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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eye lens cataract can develop by various mechanisms the details of which are not completely known. Increased level of glucose in patients with diabetes mellitus represents one of the factors accelerating cataract development. As the lens does not depend on insulin, cataract formation is induced by hyperglycaemia both in IDDM and NIDDM patients. Glucose attacks free aminogroups of proteins and glycation products are formed by multistep non-enzymatic reactions. We can discriminate early and late products. The latter are often called as advanced glycation endproducts (AGE). They can accumulate inside the lens and interfere with its optical properties. With regard to the fact that glycation reactions are accompanied by autooxidation reactions, the overall process is usually referred to as glycoxidation. Free radical oxidations of membrane lipids give similar products as do glycation reactions, and there is synergy between these two pathways. Development of eye cataract is accompanied by a decrease in lens antioxidant capacity. A new class of glycation inhibitors has been observed recently. They are called Amadorins and they have therapeutic potential in the cataract treatment.
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PMID:[Role of nonenzymatic glycation and oxidative stress on the development of complicated diabetic cataracts]. 1095 2

The aim of Diabcare-Asia project was to collect data on diabetes control, management and complication status among patients in 12 Asian countries. Information was extracted from medical records, interviews and laboratory assessment. The majority (96%) of patients were diagnosed with type 2 diabetes mellitus, with mean age (+/-SD) of 59.3+/-12.5 years and mean diabetes duration of 9.4+/-7.0 years. Mean body mass index (BMI) was 24.7+/-4.9 kg/m(2) and the majority (60%) had BMI < or =25 kg/m(2). The majority (70%) of patients were treated with oral antidiabetic drugs (OADs), 15% with insulin, 10% with insulin and OAD combination therapy and 5% with diet control. Among OADs-treated patients, most (44%) received two or more medication. Majority of patients (> or =79%) had satisfactory metabolic control of triglycerides (<2.2 mmol/l), total cholesterol (<6.5 mmol/l) and HDL cholesterol (>0.9 mmol/l). Glucose self-monitoring (either urine or blood) was only practiced by 50% of patients. Glycaemic control (HbA1c) was unsatisfactory as majority of patients had HbA1c>7.4% (73%) and 50% had fasting blood glucose (FBG)>7.8 mmol/l. Cataract (26%), neuropathy (42%) and cerebral stroke (6%) were the most frequently reported complications. Clearly, the level of glycaemic control in majority of patients is below satisfaction. Effective education must be emphasised in the management of diabetes.
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PMID:Epidemiology of diabetes mellitus in Western pacific region: focus on Philippines. 1102 81

Diagnosis and management of giant cell (temporal) arteritis (GCA) should be performed by physicians who can accurately monitor the ophthalmologic, neurologic, and systemic sequelae of the disease as well as the numerous side effects of systemic corticosteroids, which are typically necessary for treatment. When the diagnosis of giant cell arteritis is seriously entertained, early treatment with adequate doses of oral or intravenous corticosteroids should not be delayed until laboratory confirmation has been obtained. Unilateral or bilateral temporal artery biopsy should be performed on all patients with suspected GCA. A positive biopsy result mandates that higher doses of corticosteroids be used during the first 2 months, which comprise the critical period for risk of new ocular ischemia. A definitive, biopsy-proven diagnosis requires at least 6 months, and typically 12 months, of corticosteroid therapy. Common pitfalls include increasing the dose and prolonging the use of corticosteroids in response to increases in the erythrocyte sedimentation rate (ESR) unrelated to GCA or visual blurring that may be related to benign tear film abnormalities, corticosteroid-induced lens changes, and other ophthalmic conditions. The muscle stiffness of polymyalgia rheumatica (PMR) must be distinguished from the osteoarthritis and other painful conditions common in the elderly. After corticosteroid therapy has begun, continuing ophthalmologic evaluation is necessary to evaluate the effectiveness of treatment and whether ocular complications, such as glaucoma or cataract, develop. Careful attention must be given to early detection and prevention of systemic side effects of corticosteroid treatment. Patients may be given gastrointestinal protective agents, such as histamine (H(2))-blocking agents; vitamin D and calcium; oral hypoglycemic agents; and, if necessary, insulin and antihypertensive drugs. If bone density measurements warrant, hormones/supplementation to prevent or reverse osteoporosis may be prescribed. After the initial diagnosis and first 4 weeks of treatment, elevation of the ESR or C-reactive protein alone should generally not be used as signs of disease activity nor as a reason to increase the daily dose of steroids. If symptoms or signs of disease activity occur, the dose should be raised regardless of test results. Even with vigorous physician-patient education, however, a patient is occasionally unable to provide adequate historical information about response to therapy, and the physician is forced to rely on laboratory values as a measure of disease activity. After initial high-dose corticosteroid therapy, patients without a classic history and with negative biopsy results will generally receive a rapid taper to low doses of corticosteroids. The role of repeated temporal artery biopsy in the clinical management of GCA is unclear. Despite persistence of PMR and, in some cases, histologic evidence of inflammation in temporal arteries, patients do not frequently have recurrence of symptomatic GCA after 6 months or more of corticosteroid therapy. Under these circumstances, late vision loss is rare.
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PMID:Giant Cell Arteritis. 1109 95

