PubMed · 8718076
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K Gournay. Double bind.. https://pubmed.ncbi.nlm.nih.gov/8718076/
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BACKGROUND: Patients with asthma have an increased risk of developing depression, affecting their quality of life. To date, the processes contributing to this comorbidity remain unclear. METHODS: We integrated two large genome-wide association studies (88,486 patients with asthma and 447,859 controls; 412,024 patients with depression and 1,587,577 controls) with cross-sectional and longitudinal information available from the All of Us Research Program (N = 87,167) through polygenic risk scoring (PRS), Cox proportional-hazards models, one-sample Mendelian randomization (MR), and gene-set and drug-repurposing analyses. RESULTS: We observed that depression PRS was associated with increased asthma risk (hazard ratio, HR = 1.13, 95% CI = 1.09-1.17), also when accounting for comorbidity status (HR = 1.08, 95% CI = 1.04-1.12). Conversely, the effect of asthma PRS was null after accounting for comorbidity status. One-sample MR analysis showed an effect of depression genetic liability on asthma, ranging from beta = 0.36 ± 0.03 when considering a linear relationship to beta = 3.21 ± 0.31 when considering possible nonlinear relationships. Conversely, the effect of asthma genetic risk on depression was null after accounting for potential confounders. The gene-set analyses showed that asthma and depression polygenic risks share biological processes, molecular functions, and cellular components related to the immune system and the lung-brain axis. CONCLUSIONS: Genetic predisposition contributes to asthma-depression comorbidity through direct effects and shared pathogenic processes. These findings highlight the potential to develop targeted interventions to prevent and treat the co-occurrence of respiratory and neuropsychiatric disorders.
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Multiple-system atrophy (MSA) is characterized by progressive autonomic failure with cerebellar, pyramidal and extrapyramidal signs. In MSA patients laryngoscopy often reveals unilateral or bilateral abductor vocal fold palsies. Snoring is very common. However, assessment of sites of obstruction and their severity is needed. We report our clinical experience in managing a 56-year-old, obese male MSA patient (1.76 m height, 100 kg weight, BMI 32.3 kg/m2) who was admitted for evaluation of snoring and excessive daytime sleepiness. Endoscopy while awake demonstrated an incomplete abductor vocal fold palsy. Polysomnography confirmed heavy snoring with arousals (11.1/h) and an RDI of 1.4/h. Sleep efficiency was low (51.9%) due to long intermittent awake periods. Sleep videoendoscopy of the upper airway proved the entire pharynx to be open during REM and non-REM sleep. During inspiration fluttering movements of the vocal cords caused the snoring. This was regularly terminated by arousals. The further treatment is discussed. In general, glottic snoring without daytime stridor is rare and has only been described in MSA patients. However, certain of these patients will also be pharyngeal snorers. The source of the sound and site of obstruction can only be diagnosed by sleep videoendoscopy.