{"id":99652,"date":"2024-10-14T14:07:45","date_gmt":"2024-10-14T13:07:45","guid":{"rendered":"https:\/\/touchendocrinology.com\/?p=99652"},"modified":"2024-11-01T16:45:36","modified_gmt":"2024-11-01T16:45:36","slug":"dry-eye-in-diabetes-the-indian-diabetic-and-endocrine-eye-diseases-indeed-review","status":"publish","type":"post","link":"https:\/\/touchendocrinology.com\/diabetes\/journal-articles\/dry-eye-in-diabetes-the-indian-diabetic-and-endocrine-eye-diseases-indeed-review\/","title":{"rendered":"Dry Eye in Diabetes: The Indian Diabetic and Endocrine Eye Diseases (INDEED) Review"},"content":{"rendered":"
Dry eye disease (DED) is known as dry eye syndrome (DES) or keratoconjunctivitis sicca. According to the Tear Film and Ocular Surface Society\u2019s Dry Eye Workshop II (TFOS DEWS II), it constitutes a multifactorial disease of the ocular surface, characterized by a loss of homeostasis of the tear film and accompanied by ocular symptoms.1,2<\/sup><\/span>\u00a0It may cause ocular discomfort and\/or visual symptoms and inflammatory disease of the ocular surface. DED, similar to other ocular conditions such as diabetic retinopathy (DR), papillopathy, cataract and glaucoma, is associated with high morbidity. It negatively affects the quality of life, results in difficulties in performing daily activities and also reduces productivity at work.3\u20135<\/sup><\/span><\/p>\n DED is an important clinical condition, found in a large proportion of people with diabetes; it is reported in 18\u201354% of patients with\u00a0d<\/span>iabetes across India.6<\/sup><\/span>\u00a0India is home to 101 million patients with\u00a0d<\/span>iabetes, nearly 67% of whom suffer from poor glycaemic control.7,8<\/sup><\/span>\u00a0DED is an inadequately addressed condition in the diabetes management process, and the awareness among physicians regarding it is low. DED may impact self-care in patients with diabetes \u2013 it may interfere with self-confidence, physical activity and self-administration of injectable glucose-lowering drugs.9<\/sup><\/span>\u00a0Therefore, it was found imperative to address DED in patients with diabetes.5<\/sup><\/span><\/p>\n This review aims to obtain insights into the correlation between\u00a0dry eye and d<\/span>iabetes, with a focus on data published in the Indian population. The aim was to address major aspects commonly associated with DED and diabetes and make specific suggestions for the management of DED in this population so that this review could be an invaluable resource for doctors managing patients with both conditions. A comprehensive literature review was performed using\u00a0MEDLINE<\/span>\u00a0and Google Scholar, along with an internet\u2010based search of publicly available information and peer\u2010reviewed publications that may not have been indexed in these databases. The recommendations from several important societies for patients with DED have also been reviewed.<\/p>\n The worldwide prevalence studies have reported a range of 15.0%\u201354.3% DED in people with diabetes.10,11 <\/sup><\/span>Symptomatic or asymptomatic DED is present in at least half of the people with diabetes mellitus (DM) globally, which is nearly fivefold higher than the number of patients with DED and no DM.12<\/sup><\/span>\u00a0The proportion of patients with symptomatic DED is also twice as high in those with diabetes.13<\/sup><\/span>\u00a0Several studies from India have reported a significantly higher prevalence of DED in people with diabetes than those without.14\u201316<\/sup><\/span>\u00a0The eyes are exposed organs and therefore influenced by climatic and environmental factors.17<\/sup><\/span>\u00a0Previous studies have found that climatic and environmental changes have differential adverse impacts on dry eyes and likely occur in tropical countries where sunlight and wind exposure are immense.18<\/sup><\/span><\/p>\n The prevalence of DED in patients with\u00a0type 2 d<\/span>iabetes (T2D) has been reported to be between 15 and 33% in people older than 65 years, and 20% in those aged 43\u201386 