Occurrence Of Herpes Zoster Research Articles

Herpes zoster as a risk factor for stroke and TIA

Objectives:Stroke and TIA are recognized complications of acute herpes zoster (HZ). In this study, we evaluated HZ as a risk factor for cerebrovascular disease (stroke and TIA) and myocardial infarction (MI) in a UK population cohort.Methods:A retrospective cohort of 106,601 HZ cases and 213,202 controls matched for age, sex, and general practice was identified from the THIN (The Health Improvement Network) general practice database. Cox proportional hazard models were used to examine the risks of stroke, TIA, and MI in cases and controls, adjusted for vascular risk factors, including body mass index >30 kg/m2, smoking, cholesterol >6.2 mmol/L, hypertension, diabetes, ischemic heart disease, atrial fibrillation, intermittent arterial claudication, carotid stenosis, and valvular heart disease, up to 24 years (median 6.3 years) after HZ occurrence.Results:Risk factors for vascular disease were significantly increased in cases of HZ compared with controls. Adjusted hazard ratios (AHRs) for TIA and MI but not stroke were increased in all patients with HZ (AHR [95% confidence interval]: 1.15 [1.09–1.21] and 1.10 [1.05–1.16], respectively). However, stroke, TIA, and MI were increased in cases whose HZ occurred when they were younger than 40 years (AHR [95% confidence interval]: 1.74 [1.13–2.66], 2.42 [1.34–4.36], 1.49 [1.04–2.15], respectively). Subjects younger than 40 years were significantly less likely to be asked about vascular risk factors than were older patients (p < 0.001).Conclusion:HZ is an independent risk factor for vascular disease in the UK population, particularly for stroke, TIA, and MI in subjects affected before the age of 40 years. In older subjects, better ascertainment of vascular risk factors and earlier intervention may explain the reduction in risk of stroke after the occurrence of HZ.

Varicella Vaccination Alters the Chronological Trends of Herpes Zoster and Varicella

BackgroundPopulation studies on trends of varicella and herpes zoster (HZ) associated with varicella zoster vaccination and climate is limited.MethodsThis study used insurance claims data to investigate the chronological changes in incident varicella and HZ associated with varicella zoster vaccination. Poisson regression was used to estimate the occurrence of varicella associated with the occurrence of HZ and vice versa by year, season, sex, temperature, and sunny hours.ResultsThe varicella incidence declined from 7.14 to 0.76 per 1,000 person-years in 2000–2009, whereas the HZ incidence increased from 4.04 to 6.24 per 1,000 person-years. Females tended to have a higher risk than men for HZ (p<0.0001) but not varicella. The monthly mean varicella incidence was the lowest in September (160 cases) and the highest in January (425 cases), while the mean HZ incidence was lower in February (370 cases) and higher in August (470 cases). HZ was negatively associated with the incidence of varicella before and after the varicella zoster vaccination (p<0.001), increased 1.6% within one week post-vaccination. The effect of temperature on HZ was attenuated by 18.5% (p<0.0001) in association with vaccination. The varicella risk was positively associated with sun exposure hours, but negatively associated with temperature only before vaccination.ConclusionsThe varicella vaccination is effective in varicella prevention, but the incidence of HZ increases after vaccination. HZ has a stronger association with temperature and UV than with seasonality while varicella risk associated with temperature and UV is diminished.

Incidence and risk factors of herpes zoster among hiv-positive patients in the german competence network for HIV/AIDS (KompNet): a cohort study analysis

