ABSTRACT
BACKGROUND: Improving quality of life is considered to be a major endpoint and motivation for clinical intervention in patients with perennial allergic rhinitis (PAR). In addition to classical symptoms of congestion, pruritus, and rhinorrhea, patients will often complain of not being able to sleep well at night and of feeling fatigued during the day. Like sleep apnea, PAR has also been shown to cause sleep disturbance and consequently worsen daytime fatigue and somnolence. HYPOTHESIS: It is proposed that by decreasing nasal obstruction due to allergic rhinitis by treating with the topical steroid budesonide, symptoms of daytime fatigue and somnolence can be improved. METHODS: Twenty-two subjects were enrolled in a double-blind, placebo-controlled, crossover study using Baalam's design. Patients were treated with either budesonide 128 g/day or placebo. Subjective data include the Epworth Sleepiness Scale, Functional Outcomes of Sleep Questionnaire, Rhino-conjunctivitis Quality of Life Questionnaire, and a daily diary recording nasal symptoms, sleep problems, and daytime fatigue. RESULTS: The results illustrated that the topical nasal corticosteroid significantly improved daytime fatigue (P = 0.03), somnolence (P = 0.02), and quality of sleep (P = 0.05) compared to placebo in patients suffering from PAR. SUMMARY: Budesonide is able to improve congestion, sleep, and daytime somnolence.
Subject(s)
Anti-Inflammatory Agents/therapeutic use , Budesonide/therapeutic use , Disorders of Excessive Somnolence/drug therapy , Disorders of Excessive Somnolence/etiology , Rhinitis, Allergic, Perennial/complications , Rhinitis, Allergic, Perennial/drug therapy , Administration, Topical , Adult , Cross-Over Studies , Double-Blind Method , Female , Glucocorticoids , Humans , Male , Middle Aged , Nasal Obstruction/complications , Nasal Obstruction/drug therapy , Nasal Obstruction/etiology , Quality of Life , Surveys and Questionnaires , Treatment OutcomeABSTRACT
A 57-year-old woman with hyperthyroidism had a loud to-and-fro bruit which persisted when the patient was inadvertently rendered hypothyroid with antithyroid drugs. Symptoms suggestive of transient cerebral ischemia prompted an angiographic study which demonstrated both normal cerebral circulation and an enormous increase in the size of thyroid vasculature. The possibility that the enhanced blood supply to the thyroid had compromised cerebral circulation (thyroid steal syndrome) was considered. The angiographic presentation of hyperthyroidism is reviewed, and the lack of specificity of thyroid bruits as a marker of hyperthyroidism in patients on antithyroid drugs is stressed.
