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Diabetic retinopathy, treated with

Lanthony P, Cosson JP (1988) The course of color vision in early diabetic retinopathy treated with Ginkgo biloba extract. A preliminary double-blind versus placebo study. J Fr Ophtahnol ll(10) 671-674... [Pg.3412]

Jonas et al. (45) found no significant effect of intravitreal triamcinolone on blood glucose in a series of diabetic patients treated with intravitreal triamcinolone after pars plana vitrectomy for proliferative diabetic retinopathy. [Pg.78]

Looukovaara S, Immonen I, Teramo KA, Kaaja R. Progression of retinopathy during pregnancy in type 1 diabetic women treated with insulin lispro. Diabetes Care 2003 26 1193-1198. [Pg.252]

Frystyk J, Chantelau E. Progression of diabetic retinopathy during improved metabolic control may be treated with reduced insulin dosage and /or somatostatin analogue administration - a case report. Growth Horm IGF Res 2005 15 130-5. [Pg.421]

Intensive pharmacologic treatment of diabetes is known to decrease the risk for microvascular events such as nephropathy and retinopathy, but there is less evidence that it decreases macrovascular disease (28,29). DCCT/EDIC trial, however, demonstrated reduction in CVD (nonfatal Ml, stroke, death from CVD, confirmed angina, or the need for coronary-artery revascularization) in patients with type I diabetes assigned to intensive diabetes treatment compared with conventional treatment by 42% (p = 0.02) (30). Patients with lower extremity PAD and both type I and type 2 diabetes should be treated to reduce their glycosylated hemoglobin (Hb AIC) to less than 7%, per the American Diabetes Association recommendation (31). Subanalysis of the UKPDS showed no evidence of a threshold effect of Hb AIC a I % reduction in Hb Al C was associated with a 35% reduction in microvascular endpoints, an 18% reduction in Ml, and a 17% reduction in all-cause mortality. Frequent foot inspection by patients and physicians will enable early identification of foot lesions and ulcerations and facilitate prompt referral for treatment (32). [Pg.516]

In a related study, streptozotocin-induced diabetic rats were treated with pyridox-amine, vitamin E, and enalapril (7V-(l-[ethoxycarbonyl -3-phcny I propyl)-Ala-Pro), an AGE/ALE inhibitor, an antioxidant, and an ACE-inhibitor, respectively.598 Diabetic hyperglycaemia was accompanied by severe dyslipidaemia. Treatment with pyridoxamine was the most effective in reducing lipid abnormalities and in retarding nephropathy, retinopathy, and protein modification. Vitamin E was the next most effective treatment in retarding nephropathy, but did not affect retinopathy or AGE/ALE formation. Enalapril normalised blood pressure and retarded nephropathy and the accumulation of CML in the kidney, but did not affect dyslipidaemia and retinopathy. Thus pyridoxamine is the most effective therapy overall. [Pg.166]

Two years ago she developed hypertension, which was treated with ben-droflumethiazide, 5mg daily. At that time, her blood urea level was 8.2 mmol/L, serum creatinine was 80 pmol/L, and dipstick urinalysis was negative for protein. She was also noted to have non-proliferative diabetic retinopathy, and given a course of laser treatment. [Pg.361]

Diabetic retinopathy can lead to blindness becanse of an abnormally high synthesis of connective tissne to repair leaking capillaries and to form new capillaries. Twelve adult diabetics treated with 600 mg of anthocyanins per day for 2 months had a significant decrease in the biosynthesis of connective tissue, especially polymeric collagen and stracture glycoproteins in gingival tissue. ... [Pg.15]

HPI DK is a 62-year-old woman with type 2 diabetes for 5 years. She has been treated with giyburide for 4 years. She follows dietary recommendations (low fat distributes carbohydrates throughout her three meals a day) to the best of her ability and walks 30 minutes three times weekly. At a routine veit with her primary care provider, her FBG is 180 mg/dL. She does not monitor her blood glucose at home and does not have a glucose meter. She is a nonsmoker and her father has type 2 diabetes. Her only long-term diabetes complication is background diabetic retinopathy. [Pg.63]

Diabetic retinopathy (Oslo Study), motor nerve conduction and glomerular hyperfiltration were less progressive in patients treated with CSII or MDI compared with conventional insulin therapy (Dahl-Jorgensen, 1987). An improvement of retinopathy with CSII was reported in the KROC Study Group (1988) (Fig. 14). [Pg.73]

Recently, macular edema associated with uveitis (29), diabetic retinopathy (30), and central retinal vein occlusion (31,32) has been treated with intravitreal injection of triamcinolone acetonide. Macular edema decreased after treatment but recurred three to six months after injection. A sustained-release steroid delivery system may be more attractive than a simple injection of triamcinolone as it could reduce or eliminate the need for multiple intravitreal injections. [Pg.180]

Recently, intravitreal triamcinolone acetonide has been used clinically to treat retinal vascular disease (Fig. 4). A case report by Jonas and Sofker (32) described a patient with nonproliferative diabetic retinopathy and a six-month history of persistent, diffuse macular edema despite grid photocoagulation. Following one intravitreal injection of triamcinolone acetonide, the visual acuity of this patient improved from 20/200 to 20/50 over a five-month follow-up period. It was also noted that there was marked regression of macular edema on clinical examination. Martidis et al. (33,34) reported on the use of intravitreal triamcinolone for refractory diabetic macular edema. Sixteen eyes with a macular thickness of at least 300 pm despite prior photocoagulation were treated with 4 mg injections of triamcinolone. At three-month follow-up the mean decrease in central retinal thickness was 57.5%, with a visual acuity increase of 2.4 Snellen lines. Those with six-month follow-up demonstrated some recurrence of edema and visual acuity improvement was reduced to 1.3 lines. [Pg.306]

One of the hypotheses for the development of vascular occlusion that precedes proliferative diabetic retinopathy is that disturbances in the thrombocyte aggregation lead to leukostasis and formation of microthrombosis in the retinal capillaries. Consequently, attention has been focused at treating diabetic retinopathy with inhibitors of thrombocyte aggregation. However, a prospective study has shown that acetyl salicylic acid does not reduce the development of diabetic retinopathy. Additionally, this treatment does not increase the risk of developing complications such as vitreous hemorrhage. This is important evidence since inhibitors of thrombocyte aggregation are often used to reduce the risk of the development of the macrovascular complications of the disease [12]. [Pg.257]

Lasers in medicine Francis L Esperance begins using the argon-ion laser to treat patients with diabetic retinopathy. [Pg.2068]

Pituitary ablation with Y was successful in 2 of 5 patients with diabetic retinopathy but hyporesponsiveness of the hypophysis to stress caused death in 4 patients (Lomsky et al., 1966). However, such implants can control retinopathy and preserve the patient s sight (Jauregui et al., 1968). The procedure was used in 22 patients with 75% showing distinct improvement but 5 others died of complications (Ray et al., 1968). The cotton wool spots of diabetic retinopathy, when treated by Y pituitary implantation, disappear in about 2.3 months but the capillary closure persists (Kohner et al., 1969). New capOlaries arise from the optic disc after Y implantation but results are better in patients below 40 years of age (Panisset et al., 1971). Such treatment is also beneficial in cases of the thyrotoxic malignant exophthalmos but the patients may develop adrenocortical insufficiency and gonadal hypofunction (Molinatti, 1964). [Pg.577]


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