Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was conducted on 25 patients with Diabetes Mellitus (DM) having positive indication of diabetic retinopathy on ophthalmoscopic examination. The patients were examined clinically, ophthalmoscopically and with Fluorescein Angiography (FA). It was found that the maximum number of patients with retinopathy were in their 5th and 6th decade and that retinopathy was more common in Non Insulin dependent diabetics (NIDDM) than Insulin dependent Diabetics (IDDM). It was also seen that retinopathy takes longer time to develop in IDDM patients (16.37 years vs 11.7 years). Proliferative diabetic retinopathy was more common with patients having poor glycemic control and in IDDM patients. FA was very helpful in detecting microaneurysms and for exact localization of neovascularization, and other microangiopathic lesions as well as for permanent record.
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PMID:Diabetic retinopathy: a clinical study with special reference to fluorescein angiography. 184 1

Pancreatic B-cell function in relation to diabetic retinopathy was studied in 195 NIDDM patients with long-standing diabetes. Background diabetic retinopathy (BDR) was present in 95 (48.7%) and proliferative retinopathy (PDR) in 17 (8.7%) of the subjects. There was no significant difference between the BDR, PDR, and non-retinopathy groups with respect to age, age at diagnosis of diabetes and HbA1 values. Mean duration of diabetes was higher in the PDR group (p less than 0.05). Serum C-peptide values showed no correlation with the presence of retinopathy or with the duration of diabetes. The C-peptide values were widely scattered in patients with BDR and PDR showing no association between pancreatic B-cell reserve and occurrence or severity of retinopathy in NIDDM patients. Thus, decreased pancreatic B-cell reserve does not appear to be a risk factor for diabetic retinopathy in NIDDM patients.
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PMID:Pancreatic B-cell function in relation to diabetic retinopathy in Asian Indian NIDDM patients. 306 87

Several studies report increased growth hormone (GH) responses to provocative stimuli in patients with diabetic retinopathy. We studied GH responses to 1 microgram/kg body wt human pancreatic GH-releasing hormone 1-44 (hpGHRH 1-44) in 33 patients with type I diabetes mellitus, 31 patients with type II diabetes mellitus, and 2 control groups (N = 11 and 8). Based on the results of fundoscopy and fluorescein angiography, the diabetic patients were subdivided into patients without diabetic retinopathy, patients with nonproliferative diabetic retinopathy, and patients with proliferative diabetic retinopathy. Growth hormone responses to hpGHRH 1-44 in diabetic patients with proliferative or nonproliferative retinopathy or without retinopathy were not significantly different regardless of the type of diabetes. Remarkably, GH responses to hpGHRH 1-44 in type I diabetic patients without retinopathy were significantly higher than the matched controls. Our data suggest that diabetic retinopathy in type I and in type II diabetes is not associated with increased GH responsiveness to hpGHRH 1-44, whereas in type I diabetes mellitus without diabetic retinopathy, a GH hyperresponsiveness to hpGHRH seems to occur.
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PMID:No evidence for increased growth hormone responses to growth hormone-releasing hormone in patients with diabetic retinopathy. 310 Mar 67

A phacoemulsification procedure, combined with an "in-the-bag" lens implantation, was performed on ten eyes that once had proliferative diabetic retinopathy (PDR). The ten eyes were in eight patients who had a 20-plus year history of either type I or type II diabetes mellitus. All eyes had reached the "quiescent" state of diabetic retinopathy 2-13 years before the cataract surgery through either argon laser pan retinal photocoagulation and/or pars plana vitrectomy. Nine of ten eyes remained completely free of retinal neovascularization and rubeosis iridis, with follow-up periods between 1.5 and 5 years. One eye has been lost to recurrent vitreous hemorrhages and an inoperable retinal detachment.
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PMID:Phacoemulsification and implantation of posterior chamber intraocular lens in eyes with quiescent proliferative diabetic retinopathy. 365 17

