Herpes zoster



Herpes zoster


Rana Majd Mays, Erik T. Petersen, Rachel A. Gordon and Stephen K. Tyring


Evidence Levels:  A Double-blind study  B Clinical trial ≥ 20 subjects  C Clinical trial < 20 subjects  D Series ≥ 5 subjects  E Anecdotal case reports


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Reactivation of latent varicella zoster virus (VZV) produces the clinical syndrome herpes zoster (shingles), which manifests as a unilateral eruption along a single dermatome and is usually preceded by prodromal pain and paresthesia. The eruption lasts around seven to 10 days, and progresses from erythematous macules and papules to vesicles, then pustules, and finally crusts over. One of the most common complications of herpes zoster is postherpetic neuralgia (PHN), which is dermatomal pain persisting longer than 3 months.



Management strategy


Early treatment – within the first 72 hours of vesicle formation – is important for antiviral efficacy, time to lesion healing, and minimizing zoster-associated pain (although initiating treatment after 72 hours may still be effective). Acyclovir, valacyclovir, and famciclovir are guanosine analogs that are phosphorylated by thymidine kinase to a triphosphate form that inhibits viral DNA polymerase. The oral bioavailability of the antivirals determines the number of daily administrations. Patient compliance tends to decrease as the number of daily administrations increases. The most common side effects seen are nausea, headache, and gastrointestinal upset, but these drugs are otherwise safe and well tolerated. Patients with renal insufficiency will need an adjusted dose, as these medications are excreted by the kidneys.


Acyclovir-resistant VZV infections have been reported in immunocompromised patients (i.e., AIDS, transplant patients) and in these cases foscarnet (given intravenously 40 mg/kg three times daily) can be used as an alternative.


Acutely, corticosteroids may reduce zoster-associated pain, but they are associated with a risk of serious adverse events and have shown no benefit in reducing time to complete cessation of pain.


Current therapeutic options for PHN include the anticonvulsants gabapentin and pregabalin, opioid analgesics, tricyclic antidepressants (Table 101.1), lidocaine patch 5%, and capsaicin cream. Choice of therapy should be guided by considering a patient’s comorbidities, drug adverse event profiles, and preference. Combination therapy is common in clinical practice, but there is no evidence base to support this practice.



Vaccination of patients aged 50 years and over with VZV is the most promising option for the prevention of herpes zoster. Administration of gabapentin in conjunction with antivirals (and analgesics) during the acute phase of zoster may offer further protection against PHN. Asymptomatic reactivation of the VZV and contact with patients with chickenpox may enhance cell-mediated immunity.




First-line therapies


















Antiviral agents
imageAcyclovir A
imageFamciclovir A
imageValacyclovir A


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Valacyclovir compared with acyclovir for improved therapy for herpes zoster in immunocompetent adults.

Beutner KR, Friedman DJ, Forszpaniak C, Andersen PL, Wood MJ. Antimicrob Agents Chemother 1995; 39: 1546–53.


Valacyclovir is comparable to acyclovir in the resolution of zoster eruption (Table 101.2), but it accelerates the resolution of pain compared to acyclovir and is more convenient.


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Aug 7, 2016 | Posted by in Dermatology | Comments Off on Herpes zoster

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