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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A retrospective study on the role of pancreatic B-cell insulin secretory capacity in the development of proliferative diabetic retinopathy was performed in 160 diabetic patients with a duration of diabetes of more than 10 years (mean 19.5 +/- 7.9 years). Pancreatic B-cell insulin secretory capacity was assessed in terms of the quantity of C-peptide excreted into urine per day (24-h urinary C-peptide). When the patients were divided into three groups according to the quantity of 24-h urinary C-peptide (group I, C-peptide less than 30 micrograms, n = 49; group II, 30 micrograms less than or equal to C-peptide less than 80 micrograms, n = 76; and group III, C-peptide greater than or equal to 80 micrograms, n = 35), the prevalence of proliferative diabetic retinopathy was much higher in group I (26.5%) than in group II (5.3%) or group III (2.9%). The incidence of proliferative diabetic retinopathy during the follow-up period (mean 9.8 +/- 4.8 years) was also highest in group I (20.0%, 2.7%, and 2.9% in groups I, II, and III, respectively). Other factors which might affect the development of proliferative diabetic retinopathy, including duration of diabetes and past glycemic control, were comparable in these three groups. In contrast, a division of the patients according to glycemic control revealed a strong correlation between glycemic control and background diabetic retinopathy whereas no such correlation was apparent with proliferative diabetic retinopathy. These data are consistent with the view that low pancreatic B-cell insulin secretory capacity may be a risk factor for the development of proliferative diabetic retinopathy.
Diabetes Res Clin Pract 1989 Jan 03
PMID:High prevalence of proliferative retinopathy in diabetic patients with low pancreatic B-cell capacity. 264 41

Ophthalmic evolution was studied for 2 years in 17 patients with insulin-dependent diabetes mellitus and background diabetic retinopathy. Nine patients were treated with triflusal, a new platelet antiaggregant drug, and the eight remaining patients, with similar clinical and biological characteristics, were considered the control group. At the end of the study the ophthalmic evolution was different in the two groups. In the control group the degree of fluorescein leakage and the number of microaneurysms increased, while in the triflusal-treated group both parameters were reduced. There were no differences in visual acuity and computerised perimetry between the groups. Our results suggest that platelet antiaggregant therapy can be useful in the treatment of background diabetic retinopathy.
Diabetes Res Clin Pract 1989 Nov 06
PMID:Effect of treatment with an inhibitor of platelet aggregation on the evolution of background retinopathy: 2 years of follow-up. 269 31

Localization of the site of blood-retinal barrier breakdown in diabetes has been controversial. It has been particularly difficult to make assessments in clinical material where the use of tracer materials may not be practical. In this study, immunohistochemical staining for albumin was performed on paraffin-embedded eyes from patients with no known ocular disease and those with various stages of diabetic retinopathy. No extravascular albumin was detected in the retina or retinal pigment epithelium (RPE) of normal nondiabetics or diabetics with no ocular findings, but it was detected in 12.5% of mildly affected diabetics, 20% of background diabetic retinopathy cases, and 89% of proliferative diabetic retinopathy cases. The inner retinal vasculature appeared to be the primary site of leakage in diabetics because all cases demonstrating extravascular albumin-positivity expressed it in the inner retina. It usually permeated the vessel walls and spread along the inner surface of the retina. Some of these cases also contained albumin in the outer retina and RPE, suggesting that additional leakage also may occur through the RPE. A case of cytomegalovirus (CMV) retinitis showed albumin staining predominantly in the inner retina, whereas a rhegmatogenous retinal detachment showed only outer retina staining. These data suggest immunohistochemical staining for albumin may be a useful technique for localizing blood-retinal barrier breakdown.
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PMID:Immunohistochemical localization of blood-retinal barrier breakdown in human diabetics. 291 45

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

Many individual factors have been related to development of proliferative diabetic retinopathy. To evaluate possible interactions among these, a constellation of variables were studied in 22 patients with long duration of insulin-dependent diabetes mellitus for greater than 25 years, with minimal background diabetic retinopathy, and compared to 27 patients with insulin-dependent diabetes mellitus for a variable duration, but with bilateral proliferative retinopathy. The patients were compatible in age at onset of diabetes (12 +/- 2 in proliferative retinopathy group vs 12 +/- 1 yr in the background retinopathy group). Following initial standard statistical analyses, data were further analysed using Logistic Regression Analysis. In the proliferative retinopathy group males were more prevalent (2.9:1), and patients were treated with larger insulin doses (0.86 +/- 0.07 vs 0.59 +/- 0.04 U/Kg B.W., p less than 0.001). Systemic hypertension and neuropathy were more prevalent (p less than 0.02 and less than 0.004 respectively), and diastolic blood pressure was higher (87 +/- 3 vs 75 +/- 2, p less than 0.01). In the same group diet was higher in carbohydrate and the ratio of polyunsaturated to saturated fats was lower (p less than 0.03, less than 0.05 respectively). HbA1 was higher (0.127 +/- 0.004 vs 0.110 +/- 0.004%, p less than 0.004), but the mean of all available plasma glucose values was not different. Impaired renal function expressed by higher BUN, serum creatinine, and urinary protein and lower creatinine clearance was observed. Nerve conduction parameters were more significantly impaired and plasma triglycerides were higher (1.74 +/- 0.2 vs 0.85 +/- 0.1 mmol/l, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:An evaluation of factors associated with proliferative diabetic retinopathy. 383 35