years.19<\/sup><\/span>\u00a0Among children and adolescents with type 1 diabetes, the 3-year incidence rate was 22.5%.20<\/sup><\/span>\u00a0In a study from India, the age-adjusted prevalence of DED in patients with T2D was 18.4% and 23.3% in males and females, respectively.21<\/sup><\/span><\/p>\n Population-based studies have shown that poor glycaemic control has also been associated with severe DED symptoms.22,23<\/sup><\/span>\u00a0<\/sup>A significant correlation between the severity of DED and the duration of diabetes has also been reported.24<\/sup><\/span>\u00a0The prevalence of mild DED was\u00a0<\/span>~12% in those with 5\u201310 years, 37\u201339% in 11\u201320 years and\u00a0<\/span>~43% in >20 years of T2D diagnosis.24<\/sup><\/span> However, it has been argued that the symptoms of DED are less severe in patients with prolonged disease due to reduced corneal sensitivity associated with diabetic peripheral corneal neuropathy.25 <\/sup><\/span>The presence of retinopathy or macular oedema doubles the odds of DED.26,27<\/sup><\/span>\u00a0Ocular surgeries for cataract and retinopathy are also associated with DED.28<\/sup><\/span><\/p>\n A meta-analysis of four studies including the data from more than two million persons confirmed a significant association between DM and the risk of DED.29<\/sup><\/span>\u00a0Risk factors for DED in the general population also apply to people with diabetes and may increase the cumulative risk (Table 1<\/em><\/span>).27,30<\/sup><\/span><\/em><\/p>\n Table 1: <\/span>Risk factors for dry eye disease in\u00a0d<\/span>iabetes27<\/sup><\/span><\/p>\n Intrinsic factors<\/p>\n<\/td>\n Extrinsic factors<\/p>\n<\/td>\n<\/tr>\n<\/thead>\n Female gender (including post-menopausal status)<\/p>\n<\/td>\n Environmental factors, such as poor humidity, high temperatures, pollution, and excessive screen time for reading<\/p>\n<\/td>\n<\/tr>\n Advancing age<\/p>\n<\/td>\n Psychological factors, such as depression and stress<\/p>\n<\/td>\n<\/tr>\n Duration of diabetes<\/p>\n<\/td>\n<\/tr>\n Poor glycaemic control<\/p>\n<\/td>\n<\/tr>\n Diabetic retinopathy and interventions to treat it<\/p>\n<\/td>\n<\/tr>\n Pre-existing comorbidities, such as chronic viral infections and Parkinson’s disease<\/p>\n<\/td>\n<\/tr>\n Concomitant use of anticholinergic medications, beta-blockers, oestrogen, interferons and chemotherapy<\/p>\n<\/td>\n<\/tr>\n Ocular surgeries<\/p>\n<\/td>\n<\/tr>\n Blepharitis<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<\/div>\n Insulin deficiency and consequent hyperglycaemia lead to histological abnormalities in the various ocular components that increase the risk of DED.30,31<\/sup><\/span>\u00a0Insulin resistance or deficiency and chronic hyperglycaemia may reduce the meibomian gland epithelial cells and goblet cells, leading to a deficient tear film.6<\/sup><\/span>\u00a0Moreover,\u00a0<\/span>T2D leads to structural anomalies in the corneal nerve fibres, which may also result in decreased sensitivity.6<\/sup><\/span>\u00a0Recent evidence from a cross-sectional study has demonstrated impaired\u00a0m<\/span>eibomian gland and tear function in patients with T2D, which deteriorated with moderate or long diabetic duration and a high glycated haemoglobin (HbA1c) level. The values of meibomian gland parameters and the corneal fluorescein staining score were significantly lower in patients with T2D without DED than those with T2D with DED. Thus, asymptomatic\u00a0Meibomian gland dysfunction<\/span>\u00a0(MGD) may occur before the ocular discomfort, and DED develops in patients with T2D<\/sup>\u00a0(Figure 1<\/span><\/span>).31,32<\/sup><\/span><\/p>\n Figure 1: <\/span>Pathogenesis of\u00a0dry eye disease<\/span>\u00a0in patients with d<\/span>iabetes32<\/sup><\/span><\/p>\n Chronic hyperglycaemia leads to histological abnormalities in the lacrimal glands and corneal epithelium and interferes with the regulation of expression of certain mediators causing dysfunction of the lacrimal functional unit, resulting in dry eye disease.