Introduction: Sleep apnea-hypopnea syndrome (SAHS) is a multifactorial disease characterized by recurrent hypopnea or respiratory interruption during sleep, which causes intermittent hypoxemia, hypercapnia, and sleep structure disturbances. An association between ankylosing spondylitis (AS) and the type of SAHS has rarely been reported in the literature. Here, we present a case of SAHS in a patient with AS and discuss the possible mechanism underlying the type of SAHS.

Patient Concerns: A 46-year-old man presented with a 15-year history of AS. He had been receiving sulfasalazine for symptomatic relief and had never been on immunosuppressive therapy.

Diagnosis: The patient was diagnosed with SAHS in addition to AS.

Interventions: We instituted treatment with methylprednisolone (5 mg, oral, daily), leflumomide (20 mg, oral, daily), bicyclol tablets (25 mg, oral, 3 times a day), and ursodeoxycholic acid tablets (10 mg/kg, oral, daily). The patient received etanercept (50 mg, sc, once a week) as his condition deteriorated. In addition, for management of SAHS symptoms, the patient received nasal continuous positive airway pressure (CPAP) during sleep.

Outcomes: Six months after commencement of the treatment, the clinical manifestations of SAHS and AS had significantly improved.

Conclusions: We hypothesize that patients with AS are prone to sleep apnea due to airway compression, central depression of respiration, abnormal inflammatory responses. Hence, careful assessment toward potential SAHS symptoms should be considered especially in patients with AS.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7220631PMC
http://dx.doi.org/10.1097/MD.0000000000020055DOI Listing

Publication Analysis

Top Keywords

oral daily
12
sleep apnea-hypopnea
8
apnea-hypopnea syndrome
8
ankylosing spondylitis
8
patient received
8
sahs symptoms
8
sahs
7
sleep
5
syndrome caused
4
caused ankylosing
4

Similar Publications

Drug Development.

Alzheimers Dement

December 2024

Cognition Therapeutics, Purchase, NY, USA.

Background: CT1812 is an experimental therapeutic sigma-2 receptor modulator in development for Alzheimer's disease (AD) and dementia with Lewy bodies. CT1812 reduces the affinity of Aβ oligomers to bind to neurons and exert synaptotoxic effects. This phase 2, multi-center, international, randomized, double-blind, placebo-controlled trial assessed safety, tolerability and effects of CT1812 on cognitive function in individuals with AD.

View Article and Find Full Text PDF

Drug Development.

Alzheimers Dement

December 2024

Indiana University School of Medicine, Department of Psychiatry, Indianapolis, IN, USA.

Background: Major contributors to AD pathogenesis include aggregates of amyloid-β (Aβ) peptides, hyperphosphorylated tau protein, and neuroinflammation. No currently approved treatment stops or significantly slows the progression of AD. Nevertheless, one class of agents that has shown promise is metal chelators.

View Article and Find Full Text PDF

Drug Development.

Alzheimers Dement

December 2024

Anavex Life Sciences Corp., New York, NY, USA.

Background: There are no approved oral disease-modifying treatments for Alzheimer disease (AD). This study was intended to assess efficacy and safety of blarcamesine (ANAVEX2-73), an orally available small-molecule activator of the sigma-1 receptor (SIGMAR1) designed to exert neuroprotection through restoration of cellular homeostasis including autophagy enhancement.

Method: ANAVEX2-73-AD-004 is a multicenter (52 medical research centers/hospitals in 5 countries), randomized, double-blind, placebo-controlled, 48-week phase 2b/3 trial that enrolled 508 participants with early AD (mild cognitive impairment/mild dementia) from July 2018 to June 2021 (last patient visit in June 2022).

View Article and Find Full Text PDF

Drug Development.

Alzheimers Dement

December 2024

Oligomerix, Inc., Bronx, NY, USA.

Background: OLX-07010 is an oral small molecule inhibitor of tau self-association that prevented the accumulation of tau aggregates in the htau mouse model expressing wild type human CNS tau isoforms and in P301L tau JNPL3 mice using chronic treatment by administration in diet (Davidowitz et al., 2020, PMID: 31771053; 2023 PMID:37556474). A therapeutic study of JNPL3 mice with chronic treatment from 7-12 months of age inhibited the progression of tau aggregation and improved motor coordination.

View Article and Find Full Text PDF

Background: Reactive astrocytes and neuron death by excitotoxicity are observed in Alzheimer's disease (AD). DHA-H (2-hydroxy-docosahexaenoic acid; 2-OH-C22:6 n-3) is a molecule under development that has demonstrated therapeutic efficacy in both cellular and 5xFAD mouse model of AD. DHA-H is metabolized through α-oxidation to yield HPA (Heneicosapentaenoic acid; C21:5 n-3).

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!