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hsc.usc.edu
OBJECTIVES: To present a potentially life-threatening manifestation of gastroesophageal reflux disease (GERD), laryngospasm. This review covers the diagnosis and management of eight patients treated by the authors. STUDY DESIGN: A retrospective analysis of 8 consecutive patients who were referred for the evaluation of unexplained laryngospasm. The medical therapy and lifestyle modifications of treatment are discussed. METHODS: The patient records were reviewed and tabulated for age, onset of symptoms, and history of GERD; the presence of an associated upper respiratory infection with persistent cough; and the development of syncope in the presence of laryngospasm. RESULTS: All 8 patients had initial control of laryngospasm. Three had complete control without relapse, 3 had initial control with rare relapse of mild laryngospasm, and 2 patients had initial control with frequent relapses. Six of the 8 had syncopal episodes as a consequence of the laryngospasm. All patients were initially treated with a proton pump inhibitor. Five of the 8 required the addition of an esophageal prokinetic agent to control the reflux and subsequent laryngospasm. Two patients are off all medications at the time of this writing and 4 of the 8 have had rare relapses after initial control of symptoms. Once control of the laryngospasm had been achieved, there were no subsequent episodes of syncope. CONCLUSIONS: Based on the data collected in these 8 individuals, patients with reflux disease (known or unknown) can develop severe laryngospasm and possible syncope. The key factor seems to be the association of a recent or concurrent upper respiratory infection that results in a protracted cough that is more severe when supine and at times violent. The cough increases the amount of the refluxate, which is the noxious insult to the larynx.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11801981&dopt=Abstract
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med.unc.edu
OBJECTIVE: To determine the extent to which gastroesophageal reflux (GER)-initiated laryngeal chemoreflexes contribute to obstructive sleep apnea (OSA). METHODS: Prospective, nonrandomized clinical trial of an antireflux treatment protocol as a means of reducing the severity of OSA. Population consisted of 10 males aged 20 to 64 years with confirmed OSA (by overnight polysomnography) and GER (by ambulatory pH probe monitoring). Patients were treated with omeprazole and standard antireflux protocol for 30 days and pre- and posttreatment polysomnography variables were compared. RESULTS: Mean apnea index declined 31% (45-31, P = .04); mean respiratory disturbance index declined 25% (62-46, P = .06). Three patients (30%) are "treatment responders" as defined by traditional OSA treatment definitions. CONCLUSIONS: These results suggest a potential relationship between OSA and GER, the treatment of which may be an effective adjunctive in those with both disorders. Treatment of GER may significantly impact OSA in select individuals.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11802013&dopt=Abstract
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med.osaka-cu.ac.jp
BACKGROUND: In a previous study we showed that interleukin 1beta (IL-1beta) caused recurrence of gastric ulcers in rats, and that adhesion molecules (intercellular adhesion molecule 1 and leucocytic beta2 integrins) play a role in this recurrence. Although gastric acid plays an important role in many types of gastric injuries, including peptic ulcer recurrence, the mechanism(s) remains unclear. AIMS: To examine the involvement of gastric acid in induction of ulcer recurrence by IL-1beta, and to investigate the role of gastric acid in inflammatory responses during ulcer recurrence. METHODS: Rats with healed ulcers were used. Rats were given 1 microg/kg IL-1beta intraperitoneally. Another group of rats was given 20 mg/kg omeprazole for three days to inhibit acid secretion, and received IL-1beta 20 hours after the first administration of omeprazole. They were then given 0.15 N HCl or vehicle at 0, 12, 24, and 36 hours after IL-1beta treatment. Some rats were given acid alone at the same time points. Expression of adhesion molecules was examined immunohistochemically and concentrations of IL-1beta and tumour necrosis factor alpha (TNF-alpha) were measured by ELISA in scar tissue 24 hours after IL-1beta treatment. RESULTS: IL-1beta increased expression of adhesion molecules and concentrations of IL-1beta and TNF-alpha in scar tissue by 24 hours after IL-1beta treatment, and nine of 11 healed ulcers had recurred by 48 hours. Omeprazole inhibited the effects of IL-1beta. HCl acid abolished the inhibitory effects of omeprazole. Acid alone affected neither expression of adhesion molecules nor cytokine concentrations, and did not cause recurrence. CONCLUSIONS: Gastric acid is required for recurrence of gastric ulcers caused by IL-1beta, and gastric acid stimulates the inflammatory process in scarred mucosa during ulcer recurrence.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11358894&dopt=Abstract
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