<\/em><\/p>\n AGEs = advanced glycation end-products; ALS2CL =\u00a0ALS2 C-Terminal Like<\/span>; APC = antigen-presenting cells; Apo = apolipoprotein<\/span>;\u00a0ARHGEF19<\/span>\u00a0=\u00a0Rho Guanine Nucleotide Exchange Factor 19; CAMs = cell adhesion molecules;<\/span>\u00a0CD = cluster of differentiation;\u00a0IFN = interferon;\u00a0IL = interleukin<\/span>; KIAA1109 =\u00a0FSA (fragile site-associated) protein;<\/span>\u00a0LFU = lacrimal functional units; MMP = matrix metalloproteinase; NF = neuronal<\/span>\u00a0fibres; PLXNA1 = Plexin A1; POLG =\u00a0DNA polymerase subunit gamma<\/span>; SIRT = sirtuin; TH = T-helper cells; WIPI1 =\u00a0WD repeat domain, phosphoinositide interacting 1<\/span>; ZMIZ2 =\u00a0Zinc Finger MIZ-Type Containing 2<\/span>.<\/span><\/em><\/p>\n<\/div>\n Patients with DED often display signs and symptoms of ocular discomfort, such as burning sensation, photopsia, foreign body sensation, soreness, itchiness, redness and blurred vision.13<\/sup><\/span>\u00a0It may cause severe irritation to the ocular surface, predominantly the cornea, causing corneal complications.13<\/sup><\/span>\u00a0Studies have demonstrated a direct association between a higher grade of DED in those with DM compared with those without and more severe signs and symptoms in those with poor glycaemic control (high A1c) versus those with normoglycaemia.14<\/sup><\/span>\u00a0Thus, DM and DED increase the risk of corneal infection, scarring, perforation and irreparable tissue injury.32<\/sup><\/span><\/p>\n In both Caucasians and Asians, the degree of DED severity scores was found to be higher, and corneal sensitivity poorer, in patients with\u00a0d<\/span>iabetes than those without.33<\/sup><\/span>\u00a0A recently published study from India also demonstrated that corneal nerve sensitivity was reduced more in patients with diabetes and moderate DED.6<\/sup><\/span>\u00a0Histological evaluation showed a greater extent of ocular tissue abnormalities in patients with\u00a0d<\/span>iabetes and DED than in those with DED alone.33,34<\/sup><\/span>\u00a0Prospective, controlled studies comparing age- and gender-matched patients have found approximately twofold higher frequency of DED symptoms in patients with diabetes than those without.33,35<\/sup><\/span>\u00a0A recent meta-analysis including more than 3,500 participants from 59 studies across the globe indicated worse tear function scores among patients with DM than those without.36<\/sup><\/span>\u00a0These differences were maintained regardless of the type of diabetes and ethnicity.36,37<\/sup><\/span>\u00a0Thus, unlike in patients without DM, these data suggest that in patients with DM, decreased tear production and poor corneal sensitivity due to persistent hyperglycaemia-induced injury to the corneal receptors result in a more severe dry eye vicious cycle. This is corroborated by the results of this meta-analysis, which found no significant difference in tear function between patients with DM having good glycaemic control and participants without DM.36<\/sup><\/span><\/p>\n Nearly 60% of patients with diabetes have one or more of the ocular complications, which progressively increase after 5 years of a diabetes diagnosis.38<\/sup><\/span>\u00a0However, as DED is a multifactorial disease, the presence of multiple risk factors (environmental factors such as digital screens, intrinsic factors such as hypertension and concomitant therapies increasing the DED risk) in addition to diabetes may prepone the occurrence.<\/p>\n A dry eye examination, as described in detail in the TFOS DEWS II Diagnostic Methodology report, should be added to the routine monitoring of patients with DM, at least in those at high risk.2,39<\/sup><\/span><\/p>\n <\/span>All patients with diabetes should undergo comprehensive ocular screening for retinopathy, glaucoma and dry eye at least annually.<\/p>\n<\/li>\n <\/span>More frequent screening is suggested in:<\/p>\n<\/li>\n<\/ul>\n patients with long-standing diabetes and poor glycaemic control;<\/p>\n<\/li>\n patients with a previous diagnosis of DR or neuropathy;<\/p>\n<\/li>\n post-menopausal females with diabetes and those on oestrogen replacement therapy; and<\/p>\n<\/li>\n patients with comorbidities such as hypertension, Parkinson\u2019s disease and depression.