Does Bortezomib Induce De Facto Varicella Zoster Virus Reactivation in Patients With Multiple Myeloma?

Abstract BACKGROUND: Bortezomib is associated with a significant risk of Varicella zoster virus (VZV) reactivation in patients with multiple myeloma (MM). There are some reports that acyclovir or valacycclovir reduces the risk of VZV reactivation. We assessed whether VZV reactivation could be prevented by valacyclovir at a dose of 300 mg bid. PATIENTS AND METHODS: We retrospectively evaluated 108 patients with MM who received bortezomib and valacyclovir prophylaxis at the Nanfang Hospital from 2015 to 2017. Patients received valacyclovir prophylaxis orally at a dose of 300 mg bid, without cessation until finishing the whole course of bortezomib treatment. RESULTS: The median age was 56 years (range=37-84 years). 57 patients were male and 51 were female. The median bortezomib dose was 31.2 mg/m2(range=5.2-83.2 mg/m2). All patients also received corticosteroids. The median duration of valacyclovir prophylaxis was 333 days (range=38-724 days) and the median valacyclovir dose was 199.8 g (range=22.8-434.4 g). VZV reactivation did not develop in any patient during valacyclovir prophylaxis. Adverse events over grade 3 associated with valacyclovir were not observed. CONCLUSION: Valacyclovir at a dose of 300 mg bid appears to be effective at preventing VZV reactivation and was well-tolerated by patients with MM treated with bortezomib. Disclosures No relevant conflicts of interest to declare.

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Varicella Zoster Virus Reactivation in Adult Survivors of Hematopoietic Cell Transplantation: How Do We Best Protect Our Patients?

Biology of Blood and Marrow Transplantation ◽

10.1016/j.bbmt.2018.04.003 ◽

2018 ◽

Vol 24 (9) ◽

pp. 1783-1787 ◽

Cited By ~ 7

Author(s):

Catherine J. Lee ◽

Bipin N. Savani ◽

Per Ljungman

Keyword(s):

Varicella Zoster Virus ◽

Cell Transplantation ◽

Hematopoietic Cell Transplantation ◽

Adult Survivors ◽

Hematopoietic Cell ◽

Virus Reactivation ◽

Varicella Zoster

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Analysis of T Cell Responses during Active Varicella-Zoster Virus Reactivation in Human Ganglia

Journal of Virology ◽

10.1128/jvi.03445-13 ◽

2013 ◽

Vol 88 (5) ◽

pp. 2704-2716 ◽

Cited By ~ 44

Author(s):

M. Steain ◽

J. P. Sutherland ◽

M. Rodriguez ◽

A. L. Cunningham ◽

B. Slobedman ◽

...

Keyword(s):

T Cell ◽

Varicella Zoster Virus ◽

T Cell Responses ◽

Virus Reactivation ◽

Varicella Zoster ◽

Cell Responses

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A Case Report of Acute Severe Myelitis and Meningitis Secondary to Varicella Zoster Virus Reactivation in a Patient with Acquired Immunodeficiency Syndrome

International Journal of Medical Students ◽

10.5195/ijms.2021.863 ◽

2021 ◽

Author(s):

Victor A Novelo-Hernández ◽

Marco Cárdenas ◽

Claudia Torres-González ◽

Patricio Garcia-Espinosa ◽

Rómulo Ramirez ◽

...

Keyword(s):

Spinal Cord ◽

Varicella Zoster Virus ◽

Acquired Immunodeficiency Syndrome ◽

Clinical Manifestations ◽

Virus Reactivation ◽

Neck Stiffness ◽

Varicella Zoster ◽

Wide Range ◽

Acquired Immunodeficiency ◽

Immunodeficiency Syndrome

Background: Myelitis post Herpes-Zoster is a rare condition that is typically associated with immunocompromised states. It usually starts as an acute loss of sensory and motor functions below the affected spinal cord level. The condition can range in severity from a mild to a fatal presentation. Other neurological complications include meningitis, atypical presentations should encourage the search for undiagnosed immunosuppression states. The Case: We describe the case of a 42-year-old man, previously undiagnosed with HIV, who developed acute myelitis and meningitis after the appearance of the classic zoster lesions. On lumbar puncture and subsequent CSF analysis, the patient was found to have Froin’s Syndrome. The patient was initiated with ceftriaxone, vancomycin, and acyclovir regimen and prophylactic antiphymic treatment was also added. After 14 days in the hospital, the fever, headache, and neck stiffness subsided while the sphincter function and lower limb paraplegia did not improve. Conclusion: Varicella zoster virus reactivation suggests underlying immunosuppression. This case demonstrates the importance of being cognizant to the wide range of clinical manifestations that may suggest spinal cord involvement after clinical reactivation. Furthermore, physicians also need to be mindful that Acquired Immunodeficiency Syndrome (AIDS) and other immunodeficiency states could present with atypical clinical manifestations.

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Neurological Disease Produced by Varicella Zoster Virus Reactivation Without Rash

Current Topics in Microbiology and Immunology - Varicella-zoster Virus ◽

10.1007/82_2009_3 ◽

2010 ◽

pp. 243-253 ◽

Cited By ~ 43

Author(s):

Don Gilden ◽

Randall J. Cohrs ◽

Ravi Mahalingam ◽

Maria A. Nagel

Keyword(s):

Varicella Zoster Virus ◽

Neurological Disease ◽

Virus Reactivation ◽

Varicella Zoster

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Pharyngeal dysphagia due to Varicella zoster virus meningoradiculitis and full recovery: Case report and endoscopic findings

SAGE Open Medical Case Reports ◽

10.1177/2050313x18756560 ◽

2018 ◽

Vol 6 ◽

pp. 2050313X1875656

Author(s):

Paul Muhle ◽

Sonja Suntrup-Krueger ◽

Rainer Dziewas ◽

Tobias Warnecke

Keyword(s):

Varicella Zoster Virus ◽

Brain Magnetic Resonance Imaging ◽

Virus Reactivation ◽

Swallowing Function ◽

Percutaneous Gastrostomy ◽

Negative Finding ◽

Varicella Zoster ◽

Fluid Analysis ◽

Pharyngeal Dysphagia ◽

Acyclovir Treatment

Varicella zoster virus reactivation is a rare cause of pharyngeal dysphagia with long-term sequelae persisting in most cases. A 76-year-old immunocompetent woman presented with a 4-week history of dysphagia and dysphonia. Brain magnetic resonance imaging displayed a negative finding. Fiberoptic endoscopic evaluation of swallowing showed a severe dysphagia leading to a percutaneous gastrostomy eventually. Cerebrospinal fluid analysis revealed a lymphocytic pleocytosis and polymerase chain reaction amplified Varicella zoster virus DNA. Eight months after Acyclovir treatment and despite a persisting impairment of the recurrent laryngeal nerve, regular swallowing function was regained and percutaneous gastrostomy could be removed.

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