No evidence of family history as a risk factor for herpes zoster in patients with post‐herpetic neuralgia

Little is known about reactivation of latent varicella zoster virus as herpes zoster in individuals with no underlying immunosuppression. Risk factors include age, sex, ethnicity, exogenous boosting of immunity from varicella contacts, underlying cell‐mediated immune disorders, mechanical trauma, psychological stress, and immunotoxin exposure. An association between herpes zoster and family history of zoster has been proposed. A case‐control study involving patients affected by post‐herpetic neuralgia, which usually follows more severe acute herpes zoster, was performed. The patients with post‐herpetic neuralgia were enrolled at the Pain Clinic of the Policlinico Tor Vergata in Rome, Italy, within 1 year from the onset of acute zoster. The controls matched for sex and age were chosen among healthy subjects without a history of herpes zoster presenting at the Internal Medicine Outpatient Clinic for hypertension in the same time period. All the participants in the study gave informed consent and were interviewed by medically trained and blinded investigators using a questionnaire. Similar proportions of the patients and the controls reported a family history of herpes zoster irrespective of the degree of relationship, i.e., 17.4% and 18.2%, respectively, by analyzing only the first‐degree relatives [RR 1.03 (CI 95%: 0.78–1.37)], and 28.4% and 29.6%, respectively, by analyzing the total number of relatives [RR 1.03 (CI 95%: 0.81–1.31)]. Further and larger prospective cohort studies are needed to ascertain whether a family history of herpes zoster is really an independent predictor of zoster in different geographical settings. J. Med. Virol. 82:1007–1011, 2010. © 2010 Wiley‐Liss, Inc.     

Association between radical prostatectomy and risk of herpes zoster

The present study investigated the association between radical prostatectomy (RP) and the risk of herpes zoster (HZ). Male patients aged?≥?40 years and diagnosed with prostate cancer (PCa) between 2000 and 2005 were included in this study. Patients who underwent RP for the first time during 2000–2006 were included in the RP group. Randomly selected individuals from among the remaining patients with PCa who did not undergo RP were included in the non-RP group. Univariate and multivariate Cox regression models were used to analyze the association between PCa and HZ. In addition, the association between RP and the risk of HZ in different subgroups was evaluated after stratification by age, comorbidities, and hormone therapy (HoT) status. Furthermore, the combined effect of RP and HoT on the risk of HZ was evaluated. This study included 1,380 patients with PCa who newly underwent RP and 1,371 patients with PCa who did not undergo RP. During follow-up, 96 and 104 patients in the RP and non-RP groups, respectively, developed HZ. Patients who underwent both RP and HoT showed a significantly reduced risk of HZ, compared with patients who did not undergo both RP and HoT. RP is not associated with an increased risk of HZ. However, prostate-specific antigen levels should be monitored routinely during follow-up to detect PCa recurrence.     

JC polyomavirus reactivation is not associated with herpes zoster

Herpes zoster (HZ) is a neurocutaneous disease caused by Varicella-zoster virus (VZV) as a consequence of declined cell-mediated immunity, immune suppression and immunodeficiency. As reactivation of JC polyomavirus (JCPyV) might be linked with immunodeficiency or immunosuppressive therapy, the relationship between HZ and JCPyV reactivation was investigated. The incidence of JCPyV in urine samples from 102 patients with HZ and 100 healthy individuals from South Korea was determined by PCR. The incidence values for HZ patients and control individuals did not differ significantly (24.5% vs. 20.0%, respectively, P = 0.5391). When different age groups were monitored, the positivity values of 21.1%, 20.0%, and 30% were found for 20-39, 40-59 and over 60 year-old patients, respectively. In order to determine the genotype of JCPyV isolates, their VP1-large T antigen (VT)-intergenic region was PCR amplified, sequenced and analyzed. Three distinct types, namely 1, 2A and 7B were found in 8%, 24%, and 68% of were found among 25 isolates from HZ patients. Using phylogenetic analysis, the type 1 isolates were assigned to the 1C subtype. These results indicate that HZ does not play an important role in JCPyV reactivation and is not associated with JCPyV.     

Increased risk of chronic fatigue syndrome following herpes zoster: a population-based study

Chronic fatigue syndrome (CFS) is a complex disorder accompanied by unexplainable persistent fatigue, in which several etiological factors exist, such as viral infections. Using the National Health Insurance Research Database (NHIRD) of Taiwan, this study evaluated the association between herpes zoster (HZ) infection and the risk of CFS, and examined the possibility of patients developing postviral fatigue effects, including the possibility of developing other unexplainable chronic fatigue conditions. In this prospective cohort study using the NHIRD, we identified 9,205 patients with HZ infection [ICD-9 (International Classification of Disease, Ninth Revision), code 053] and 36,820 patients without HZ infection (non-HZ) from 2005 to 2007, and followed up to the end of 2010. The incidence rate of CFS was higher in the HZ cohort than in the non-HZ cohort (4.56 vs. 3.44 per 1,000 person-years), with an adjusted hazard ratio of 1.29 [95 % confidence interval (CI) = 1.09–1.53]. It was shown that the risk of CFS without comorbidity for each patient increased from 1.25- to 1.36-fold between the CFS and non-CFS cohorts; with long-term follow-up, the HZ cohort showed a significantly higher cumulative incidence rate of developing CFS than the non-HZ patients. We propose that patients with chronic fatigue might exist in a subset of patients that would be associated with HZ infection. The actual mechanism of development of CFS that is attributed to HZ infection remains unclear. The findings of this population cohort study provide pivotal evidence of postviral fatigue among patients with HZ infection.     