<\/p>\n<\/li>\n<\/ul>\n Diagnosis of DED is based on the use of a combination of subjective and objective assessment.2<\/sup><\/span>\u00a0The DEWS report recommends implementing one of the questionnaires for subjective evaluation in the clinical setting for screening purposes.2<\/sup><\/span>\u00a0Objective diagnostic methods have evolved over the years. Based on the availability and patient inclination, tests yielding specific information to aid early treatment should be preferred. Additional tests should be chosen such that they identify DED subtypes and guide the treatment strategy significantly. Once a DED diagnosis is confirmed, aqueous deficient dry eye and evaporative dry eye can be distinguished based on the results of relevant tests.<\/p>\n The degree of tear function is governed by glycaemic control; therefore, glycaemic control in patients with DM is critical for maintaining tear function.36<\/sup><\/span><\/p>\n In patients with uncontrolled plasma glucose, dry eye symptoms were reported to be severe.14<\/sup><\/span>\u00a0A 12-month observational study in patients with diabetes found that the severity of DED (assessed by Ocular Surface Disease Index [OSDI] score) was linearly associated with A1C.40,41<\/sup><\/span>\u00a0The OSDI score was 4 for A1c 6.0\u20137.0%, 10 for A1c 7.1\u20138.0%, 22 for A1C 8.1\u20139.0% and 28 for A1C >9.0%.40<\/sup><\/span> Overall, the OSDI score was less than 12 for patients with A1C less than 8.0% and greater than 12.0% for A1C greater than 8.0%. An open-label 6-week study found that in patients with severely uncontrolled plasma glucose (A1c >12.0%), the mean levels of OSDI score (>28.0), tear film osmolarity <\/span>(TFO) measurement (>349.0 mOsm\/L), tear breakup time (TBUT) test (>6.0\u00a0<\/span>s) and Schirmer\u2019s test (>8.0 mm) were considerably beyond the cut-offs.42<\/sup><\/span>\u00a0These values significantly reduced by approximately 10.0\u201340.0% when plasma glucose was reduced by 50.0% (fasting blood glucose [FBG] 300.0\u2013153.0 mg\/dL) and post-prandial blood glucose (PPBG; 431.0\u2013252.0 mg\/dL)] and HbA1c reduced by 25.0% (from 12.0 to 9.0%).42<\/sup><\/span><\/p>\n In addition to the direct impact of poor glycaemic control on DED, microvasculopathy, such as retinopathy and neuropathy, which also occur as a consequence of long-standing hyperglycaemia, affects the severity of DED. Patients with reduced corneal sensitivity may remain asymptomatic and thus may not seek medical advice, leading to worsening of DED and increasing the risk of complications. Thus, patients with DED and either retinopathy or neuropathy due to prolonged hyperglycaemia also experience poor scores on DED parameters than those with DED alone.<\/p>\n Thus, poor glycaemic control, directly and indirectly, affects the severity of DED in patients with diabetes. Therefore, treatment of DED in patients with diabetes should focus not only on symptomatic relief, but also on glycaemic control.<\/p>\n DED can cause loss of visual acuity, which may complicate diabetes self-management.43<\/sup><\/span>\u00a0Clinical studies and population-based surveys have shown that symptomatic DED impacts the quality of vision because of the abnormalities of the tear film and associated optical refracting surfaces and, consequently, decreases the ability to perform self-care activities.44<\/sup><\/span>\u00a0Among the various affected activities are cooking healthy food, exercising, monitoring blood glucose and taking insulin and medications that help patients maintain a stable plasma glucose level.44<\/sup><\/span>\u00a0It also affects the ability to navigate spaces, which could limit movement. Thus, DED in patients with diabetes could affect the entire self-care regimen. Consequently, reduced adherence to the use of medications prescribed for diabetes, as well as reduced physical activity, could negatively affect glycaemic control, which could, in