BackgroundHIV infection is a risk factor for the development of Herpes zoster (HZ) and its complications. Prior to antiretroviral therapy (ART), HZ incidence in HIV-infected individuals ranged from 2.9–5.1/100 person-years. There is limited evidence for the impact of ART on HZ occurrence among HIV-infected adults. We analysed the incidence of, and risk factors for, HZ in a large cohort of German HIV-positive patients.MethodsThe study population was taken from the German KompNet cohort, a nationwide multicenter HIV cohort study. The study population was defined by age (≥ 18 years), year of first positive HIV diagnosis, CD4 values ± 6 months from HIV diagnosis (t0), and month of HZ diagnosis. Incidences were estimated using a Poisson distribution, and uni- and multivariate Cox proportional Hazard ratio (HR) regression models were fitted to identify risk factors for developing an initial HZ episode. Independent variables were sex, age at HIV diagnosis, route of HIV transmission, ART status, CD4 count before HZ episode, immunosuppressive medication, and mode of data documentation (retrospective or prospective).ResultsHZ incidence in the overall study population was 1.2/100 person-years. In a subset of patients for that we were able to examine risk factors the following was observed: We examined 3,757 individuals whose mean age at t0 was 38 years. Of those individuals, 96% were diagnosed with HIV in 1996 or later, with a mean observation time of 5.8 years. HZ episodes (n = 362) were recorded in 326 patients (8.7%), resulting in annual HZ incidences of 1.7/100 person-years overall, and 1.6/100 person-years for initial HZ cases. The main risk factors associated with an initial HZ episode were: not partaking in ART compared with an ART regimen containing a non-nucleoside reverse-transcriptase inhibitor (HR 0.530, p < 0.001) or a protease inhibitor (HR 0.624, p = 0.004); and lower CD4 count by 100 cells/μl (HR 0.918, p=0.001).ConclusionsHZ incidence was 4-11-fold higher than in non HIV-infected individuals, but in our study HZ incidences were lower than in previous studies relating to HIV-positive patients. We showed that ART is an important protective factor for HZ episodes.

P2.120 Incidence and Risk Factors of Herpes Zoster Among HIV-Positive Patients in the Cohort of the German Competence Network For HIV/AIDS (KompNet)

Background HIV infection is a risk factor for development of Herpes Zoster (HZ) and its complications. There is limited evidence on the impact of antiretroviral therapy (ART) on the occurrence of HZ among HIV-infected adults. Methods Study population was drawn from the KompNet HIV cohort. Inclusion criteria were: age ≥ 18 years, record of HIV diagnosis date (t0), record of CD4 count available ± 6 months from t0. Patients without month of HZ diagnoses were excluded. Study period was 1.1.1985–1.7.2010. Incidences of all HZ events were estimated assuming Poisson distribution, uni-/multivariate Cox proportional Hazard ratio (HR) regression models were fitted to identify risk factors for a first HZ event. Independent variables were: sex, age at HIV diagnosis, HIV transmission route, ART status, CD4-value before HZ episode, immunosuppressive medication, mode of data documentation (retrospective/prospective). Results Study population comprised 3,757 subjects (86% male, 66% MSM, 3% IVDU, 92% Caucasian), mean age at HIV diagnosis was 38 years, mean observation time was 5.8 years. 362 HZ events were recorded in 326 patients (8.6%), resulting in an HZ incidence of 16.7/1,000 PY overall and 16.1/1,000 PY for first HZ cases. Main risk factors associated with first HZ event were: no ART compared to an ART containing a non-nucleoside reverse-transcriptase inhibitor (NNRTI vs no ART; HR 0.530, p Conclusions According to former studies incidence of HZ in HIV-infected individuals was ∼5 times higher than in the general population. Our study showed ART as important protective associated factor for HZ events. Reasons may be earlier HIV-diagnosis, more recent picturing of ART, and low IVDU proportion in our study.

SAT0463 Incidence of Herpes Zoster Infections in Juvenile Idiopathic Arthritis Patients – Experience of the Biker Registry

BackgroundAn increased risk of herpes zoster among patients with juvenile idiopathic arthritis (JIA), especially with exposure to immunosuppressant medications and biologics have been described.ObjectivesWe determined incidence rates of herpes zoster...

Leg paralysis due to herpes zoster: segmental paralysis or viral vasculopathy and stroke?

