Aseptic Meningitis after Amenamevir Treatment for Herpes Zoster in the First Branch of the Trigeminal Nerve

Itoh, Kazuhiro; Mitsuke, Yasuhiko; Wakahara, Mami; Yoshioka, Takayuki; Otsuki, Nozomi; Suzuki, Yusuke; Kiriba, Chiyo; Kuwata, Atsushi; Sakamaki, Ippei; Iwasaki, Hiromichi; Tsutani, Hiroshi

doi:10.2169/internalmedicine.8581-21

Cited by 5 publications

(4 citation statements)

References 13 publications

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“…We experienced three cases of aseptic meningitis by VZV and one case of VZV myelitis after HZ dermatitis during treatment with amenamevir for HZ in various immunological backgrounds (Table 1). Table 2 summarizes six HZ cases treated with amenamevir with CNS complications that were previously reported [2][3][4][5][6]. While three cases in our report are regarded as immunocompromised hosts (two cases were taking immunosuppressive drugs, and one case had sigmoid colon cancer as an underlying disease), one case was immunocompetent.…”

Section: Discussionmentioning

confidence: 76%

“…In the outpatient setting, amenamevir may be a more frequent prescription choice, especially for elderly patients with HZ, as no volume adjustment based on creatinine clearance is necessary. However, for immunocompromised patients, such as those taking immunosuppressive medications, or for ocular HZ patients at a high risk of CNS complications, as in the present cases, it may be preferable to use acyclovir or valacyclovir to reduce the risk of complications [ 5 ]. Additionally, Skripuletz et al conducted a study on VZV CNS complications and found that cardiovascular diseases were the most common comorbidity, followed by impaired renal function [ 17 ].…”

Section: Discussionmentioning

confidence: 99%

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Varicella-Zoster Meningitis and Myelitis After Herpes Zoster Dermatitis Treatment With Amenamevir: A Case Series and Literature Review

Tada,

Kaito,

Watanabe

et al. 2024

Cureus

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Varicella-zoster virus (VZV), known for causing chickenpox, establishes latent infections in neural tissues. Reactivation of VZV can lead to herpes zoster (HZ) and various neurological complications. In this report, we present four cases of VZV meningitis and myelitis following amenamevir treatment for HZ dermatitis with positive VZV DNA in cerebrospinal fluid (CSF) revealed by polymerase chain reaction (PCR). Three of them were considered immunocompromised hosts given the fact that two of these patients were taking immunosuppressive drugs for rheumatoid arthritis, and one patient had a history of sigmoid colon cancer (four months after resection). After HZ onset, amenamevir, which has poor CSF transfer, was prescribed for all the patients, and all of them developed central nervous complications by VZV (meningitis in three cases and myelitis in one case) confirmed by PCR. All the patients were treated with acyclovir, which has a higher CSF transfer, and fully recovered. We speculate that amenamevir might have failed to prevent VZV infection in the central nervous system (CNS) and think that consideration should be given to administering acyclovir in preference to amenamevir for ΗΖ patients at high risk of CNS VZV infection, such as immunocompromised hosts.

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Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Varicella-Zoster Meningitis and Myelitis After Herpes Zoster Dermatitis Treatment With Amenamevir: A Case Series and Literature Review

Tada,

Kaito,

Watanabe

et al. 2024

Cureus

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“…These symptoms result from the inflammatory processes and the resulting irritation of the meninges and surrounding nervous tissue. 147 The diagnosis of VZV-associated aseptic meningitis often involves the detection of VZV-specific antibodies or viral DNA in the CSF. Antiviral therapy, along with supportive care and management of symptoms, is essential in reducing viral replication, controlling the inflammatory response, and improving clinical outcomes in affected individuals.…”

Section: Aseptic Meningitismentioning

confidence: 99%

“…Aseptic meningitis associated with VZV infection typically presents with symptoms such as headache, fever, neck stiffness, photophobia, and neurological deficits. These symptoms result from the inflammatory processes and the resulting irritation of the meninges and surrounding nervous tissue 147 . The diagnosis of VZV‐associated aseptic meningitis often involves the detection of VZV‐specific antibodies or viral DNA in the CSF.…”

Section: Role Of Vzv Infection In Inflammatory Neurological Diseasesmentioning

confidence: 99%

Varicella‐zoster virus‐related neurological complications: From infection to immunomodulatory therapies

Hakami,

Khan,

Abdulaziz

et al. 2024

Reviews in Medical Virology

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The Varicella‐zoster virus (VZV), classified as a neurotropic member of the Herpesviridae family, exhibits a characteristic pathogenicity, predominantly inducing varicella, commonly known as chickenpox, during the initial infectious phase, and triggering the reactivation of herpes zoster, more commonly recognized as shingles, following its emergence from a latent state. The pathogenesis of VZV‐associated neuroinflammation involves a complex interplay between viral replication within sensory ganglia and immune‐mediated responses that contribute to tissue damage and dysfunction. Upon primary infection, VZV gains access to sensory ganglia, establishing latent infection within neurons. During reactivation, the virus can spread along sensory nerves, triggering a cascade of inflammatory mediators, chemokines, and immune cell infiltration in the affected neural tissues. The role of both adaptive and innate immune reactions, including the contributions of T and B cells, macrophages, and dendritic cells, in orchestrating the immune‐mediated damage in the central nervous system is elucidated. Furthermore, the aberrant activation of the natural defence mechanism, characterised by the dysregulated production of immunomodulatory proteins and chemokines, has been implicated in the pathogenesis of VZV‐induced neurological disorders, such as encephalitis, myelitis, and vasculopathy. The intricate balance between protective and detrimental immune responses in the context of VZV infection emphasises the necessity for an exhaustive comprehension of the immunopathogenic mechanisms propelling neuroinflammatory processes. Despite the availability of vaccines and antiviral therapies, VZV‐related neurological complications remain a significant concern, particularly in immunocompromised individuals and the elderly. Elucidating these mechanisms might facilitate the emergence of innovative immunomodulatory strategies and targeted therapies aimed at mitigating VZV‐induced neuroinflammatory damage and improving clinical outcomes. This comprehensive understanding enhances our grasp of viral pathogenesis and holds promise for pioneering therapeutic strategies designed to mitigate the neurological ramifications of VZV infections.

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Aseptic meningitis after amenamevir treatment for herpes zoster ophthalmicus with oculomotor nerve palsy in a patient taking immunosuppressant

Omiya

Nishiguchi

Moriya

et al. 2023

Journal of Infection and Chemotherapy

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Aseptic Meningitis after Amenamevir Treatment for Herpes Zoster in the First Branch of the Trigeminal Nerve

Cited by 5 publications

References 13 publications

Varicella-Zoster Meningitis and Myelitis After Herpes Zoster Dermatitis Treatment With Amenamevir: A Case Series and Literature Review

Varicella-Zoster Meningitis and Myelitis After Herpes Zoster Dermatitis Treatment With Amenamevir: A Case Series and Literature Review

Varicella‐zoster virus‐related neurological complications: From infection to immunomodulatory therapies

Aseptic meningitis after amenamevir treatment for herpes zoster ophthalmicus with oculomotor nerve palsy in a patient taking immunosuppressant

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