Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute ingestion of ethanol induces vasodilation and swelling of respiratory mucosa; it depresses respiratory centers resulting in hypotonia of oropharyngeal dilator muscles and inducing or aggravating sleep apnea. However, no association between the sleep apnea syndrome (SAS) and Alcohol Use Disorders (AUD) has been demonstrated.
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PMID:Alcohol and sleep apnea. 191 44

A 61-year-old patient with alcohol use disorder (AUD) was referred for suspicion of sleep apnea syndrome (SAS). He had incurred three road accidents attributed to sleepiness over the previous year, shortly after initiation of high-dose (100 mg b.i.d.) treatment with baclofen, a molecule increasingly used in the management of AUD. Polysomnography revealed a severe central SAS (CSAS) with an apnea-hypopnea index (AHI) of 81.6/h. Baclofen was suggested as a possible cause of the CSAS, and after its withdrawal, a second polysomnography was done, showing the disappearance of the central apneas and a shift to severe obstructive SAS (AHI 43.9/h), for which a positive airway pressure (CPAP) treatment was initiated. A third polysomnography was performed under CPAP after reintroduction of baclofen (50 mg b.i.d.) by the patient, showing reappearance of the CSAS (AHI 42.1/h). This case report illustrates the deleterious effect of baclofen on breathing physiology during sleep. Since it is typically prescribed off label at high doses to a population of patients potentially using other substances that inhibit the ventilatory drive, this possible adverse effect is a major concern. When considering the use of baclofen in patients with AUD, the potential for sleep-disordered breathing should be weighed and carefully monitored.
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PMID:Baclofen-Associated Onset of Central Sleep Apnea in Alcohol Use Disorder: A Case Report. 2639 Jan 41

Since the early 2000s, the gamma-aminobutyric acid type B (GABA-B) receptor agonist baclofen has been extensively used for treating alcohol use disorder (AUD). In some countries, like France, Australia, or Germany, baclofen has been used at patient-tailored dose regimens, which can reach 300 mgpd or even more in some patients. The GABA-B-related pharmacology of baclofen expose patients to a specific profile of neuropsychiatric adverse drug reactions (ADRs), primarily some frequent sedative symptoms whose risk of occurrence and severity are both related to the absolute baclofen dosing and the kinetics of dose variations. Other frequent neuropsychiatric ADRs can occur, i.e., tinnitus, insomnia, or dizziness. More rarely, other serious ADRs have been reported, like seizures, manic symptoms, or sleep apnea. However, real-life AUD patients are also exposed to other sedative drugs, like alcohol of course, but also benzodiazepines, other drugs of abuse, or other sedative medications. Consequently, the occurrence of neuropsychiatric safety issues in these patients is essentially the result of a complex multifactorial exposure, in which baclofen causality is rarely obvious by itself. As a result, the decision of initiating baclofen, as well as the daily dose management should be patient-tailored, according the medical history but also the immediate clinical situation of the patient. The overall safety profile of baclofen, as well as the clinical context in which baclofen is used, have many similarities with the use of opiate substitution medications for opiate use disorder. This empirical statement has many implications on how baclofen should be managed and dosing should be adjusted. Moreover, this constant patient-tailored adjustment can be difficult to adapt in the design of clinical trials, which may explain inconsistent findings in baclofen-related literature on AUD.
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PMID:Safety Challenges of Using High Dose Baclofen for Alcohol Use Disorder: A Focused Review. 3018 87