Herpes zoster (HZ) is caused by a ubiquitous, exclusively human, highly neurotropic virus called varicella-zoster virus (VZV), which can affect the entire neuraxis. It usually presents with a characteristic unilateral vesicular rash and radicular pain in a dermatomal distribution. Eventhough in most of the cases only a single or two adjacent dermatomes are affected, multiple contiguous dermatomes can be involved in some patients. Somatic and autonomic neuropathy leading to a segmental zoster paresis/paralysis and autonomic motor complications has also been recognized as a part of the herpes zoster syndrome [1]. Other neurological complications such as stroke, transient ischemic attack, and myelopathy have also been described [2, 3]. On the other hand, disseminated HZ is usually defined as a generalized eruption of more than 20 extradermatomal vesicles occurring within a week of classic dermatomal herpes zoster [4]. It occurs mainly in patients with decreased VZV specific cell-mediated immune response, such as elderly individuals, patients with underlying malignancy, patients on immunosuppressive therapy, and patients with acquired immunodeficiency syndrome. Recently, we read an article published in the Internal and Emergency Medicine journal by Nicoli et al. [5] describing a case of herpetic leg paralysis, abdominal ileus, and urinary retention in a patient with idiopathic myelofibrosis. Although the case was very interesting, we have a few concerns regarding the description and discussion of this case. First, in this case report, the authors claim that a systemic widespread VZV infection involving the central nervous system and VZV encephalitic vasculopathy could precipitate the right lower limb paralysis. In adults, the typical clinical presentation of stroke caused by VZV is the occurrence of cranial nerve distribution HZ followed by acute contralateral hemiplegia weeks to months later. This patient had HZ involving the lumbosacral segments. Although the authors did not report a specific dermatomal distribution, judging by the description of the case it appeared as if the L2–L3 dermatomes were affected. Furthermore, a detailed strength examination was not performed to identify muscle weakness in the different muscle groups of the lower and upper limbs. Second, in patients with VZV vasculopathy, brain imaging reveals ischemic or hemorrhagic infarction in virtually all cases [2]. This particular patient had a negative computed tomography scan of the brain, which rules against VZV vasculopathy. Unfortunately, magnetic resonance imaging (MRI) of the brain, which could have added more information regarding the case, was not performed due to the contraindication of the presence of his pacemaker. In addition, MRI of the spinal cord would be another test to possibly assist in the differential diagnosis, as cases of myelopathy, polyradiclopathy, and polyradiculoneuropathy may be detected. Third, this case most likely does not represent systemic disseminated VZV infection, because there was no finding I. Chernev Physical Medicine and Rehabilitation, Beckley Appalachian Regional Healthcare, Beckley, WV, USA

The risk of herpes zoster in the anti-TNF-α era: a case report and review of the literature

Tumor necrosis factor-α (TNF-α) inhibitors represent efficacious therapeutic agents in many chronic inflammatory diseases such as psoriasis and rheumatoid arthritis. However they have been connected with increased risk of infection and reactivation of a variety of infectious agents, such as viruses. The reactivation of varicella zoster virus infection causes herpes zoster (HZ), a self-limiting, dermatomally localized, vesicular rash that can be accompanied by postherpetic neuralgia and severe neurological complications. Limited information has been published regarding HZ during therapy with TNF-α inhibitors especially for the occurrence of HZ during adalimumab treatment. We report the case of a 58-year-old immunocompetent man with a 18-year history of plaque psoriasis who develops ophthalmic HZ during treatment with adalimumab. We report this case to enrich the literature and to highlight the increased risk of HZ infections in patient on anti-TNF-α therapy (incidence of HZ is about 3-fold increased respect to general population). Clinically, these infections often have atypical presentations that may hamper prompt diagnosis. Therefore, it is very important to identify early signs and symptoms of herpes zoster in patients on biologic therapy in order to start prompt efficient antiviral treatment to prevent the development of severe complications.

Herpes zoster complicating bortezomib therapy of relapsed/refractory indolent B-cell and mantle cell lymphoma: an analysis of two phase II trials

The incidence of herpes zoster (HZ) in patients with non-Hodgkin lymphoma (NHL) receiving bortezomib-based therapy has not been well studied. We reviewed data from two phase II trials in which bortezomib was administered to 236 patients, median age 65 years, with relapsed/refractory mantle cell or indolent NHL. HZ occurred in 24 patients (10.2%) overall, with a comparable incidence in NHL histologic subgroups. Median time to HZ was 39 (range, 11–206) days. In total, 71% of patients who developed HZ were aged ≥ 65 years, compared to 48% without HZ (p = 0.03). Patients with HZ were more likely to have had received ≥ 2 lines of therapy (63% vs. 47%, p = 0.16). Six (25%) of the patients who developed HZ had received purine analogs, compared with 34 (16%) patients without HZ (p = 0.27). As the occurrence of HZ may complicate the course of indolent or mantle cell NHL in patients receiving bortezomib-based therapies, these patients, especially the elderly, should be strongly considered for antiviral prophylaxis.

