingles) which is often complicated by chronic pain (postherpetic neuralgia), cranial nerve palsies, zoster paresis, meningoencephalitis and cerebellitis, myelopathy, vasculopathy and multiple ocular disorders. The cardinal pathological features of zoster are characterized by inflammation and hemorrhagic necrosis with associated neuritis, localized leptomeningitis, unilateral segmental poliomyelitis and degeneration of related motor and sensory roots (57).
Zoster paresis (weakness) may present with arm weakness or diaphragmatic paralysis after cervical distribution rash, leg weakness after lumbar or sacral distribution rash, or urinary retention after sacral distribution rash. Dermatomal-distribution pain persisting for more than 3 months after zoster is operationally defined as postherpetic neuralgia (PHN).
The optimal approach to the management of herpes zoster is analgesia for pain and antivirals to speed healing of rash and shorten the duration of acute pain. Oral acyclovir, famciclovir and valacyclovir have similar clinical efficacy in herpes zoster in immunocompetent patients if started within 72 hours of rash. In contrast, zoster during pregnancy does not pose any risks for intrauterine infection (34) and should only be treated with acyclovir in cases of severe disease (107).
Randomized placebo-controlled studies have shown that oral acyclovir reduces new lesion formation and significantly accelerates rash healing in normal hosts with herpes zoster (60, 133). In a randomized, double-blind study of 1141 immunocompetent adults of age ≥50 years with herpes zoster that compared the safety and efficacy of valacyclovir to acyclovir, valacyclovir significantly accelerated resolution of zoster-associated pain (median pain durations were 38 and 44 days, respectively, vs. In a placebo-controlled trial of 429 immunocompetent adults with herpes zoster treated within 72 hours of rash (120), famciclovir accelerated lesion healing and reduced the duration of viral shedding.
Overall, clinical trials demonstrate that treatment of zoster with acyclovir, famciclovir or valacyclovir reduces the duration of viral shedding and new lesion formation and accelerates rash healing.
Administration of corticosteroids during acute zoster has been shown to be efficacious in large double-blind studies (36, 132). A newer potentially promising treatment for PHN is percutaneous peripheral nerve field stimulation. All of these neurological complications of VZV reactivation can occur after zoster, but may also occur in the absence of zoster rash, as demonstrated by reports of VZV meningitis (52), meningoradiculitis (51) and cerebellitis (79) in which diagnosis was confirmed by the detection of VZV DNA and anti-VZV antibody in CSF.
Zoster sine herpete was first described in a report of multiple patients with dermatomal distribution radicular pain in areas distinct from pain with rash in zoster (67).
Zostavax® (highly potent attenuated VZV) is indicated for prevention of zoster in individuals age 60 and older. The Shingles Prevention Study (SPS) of the licensed zoster vaccine was a placebo-controlled, double-blind study of more than 38,000 adults over the age of 60.
Like varicella vaccine, zoster vaccine should not be administered to immunocompromised individuals. While VZV DNA can be found on surfaces such as door knobs, toys, air-conditioning filters and tables in rooms where children or adults have active varicella or zoster, enveloped VZV is highly sensitive to desiccation such that infection is typically acquired through inhalation of aerosolized virus. Humans are the only reservoir for VZV, and anyone with varicella or zoster can transmit disease to seronegative individuals, often by the respiratory route. Unlike varicella, which occurs most often in the winter and early spring, zoster is not seasonal because it originates from reactivation of latent virus.
Levels of acyclovir in CSF after treatment with acyclovir or valacyclovir are 25-50% of that in plasma (112, 124).


Clinical benefit from acyclovir is only modest and does not reduce the risk of complications (27); thus, the American Academy of Pediatrics (AAP) does not recommend routine antiviral treatment of uncomplicated varicella in otherwise healthy children (3). Magnetic resonance imaging (MRI) of patients with zoster paresis reveals involvement of both anterior and posterior roots at spinal levels corresponding to clinical deficit.
Current guidelines recommend treating zoster with famciclovir 500 mg 3 times daily, valacyclovir 1 g 3 times daily or acyclovir 800 mg 5 times daily.
This so-called post-infectious myelitis usually occurs in immunocompetent patients, days to weeks after acute varicella or zoster. The first two virologically confirmed cases of zoster sine herpete were verified by detection of VZV DNA in CSF (47). DNA sequencing has shown that zoster (20, 43), as well as VZV meningitis and multifocal VZV vasculopathy (104) can develop after reactivation of vaccine strain VZV. Zoster vaccine increases CD4 and CD8 T cells (effector and memory), and the half-life of the boost in T-cell immunity to VZV is at least 5 years.
Rarely, clinical deficit in cervical zoster paresis extends to the brachial plexus, confirmed by both electrodiagnostic testing and MRI.
Among persons older than 50 and 80 years, the incidence of PHN in zoster patients is 18% and 33%, respectively. While the dosing of acyclovir requires treatment 5 times a day, it is considerably cheaper than valacyclovir or famciclovir.
A placebo-controlled study of treatment with acyclovir and prednisone showed that combination therapy significantly shortened the duration of rash and increased quality of life, but did not affect resolution of pain during a 6-month period (131). A third case of thoracic-distribution zoster sine herpete, in which electromyography of paraspinal muscles demonstrated frequent fibrillation potentials restricted to chronically painful thoracic root segments, was confirmed by detection of VZV DNA in blood MNCs and anti-VZV IgG antibody in CSF (4). Zoster vaccine also boosts VZV-specific immunity in adults with a history of zoster or with chronic illness.
Endpoints included the burden of illness due to zoster and zoster-associated pain as well as the incidence of PHN.
Another case of virologically confirmed zoster sine herpete with electrophysiologic correlation. A single dose of gabapentin reduces acute pain and allodynia in patients with herpes zoster.
Valaciclovir compared with acyclovir for improved therapy for herpes zoster in immunocompetent adults. Zoster sine herpete: virological verification by detection of anti-VZV IgG antibody in CSF. The effects of pre-emptive treatment of postherpetic neuralgia with amitriptyline: a randomized, double-blind, placebo-controlled trial. Pregabalin for the treatment of postherpetic neuralgia: a randomized, placebo-controlled trial.
Consequences of varicella and herpes zoster in pregnancy: prospective study of 1739 cases. Aseptic meningitis and optic neuritis preceding varicella zoster progressive outer retinal necrosis in a patient with AIDS. The effect of treating herpes zoster with oral acyclovir in preventing postherpetic neuralgia.
Increased risk of stroke after a herpes zoster attack: a population-based follow-up study. Varicella zoster virus infections of the nervous system: clinical and pathologic correlates.
Emergence of acyclovir-resistant varicella zoster virus in an AIDS patient on prolonged acyclovir therapy. VZV multifocal vasculopathy with ischemic optic neuropathy, acute retinal necrosis and temporal artery infection in the absence of zoster rash. The varicella zoster virus vasculopathies: clinical, CSF, imaging and virological features.


