Posterior reversible encephalopathy syndrome as a complication of acute lupus activity.

OBJECTIVES: We aimed to describe the clinical and imaging characteristics; associated risk factors and neurological outcome of posterior reversible encephalopathy syndrome (PRES) in patients with systemic lupus erythematosus (SLE). METHODS: From October 2001 to January 2007, we identified patients with SLE and the criteria for PRES in our institution, which is a tertiary-care referral center for patients with SLE; the patients were evaluated at baseline and followed to determine the clinical outcome. RESULTS: We identified 22 episodes of PRES in 21 patients; 20 (95.2%) were women, mean age of onset was 24.9+/-8.6 years, all patients had high systemic activity (SLEDAI scores from 12 to 39). Acute hypertension was observed in 18 episodes (81.8%), and renal failure in 16 (72.7%); only 3 patients were on cyclophosphamide at the time of the onset of PRES. Persistent neurological deficit was observed in 2 cases; one patient died during the acute episode. CONCLUSIONS: PRES is a central nervous system syndrome that is observed in SLE patients. It was associated mainly to high systemic activity, acute hypertension, and renal failure. Although reversibility is common, residual neurological damage may be observed.

Renal failure is a risk factor for cefepime-induced encephalopathy.

BACKGROUND: Cefepime is a widely used antibiotic. However, it can cause encephalopathy, which has been increasingly described in the literature, occurring mainly in patients with impaired renal function. The primary objective in this study was to measure the incidence of cefepime-induced encephalopathy and determine potential risk factors for its occurrence. METHODS: In the period from February 2005 to February 2006, a prospective cohort study was conducted, which followed 498 patients using cefepime. Other metabolic problems were ruled out for all patients with clinical suspicion of encephalopathy and, when cefepime was the probable cause, electroencephalographic (EEG) tests were performed to assist in the diagnosis, with the first performed during cefepime use and another performed at least 48 hours following drug discontinuation and/or clinical improvement. RESULTS: Among patients selected for this study (n=498), 5 were diagnosed with cefepime-induced encephalopathy, thus indicating a cumulative incidence of approximately 1% (0.01), 387 had glomerular filtration rate (GFR) >or=60 ml/min and 111 had GFR <60 ml/min. Among the latter, 5 patients developed cefepime-induced encephalopathy. Mean GFR value in patients with encephalopathy (n=5) was 17.20 ml/min (SD +/-10.75 ml/min) and, in patients without encephalopathy (n=106) it was 32.59 ml/min (SD +/-14.89 ml/min) (p=0.025). CONCLUSION: The development of cefepime-induced encephalopathy seems to be related to the severity of impairment in glomerular filtration.

Brain damage in glycogen storage disease type I.

OBJECTIVE: To investigate brain morphology and function in patients with glycogen storage disease type I (GSDI). STUDY DESIGN: Nineteen patients (13 females and 6 males, aged 0.9-22.6 years) and 38 sex- and age-matched controls entered the study. Neurological examinations, psychometric tests (IQ, tests of performance and verbal abilities), standard electroencephalogram (EEG), somatosensory (SEPs), visual (VEPs), and brain-stem auditory evoked potentials (BAEPs), and brain magnetic resonance imaging (MRI) were performed. RESULTS: The results of tests of performance ability were lower in patients than in controls (P <.05). The prevalence of abnormal EEG findings (26.3% versus 2.6%), VEPs (38.4% versus 7.7%), SEPs (23.0% versus 0%), and BAEPs abnormalities (15.7% versus 0%) was higher in patients than in controls (P <.05). MRI pattern was altered in 57.1% of patients and was normal in all controls (P <.05). Both results of tests of performance ability and BAEPs abnormalities significantly correlated with the frequency of admissions for hypoglycemia, whereas EEG abnormalities correlated with dietary compliance (P <.05). CONCLUSIONS: Brain damage, probably caused by recurrent severe hypoglycemia, may be present in patients with GSDI.