Ramsay Hunt syndrome

Ramsay Hunt syndrome is defined as herpes zoster oticus associated with an acute peripheral facial nerve paresis and quite often with other cranial nerve lesions. The combination of motor, sensory and autonomic involvement leads to a variety of neurological damage patterns, i. e. facial muscle paresis, hearing and balance disorders, sensory problems and disturbances of taste as well as lacrimal and nasal secretion. Additional variability of the clinical picture of Ramsay Hunt syndrome is produced by varying patterns of skin involvement explained by individual anastomoses between cranial and cervical nerves. Knowledge of these findings and an early diagnosis of Ramsay Hunt syndrome are important as prognosis of cranial nerve damage depends on the time at which acyclovir-corticosteroid therapy is started.

Efficacy, Safety, and Tolerability of Herpes Zoster Vaccine in Persons Aged 50-59 Years

Herpes zoster (HZ) adversely affects individuals aged 50-59, but vaccine efficacy has not been assessed in this population. This study was designed to determine the efficacy, safety, and tolerability of zoster vaccine for preventing HZ in persons aged 50-59 years. This was a randomized, double-blind, placebo-controlled study of 22 439 subjects aged 50-59 years conducted in North America and Europe. Subjects were given 1 dose of licensed zoster vaccine (ZV) (Zostavax; Merck) and followed for occurrence of HZ for ≥1 year (mean, 1.3 years) postvaccination until accrual of ≥96 confirmed HZ cases (as determined by testing lesions swabs for varicella zoster virus DNA by polymerase chain reaction). Subjects were followed for all adverse events (AEs) from day 1 to day 42 postvaccination and for serious AEs (SAEs) through day 182 postvaccination. The ZV reduced the incidence of HZ (30 cases in vaccine group, 1.99/1000 person-years vs 99 cases in placebo group, 6.57/1000 person-years). Vaccine efficacy for preventing HZ was 69.8% (95% confidence interval, 54.1-80.6). AEs were reported by 72.8% of subjects in the ZV group and 41.5% in the placebo group, with the difference primarily due to higher rates of injection-site AEs and headache. The proportion of subjects reporting SAEs occurring within 42 days postvaccination (ZV, 0.6%; placebo, 0.5%) and 182 days postvaccination (ZV, 2.1%; placebo, 1.9%) was similar between groups. In subjects aged 50-59 years, the ZV significantly reduced the incidence of HZ and was well tolerated. NCT00534248.

Increased Risk of Multiple Sclerosis Following Herpes Zoster: A Nationwide, Population-Based Study

(See the editorial commentary by Corona and Flores, on pages 177-8.) Varicella zoster virus (VZV) has been proposed to be involved in the pathogenesis of multiple sclerosis (MS). However, the epidemiological data regarding the MS occurrence rate following herpes zoster are still scanty. The goal of this study is to investigate the frequency and risk for MS following occurrence of herpes zoster. This study used the Taiwan National Health Insurance Research Database. A total of 315,550 patients with herpes zoster were included as the study group, and the control group consisted of 946,650 randomly selected subjects. The stratified Cox proportional hazard regression was performed to calculate the 1-year MS-free survival rate. Of 1,262,200 sampled patients, 29 from the study group (.009%) and 24 from the control group (.003%) had MS during the 1-year follow-up period. After adjusting for monthly income and geographic region, the hazard of MS was 3.96 times greater (95% CI = 2.22-7.07, p < 0.001) for the study group than controls. Our findings support the notion that occurrence of MS could be associated with herpes zoster attack. We found a significantly higher risk for MS within 1 year of herpes zoster attack compared with the control population.

Herpes Zoster Recurrences More Frequent Than Previously Reported

To present population-based estimates of herpes zoster (HZ) recurrence rates among adults. To identify recurrent cases of HZ, we reviewed the medical records (through December 31, 2007) of all Olmsted County, Minnesota, residents aged 22 years or older who had an incident case of HZ between January 1, 1996, and December 31, 2001. Kaplan-Meier curves and Cox regression models were used to describe recurrences by age, immune status, and presence of prolonged pain at the time of the incident HZ episode. Of the 1669 persons with a medically documented episode of HZ, 95 had 105 recurrences (8 persons with >1 recurrence) by December 31, 2007, an average follow-up of 7.3 years. The Kaplan-Meier estimate of the recurrence rate at 8 years was 6.2%. With a maximum follow-up of 12 years, the time between HZ episodes in the same person varied from 96 days to 10 years. Recurrences were significantly more likely in persons with zoster-associated pain of 30 days or longer at the initial episode (hazard ratio, 2.80; 95% confidence interval, 1.84-4.27; P<.001) and in immunocompromised individuals (hazard ratio, 2.35; 95% confidence interval, 1.35-4.08; P=.006). Women and anyone aged 50 years or older at the index episode also had a greater likelihood of recurrence. Rates of HZ recurrence appear to be comparable to rates of first HZ occurrence in immunocompetent individuals, suggesting that recurrence is sufficiently common to warrant investigation of vaccine prevention in this group.