turn, aggravate DED symptoms. Thus, patients with both DED and diabetes are at risk of a vicious cycle of negative health outcomes.43<\/sup><\/span><\/p>\n Marked symptoms in the absence of clinically observable signs may indicate the possibility of neuropathic pain, which is prevalent in patients with diabetes. Therefore, DED signs alone may still warrant management to prevent DED manifestation.45<\/sup><\/span>\u00a0The prevention of DED involves the identification of risk factors, such as poor glycaemic control in patients with diabetes, educating patients regarding these and other environmental risk factors and managing based on DED severity.<\/sup>5,8,30,46<\/sup><\/span><\/p>\n The goal of DED management in diabetes is to re-establish homeostasis of the ocular surface by interrupting the vicious cycle of the disease. It also includes the use of sustainable alternatives to avoid a return to the pathophysiological cycle and re-emergence of symptoms. To achieve this successfully, it is essential to target all contributing factors and not rely only on tear replacement.45,46<\/sup><\/span><\/p>\n Case\u2013control studies conducted in India have shown a possibility that environmental factors, such as air pollution, wind, humidity and altitude, may affect the signs and symptoms of DED.17<\/sup><\/span><\/sup><\/sup>\u00a0Therefore, lid hygiene plays an important role in the management of DED. The lid hygiene management has been studied in various clinical studies described by DEWS. It includes eyelid warming, massaging and cleaning using a lid scrub, wipes, neutral shampoo or a combined lid cleanser and artificial tears. These studies have demonstrated improvement in signs and symptoms, TBUT and eyelid margin status.41,46,47<\/sup><\/span><\/p>\n It helps to decrease dry eye symptoms, re-establish tear film stability, improve\u00a0Meibomian gland<\/span>\u00a0(MG) secretion, increase tear film lipid layer thickness and reverse MG dropout.<\/p>\n Long-term treatment adherence is challenging due to patient-centred factors (compliance is 54%).43,48<\/sup><\/span><\/p>\n Patient education plays an important role in the management of patients with both diabetes and DED (Table 2<\/em><\/span>).<\/p>\n Table 2: <\/span>Patient education: Dry eye disease in\u00a0d<\/span>iabetes<\/p>\n Dry eye disease<\/p>\n<\/td>\n Diabetes and other risk factors<\/p>\n<\/td>\n<\/tr>\n<\/thead>\n The patient should be educated and reassured that even though DED is chronic and not curable, it can be well controlled with appropriate treatment and does not generally lead to loss of vision<\/p>\n<\/li>\n<\/ul>\n<\/td>\n Patients should be educated on the association between glycaemic control and severity of DED and other ocular complications and therefore encouraged to remain adherent to lifestyle changes and pharmacotherapy for both DED and diabetes<\/p>\n<\/li>\n<\/ul>\n<\/td>\n<\/tr>\n Appropriate instruction regarding the use of medications should be provided<\/p>\n<\/li>\n<\/ul>\n<\/td>\n<\/tr>\nPrevalence,\u00a0risk factors and pathogenesis<\/span>\u00a0of dry eye disease in\u00a0diabet<\/span>es<\/h1>\n
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\n \n\n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n <\/p>\n
Clinical\u00a0m<\/span>anifestations of dry eye disease in\u00a0d<\/span>iabetes<\/h1>\n
Screening of dry eye disease in\u00a0p<\/span><\/span>atients with\u00a0d<\/span>iabetes<\/h1>\n
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Bidirectional\u00a0a<\/span>ssociation between dry eye disease and\u00a0d<\/span>iabetes<\/h1>\n
Clinical\u00a0e<\/span>vidence:\u00a0I<\/span>mpact of\u00a0poor glycaemic control on\u00a0<\/span><\/span>dry eye disease<\/span><\/span><\/h1>\n
Impact of\u00a0dry eye disease<\/span><\/span>\u00a0on glycaemic control<\/span><\/span><\/h1>\n
Prevention and\u00a0t<\/span>reatment of dry eye disease<\/h1>\n
Prevention of dry eye disease<\/h2>\n
Treatment of dry eye disease<\/h2>\n
Lid hygiene management<\/h2>\n
Advantages<\/h2>\n
Limitations<\/h2>\n
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