Gender is a risk factor for lung cancer

Results of epidemiological studies suggest that, after one controls for the number of cigarettes smoked, women have a three times higher risk of getting lung cancer than men. Although the mechanism(s) explaining this gender-dependent difference in lung cancer risk is not known, it is thought that endocrine factors may play an important role. Normal human bronchial epithelial cells contain estrogen receptors and synthesize 17β-estradiol (E(2)) and estrone (E(1)), which can undergo further metabolism into the catechol estrogens, 4-hydroxyestradiol (4-OHE(2)) and 4-hydroxyestrone (4-OHE(1)), respectively. Catechol estrogens are formed from E(2) by the actions of cytochrome p450 1B1 (CYP1B1). CYP1B1 is present in normal human bronchial epithelial) cells, and its activity is increased by cigarette smoking. Both 4-OHE(1) and 4-OHE(2) are mutagenic and carcinogenic and may exert their biological effects by inducing DNA adducts in cancer-related genes, including the tumor suppressor gene p53 and the proto-oncogene K-ras. Women with lung cancer have a different p53 mutational spectrum and a higher frequency of K-ras mutations than do men with lung cancer. Both clinical and basic research studies support the hypothesis that E(2) and cigarette smoking are cofactors in lung carcinogenesis in women. More specifically, cigarette smoke stimulates metabolism of E(2) into the genotoxic metabolites, 4-OHE(1) and 4-OHE(2,) which interact with DNA in cancer-related genes, including the tumor suppressor gene, p53, and the proto-oncogene K-ras, two genes frequently mutated in patients with lung cancer. E(2) may stimulate cellular proliferation and enhance tumor growth.     

Homocysteinemia is a risk factor for aortic dissection

There are significant associations between moderate increases in serum homocysteine and three cardiovascular diseases: ischemic heart disease, deep vein thrombosis and pulmonary embolism, and stroke. An association between the presence of abdominal aortic aneurysm and elevated homocysteine plasma levels has been indicated. Although chronic systemic hypertension is the most common factor predisposing the aorta to dissection, homocysteinemia has never been known as the risk for aortic dissection except for that with Marfan syndrome. Homocysteinemia is suggested to be the risk for aortic dissection in Marfan syndrome and spontaneous cervical artery dissection. Reduced fibrillin-1 deposition into the extracellular matrix is found not only in Marfan syndrome but also in isolated ascending aortic aneurysm and dissection. The reduced matrix deposition produces a mild form of weakness of elastic tissue, which predisposes to ascending aortic aneurysm and dissection in patients who do not have the Marfan syndrome. The defect in fibrillin-1 leads to: (1) formation of elastin that is abnormally aggregated and more easily degraded by matrix metalloproteinases than is normal elastin; (2) upregulation of the synthesis of matrix metalloproteinases; (3) progressive destruction of connective tissue by these enzymes; (4) development of thoracic aortic aneurysms. Homocysteine causes premature breakdown in the arterial elastic fibers by activation of the elastolytic activities. Irreversible homocysteinylation of long-lived proteins should lead to cumulative damage and progressive clinical manifestations, and fibrillin-1 is seen as the paradigm of extracellular connective tissue proteins that are specially susceptible to homocysteine (and presumably homocysteine thiolactone) attack. The authors hereupon propose a novel hypothesis that homocysteine plays an important role in development of aortic dissection and that homocysteinemia is one of the risk factors for aortic dissection.     

Is herpes zoster a marker for occult or subsequent malignancy?

BACKGROUND: It has been suggested that herpes zoster may be a marker for occult malignancy. AIM: To examine the emergence of a subsequent cancer diagnosis in patients with and without herpes zoster. DESIGN OF STUDY: Retrospective cohort study. SETTING: Results were based on the database of Intego, an ongoing Belgian general practice-based morbidity registry, covering 37 general practitioners and including about 311 000 patient years between the years 1994 and 2000. METHOD: Survival analysis comparing the emergence of malignancy in patients with and without herpes zoster. RESULTS: The number of patients below the age of 65 years with herpes zoster, cancer or both was too low to draw any sensible conclusions. Above the age of 65 years we identified a significant increase of cancer emergence in the whole group and in females (hazard ratio = 2.65, 95% confidence interval = 1.43 to 4.90), but not in males. No difference could be identified in the first year after the herpes zoster infection. CONCLUSION: Our results do not justify extensive testing for cancer in herpes zoster patients. The association we identified, however, leaves open a number of questions with respect to the physiopathology behind it.     

Recurrent herpes zoster myelitis.

Recurrent zoster myelitis is quite rare. We present a previously healthy 27-year-old woman who developed recurrent attacks of myelopathy shortly after the characteristic skin rashes of herpes zoster. Magnetic resonance imaging studies demonstrated each lesion in the spinal cord at the same segments as the skin lesions. She had two attacks at opposite sites at the same spinal cord level and complete recovery after being treated with intravenous acyclovir. We suspect that direct invasion of varicella zoster virus was the cause of recurrent myelopathy in our patient.