Herpes Zoster and Diabetes Mellitus: A Review

Abstract

Accumulating evidence suggests that diabetes mellitus (DM) represents an important risk factor for both herpes zoster and post-herpetic neuralgia. Moreover, post-herpetic neuralgia appears to be more severe and persistent in diabetic patients. On the other hand, a novel vaccine against varicella-zoster virus (VZV) was recently introduced in clinical practice. Given the increased risk and severity of herpes zoster infection in patients with DM, this vaccine might be useful in this population. However, there are limited data regarding the efficacy and safety of vaccination against herpes zoster in the diabetic population. The aim of the present review is to discuss the incidence and consequences of herpes zoster infection in DM and to comment on the role of vaccination against VZV in these patients.

Herpes Zoster Infection as a Presentation for Hidden Diabetes Mellitus

“…HZ shows an aggressive course in patients with DM, with higher health-related resource consumption, poor glycemic control, and reduced quality of life. This will reflect negatively on the number of outpatient visits, hospitalizations, and medication for diabetes after the HZ episode, as well as an increase in HbA1c levels [3,6].…”

“…There are inconclusive results regarding the role of severe immunosuppression as a risk factor for PHN which can be seen in about 10% -50% of patients with HZ, especially in diabetic individuals [2,[11][12]15]. The risk of PHN increases with increasing age (particularly over the age of 50) and is more significant in persons with severe pain at the onset of HZ or a severe rash with a large number of lesions [2][3]12].…”

“…Hyperglycemia may predict future PHN [3,11]; yet, it does not correlate with the severity of CMI impairment in patients with HZ or PHN [7].…”

“…The data are sparse regarding the preferred glucoselowering regimen of choice in HZ with DM or stress hyperglycemia [9]. Recent studies have demonstrated an increased risk for acquiring HZ in patients with established DM when they used thiazolidinediones, alpha-glucosidase inhibitors, and dipeptidyl peptidase-4 (DPP-4) inhibitors which appear to increase the risk of HZ, whereas metformin and sulphonylureas did not [3,14].…”

“…Herpes zoster (HZ) infection (shingles) occurs due to reactivation of a previous infection with varicella-zoster virus (VZV), due to decreased VZV-specific cell-mediated immunity (CMI), with aging or in individuals with immunosuppressive disorders [1]. Usually, a latency period (which reflects the host-virus interaction) of several years follows and then replication of the virus occurs [2][3].…”