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Context: Patients with chronic fatigue syndrome (CFS) are more likely than healthy persons to develop neurally mediated hypotension (NMH) in response to prolonged orthostatic stress., Objective: To examine the efficacy of fludrocortisone acetate as monotherapy for adults with both CFS and NMH., Design: Randomized, double-blind, placebo-controlled trial conducted between March 1996 and February 1999., Setting: Two tertiary referral centers in the United States., Patients: One hundred individuals aged 18 to 50 years who satisfied Centers for Disease Control and Prevention criteria for CFS and had NMH provoked during a 2-stage tilt-table test. Eighty-three subjects had adequate outcome data to assess efficacy., Intervention: Subjects were randomly assigned to receive fludrocortisone acetate, titrated to 0.1 mg/d (n = 50) or matching placebo (n = 50) for 9 weeks, followed by 2 weeks of observation after discontinuation of therapy., Main Outcome Measure: Proportion of subjects in each group with at least a 15-point improvement on a 100-point global wellness scale., Results: Baseline demographic and illness characteristics between the groups were similar; CFS had been present for at least 3 years in 71%. Using an intention-to-treat analysis, 7 subjects (14%) treated with fludrocortisone experienced at least a 15-point improvement in their wellness scores compared with 5 (10%) among placebo recipients (P =.76). No differences were observed in several other symptom scores or in the proportion with normal follow-up tilt test results at the end of the treatment period., Conclusions: In our study of adults with CFS, fludrocortisone as monotherapy for NMH was no more efficacious than placebo for amelioration of symptoms. Failure to identify symptomatic improvement with fludrocortisone does not disprove the hypothesis that NMH could be contributing to some of the symptoms of CFS. Further studies are needed to determine whether other medications or combination therapy are more effective in treating orthostatic intolerance in patients with CFS.

Context: The effectiveness of glucocorticoids for patients with croup is well established but it remains uncertain which glucocorticoid regimen is most effective., Objective: To determine the effectiveness of 3 glucocorticoid regimens in patients with croup., Design: Randomized controlled trial with parallel design., Setting: Emergency departments of 2 Canadian pediatric tertiary care hospitals., Participants: Children with a clinical syndrome consistent with croup, aged 3 months to 5 years, with a croup score of 2 or greater following at least 15 minutes of mist therapy., Interventions: Oral dexamethasone, 0.6 mg/kg, and nebulized placebo; oral placebo and nebulized budesonide, 2 mg; or oral dexamethasone, 0.6 mg/kg, and nebulized budesonide, 2 mg., Main Outcome Measures: Westley croup score (primary outcome), hospital admission rates, time spent in the emergency department, return visits to the emergency department, or ongoing symptoms at 1 week., Results: The mean change in the croup score from baseline to the final study assessment was -2.3 (95% confidence interval [CI], -2.6 to -2.0) in the budesonide group (n = 65), -2.4 (95% CI, -2.6 to -2.2) in the dexamethasone group (n = 69), and -2.4 (95% CI, -2.7 to -2.1) in the budesonide and dexamethasone group (n = 64, P = .70)., Conclusions: Based on the similar outcomes in the 3 groups, oral dexamethasone is the preferred intervention because of its ease of administration, lower cost, and more widespread availability.

Objective: To compare the clinical symptoms and response evoked by upright tilt-table testing in healthy individuals and in a sample of those satisfying strict criteria for chronic fatigue syndrome., Design: Case-comparison study with mean (SD) follow-up of 24 (5) weeks., Setting: Tertiary care hospital., Patients and Other Participants: A sample of 23 patients with chronic fatigue syndrome (five men and 18 women; mean age, 34 years), each of whom fulfilled the strict diagnostic criteria of the Centers for Disease Control and Prevention, was recruited from regional chronic fatigue support groups and from the investigators' clinical practices. There were 14 healthy controls (four men and 10 women; mean age, 36 years)., Interventions: Each subject completed a symptom questionnaire and underwent a three-stage upright tilt-table test (stage 1, 45 minutes at 70 degrees tilt; stage 2, 15 minutes at 70 degrees tilt with 1 to 2 micrograms/min of isoproterenol; and stage 3, 10 minutes at 70 degrees with 3 to 4 micrograms/min of isoproterenol). Patients were offered therapy with fludrocortisone, beta-adrenergic blocking agents, and disopyramide, alone or in combination, directed at neurally mediated hypotension., Main Outcome Measures: Response to upright tilt and scores on symptom questionnaires prior to and during follow-up., Results: An abnormal response to upright tilt was observed in 22 of 23 patients with chronic fatigue syndrome vs four of 14 controls (P < .001). Seventy percent of chronic fatigue syndrome patients, but no controls, had an abnormal response during stage 1 (P < .001). Nine patients reported complete or nearly complete resolution of chronic fatigue syndrome symptoms after therapy directed at neurally mediated hypotension., Conclusions: We conclude that chronic fatigue syndrome is associated with neurally mediated hypotension and that its symptoms may be improved in a subset of patients by therapy directed at this abnormal cardiovascular reflex.

Genetic disorders were identified infrequently among children presenting with Reye's syndrome in the past. During a two-year period, we evaluated four consecutive patients referred for intensive care of Reye's syndrome. A standard investigation for inborn errors of metabolism revealed that two patients had enzymatic defects of fatty acid oxidation, and the other two had partial deficiencies of ornithine transcarbamoylase. None had experienced a previous episode of Reye's syndrome, and three of the four had been entirely healthy in the past. Our experience suggests that as the incidence of Reye's syndrome has decreased, patients with its clinical features are now more likely to have manageable inborn errors of metabolism (eg, disorders of ureagenesis, ketogenesis, and branched-chain amino acids).