We examined the effects of high-fructose (FR) feeding on the development of diabetic complications in the lens and the kidney of streptozotocin (STZ)-diabetic rats. Male Wistar Furth rats were treated with one of two doses of STZ (HIGH STZ, 55 mg/kg body weight; MOD STZ, 35 mg/kg body weight) or vehicle alone (SHAM) and were then assigned to a control (CNTL) or 400 g FR/kg diet for 12 weeks. At the end of the study, body weight, plasma glucose and insulin concentrations differed among STZ groups (HIGH v. MOD v. SHAM, P < 0.001) but did not differ due to diet. Plasma FR concentrations were significantly higher in FR-fed v. CNTL-fed groups (P < 0.0001) and in HIGH-STZ groups v. MOD-STZ and SHAM groups (P < 0.0004 and P < 0.0001 respectively). Focal length variability of the lens, a quantitative measure of cataract formation, was increased in the HIGH STZ, FR group compared with the HIGH STZ, CNTL group (P < 0.01). The concentration of H2O2 in kidney microsomes was significantly higher in HIGH STZ, FR rats v. HIGH STZ, CNTL rats (P < 0.01). Micro-albuminuria was not observed in any of the groups examined, and there was no evidence of extensive histological damage in the kidney from any rats. Under conditions of severe hyperglycaemia, high FR intake promotes the development of cataracts in the lens of the eye, and results in increased concentrations of substances indicative of oxidative stress in the kidney. Although FR has been suggested as a carbohydrate source for diabetics, a high FR diet coupled with hyperglycaemia produces effects that may promote some of the complications associated with diabetes.
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PMID:High-fructose feeding of streptozotocin-diabetic rats is associated with increased cataract formation and increased oxidative stress in the kidney. 1110 29

Neonatal diabetes mellitus is defined as hyperglycemia detected in the first month of life of more than 2 weeks' duration, requiring insulin treatment. It is extremely uncommon (1/500,000 neonates) and is permanent in only 30% of cases. Several hypotheses concerning its etiology have been postulated, such as pancreatic immaturity, paternal uniparental isidisomy of chromosome 6, and the existence of a gene located in the 6 q 22-23 chromosome region subjected to imprinting and exclusively of paternal expression. The management of these patients is usually difficult. These neonates are underweight for their gestational age, and neither anti-insulin antibodies nor anti-islets are detected. We studied a neonate hospitalized because of low weight for his gestational age with dimorphic features and hyperglycemia since the 17 th day of life. Clinical and anatomical follow-up has been periodically performed to the present date. The child presents permanent neonatal diabetes with negative antibodies. Although various insulin patterns have been used since the onset of the syndrome, management remains difficult. The child presents hypothyroidism, bilateral neurosensory deafness, bilateral congenital cataract, myopia, dimorphic features, congenital stridor and slow weight-stature curve. The results of muscle biopsy and metabolic studies were normal. Wolfram's syndrome and mitochondrial diabetes were ruled out. This is an exceptional case of permanent neonatal diabetes associated with other malformations corresponding to no known syndromic patterns.
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PMID:[Permanent neonatal diabetes associated with other anomalies]. 1133 81