Decrease in CD4+ T-Cell Counts in Patients With Multiple Myeloma Treated With Bortezomib

Bortezomib is highly effective in multiple myeloma and is widely used in this disease. Recently, an increased incidence of varicella zoster virus (VZV) reactivation was reported in patients with myeloma undergoing bortezomib treatment. We investigated the influence of bortezomib on T-cell subpopulations in 53 patients with myeloma before initiation of bortezomib and during therapy. A decrease of CD4+ T cells was seen in 41 of 53 patients (77%). The median CD3+/CD4+ lymphocyte counts declined from 494/microL (range, 130-2187/microL) to 274/microL (range, 41-1404/microL) during bortezomib treatment (P < .001). In the majority of patients (40 of 53 patients, 75%), CD4+ lymphocytes dropped to < 400/microL during bortezomib treatment, and in 18 of 53 patients (33.9%) the CD4+ T cells fell below 200/microL. The minimum CD4S+ cell count was observed at a median of 6 weeks (range, 2-22 weeks) after initiation of treatment. The incidence of herpes zoster reactivation was 5.7% in the whole population of patients with myeloma receiving bortezomib. Nineteen of 53 patients received acyclovir at a dose of 400 mg daily as prophylaxis against VZV reactivation. In this group, none of the patients developed herpes zoster. The incidence of VZV reactivation in patients not receiving acyclovir was 3 of 34 (8.8%). Importantly, occurrence of herpes zoster was associated with reduced CD4+ T-cell subpopulation: all patients who developed herpes zoster had CD4+ lymphocytes < 400/microL. Our results show that bortezomib leads to a transient decrease in CD4+ lymphocytes, accompanied by an increased incidence of VZV infections. The antiviral prophylaxis with acyclovir is effective in patients with myeloma treated with bortezomib.

Decrease in CD4+ T Cells in Multiple Myeloma Patients Receiving Bortezomib.

Abstract 3865Poster Board III-801The proteasome inhibitor bortezomib is highly effective in multiple myeloma and widely used in this disease. Recently, an increased incidence of opportunistic infections, particularly varicella zoster virus (VZV) reactivation (herpes zoster), was reported in myeloma patients undergoing treatment with bortezomib. We therefore analyzed the influence of bortezomib on lymphocyte subsets, particularly T-cell subpopulations, in the peripheral blood of myeloma patients before initiation and during the treatment. In addition, the results were correlated with the incidence of VZV reactivation. Peripheral blood samples from 53 multiple myeloma patients treated with bortezomib were collected. Eight of the patients were previously untreated and received bortezomib as front-line therapy, whereas 45 patients were treated in the relapse setting. Different subsets of lymphocytes in the peripheral blood were analyzed by four-color flow cytometry. A decrease of CD4+ T-cells was seen in 42/53 patients (77%). The median numbers of CD4+ T-cells decreased by 45% from 494/μl (range 130-2187) to 274/μl (range 41-1404) during therapy with the proteasome inhibitor (p < 0.001). In the majority of the patients (76%), CD4+ lymphocytes dropped to < 400/μl during bortezomib treatment, and in 18/53 patients (33.9%) the CD4+ T cells fell below 200/μl. The minimum CD4+ cell count was seen at a medium of 6 weeks (range 2-22) after the initiation of treatment, but recovered within a few weeks. The median number of circulating CD3+/CD8+ T-cells decreased by 33.6% from 420/μl (range 48-1518) to 279/μl (range 19-1693) during bortezomib therapy (p < 0.001). This was accompanied by a slight decrease of the median CD4/CD8 ratio from 1.17 (range 0.23-6.0) to 1.0 (range 0.15-4.18). Importantly, all of the patients receiving bortezomib as first-line treatment had a normal CD4+ lymphocyte count before initiation of treatment, and all of them showed a decrease of CD3+/ CD4+ cells during the therapy. The median number of circulating CD4+ T-cells in this subgroup decreased by 70% from 924/μl (range 479-1579) to 276/μl (range 80-626) (p < 0.01). The incidence of herpes zoster reactivation was 5.3% in the whole population of myeloma patients receiving bortezomib. 19/53 patients received acyclovir at a dose of 400mg daily as prophylaxis against VZV reactivation. In this group, none of the patients developed herpes zoster. The incidence of VZV reactivation in patients not receiving acyclovir was 3/34 (8.8%). Importantly, occurrence of herpes zoster was associated with reduced CD4+ T cell subpopulation: all patients who developed herpes zoster had CD4+ lymphocytes < 400/μl. In conclusion, our results show that bortezomib leads to a transient decrease in CD4+ lymphocytes, accompanied by an increased incidence of VZV infections. The antiviral prophylaxis with acyclovir is effective in myeloma patients treated with bortezomib. Disclosures:No relevant conflicts of interest to declare.

