Diabetes mellitus suppresses hemodialysis-induced increases in tear fluid secretion

Nakata, M.; Okada, Yoshinori; Kobata, Hirotsugu; Sügimura, Takashi; Reinach, Peter S.; Tomoyose, Katsuo; Saika, Shizuya

doi:10.1186/1756-0500-7-78

Cited by 12 publications

(10 citation statements)

References 25 publications

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“…Excessive levels of cytokines in DED inhibit the release of acetylcholine from the nerve endings and auto autoantibody blockade of M3AChR, disturbing the neuronal stimuli transmission to the secretory component of the OSM [ 117 , 118 ]. Moreover, diabetes can cause lachrymal and corneal neuropathy, and ultimately induce the change of OSM and dry eye [ 119 , 120 ]. Some ophthalmologic surgeries such as refractive surgery and cataract surgery could cause corneal nerve transection which results in decreased feedback to the lacrimal gland leading to reduced tear production [ 121 , 122 , 123 ].…”

Section: Ocular Surface Microenvironment Change In Dry Eyementioning

confidence: 99%

Dry Eye Management: Targeting the Ocular Surface Microenvironment

Zhang

et al. 2017

IJMS

195

185

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Dry eye can damage the ocular surface and result in mild corneal epithelial defect to blinding corneal pannus formation and squamous metaplasia. Significant progress in the treatment of dry eye has been made in the last two decades; progressing from lubricating and hydrating the ocular surface with artificial tear to stimulating tear secretion; anti-inflammation and immune regulation. With the increase in knowledge regarding the pathophysiology of dry eye, we propose in this review the concept of ocular surface microenvironment. Various components of the microenvironment contribute to the homeostasis of ocular surface. Compromise in one or more components can result in homeostasis disruption of ocular surface leading to dry eye disease. Complete evaluation of the microenvironment component changes in dry eye patients will not only lead to appropriate diagnosis, but also guide in timely and effective clinical management. Successful treatment of dry eye should be aimed to restore the homeostasis of the ocular surface microenvironment.

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Section: Ocular Surface Microenvironment Change In Dry Eyementioning

confidence: 99%

Dry Eye Management: Targeting the Ocular Surface Microenvironment

Zhang

et al. 2017

IJMS

195

185

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“…Hyperglycaemia-induced AGE and sorbitol accumulation within the cells leads to cellular oedema and dysfunction, resulting in structural and functional damage of the lacrimal gland [69]. Additionally, diabetic neuropathy impairs the autonomic control of the lacrimal gland [70]. Consequently, both these factors decrease the capacity of the lacrimal gland to produce tears.…”

Section: Tear Film Functionmentioning

confidence: 99%

Diabetic Corneal Neuropathy

Mansoor¹,

Tan

Lin

et al. 2020

JCM

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Diabetic keratopathy (DK) is a common, but underdiagnosed, ocular complication of diabetes mellitus (DM) that has a significant economic burden. It is characterised by progressive damage of corneal nerves, due to DM-induced chronic hyperglycaemia and its associated metabolic changes. With advances in corneal nerve imaging and quantitative analytic tools, studies have shown that the severity of diabetic corneal neuropathy correlates with the status of diabetic peripheral neuropathy. The corneal nerve plexus is, therefore, considered as an important surrogate marker of diabetic peripheral neuropathy and helps in the evaluation of interventional efficacy in the management of DM. The clinical manifestations of DK depend on the disease severity and vary from decreased corneal sensitivity to sight-threatening corneal infections and neurotrophic ulcers. The severity of diabetic corneal neuropathy and resultant DK determines its management plan, and a step-wise approach is generally suggested. Future work would focus on the exploration of biomarkers for diabetic corneal neuropathy, the development of new treatment for corneal nerve protection, and the improvement in the clinical assessment, as well as current imaging technique and analysis, to help clinicians detect diabetic corneal neuropathy earlier and monitor the sub-clinical progression more reliably.

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“…Diabetic neuropathy may be an important risk factor for lacrimal gland dysfunction. Nakata et al demonstrated that diabetes suppresses hemodialysis-induced increases in tear fluid secretion, which suggests that autonomic control of lacrimal gland function may be compromised by neuropathy in patients with DM [ 19 ].…”

Section: Etiology Of Diabetes Mellitus Associated Dry Eye Syndromementioning

confidence: 99%

Dry Eye Syndrome in Patients with Diabetes Mellitus: Prevalence, Etiology, and Clinical Characteristics

Zhang

Zhao

Deng

et al. 2016

Journal of Ophthalmology

155

127

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There has been substantial progress in our understanding of the ocular surface system/lacrimal function unit in the past 15 years. Keratoconjunctivitis sicca, more commonly referred to as dry eye syndrome (DES), is the most frequently encountered condition and diabetes mellitus (DM) has been identified as one of the leading causes of DES. Poor glycemic control affects both the anterior and the posterior segments of the eye and increasing prevalence of diabetes-associated DES (DMDES) has been reported in recent years. The pathogenesis and specific features of DMDES remain uncertain and interventions are limited to those used in DES. This review outlines the pathogenesis, clinical manifestations, and the current preventive and treatment strategies for diabetes-related DES.

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Diabetes mellitus suppresses hemodialysis-induced increases in tear fluid secretion

Cited by 12 publications

References 25 publications

Dry Eye Management: Targeting the Ocular Surface Microenvironment

Dry Eye Management: Targeting the Ocular Surface Microenvironment

Diabetic Corneal Neuropathy

Dry Eye Syndrome in Patients with Diabetes Mellitus: Prevalence, Etiology, and Clinical Characteristics

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