The effect of plasma glucose control on retinal morphology, urinary albumin excretion and related haematological and lipid measurements was studied prospectively for 30 weeks in 17 patients with insulin-dependent diabetes mellitus. All had background diabetic retinopathy (BDR) and absence of albustix positive proteinuria: 9 were allocated to a continuous subcutaneous insulin infusion (CSII) group and 8 to a conventional therapy (CT) group. There was a sustained reduction (p less than 0.01) in haemoglobin A1 (HbA1) in the CSII group, but not in the CT group. Mean HbA1 over the 30 week study period was lower (p less than 0.05) in the CSII (8.9 +/- 0.3%) than the CT group (10.2 +/- 0.5%). Retinal morphology assessed by fluorescein angiography improved after 30 weeks in one patient in the CSII group, but in most patients it remained the same or deteriorated. The patient with the best plasma glucose control developed a small area of neovascularisation. Less deterioration in retinopathy was not related to better plasma glucose control. Urinary albumin excretion, plasma viscosity, plasma fibrinogen, red cell deformability and plasma lipids did not change in either the CSII or CT group. In the 7 patients selected from both groups who achieved the best control there was a reduction in urinary albumin and LDL cholesterol.
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PMID:The effect of plasma glucose control by continuous subcutaneous insulin infusion or conventional therapy on retinal morphology and urinary albumin excretion. 389 66

The brachial artery pressure and retinal artery pressure responses to a one-minute cold pressor test were evaluated simultaneously in 14 patients with type I diabetes mellitus (six with and eight without diabetic retinopathy) and 10 age-matched control subjects. Five patients with type I diabetes had autonomic neuropathy. Mean baseline brachial artery pressure and retinal artery pressure were similar in patients with type I diabetes and control subjects. After cold pressor testing, the brachial artery pressure increased significantly (p less than 0.01) compared with baseline values in both groups. Retinal mean arterial pressures increased significantly (p less than 0.001) after cold pressor testing compared with the baseline values only in patients with type I diabetes. Positive correlation was found between the brachial and retinal mean arterial pressures after cold pressor testing (r = 0.48; p less than 0.05) in the diabetic patients but not in the control subjects (r = 0.10; p = NS). No correlation was found between the retinal artery pressure and age of onset of diabetes, duration of diabetes, the presence or absence of diabetic retinopathy, and glycemic control. Four patients with autonomic neuropathy and low retinal artery pressures, which remained unchanged after cold pressor testing, had no diabetic retinopathy. The fifth patient with autonomic neuropathy and exaggerated systolic brachial artery pressure (175 mm Hg) and retinal artery pressure (more than 80 mm Hg) responses had severe background diabetic retinopathy. In conclusion, abnormal retinal artery responses to stress are present in patients with type I diabetes. This may be modified by the presence or absence of both autonomic neuropathy and hypertension. The biologic significance of these findings is yet to be determined.
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PMID:Abnormal retinal artery responses to stress in patients with type I diabetes. 398 37

Three patients (a 44-year-old woman, a 65-year-old man, and a 39-year-old woman) who had had diabetes mellitus for an average of 17 years had good vision and mild to moderate background diabetic retinopathy. These patients developed severe iron deficiency anemia from varying causes and their conditions rapidly progressed to a severe proliferative phase that necessitated panretinal photocoagulation and pars plana vitrectomy in two cases.
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PMID:Anemia and diabetic retinopathy. 403 31

The potential complications of cataract surgery in the general population are well known. In addition, cataract extraction in the patient with diabetes mellitus is associated with other potential complications common to this disease: neovascular glaucoma and acceleration of proliferative diabetic retinopathy with or without vitreous hemorrhage. We analyzed the records of 154 patients with diabetes mellitus who had undergone standard intracapsular cataract extraction in one eye only with the other eye serving as the unoperated control eye. We were able to determine the status of the diabetic retinopathy before the operation and to note the development of vitreous hemorrhage and rubeosis iridis/neovascular glaucoma after the operation. If either event occurred within six weeks of the surgery, it was considered to be a complication of the cataract extraction. Intracapsular cataract extraction in this diabetic population, without regard of the preoperative status of the retinopathy, was associated with a statistically significant incidence of postoperative rubeosis iridis/neovascular glaucoma (7.8% vs 0%). In patients with preoperative active proliferative diabetic retinopathy, the risk of developing postoperative rubeosis iridis/neovascular glaucoma was even higher (40% vs 0%). There was also a statistically significant incidence of vitreous hemorrhage after surgery in eyes with no diabetic retinopathy or background diabetic retinopathy (6.5% vs 0%). In patients with active proliferative diabetic retinopathy, there was an increased incidence of vitreous hemorrhage after surgery (20% vs 6.5%), but this was not statistically significant due to the small number of patients studied. Possible explanations for these findings are explored and therapeutic and prophylactic measures recommended.
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PMID:Neovascular glaucoma and vitreous hemorrhage following cataract surgery in patients with diabetes mellitus. 619 91

Recent investigations of retinal vascular cells in tissue culture, animal models, and diabetic human subjects suggest several potential pathogenetic mechanisms for diabetic retinopathy. These include the enzyme aldose reductase, which appears to be responsible for basement membrane thickening in galactosemic rats (since the lesion is prevented by an aldose reductase inhibitor), and a picture, in galactosemic dogs, that closely resembles early, background diabetic retinopathy; insulin, which stimulates, and elevated glucose levels, which inhibit in vitro proliferation of retinal pericytes. Various hormones, including the sex hormone, the insulin-like growth factors and, perhaps independently, growth hormones, may influence the later stages of diabetic retinopathy. Chronic hyperglycemia appears to be the primary pathogenetic agent in diabetic retinopathy as well as in other complications of diabetes, but the different rates of onset and progression of these complications suggest that glucose acts through different biochemical pathways that are probably under different genetic control. Finally, the locus of the primary biochemical lesion in diabetic retinopathy may reside in the neuronal or glial cells of the retina, with the retinal blood vessels only secondarily involved.
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PMID:On the pathogenesis of diabetic retinopathy. 620 41


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