Varicella‐Zoster Virus–Specific Immune Responses to Herpes Zoster in Elderly Participants in a Trial of a Clinically Effective Zoster Vaccine

The objectives of this study were to evaluate the association between varicella-zoster virus (VZV)-specific humoral and cell-mediated immunity (CMI) to herpes zoster (HZ) and protection against HZ morbidity and to compare immune responses to HZ and zoster vaccine. In 981 elderly persons who developed HZ during a zoster vaccine efficacy trial (321 vaccinees and 660 placebo recipients) and 1362 without HZ (682 vaccinees and 680 placebo recipients), CMI was measured by VZV responder cell frequency and interferon-gamma enzyme-linked immunospot, and antibodies were measured by VZV enzyme-linked immunosorbent assay against affinity-purified VZV glycoproteins (gpELISA). Robust VZV CMI at HZ onset correlated with reduced HZ morbidity, whereas VZV gpELISA titers did not. Three weeks after HZ onset, gpELISA titers were highest in those with more severe HZ and were slightly increased in placebo recipients (compared with zoster vaccine recipients) and in older individuals. VZV CMI responses to HZ were similar in zoster vaccine and placebo recipients and were not affected by demographic characteristics or antiviral therapy, except for responder cell frequency at HZ onset, which decreased with age. When responses to zoster vaccine and HZ could be compared, VZV CMI values were similar, but antibody titers were lower. Higher VZV CMI at HZ onset was associated with reduced HZ severity and less postherpetic neuralgia. Higher antibody titers were associated with increased HZ severity and occurrence of postherpetic neuralgia. HZ and zoster vaccine generated comparable VZV CMI.

Herpes zoster in patients taking TNFα antagonists for chronic inflammatory joint disease

Objective To assess the rate of occurrence and outcomes of herpes zoster in patients taking TNFα antagonists. Methods Retrospective review of the medical records of 300 patients who received TNFα antagonists to treat chronic inflammatory joint disease. Results We identified 9 (9/300, 3%) patients who experienced herpes zoster, 6 women and 3 men, with rheumatoid arthritis ( n = 7) or ankylosing spondylitis ( n = 2). The drug was infliximab in 4 patients, adalimumab in 2 patients, and etanercept in 3 patients, including 2 patients with a prior history of infliximab therapy (for 12 and 36 months, respectively). Mean treatment duration at the occurrence of herpes zoster was 27 months (range, 6–42 months). Discussion Glucocorticoid therapy ( n = 7) and methotrexate therapy ( n = 6) were the only risk factors identified in our study. Mean follow-up was 26 months. All 9 patients achieved a full recovery with antiviral treatment and interruption of the TNFα antagonist. One patient experienced a recurrence after resuming TNFα antagonist therapy. Conclusion The scant data in the literature suggest a higher risk of herpes zoster with anti-TNFα antibodies than with the soluble receptor. The role for concomitant treatments (glucocorticoids and methotrexate) should be taken into account.

