Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obstructive sleep apnea-hypopnea syndrome (OSAHS) is becoming widely accepted as a risk factor for glaucoma. We discuss the proposed mechanism involved in the pathogenesis of glaucoma in OSAHS, and review the published data on the association between these two conditions, as well as papers regarding functional and structural tests related with glaucomatous damage. There is increasing evidence that the prevalence of glaucoma is higher in OSAHS patients, especially in those with severe disease with apnea-hypopnea index (AHI) >30, and also that sleep disorders may be more frequent in patients with glaucoma, especially in those with normal tension glaucoma (NTG). Several ophthalmic signs and symptoms have been associated with this condition. Raised intraocular pressure (IOP), possibly related to increased body mass index, thinning of retinal nerve fiber layer (RNFL), and alteration of visual field (VF) indices has been demonstrated in many studies, in patients with no history of glaucoma or evidence of glaucomatous changes in the ophthalmic examination. A correlation of AHI with RNFL and VF indices has been described in some studies. Finally, corneal thinning, suspicious glaucomatous disc changes and anomalies in electrophysiological tests such as multifocal visual evoked potential have been described in patients with OSAHS, even in patients with normal findings in the optic nerve and VF, suggesting subclinical optic nerve involvement not detectable in conventional ophthalmic examinations. The pathogenesis of optic nerve involvement has been related to vascular and mechanical factors. Vascular factors include recurrent hypoxia with increased vascular resistance, autonomic deregulation, oxidative stress and inflammation linked to hypoxia and subsequent reperfusion, decreased cerebral perfusion pressure and direct hypoxic damage to the optic nerve. Proposed mechanical factors include increased IOP at night related to supine position and obesity, raised intracranial pressure and elastic fiber depletion in the lamina cribosa and/or trabeculum. In conclusion, ophthalmic evaluation should be recommended in patients with severe OSAHS, and the presence of sleep disorders should be investigated in patients with glaucoma, especially in NTG patients and in those with progressive damage despite controlled IOP, as treatment with continuous positive airway pressure may contribute to stabilizing the progression of glaucomatous damage.
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PMID:Obstructive sleep apnea-hypopnea syndrome (OSAHS) and glaucomatous optic neuropathy. 2485 87

Aims: To investigate the impact of thinning at individual grids of macular neuroretinal layers, clinical factors, and inadequate light exposure on the specific components of sleep disorder in patients with type 2 diabetes. Methods: One hundred twenty-four patients with type 2 diabetes without clinical evidences of diabetic retinopathy and neuropathy (HbA1c: 8.3%, diabetes duration; 8.7 years) and 54 age- and sex-matched control subjects (HbA1c: 5.6%) underwent detailed clinical, neurological, and ophthalmological examinations. The sleep disorder was assessed by the Pittsburgh Sleep Quality Index Japanese Version (PSQI-J). The temporal structures of daily life were assessed by the Munich Chronotype Questionnaire Japanese Version. The thickness at nine grids defined by the Early Treatment Diabetic Retinopathy Study of nine macular neuroretinal layers was determined by swept-source optical coherence tomography and OCT-Explorer. The associations between the individual components of sleep disorders and the thickness at each grid of macular neuroretinal layers, clinical factors, or the temporal structures of daily life were examined. Results: The prevalence of the sleep disorder, global score, and four individual PSQI-J scores in patients with type 2 diabetes were higher than control subjects. The thickness of two and five grids of two inner retinal layers and four to seven grids of four outer retinal layers in patients with type 2 diabetes was thinner than those in control subjects. The thickness at one to eight grids of four outer retinal layers in type 2 diabetic patients was inversely associated with global score and five individual scores of sleep disorder. The thinning at one to two grids of the inner plexiform layer was related to three high individual scores of sleep disorder. The inappropriate light exposure was associated with the sleep disorder and altered macular neuroretinal layers. The high HbA1c and LDL-cholesterol levels were related to the high global score and two individual scores of sleep disorder, respectively. Conclusion: In patients with type 2 diabetes, the thinning at grids of the inner plexiform layer and outer retinal layers was associated with the high scores of specific components of the sleep disorder. The sleep disorder was also related to hyperglycemia, dyslipidemia, and inappropriate light exposure.
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PMID:Thinning of Macular Neuroretinal Layers Contributes to Sleep Disorder in Patients With Type 2 Diabetes Without Clinical Evidences of Neuropathy and Retinopathy. 3218 58