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

Of 148 adults with sickle cell hemoglobin C (SC) disease seen at Cook County Hospital and Clinics, Chicago, Illinois, eight patients had coexistent noninsulin-dependent diabetes mellitus. The clinical findings were notable for the paucity of retinal vascular changes. No patient showed proliferative diabetic retinopathy; one patient showed background diabetic retinopathy consisting of a few microaneurysms. Six of the eight patients showed no lesions of proliferative sickle retinopathy. Coexistence of noninsulin-dependent diabetes mellitus and SC disease does not appear to have an additive adverse effect on the presence or severity of proliferative retinopathy in the affected patient.
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PMID:Concurrent sickle cell hemoglobin C disease and diabetes mellitus: no added risk of proliferative retinopathy? 796 31

The development of drugs in order to block metabolic pathway of glucose responsible for diabetic vascular dysfunction is in progress. Aldose reductase inhibitors prevent or reduce the different components of vascular dysfunction, cataract, neuropathy and nephropathy in animal models of diabetes. Promising results have been observed in diabetic patients concerning the prevention of neuropathy and of retinopathy. Larger scale studies with the second generation compounds are in progress. Glycation inhibitors, mainly aminoguanidine, have been shown to prevent or reduce vascular dysfunction and microvascular complications in animal models. Trials in diabetic patients with aminoguanidine are just beginning. Anti-oxidant therapy is also at its early stage of development (vitamin E, vitamin C, alpha lipoic acid). Antiplatelet agents (aspirin, ticlopidine) have been demonstrated to reduce the progression of non proliferative diabetic retinopathy. Angiotensin converting enzyme inhibitors are of particular interest in preventing diabetic glomerulopathy.
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PMID:[Preventive treatment of diabetic microangiopathy: blocking the pathogenic mechanisms]. 800 9

Vitreous haemorrhage is a serious complication of proliferative diabetic retinopathy: it provides evidence of the severity of at proliferative retinopathy at stake and precludes laser photocoagulation. In some cases of moderate vitreous haemorrhage, panretinal photocoagulation remains possible especially using longer wavelengths such as krypton red; cryotherapy under ophthalmoscopic control may be an alternative to panretinal photocoagulation. Development of pars plana vitrectomy, however, has been the main break the rough in the management of severe vitreous haemorrhage. Pars plana vitrectomy was first reserved to massive, long-standing vitreous haemorrhage; improvements in instrumentation and techniques, as well as observations of the favourable effect of vitrectomy on the progression of proliferative retinopathy led to enlarged indications for pars plana vitrectomy. Beyond severity and duration of visual loss, main arguments for pars plana vitrectomy are bilaterality, lack of previous panretinal photocoagulation, iris neovascularization, Type 1 diabetes, and severity of fibrovascular proliferation.
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PMID:[Vitreous hemorrhage: attitudes in therapy, vitrectomy]. 805 23

We measured the breakdown of the blood-aqueous barrier in 63 patients with diabetes (126 eyes) by using a laser flare meter. Of 126 eyes, 40 had no retinopathy, 34 had proliferative retinopathy, 24 had regressed proliferative retinopathy, 14 had background retinopathy, and 14 had maculopathy. Eyes were classified into one category only. Mean flare was greater for proliferative retinopathy compared to background retinopathy (P = .0065), no retinopathy (P = .0001), and maculopathy (P = .0189). Flare values were greater for regressed proliferative retinopathy compared to no retinopathy (P = .0118) (paired Student's t-test). Diabetic eyes without demonstrable retinopathy still had higher flare values than control eyes without diabetes. The length of diabetes was greater for those eyes with proliferative diabetic retinopathy (P = .0195), regressed proliferative diabetic retinopathy (P = .0625), and background diabetic retinopathy (P = .006) compared to those with no retinopathy. No significant difference was noted in duration of diabetes for eyes with diabetic maculopathy when compared to those with no retinopathy (P = .5788). Breakdown of the blood-aqueous barrier precedes the development of retinopathy, and the more severe proliferative forms have greater blood-aqueous barrier dysfunction.
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PMID:Studies of the blood-aqueous barrier in diabetes mellitus. 782 83