Hyperglycemia leads to vascular disease specific to diabetes mellitus. This pathology, which results from abnormal proliferation of smooth muscle cells in arterial walls, may lead to cataract, renal failure, and atherosclerosis. The hexosamine biosynthetic pathway is exquisitely responsive to glucose concentration and plays an important role in glucose-induced insulin resistance. UDP-GlcNAc: polypeptide O-N-acetylglucosaminyltransferase (O-GlcNAc transferase; OGTase) catalyzes the O-linked attachment of single GlcNAc moieties to serine and threonine residues on many cytosolic or nuclear proteins. Polyclonal antibody against OGTase was used to examine the expression of OGTase in rat aorta and aortic smooth muscle (RASM) cells. OGTase enzymatic activity and expression at the mRNA and protein levels were determined in RASM cells cultured at normal (5 mM) and at high (20 mM) glucose concentrations. OGTase mRNA and protein are expressed in both endothelial cells and smooth muscle cells in the aorta of normal rats. In both cell types, the nucleus is intensely stained, while the cytoplasm stains diffusely. Immunoelectron microscopy shows that OGTase is localized to euchromatin and around the myofilaments of smooth muscle cells. In RASM cells grown in 5 mM glucose, OGTase is also located mainly in the nucleus. Hyperglycemic RASM cells also display a relative increase in OGTase's p78 subunit and an overall increase protein and activity for OGTase. Biochemical analyses show that hyperglycemia qualitatively and quantitatively alters the glycosylation or expression of many O-GlcNAc-modified proteins in the nucleus. These results suggest that the abnormal O-GlcNAc modification of intracellular proteins may be involved in glucose toxicity to vascular tissues.
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PMID:Hyperglycemia and the O-GlcNAc transferase in rat aortic smooth muscle cells: elevated expression and altered patterns of O-GlcNAcylation. 1133 5

To prevent cataracts induced by glucocorticoids (GC) as a systemic disease, the suppression of oxidative stress caused by GC in the hepatic metabolism is of significant interest. In this study, to elucidate the formative mechanism of GC-induced cataracts, we examined the preventive effect and then analysed the mechanisms of thyroxine on GC-induced cataract formation. Fifteen day old chick embryos were administered with 0.25 micromol hydrocortisone succinate sodium (HC), and then 12-30 nmol of thyroxine 4 hr after HC administration. At the indicated time after HC treatment, we examined the incidence of cataract formation, the levels of serum glucose and lipids, lenticular and hepatic glutathione (GSH), and lipid peroxide (LPO) in the lens, blood and liver. Almost all lenses (96%) removed 48 hr after HC administration were opaque. Thyroxine prevented HC-induced cataract formation effectively, and suppressed the elevations of serum glucose and LPO in the lens, blood and liver. The treatment prevented the decreased lenticular GSH level at 48 hr, but the hepatic GSH level at 24 hr remained lowered in contrast to the results of previous studies using insulin. Moreover, thyroxine did not decrease the elevated serum lipid level (triglyceride and non-esterified fatty acid) caused by HC. Under thyroxine treatment, in constant to insulin, acceleration of GSH-GSSG cycle rather than GSH de novo synthesis keeps a certain level of hepatic GSH necessary for diminishing the elevation of LPO as a risk factor of GC-induced cataract formation. The regulation of metabolic changes ensured the maintenance of hepatic GSH level, which is necessary to reduce oxidative stress produced by GC and to protect the lens from oxidative stress leading to opacification.
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PMID:Suppressive effects of thyroxine on glucocorticoid (gc)-induced metabolic changes and cataract formation on developing chick embryos. 1138 52

