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17.01.2015

How to treat herpes zoster, antiviral for herpes - PDF Review

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Significant scarring may result from cutaneous herpes zoster and this is most problematic with facial involvement. In most circumstances, the diagnosis of cutaneous herpes zoster is made on clinical grounds.
The following treatment recommended for varicella and zoster are based on the 2009 document Guidelines for Prevention and Treatment of Opportunistic Infections in HIV-Infected Adolescents and Adults[4]. In general, HIV-infected patients with uncomplicated varicella infection can be treated with oral antiviral therapy. The recommendations regarding the use of the varicella vaccine (Varivax) and zoster vaccine (Zostavax) are discussed in the in Case 4 (Appropriate Vaccinations) in the section Initial Evaluation. These extensive zoster lesions on the buttock and posterior leg have crusted and show no sign of secondary bacterial infection.
Herpes zoster infection (shingles) results from the reactivation of varicella zoster virus infection. Anticonvulsants have been shown to be equally efficacious; however, drug selection may involve trial and error. Given the widespread prevalence of varicella-zoster virus (VZV) infection in adults, most HIV-infected adults are at risk of developing VZV reactivation and herpes zoster.
The factors governing the maintenance of latency or the progression to viral replication remain poorly understood, but the increased incidence of zoster among immunocompromised persons suggests that cell-mediated immunity probably plays a critical role.
Reactivation of herpes zoster in the trigeminal ganglia may lead to the development of herpes zoster ophthalmicus, a condition that includes a number of inflammatory manifestations in the eye, such as conjunctivitis, episcleritis, keratitis, and iritis. All patients with an acute episode of varicella or zoster should promptly receive antiviral treatment[4].
In contrast, HIV-infected persons with complicated primary varicella infection, including involvement of visceral organs, retina, or the central nervous system, should receive treatment with intravenous acyclovir and undergo hospitalization for observation (Figure 7). The recommended antiviral treatment options (Figure 8) for localized dermatomal zoster in HIV-infected persons consist of valacyclovir (Valtrex), famciclovir (Famvir), or acyclovir (Zovirax)[4].
In the rare instance when an HIV-infected person who is non-immune to VZV has significant exposure to a patient with active varicella or zoster, varicella zoster immune globulin (VZIG) should be administered within 96 hours of exposure (preferably within 48 hours). Guidelines for prevention and treatment of opportunistic infections in HIV-infected adults and adolescents: recommendations from CDC, the National Institutes of Health, and the HIV Medicine Association of the Infectious Diseases Society of America. In excess of 60% of people older than 60 years, especially those with diminished immunity due to diabetes and cancers, are afflicted by herpes zoster. Prednisone use in conjunction with acyclovir resulted in the reduction of the pain associated with acute herpes zoster. The outcome of treatment of shingles is often unsatisfactory, although the antiviral medications reduce the duration of pain during the acute phase but do not prevent PHN complications and pain.


The incidence of zoster among HIV-infected adults is more than 15-fold higher than age-matched VZV-infected immunocompetent persons, with nearly 30 cases per year observed for every 1,000 HIV-infected adults[2].
Patients with herpes zoster often present with dysesthesias of the skin several days prior to the onset of cutaneous lesions.
Post-herpetic neuralgia (defined as pain that persists longer than 30 days after the onset of the rash) is a significant problem associated with herpes zoster infection, but, after adjusting for age, the risk of post-herpetic neuralgia does not differ significantly among HIV-infected persons compared with immunocompetent persons[7]. The direct fluorescent antibody (FA) assessment of a cellular rich sample from the base of the lesion offers the most sensitive, specific, and rapid diagnosis for herpes zoster.
Note these antiviral medications are administered at doses higher than those commonly used for the treatment of uncomplicated herpes simplex virus infections.
One report described 18 HIV-infected patients with advanced immunosuppression and acyclovir-resistant VZV-related skin lesions that failed to heal despite treatment with acyclovir[15]; most of these patients had an excellent respond to treatment with foscarnet (Foscavir). Initially, the host is able to produce varicella zoster virus—specific, cell-mediated immunity during the infection. The second objective is to treat the associated pain in the acute phase and in PHN, and the third objective is to prevent the occurrence of PHN and other complications.
The diagnosis of herpes zoster should prompt the clinician to consider HIV testing, particularly in persons with known HIV risk factors, those younger than 50 years of age, or those who develop multi-dermatomal herpes zoster. Post-herpetic neuralgia manifests as chronic (more than 30 days after the onset of lesions) severe skin pain along the distribution of the initial zoster outbreak[8].
In these cases of complicated varicella, if the patient responds well to intravenous acyclovir, they can typically switch to oral antiviral therapy to finish their treatment course[4].
Low levels of immune globulin have been shown to predispose patients to recurring herpes zoster infection.
Despite the usefulness of prednisone in managing the associated pain with herpes zoster infection, it has not been shown to decrease or prevent the incidence of PHN. I believe it is a neurologic condition and that it should be aggressively treated with some kind of physiologic treatments by a neurologist. Postherpetic neuralgia is very resistant to treatment and results in decreased quality of life.
In addition, the incidence of zoster increases within the first 4 months after initiating highly active antiretroviral therapy (mean 5 weeks), probably related to immune reconstitution[6]. Although herpes zoster can occur anywhere on the body, the skin of the thorax is the most frequently involved region. Bacterial superinfection of vesicles can also complicate cutaneous herpes zoster (Figure 6). The CDC Advisory Committee on Immunization Practices recommends routine vaccination of all persons age >60 years with one dose of zoster vaccine.


Accordingly, the use of corticosteroids as part of the treatment for herpes zoster in HIV-infected persons is not recommended[4].
Occasionally, zoster can cause motor weakness in noncranial nerve distributions, calledzoster paresis. The pain is stipulated to be due to persistent C-fiber nociceptor activity in the nerve cells, although studies have shown chronic neural loss and scarring in nerves affected by herpes zoster injury. Lidocaine patches were superior to both no treatment and vehicle patches in averaged category pain relief scores.
Combining TCAs with antiviral drugs during herpes zoster infection has been shown to decrease the intensity of PHN pain but does not prevent it. Although other infections, such as herpes simplex virus and smallpox, may cause similar appearing vesicular lesions, the characteristic dermatomal distribution of herpes zoster helps to distinguish herpes zoster from these other disorders. Treating acute zoster-associated neuropathic pain or post-herpetic neuralgia is an important component of the management of patients with VZV infection. One specific risk for patients who are immunocompromised is dissemination of the zoster rash. Zoster vaccination is not indicated to treat acute zoster, to prevent persons with acute zoster from developing PHN, or to treat ongoing PHN. Cutaneous dissemination generally occurs only among immunocompromised patients, occurring in up to 37% of zoster cases in the absence of antiviral treatment. Valacyclovir appears to be more efficacious in decreasing the severity of pain associated with acute herpes zoster and the duration of the PHN when compared to acyclovir.
Before routine administration of zoster vaccine, it is not necessary to ask patients about their history of varicella (chickenpox) or to conduct serologic testing for varicella immunity.
Rarely, patients will experience acute focal neurologic deficits weeks to months after resolution of the zoster rash, involving the trigeminal distribution contralateral to the initial rash. When antiviral therapy starts within 72 hours of the onset of herpes zoster, acyclovir, valacyclovir, and famciclovir have been shown to significantly shorten the periods of acute pain, virus shedding, rash, and acute and late-onset complications. Other rare neurologic complications of herpes zoster include myelitis, aseptic meningitis, and meningoencephalitis. The risk for neurologic zoster complications is generally increased in immunocompromised persons.



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