Rates and predictors of ACE inhibitor discontinuation subsequent to elevated serum creatinine: a retrospective cohort study.

OBJECTIVES: ACE inhibitors (ACEI) are underutilised despite cardiovascular benefits, in part due to concerns of known transient elevations in serum creatinine (SCr) after initiation. Our objectives were to evaluate rates and predictors of ACEI discontinuation after SCr elevation post-ACEI initiation since limited data are available that examine this issue. SETTING: Primary and tertiary Veterans healthcare system in Los Angeles, California, USA PARTICIPANTS: 3039 outpatients initiating an ACEI with a SCr measured within 6 months prior to and approximately 3 months after initiating an ACEI. Patients were divided into three groups (SCr <1.5, 1.5­2 and >2). PRIMARY AND SECONDARY OUTCOME MEASURES: Rates and factors associated with ACEI discontinuation subsequent to SCr elevation after ACEI initiation and for patients with baseline SCr >2 mg/dL, the change in SCr associated with chronic use. Predictors were identified using multivariate logistic regression modelling. RESULTS: At 3 months follow-up, for those with an increase in SCr, the mean increase post-ACEI initiation was 26%, ranging from −0.01 mg/dL to 0.42 mg/dL varying according to a level of baseline renal function. ACEI discontinuation was higher in patients with elevated baseline SCr (19/165, 11.5%) compared with those with SCr <1.5 (135/2497, 5.4%), and those with SCr 1.5­2.0 (28/377, 7.4%). Male patients, and those with heart failure were less likely to discontinue ACEI after an elevation of SCr post-ACEI initiation, while those taking non-steroidal anti-inflammatory drugs, diuretics and ß-blockers were more likely to discontinue ACEI. CONCLUSIONS: SCr increases <30% on average within 3 months of ACEI initiation, with subsequent discontinuation rates varying by baseline SCr. Elevation in SCr was not associated with ACEI discontinuation rates. In patients with SCr >2 mg/dL at baseline, despite an acute increase in SCr after ACEI initiation, chronic ACEI use was associated with a decrease in SCr in most patients.

Occipital hypometabolism demonstrated by positron emission tomography after temporal lobectomy for refractory epilepsy.

BACKGROUND: Epilepsy surgery involves well-planned discrete injury to the brain and may create visual deficits. This study seeks to evaluate the indirect effects of temporal lobectomy on brain metabolism by correlating visual field defects and glucose metabolism in the visual cortex of patients before and after undergoing epilepsy surgery. METHODS: A retrospective survey of 11 patients who had undergone temporal lobectomy for refractory epilepsy in a single institution from 1986 to 1989, and who had pre-lobectomy and post-lobectomy visual field examinations and F-18 2-fluorodeoxyglucose positron emission tomography (FDG-PET) as part of a standard comprehensive epilepsy surgery evaluation. The PET images were analyzed to provide a correlation with the visual field defects that developed after the temporal lobectomy. RESULTS: Occipital hypometabolism in the absence of structural lesions of the occipital lobe was noted in seven patients with contralateral visual field defects and in one of four patients without a visual field defect. FDG-PET studies in three patients repeated for as long as 20 months after lobectomy showed no significant change in the occipital hypometabolism pattern. CONCLUSIONS: Although the occipital cortex was not directly injured during temporal lobectomy, the resulting hypometabolism correlates with the clinical findings of visual field defects. The hypometabolism may be due to deafferentation after interruption of the optic pathways and appears to be persistent.