Prostacyclin (PGI2) is the most potent endogenous inhibitor of platelet aggregation yet discovered. Thromboxane (TXA2) promotes aggregation and degranulation of platelets. It is hypothesized that an homeostasis exists between these pathways that is protective against vascular damage and is disturbed in several diseases such as diabetes. Circulating levels of PGI2-TXA2 in 35 patients with adult onset diabetes and 15 controls have been assayed. Twenty patients had background retinopathy, and 15 had proliferative retinopathy. Circulating levels of PGI were found to be elevated in 9/15 patients with proliferative diabetic retinopathy, 2/20 diabetic patients with background or no retinopathy, and 0/15 controls. PGI levels may correlate, therefore, with the severity of the retinopathy.
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PMID:Circulating prostacyclin and thromboxane levels in patients with diabetic retinopathy. 675 Apr 95

The prevalence of vascular complications was assessed in 726 South Indian non-insulin dependent diabetes mellitus (NIDDM) patients with over 25 years' duration of diabetes. Retinopathy was detected in 52.0% of patients which included 41.7% with non-proliferative and 10.3% with proliferative diabetic retinopathy. Nephropathy was present in 12.7% and neuropathy in 69.8% of patients. While 32.8% of patients had ischaemic heart disease, the prevalence of peripheral vascular disease was only 15.4%. Multivariate logistic regression analyses showed that serum creatinine was associated with retinopathy, creatinine and post-prandial plasma glucose with nephropathy and post-prandial plasma glucose and age with neuropathy. This is one of the first reports on vascular complications in long-term diabetes from the Indian sub-continent.
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PMID:Vascular complications in long-term south Indian NIDDM of over 25 years' duration. 879 13

A cohort of 6792 NIDDM patients attending a diabetes centre at Madras in South India was screened using a combination of retinal photography and clinical examination by retinal specialists. A total of 2319 patients (34.1%) had evidence of retinopathy. This included 2090 patients (30.8%) with non-proliferative diabetic retinopathy including 435 patients (6.4%) with maculopathy and 229 patients (3.4%) with proliferative diabetic retinopathy. Multiple logistic regression analyses showed that duration of diabetes, glycosylated haemoglobin, type of treatment (insulin treatment versus non-insulin treatment), systolic and diastolic blood pressures and serum creatinine, showed a positive association with retinopathy while body mass index (BMI) showed an inverse association. The prevalence rates of retinopathy in Southern Indians are comparable to those seen in Europeans. However in view of the high prevalence of diabetes in the Indian sub-continent, diabetic retinopathy could become a formidable challenge in the future.
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PMID:Prevalence of retinopathy in non insulin dependent diabetes mellitus at a diabetes centre in southern India. 896 88

To study the progression of diabetic retinography in relation to diabetes treatment and glycaemic control in patients with non-insulin dependent (Type 2) diabetes mellitus (NIDDM), we performed a prospective study in a cohort of 1378 diabetic patients, aged > or = 40 years at diagnosis, of whom 333 were treated with insulin, and 1045 with oral antihyperglycaemic agents or diet alone. In the latter group 174 patients changed to insulin therapy during follow-up. We used the Wisconsin scale to grade retinopathy, recorded blindness (visual acuity < or = 0.1) and visual impairment (visual acuity 0.2-0.4), and measured the average HbA1c for each patient during a mean 3.1 year study period. In a multivariate analysis, patients who changed treatment from oral agents or diet alone to insulin therapy had a relative risk of 2.0 (95% confidence interval 1.7-2.3) for progression of retinopathy > or = 3 levels compared with all other patients in the study. The increase in risk remained even after controlling for mean HbA1c (relative risk 1.6; 95% confidence interval 1.3-1.9). Progression > or = 3 levels was significantly associated with a higher incidence of macular oedema and deterioration of visual acuity (p < 0.001). The relative risk for blindness/visual impairment due to retinopathy was 2.7 (95% confidence interval 1.8-4.0) in the group with changed treatment compared with all the other patients in the study. Poor glycaemic control (Hba1c%) before the start of insulin therapy and any retinopathy at baseline were significant risk factors for progression in the group with changed treatment (both p < 0.01). In the whole study group, poor glycaemic control was significantly associated with retinopathy progression > or = 3 levels; the relative risk for those having mean HbA1c above the median being 1.7 (95% confidence interval 1.4-2.1), compared to those with a HbA1c value below the median. Moderate non-proliferative diabetic retinopathy at baseline was also associated with progression (relative risk 2.5; 95% confidence interval 1.4-4.5). In contrast, insulin treatment at baseline was not associated with an increased risk of retinopathy progression. In conclusion, while hyperglycaemia was a risk factor for the progression of retinopathy in all patients, change of treatment from oral drugs to insulin was associated with a 100% increased risk of retinopathy progression and a 3-fold increased risk of blindness/visual impairment.
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PMID:The effect of glycaemic control and the introduction of insulin therapy on retinopathy in non-insulin-dependent diabetes mellitus. 927 3