Treatment response in antidepressant-naive postherpetic neuralgia patients: double-blind, randomized trial. Zoster occurs primarily in the elderly as cell-mediated immunity to VZV declines with age, as well as in individuals whose immune system is compromised by human immunodeficiency virus (HIV) infection or by treatment with corticosteroids or immunosuppressive drugs.
Mortality can be as high as 45% in untreated pregnant women (55, 107), but decreases to 14% with acyclovir treatment (16). Because VZV becomes latent in ganglia along the entire neuraxis, zoster can develop anywhere on the body. Thoracic zoster has been associated with abdominal muscle weakness, resulting in abdominal hernia. Table 1 lists treatments for zoster and its neurological complications; the choice of drug may depend on dosing and drug price.
For patients who present >72 hours after rash, the benefit of antiviral therapy is unclear, but treatment should be considered in elderly patients, particularly those with severe pain, continued new vesicle formation or neurological complications (29).
Corticosteroids should be considered for patients with moderate to severe pain and for patients with neurological complications of zoster (29).
A study of HIV seropositivity with various clinical manifestation of herpes zoster among patients from Karnataka, India. Another meta-analysis that included one additional trial also demonstrated that acyclovir treatment reduced PHN by 46% at 6 months (60).
PORN may be preceded by retrobulbar optic neuritis and aseptic meningitis (39), central retinal artery occlusion or ophthalmic-distribution zoster (76), and may occur together with multifocal vasculopathy or myelitis.
By 2008, three years after zoster vaccine was licensed and recommended by the Advisory Committee on Immunization Practices for persons age 60 and older, less than 7% of the age group in the U.S. There are no well-controlled studies on the teratogenicity of acyclovir; the AAP does not recommend treatment of uncomplicated varicella during pregnancy. Topical corticosteroids aid resolution of episcleritis, scleritis or iritis in patients with ophthalmic-distribution zoster (94). It is essential to differentiate GCA from multifocal VZV vasculopathy because treatment with corticosteroids for presumed GCA may potentiate VZV infection and lead to loss of vision. A later study confirmed the benefits of valacyclovir over acyclovir irrespective of whether treatment was started 48 to 72 hours after rash onset (135). Importantly, diagnosis of this treatable cause of stroke is often missed because there is no history of zoster rash in one-third of subjects, the CSF is normal in one-third of subjects, there is an average 4.2-month delay from zoster to neurological symptoms and signs, and VZV DNA is often not present in CSF.
In contrast, patients with multifocal VZV vasculopathy require immediate antiviral (intravenous acyclovir) treatment. Varicella-like rashes at the injection site were more common in recipients of zoster vaccine than in placebo recipients (0.1% vs. Further evidence that postherpetic neuralgia may be produced by low-level ganglionitis has come from the detection of VZV DNA and proteins in blood MNCs of many patients with postherpetic neuralgia and from the favorable response of some postherpetic neuralgia patients to antiviral treatment. The mean age at onset of zoster among adults (age 22 years and older) is 59.4 years, with 68% of cases occurring in those 50 years and older. Subjects in the immunization group who developed zoster reported significantly less pain and discomfort than those in the placebo group and PHN was less frequent (an overall 61% lower burden of pain). Early diagnosis and aggressive treatment with intravenous acyclovir have been helpful, even in immunocompromised patients (26). Based upon these age-specific rates, ~1 million new episodes of zoster have been estimated to occur in the U.S.
Children or adolescents who acquired primary VZV infection in utero or in the first year of life are 20.9 times more likely to develop zoster before age 20 (8, 17, 50). Recurrent zoster has 3 to 5% lifetime risk to 6.2% over 8 years (137), and is associated with decreased immune competency.



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