Background and Purpose—: Vertigo is a common presenting symptom in ambulatory care settings, and stroke is its leading and most challenging concern. This study aimed to determine the risk of stroke in vertigo patients in a 4-year follow-up after hospitalization for acute isolated vertigo. Methods—: The study cohorts consisted of all patients hospitalized with a principal diagnosis of vertigo (n=3021), whereas patients hospitalized for an appendectomy in 2004 (n=3021) comprised the control group and surrogate for the general population. Cox proportional hazard model was performed as a means of comparing the 4-year stroke-free survival rate between the 2 cohorts after adjusting for possible confounding and risk factors. Among vertigo patients, there was further stratification for risk factors to identify the group at high risk for stroke. Results—: Of the 243 stroke patients, 185 (6.1%) were from the study cohort and 58 (1.9%) were from the control group. Comparing the 2 groups, patients with vertigo symptoms had a 3.01-times (95% CI, 2.20–4.11; P <0.001) higher risk for stroke after adjusting for patient characteristics, comorbidities, geographic region, urbanization level of residence, and socioeconomic status. Vertigo patients with ≥3 risk factors had a 5.51-fold higher risk for stroke (95% CI, 3.10–9.79; P <0.001) than those without risk factors. Conclusions—: Vertigo patients are at higher risk for stroke than the general population. They should have a comprehensive neurological examination, vascular risk factors survey, and regular follow-up for several years after hospital discharge after treatment of isolated vertigo.

Excessive production of cytokines by microglia may cause cognitive dysfunction and long‐lasting behavioral changes. Activating the peripheral innate immune system stimulates cytokine secretion in the central nervous system, which modulates cognitive function. Histone deacetylases (HDACs) modulate cytokine synthesis and release. Trichostatin A (TSA), an HDAC inhibitor, is documented to be anti‐inflammatory and neuroprotective. We investigated whether TSA reduces lipopolysaccharide‐ (LPS‐) induced neuroinflammation and cognitive dysfunction. ICR mice were first intraperitoneally (i.p.) injected with vehicle or TSA (0.3 mg/kg). One hour later, they were injected (i.p.) with saline or Escherichia coli LPS (1 mg/kg). We analyzed the food and water intake, body weight loss, and sucrose preference of the injected mice and then determined the microglia activation and inflammatory cytokine expression in the brains of LPS‐treated mice and LPS‐treated BV‐2 microglial cells. In the TSA‐pretreated mice, microglial activation was lower, anhedonia did not occur, and LPS‐induced cognitive dysfunction (anorexia, weight loss, and social withdrawal) was attenuated. Moreover, mRNA expression of HDAC2, HDAC5, indoleamine 2,3‐dioxygenase (IDO), TNF‐α, MCP‐1, and IL‐1β in the brain of LPS‐challenged mice and in the LPS‐treated BV‐2 microglial cells was lower. TSA diminished LPS‐induced inflammatory responses in the mouse brain and modulated the cytokine‐associated changes in cognitive function, which might be specifically related to reducing HDAC2 and HDAC5 expression.

Chronic hepatitis B virus (HBV) infection and chronic kidney disease (CKD) have high prevalences in Taiwan and worldwide. However, the association of untreated chronic hepatitis B virus (HBV) infection with chronic kidney disease (CKD) remains unclear. This cohort study used claims data in the Taiwan National Health Insurance Research Database in 1996–2010, in which all diseases were classified by ICD-9-CM codes. We identified 17796 adults who had chronic HBV infection and did not take nucleos(t)ide analogues from 1998 to 2010 and also randomly selected 71184 matched controls without HBV in the same dataset. Cumulative incidences and adjusted hazard ratio (aHR) of incident CKD were evaluated through the end of 2010 after adjusting for competing mortality. The risk of CKD was significantly higher in the HBV cohort (13-year cumulative incidence, 6.2 %; 95 % confidence interval [CI], 5.4–7.1 %) than in the non-HBV cohort (2.7 %; 95 % CI, 2.5–3.0 %) (p < 0.001), and the aHR was 2.58 (95 % CI, 1.95-3.42; p < 0.001). Multivariable stratified analysis further verified significant associations of CKD with HBV in men of any age (aHR, 2.98; 95 % CI, 2.32–3.83, p < 0.001 for men aged <50 years; aHR, 1.58; 95 % CI, 1.31–1.91, p < 0.001 for men aged ≧50 years) and women under the age of 50 (aHR, 2.99; 95 % CI, 2.04–4.42, p < 0.001), but no significant association in women aged 50 or over. Untreated chronic HBV infection is associated with increased risk of CKD. Hence, high-risk HBV-infected subjects should have targeted monitoring for the development of CKD.