Parameters of fibrinolysis, including basal plasma tissue type plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) antigen levels were studied in 49 non-insulin dependent diabetic patients (23 men, 26 women: ages 51.3 +/- 14.9 years) and 16 age matched non-diabetic subjects (9 men, 7 women ages 49.8 +/- 12.2 years) as a control group. Compared to a control group, the diabetic patients had a significantly higher mean plasma t-PA antigen (4.94 +/- 2.68 vs 3.20 +/- 2.30 ng/ml) and PAI-1 antigen (34.86 +/- 16.71 vs. 17.60 +/- 15.36 ng/ml) levels (P < 0.05). Significant univariate correlations were observed between t-PA and body mass index (BMI) (P = 0.0009, r = 0.7217), and PAI-1 were positively correlated with BMI and FBS (fasting blood sugar) in the total diabetic patients (P = 0.0003, r = 0.7217; P = 0.0477, r = 0.2858, respectively). In diabetic patients with proliferative diabetic retinopathy, both PAI-1 and t-PA antigen levels were significantly lower than those of diabetic patients with negative or background retinopathy (P = < 0.05). There were no significant differences of the plasma t-PA and PAI-1 levels between diabetic patients with micro- and macroproteinuria. This study conducted on non-insulin dependent diabetic patients suggests that they have significantly higher t-PA and PAI-1 antigen levels than do control subjects, and these findings appear to correlate negatively with proliferative retinopathy observed among the patients studied.
Diabetes Res Clin Pract 1994 Jan
PMID:Plasma t-PA and PAI-1 antigen concentrations in non-insulin dependent diabetic patients: implication for diabetic retinopathy. 820 Feb 93

Lipid peroxide (LPO) levels, as determined by high-performance liquid chromatography (HPLC) and by the thiobarbituric acid (TBA) method, and myeloperoxidase (MPO) activity in vitreous of patients vitrectomized because of proliferative diabetic retinopathy were compared with LPO levels and MPO activity in vitreous of patients with no vitreoretinal proliferation. Both LPO levels and MPO activity were significantly elevated in the vitreous of patients with fibrovascular vitreoretinal proliferations secondary to diabetes. The TBA method produced higher values for LPO levels than did the HPLC method. The correlation between the two methods was 0.94. Our results suggest that both oxygen-free radicals and inflammation-related reactions can participate in the pathogenesis of diabetic retinopathy.
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PMID:Increased lipid peroxide levels and myeloperoxidase activity in the vitreous of patients suffering from proliferative diabetic retinopathy. 825 99

The prevalence of retinopathy was studied in a group of 1179 diabetic patients attending 11 diabetologic centres in Gallica (Northwest of Spain). The age of the patients was 61.7 +/- 13.8 years, 43.8% were males and 56.2% females. The patients had had diabetes from 8.4 +/- 7.5 years, 30.4% were being treated with insulin, and 69.6% with oral antihyperglycaemics. 16.1% were aged under 40 years at onset as against 83.9% aged over 40 years. The prevalence of retinopathy was 44.7, in the whole group. Stepwise multiple regression analysis identified treatment time since onset and age at onset as the factors affecting prevalence, which was 61.8% in the insulin-treated subgroup vs 37% among those treated with oral antihyperglycaemics (p < 0.0001). The prevalence of proliferative diabetic retinopathy was 5.8% in the whole group.
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PMID:The prevalence of diabetic retinopathy in northwest Spain. An epidemiological study of diabetic retinopathy in Galicia. I. 847 9

