Valacyclovir in the Treatment of Herpes Simplex, Herpes Zoster, and other Viral Infections

We have analysed zoster-associated pain treated with valaciclovir (VCV) in immunocompetent patients with acute herpes zoster over 6 months, and evaluated the safety of VCV. We know of no reports that evaluate postherpetic neuralgia (PHN) treated with VCV for 6 months. Predisposing factors that influence PHN were age (over 60 years), clustered vesicles, severity of eruption, sleep disturbance, and hypesthesia. Timing of the administration of VCV before or after the onset of rash did not influence the incidence of PHN. No serious adverse reactions were observed during the administration of VCV.

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“…Wu et al. (11) reported that PHN was seen in 28% of patients. The incidence of PHN was similar to our result (24.7%).…”

Section: Discussionmentioning

confidence: 99%

The change in zoster-associated pain treated with oral valaciclovir in immunocompetent patients with acute herpes zoster

Kurokawa

Murakawa

Kumano

2007

International Journal of Clinical Practice

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Targeting Infectious Agents as a Therapeutic Strategy in Alzheimer’s Disease

et al. 2020

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Alzheimer's disease (AD) is the most prevalent dementia in the world. Its cause(s) are presently largely unknown. The most common explanation for AD, now, is the amyloid cascade hypothesis, which states that the cause of AD is senile plaque formation by the Amyloid β peptide, and the formation of neurofibrillary tangles by hyperphosphorylated tau. A second, burgeoning theory by which to explain AD is based on the infection hypothesis. Much experimental and epidemiologic data support an involvement of infections in the development of dementia. According to this mechanism, the infection either directly, or via microbial virulence factors, precedes the formation of Amyloid β plaques. The amyloid β peptide, possessing antimicrobial properties, is beneficial at an early stage of AD, but becomes detrimental with the progression of the disease, concomitantly with alterations to the innate immune system at both the peripheral and central levels. Infection results in neuroinflammation, leading to and sustained by systemic inflammation, causing eventual neurodegeneration, and the senescence of the immune cells. The sources of AD-involved microbes are various body microbiome communities from the gut, mouth, nose, and skin. The infection hypothesis opens a vista to new therapeutic approaches, either by treating the infection itself, or modulating the immune system, its senescence, or the body's metabolism, either separately, in parallel, or in a multi-step way. Key points:1. Experimental and epidemiologic data support an involvement of infections in the development of Alzheimer's Disease (AD) and the sources of AD-involved microbes are various body microbiome communities from the gut, mouth, nose, and skin; 2. The amyloid β peptide, possessing antimicrobial properties, is beneficial at an early stage of AD, but becomes detrimental with the progression of the disease; 3. Infection results in neuroinflammation, leading to and sustained by systemic inflammation, causing neurodegeneration, and the senescence of the immune cells preceding the clinical manifestations; 4. The infection hypothesis and the antimicrobial protection hypothesis of AD opens the way to new therapeutic approaches.

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Transverse Myelitis Caused by Varicella Zoster Virus

Arı¹,

Karaci²,

Domaç³

et al. 2019

Infect Dis Clin Pract

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Introduction The varicella zoster virus (VZV) infection causes chickenpox and herpes zoster. Primary infection occurs more frequently in the pediatric age as chickenpox. Virus can be latent in cranial nerve or dorsal root ganglia and reactivate several decades later as the form of herpes zoster generally in immunosuppressed patients. Varicella zoster virus is associated with severe neurological complications, including post herpetic neuralgia, aseptic meningitis, polyneuropathy, cranial nerve palsy, meningoencephalitis, vasculopathy, encephalitis, and transverse myelitis. The transverse myelitis caused by VZV is reported rarely. Case Report A 77-year-old immunocompetent patient presented with muscle weakness and sensation loss due to the demyelinating lesion caused by VZV on C5 dermatome. Proprioception and vibratory sensation loss were also marked. Cervical spinal magnetic resonance imaging showed expansive intramedullary high-signal intensity lesion on C5 with focal swelling on T2-weighted images and gadalinium enhancement on T1-weighted images. cerebrospinal fluid viral antibody test was positive for immunoglobulin G of VZV but negative for VZV DNA. The patient was treated with oral valacyclovir (1 g) 3 times daily for 7 days and with methylprednisolone (1.0 g) every day for 5 days. After treatment, his muscle strength increased but sensorial loss and neuropathic pain did not recover. Conclusions About 40% of transverse myelitis cases are caused by viral infections, some of them are herpes viruses and poliovirus. Varicella zoster infection is a common disease but not a common cause of transverse myelitis particularly in immuncompetent patients. The clinicians must be aware of this rare complication of VZV.

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Valacyclovir in the Treatment of Herpes Simplex, Herpes Zoster, and other Viral Infections

Abstract: Valacyclovir is safe and effective in the therapy of patients with herpes simplex and herpes zoster and may be useful in other viral infections.

Cited by 4 publications

References 48 publications

The change in zoster-associated pain treated with oral valaciclovir in immunocompetent patients with acute herpes zoster

The change in zoster-associated pain treated with oral valaciclovir in immunocompetent patients with acute herpes zoster

Targeting Infectious Agents as a Therapeutic Strategy in Alzheimer’s Disease

Transverse Myelitis Caused by Varicella Zoster Virus

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