Summary Purpose:  Long‐term therapy with antiepileptic drugs (AEDs) has been associated with metabolic consequences that lead to an increase in risk of atherosclerosis in patients with epilepsy. We compared the long‐term effects of monotherapy using different categories of AEDs on markers of vascular risk and the atherosclerotic process. Methods:  One hundred sixty adult patients who were receiving AED monotherapy, including two enzyme‐inducers (carbamazepine, CBZ; and phenytoin, PHT), an enzyme‐inhibitor (valproic acid, VPA), and a noninducer (lamotrigine, LTG) for more than 2 years, and 60 controls were enrolled in this study. All study participants received measurement of common carotid artery (CCA) intima media thickness (IMT) by B‐mode ultrasonography to assess the extent of atherosclerosis. Other measurements included body mass index, and serum lipid profile or levels of total homocysteine (tHcy), folate, uric acid, fasting blood sugar, high sensitivity C‐reactive protein (hs‐CRP), or thiobarbituric acid reactive substances (TBARS). Key Findings:  Long‐term monotherapy with older‐generation AEDs, including CBZ, PHT, and VPA, caused significantly increased CCA IMT in patients with epilepsy. After adjustment for the confounding effects of age and gender, the CCA IMT was found to be positively correlated with the duration of AED therapy. Patients with epilepsy who were taking enzyme‐inducing AED monotherapy (CBZ, PHT) manifested disturbances of cholesterol, tHcy or folate metabolism, and elevation of the inflammation marker, hs‐CRP. On the other hand, patients on enzyme‐inhibiting AED monotherapy (VPA) exhibited an increase in the levels of uric acid and tHcy, and elevation of the oxidative marker, TBARS. However, no significant alterations in the markers of vascular risk or CCA IMT were observed in patients who received long‐term LTG monotherapy. Significance:  Patients with epilepsy who were receiving long‐term monotherapy with CBZ, PHT, or VPA exhibited altered circulatory markers of vascular risk that may contribute to the acceleration of the atherosclerotic process, which is significantly associated the duration of AED monotherapy. This information offers a guide for the choice of drug in patients with epilepsy who require long‐term AED therapy, particularly in aged and high‐risk individuals.

SUMMARYPurpose: Long-term antiepileptic drug (AED) therapy has been associated with an increase in risk of atherosclerosis. At issue is whether this risk is related to the duration of AED therapy. We evaluated the hypothesis that the cumulative effect of long-term exposure to AEDs plays a pivotal role in the pathogenesis of atherosclerosis in patients with epilepsy. Methods: One hundred ninety-five patients under long-term AED therapy and 195 healthy age-and sex-matched control subjects received measurement of intima media thickness (IMT) at the far wall of the common carotid artery (CCA) by Bmode ultrasonography to assess the extent of atherosclerosis. Other measurements included body mass index (BMI) and blood lipid profile or homocysteine, folic acid, uric acid, fasting blood sugar, high sensitivity C-reactive protein (hs-CRP), thiobarbituric acid reactive substances (TBARS), and total reduced thiols.Results: CCA IMT was significantly increased in patients with epilepsy, with male subjects exhibiting thicker IMT than their female counterparts. Whereas BMI, homocysteine, hs-CRP, and TBARS were significantly elevated, folic acid and thiols were significantly reduced in patients with epilepsy. Multiple linear regression analysis further revealed that duration of AED therapy, age, gender, and TBARS level (index for oxidative stress) were independently associated with CCA IMT. In addition, the log-transformed CCA IMT increased linearly with duration of AED therapy after adjustments for age, gender, and TBARS level. Discussion: The duration of AED therapy is significantly associated with the acceleration of atherosclerosis in patients with epilepsy, alongside independent contributions of age, gender, and oxidative stress to the atherosclerotic process.

This study revealed a change in the epidemiologic trend of ABM, with an increase in the number of patients with a postneurosurgical state and a rising incidence of Acinetobacter and staphylococcal infections. Clinicians should pay greater attention to these changes, which may affect their management of ABM.

No abstract

No abstract

No abstract

No abstract

12 adult patients suffering from bacterial meningitis caused by mixed infection were identified at Kaohsiung Chang Gung Memorial Hospital over a period of 13 years (1986-1998), and they accounted for 6.5% (12/184) of our culture-proven adult bacterial meningitis. The 12 cases included seven males and five females, aged 17-74 years. Six of the 12 cases had community-acquired infections and the other six had nosocomially-acquired infections. Ten of the 12 cases had associated underlying diseases, with head trauma and/or neurosurgical procedure being the most frequent. Both gram-negative and gram-positive pathogens were identified in these 12 cases with gram-negative pathogens outnumbering the gram-positive ones. The implicated pathogens, starting with the most frequent, included Enterobacter species (Enterobacter cloacae, Enterobacter aerogenes), Klebsiella species (Klebsiella pneumoniae, Klebsiella oxytoca), Escherichia coli, Staphylococcus species (Staphylococcus aureus, Staphylococcus haemolyticus), Pseudomonas aeruginosa, Acinetobacter baumannii, Enterococcus, Serratia marcescens, Citrobacter diversus, Proteus mirabilis, Streptococcus viridans and Neisseria meningitidis. Six of the 12 cases were found to have multi-antibiotic-resistant strains, which included E. cloacae in one, A. baumannii in one, K. pneumoniae in one and S. aureus in three. The management of these 12 cases included appropriate antibiotics and neurosurgical procedures including shunt revision. Despite the complexity of implicated pathogens and the high incidence of emergence of resistant strains, the overall mortality rate (8.3%, 1/12) was not higher than that in adult bacterial meningitis. However, complete recuperation was difficult in adult patients with mixed bacterial meningitis.