A new spontaneously diabetic strain of the Sprague-Dawley rat was established in 1997 and named the SDT (Spontaneously Diabetic Torii) rat. In this research, we investigated the characteristics of the disease condition in the SDT rats. The time of onset of glucosuria was different between male and female SDT rats; glucosuria appeared at approximately 20 weeks of age in male rats and at approximately 45 weeks of age in female rats. A cumulative incidence of diabetes of 100% was noted by 40 weeks of age in male rats, while it was only 33.3% even by 65 weeks of age in female rats. The survival rate up to 65 weeks of age was 92.9% in male rats and 97.4% in female rats. Glucose intolerance was observed in male rats from 16 weeks of age. The clinical characteristics of the male SDT rats were (1) hyperglycemia and hypoinsulinemia (from 25 weeks of age); (2) long-term survival without insulin treatment; (3) hypertriglyceridemia (by 35 weeks of age); however, no obesity was noted in any of the male rats. The histopathological characteristics of the male rats with diabetes mellitus (DM) were (1) fibrosis of the pancreatic islets (by 25 weeks of age); (2) cataract (by 40 weeks of age); (3) tractional retinal detachment with fibrous proliferation (by 70 weeks of age) and (4) massive hemorrhaging in the anterior chamber (by 77 weeks of age). These clinical and histopathological characteristics of the disease in SDT rats resemble those of human Type 2 diabetes with insulin hyposecretion. In conclusion, SDT rat is considered to be a potentially useful model for studies of diabetic retinopathy encountered in humans.
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PMID:A new spontaneously diabetic non-obese Torii rat strain with severe ocular complications. 1146 1

The relationship between the polyol pathway and sugar cataracts has been studied extensively using streptozotocin-induced diabetic rats and galactose fed rats as animal models for insulin-dependent diabetes mellitus (IDDM). In these models, sugar cataracts progress quickly, leading to rapid lenticular polyol accumulation in the early stages of cataract formation. In 1992, a new animal model of non-insulin-dependent diabetes mellitus (NIDDM), the Otsuka Long-Evans Tokushima Fatty (OLETF) rat, was established. In the present study, we examined both biochemical and morphological changes in the lenses of the OLETF rats to determine whether these changes reflect those associated with diabetic cataract formation and to clarify their relationship with the polyol pathway. For the biochemical analysis, we measured the enzyme activity of aldose reductase (AR) and sorbitol dehydrogenase (SDH) and the sorbitol levels using 20, 40 and 60 week old OLETF or control Long-Evans Tokushima Otsuka (LETO) rats. Enzyme activities of AR and SDH, which were lower in 20 week old OLETF rats than in LETO rats, were increased in 60 week old OLETF rats. The lenticular sorbitol level of the OLETF rats was similar to the control level at 20 weeks of age, but it was markedly increased at 40 weeks of age, and slightly decreased at 60 weeks of age compared with rats at 40 weeks but not compared with controls. Slight lens fiber swelling was observed in the anterior and/or posterior subcapsular regions of 40 week old OLETF rats, accompanying elevated sorbitol level and slightly increased SDH activity in the lens. Swelling and liquefaction of lens fibers were observed in the subcapsular and supranuclear region of 60 week old OLETF rats, as well as decreased lenticular sorbitol, and markedly increased SDH activity compared with rats at 40 weeks. AR activity was also increased causing the elevation of sorbitol in lenses of OLETF rats during the early stages of cataract formation. Despite differences in the etiology of diabetes mellitus, the strain of rat and the rate of disease progression in the OLETF rat model compared with other diabetic models, the present results support the theory that the polyol pathway via AR is a factor in the development of sugar cataracts.
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PMID:Biochemical and morphological changes during development of sugar cataract in Otsuka Long-Evans Tokushima fatty (OLETF) rat. 1152 Jan 12

The majority of diabetic dogs appear to have a form of type 1 diabetes analogous to the latent autoimmune diabetes of adults (LADA) in humans. Evidence of acute or chronic pancreatitis occurs in about 40% of diabetic dogs. Blindness caused by cataract formation eventually occurs in the majority of diabetic dogs and is not dependent on glycemic control. Insulin is the mainstay of therapy for diabetic dogs, and a conservative approach to insulin therapy is crucial. Most diabetic dogs require twice-daily dosing with lente or NPH insulin to adequately control their clinical signs. The diet fed should primarily be palatable and nutritionally balanced. Improved glycemic control may be achieved in some dogs if the diet contains increased insoluble fiber.
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PMID:Management of canine diabetes. 1157 Jan 30


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