Diabetic retinopathy is the main cause of decreased visual acuity in non-proliferative or proliferative diabetic retinopathy. The frequency of maculopathy rises with age and the duration of diabetes, and now represents the major therapeutic problem following the control of neovascular proliferation through pan-retinal photocoagulation. Oedematous maculopathy, focal or diffuse, and cystoid macular oedema are improved by laser photocoagulation, either focal or grid. Laser photocoagulation is not indicated for predominantly ischaemic maculopathy. The laser treatment should be carried out early in the stage of clinically significant oedema, and applied either focally or in a grid depending on the clinical and angiographic features of the diabetic maculopathy. If pan-retinal photocoagulation is also indicated it should be performed after the focal macular treatment. Laser treatment should always be accompanied by a general medical assessment, emphasising optimal glycemic control and control of associated risk factors, especially arterial hypertension.
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PMID:[Laser photocoagulation treatment of diabetic maculopathy]. 858 Dec 35

The aim of the study was to define the relationship between the presence of proliferative diabetic retinopathy and nephropathy with objectively defined autonomic neuropathy in non-insulin-dependent diabetes mellitus (NIDDM) patients. The research design used was a cross-sectional, case control study. A cohort of NIDDM patients was classified, according to five cardiovascular autonomic tests described by Ewing, as: (1) no involvement--no abnormal tests (n = 17); (2) cardiovascular autonomic neuropathy--two out of five abnormal tests (n = 18). Age, age at diagnosis, plasma creatinine, fasting plasma glucose, glycated haemoglobin and blood pressure measurements were not statistically different among the two groups. According to indirect ophthalmoscopy and the presence of macroproteinuria and microalbuminuria, respectively, patients were also classified as having proliferative, non-proliferative or no retinopathy and with or without nephropathy. The results showed a striking relationship between cardiovascular autonomic neuropathy and proliferative diabetic retinopathy. Relative odds for nephropathy, non-proliferative diabetic retinopathy and proliferative retinopathy were, respectively, 16.0, 10.1 and 34.7. When odds ratios were adjusted for the presence of nephropathy, hypertension, non-proliferative and proliferative retinopathy, only proliferative retinopathy was significantly associated (odds ratio, 7.1). It was concluded that in NIDDM the presence of cardiovascular autonomic neuropathy is strongly associated with proliferative retinopathy. Long-term prospective studies on large cohorts of patients must be done to evaluate if having autonomic dysfunction would be a risk factor or a risk indicator of an etiologic process underlying the development of proliferative retinopathy.
Diabetes Res Clin Pract 1995 Sep
PMID:Proliferative diabetic retinopathy is related to cardiovascular autonomic neuropathy in non-insulin-dependent diabetes mellitus. 859 8

In Caucasian patients with insulin-dependent diabetes mellitus (IDDM) proliferative diabetic retinopathy (PDR) and persistent proteinuria (PP) are associated, and major risk factors for development of microangiopathy have been identified. The aim of the present study was to evaluate whether these risk factors are also relevant and whether an association exists between the microangiopathic complications in Japanese IDDM-patients. A clinic-based cohort of 324 Japanese IDDM-patients was followed (a mean follow-up of 7 years). Annual examination for development of PDR and PP was performed. Fifty-eight patients developed PDR and 24 developed PP. Development of PDR was associated to high HbA1c-levels, i.e., the 4th quartile (RR 7.9, P < 0.0001), background retinopathy at admission (RR 9.9, P < 0.0001), high age at diabetes onset (RR 2.9, P < 0.0001) and female gender (RR 1.7, P < 0.05). Development of PP was associated to high HbA1c-levels (RR 2.8, P < 0.001) and background background retinopathy at admission (RR 7.9, P < 0.0001). The risk of developing PP was 9 times higher in patients developing PDR than in patients not developing PDR (P < 0.0001). The effect of metabolic control in our cohort was similar to that found in the DCCT and SDIS studies. In conclusion, development of PP is closely associated with PDR, also in Japanese IDDM-patients. The effect of metabolic control is the same as in Caucasian patients. Development of malignant angiopathy in IDDM-patients is not confined to Caucasian IDDM-patients, and the incidence rates are comparable to those found in Caucasian IDDM.
Diabetes Res Clin Pract 1995 Sep
PMID:Metabolic regulation and microangiopathy in a cohort of Japanese IDDM-patients. 859 14


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