Baskaran, Berty

Abstract Introduction Bronchiectasis (BE) is characterized by recurrent infections and dilated airways and has been associated with recurrent exacerbations and hospitalizations affecting quality of life. Approximately 40-60% of patients with BE have concomitant OSA, with an increased AHI (apnea-hypopnea index) in BE patients with Pseudomonas infections. We hypothesize that patients with BE are less tolerant of PAP therapies, contributing to worsening quality of life related to either condition. We aim to determine differences in PAP adherence and treatment response in patients with BE and OSA compared with a matched OSA-control group. Methods A retrospective cohort analysis was conducted on adult patients evaluated at Mayo Clinic Center for Sleep Medicine between January 2000 to December 2020. Inclusion criteria were patients greater than 18 years old diagnosed with BE and OSA per current guidelines and were prescribed PAP therapy. Control OSA patients were matched to BE/OSA patients by gender, BMI, and AHI severity. Exclusion criteria included cystic fibrosis, hospice enrollment, active lung transplant evaluation, and lack of sleep clinic follow-up. Follow-up visits determined PAP compliance and change in quality-of-life metrics over 3 years. Results We compared 50 patients with BE/OSA with 74 OSA matched controls. The etiology of BE in these cases included COPD (32%) or other etiologies (34%). Baseline characteristics were not statistically different in gender, BMI, and AHI severity across groups. Median treatment follow-up for the BE/OSA group was 3 years [IQR 2 to 4]. Importantly, there was no statistically significant difference in PAP adherence in patients with BE/OSA compared to OSA controls regardless of etiology of BE, but these patients more often required supplemental oxygen therapy. Interestingly, there was a statistically significant increase in MRC and decrease in FEV1 over time in BE patients compliant to therapy. Conclusion There was no significant difference in baseline OSA characteristics, treatment response, and PAP adherence, except for need of oxygen supplementation in BE patients with OSA compared with matched non-BE OSA controls. FEV1 values decreased, and dyspnea score increased in BE patients compliant to PAP therapy; however, future larger studies should include longer-term follow-up to further assess the impact of PAP therapy on BE progression and outcomes. Support (if any)

Abstract Introduction Restless leg syndrome (RLS/WED) is a neurological sleep condition which is characterized by an uncontrollable urge to move an individual’s legs and sometimes arms when at rest. Symptoms typically arise in the evening and nighttime hours and can be associated with severe insomnia and negative impact on quality of life. Here we present a case of severe RLS/WED exacerbations temporally associated with androgen receptor inhibitor therapy. Report of case(s) A 58 year old male was referred to the sleep medicine clinic for refractory RLS/WED. He was previously treated with high dose ropinirole, which was associated with severe augmentation. Trials of gabapentin, pregabalin, tramadol, and hydrocodone were associated with persistence of severe symptoms. He was eventually treated with methadone at a dose of 10 mg in addition to Rotigotine patch at a dose of 2 mg, with adequate symptom relief. He was later diagnosed with prostate cancer, and initiated on enzalutamide, an androgen receptor inhibitor. Within two weeks of starting this medication, he had a severe exacerbation of his RLS symptoms and associated insomnia. The medication was discontinued, with subsequent abatement of RLS symptoms. He was then switched to apalutamide by his urologist (another androgen receptor inhibitor), but again developed severe RLS exacerbation. Dosing of the Rotigotine patch and methadone were increased to 4 mg and 12.5 mg daily respectively. In addition, he was started on pramipexole 0.25 mg, which was later increased to 0.5 mg, but he continued to have severe residual symptomatology. After discussing with his oncologist, he went on a trial of 3-4 weeks where apalutamide was discontinued. During this time, his RLS symptoms resolved, and he was sleeping well. He then restarted apalutamide and again experienced a similar a severe RLS flare. Conclusion Our case demonstrates an association between androgen receptor inhibitor therapy and RLS exacerbations. Further work is needed to understand the possible relationships between RLS and these common treatments for prostate cancer. Support (if any)