Herpes zoster infection after liver transplantation in patients receiving induction therapy with alemtuzumab

The incidence of herpes zoster (HZ) infection in liver transplant recipients prior to the use of induction therapy with monoclonal antibodies has been reported as being 1.2-18%. We studied the occurrence of HZ in liver transplant recipients that received induction therapy with alemtuzumab (Campath 1H). This was a retrospective review of primary liver transplant recipients who received alemtuzumab as induction therapy at our center. HZ infection was diagnosed clinically as the presence of a characteristic vesicular rash in a dermatomal distribution without any further virological confirmation. A total of 118 liver transplant recipients were treated with alemtuzumab between August 2002 and August 2005. Twelve patients developed HZ infection, and the cumulative probability of a patient developing HZ infection by 36 months post-transplant +/-1 SE was estimated as 16.5 +/- 5.0%. The median time for onset of the infection was 10.2 months (range 4.7-30.7) after the transplant. All patients had only one dermatomal distribution, and none developed systemic infection or complications such as postherpetic neuropathy. All patients except one were treated with systemic intravenous acyclovir. One patient received famciclovir. All of the patients had received ganciclovir during the post-transplant period but were not receiving any other antiviral medication at the time of the infection. Herpes zoster infection has previously been reported as a frequent complication of liver transplantation. Our study suggests that it occurs in approximately 16% of patients receiving induction therapy with alemtuzumab. Although alemtuzumab is a powerful immunosuppressive agent and there is still little information regarding its long-term safety when used in liver transplantation, our data do not suggest any increase in the occurrence and complications of HZ.

Impact of CCR5 Δ32/+ Deletion on Herpes Zoster Among HIV-1-Infected Homosexual Men

The association between the presence of CCR5 Delta32 heterozygosity and incidence of clinical herpes zoster was studied among 296 homosexual men from the Amsterdam cohort study (ACS) infected with human immunodeficiency virus type I (HIV-1) with an estimated date of seroconversion. Of them 63 were CCR5 Delta32 heterozygotes and 233 CCR5 wild-type. The incidence rate of a first episode of herpes zoster was 4.2% and 5.3% per person-year, respectively. A higher occurrence of herpes zoster was strongly related to a lower CD4 + cell count. After adjustment for age, presence of CCR2b 64I heterozygosity, HIV RNA load, time since seroconversion, and CD4 + cell count, the rate ratio for herpes zoster of CCR5 Delta32 was 0.9 (95%CI 0.5-1.6). In conclusion, in HIV-1-infected homosexual men, a CCR5 Delta32 heterozygous genotype has no protective effect on the incidence of herpes zoster.

Gender as an Independent Risk Factor for Herpes Zoster: A Population-Based Prospective Study

Several studies reported a difference in herpes zoster (HZ) incidence between males and females, but limitations in design and analysis impeded the assessment of gender as an independent risk factor for HZ. This study examines the independent etiologic association between gender and HZ. A total of 335,714 persons were observed prospectively during 2001. We registered gender and HZ occurrence, as well as other risk factors for HZ. We calculated overall crude and adjusted odds ratios (ORs) and stratified to age. The HZ incidence in females was 3.9/1000 patients/year (95% confidence interval [CI], 3.6-4.2), and in males, 2.5/1000 patients/year (95% CI, 2.3-2.8), with a crude OR of 1.53 (95% CI, 1.36-1.74). After adjustment for potential confounders, the adjusted OR was 1.38 (95% CI, 1.22-1.56). The incidence was greater in females in the middle-aged (age, 25 to 64 years; OR range, 1.36 to 1.83) and youngest group (OR, 1.31; 95% CI, 0.90-1.89). Gender effect was inverse in young adults (age, 15 to 24 years; OR, 0.64; 95% CI, 0.41-1.03). Female gender is an independent risk factor for HZ in the 25- to 64-year-old age groups.

歯痛や歯周病症状を初発症状とした顔面領域の帯状疱疹の３例

We describe three patients (1 man and 2 women; age, 28 to 83 years) with herpes zoster of the trigeminal nerve that developed after dental treatment. The patients presented with toothache or periodontal disease as initial symptoms. Ten cases of herpes zoster occurring after dental treatment, have been reported previously. The initial symptom was toothache or periodontal tissue discomfort in most cases, and the age of the patients ranged from 7 to 73 years. Symptoms of herpes zoster appeared within 2 days after dental treatment in half of the patients. Although the relation between dental treatment and the occurrence of herpes zoster is unclear, we should include herpes zoster in the differential diagnosis when a patient presents with toothache or periodontal tissue discomfort.