Vascular endothelial growth factor (VEGF) plays a major role in the development of neovascularization in proliferative diabetic retinopathy (PDR). The source of intravitreous VEGF is presumably ischaemic retina, but increased levels derived from serum cannot be excluded. The aim of the study is to determine the intravitreous concentrations of VEGF in diabetic patients with PDR and to investigate whether serum VEGF could contribute to the intravitreous concentration. For this purpose, we studied 20 diabetic patients (5 IDDM and 15 NIDDM) with PDR in whom a vitrectomy was performed (group A). Non-diabetic patients (n = 13) with other conditions requiring vitrectomy served as a control group (group B). In both groups, VEGF was determined in serum and undiluted vitreous samples obtained simultaneously. Furthermore, serum VEGF was determined in 69 healthy control subjects (group C) and 39 diabetic patients without microvascular complications (group D). Vitreous and serum VEGF was determined by ELISA (R & D Systems, Abingdon, UK); intra-assay CV 3.8%, interassay CV 5.1%. Intravitreous concentrations of VEGF were strikingly higher in group A (median 1.75 ng/ ml, range 0.33-6.66) in comparison with group B (median 0.009 ng/ml, range 0.009-0.038); p < 0.0001. This difference remained significant after adjusting for intravitreous protein concentration (p < 0.05). Differences in serum VEGF among the groups included in the study were not found. We conclude that the high vitreous levels of VEGF observed in diabetic patients with PDR cannot be attributed to serum diffusion across the blood-retinal barrier. Therefore, intraocular synthesis is the main contributing factor for the high vitreous VEGF concentrations observed in PDR.
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PMID:Vitreous levels of vascular endothelial growth factor are not influenced by its serum concentrations in diabetic retinopathy. 930 Feb 49

Proliferative diabetic retinopathy is an important cause of visual impairment. We investigated whether the polymorphism of the beta 3-adrenoreceptor (beta 3-AR) gene, which is associated with insulin resistance and an earlier onset of NIDDM, was associated with proliferative diabetic retinopathy (PDR) in 215 Japanese NIDDM patients with a duration of diabetes of > or = 10 years. The polymorphism of the beta 3-AR gene was determined by polymerase chain reaction-restriction fragment length polymorphism analysis. The Trp64Arg allele of the beta 3-AR gene was significantly more frequent in the NIDDM patients with PDR (P = 0.002), but not in those with non-PDR (P = 0.151), than in NIDDM patients without diabetic retinopathy. Those with the mutation had an earlier onset of diabetes, a longer duration of diabetes, and higher current and maximal BMI values, compared with those without the mutation. Moreover, this mutation was also associated with higher serum triglyceride and decreased HDL-cholesterol levels. When adjustment was made for age, age at diagnosis, duration of diabetes, current BMI, systolic blood pressure, HbA1e, and serum lipids in a multiple regression analysis, a significant association was found between the Trp64Arg allele and diabetic retinopathy (P = 0.039). The Arg/Arg or Arg/Trp genotype was significantly associated with PDR, compared with the Trp/Trp genotype, with an odds ratio of 2.55 (95% CI 1.25-5.16). We concluded that the beta 3-AR gene polymorphism is a newly identified risk factor for PDR.
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PMID:Beta 3-adrenoreceptor gene polymorphism: a newly identified risk factor for proliferative retinopathy in NIDDM patients. 931 61


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