Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have recently described heterogeneity in renal structure in non-insulin-dependent diabetic patients (NIDDM) with microalbuminuria (MA; defined as albumin excretion rate from 20 to 200 micrograms/min). Thus, at variance with IDDM patients, "typical" diabetic glomerulopathy by light microscopy is observed only in a third of NIDDM with MA (Category II, CII). Further, despite persistent MA, 30% of NIDDM have normal or near normal renal structure (Category I, CI). Another one-third shows "atypical" patterns of renal injury with absent or mild diabetic glomerular changes, associated with disproportionately severe tubulointerstitial lesions and/or arteriolar hyalinosis and global glomerular sclerosis (Category III, CIII). The aims of this study were to evaluate whether similar patterns of renal lesions could be confirmed in a larger group of NIDDM with MA and to investigate tubular function in order to understand the mechanisms underlying MA in NIDDM patients. Renal biopsies were performed in 53 NIDDM with MA. Categories I, II and III were found in 41%, 26% and 33% of NIDDM with MA, respectively. All 8 patients with proliferative diabetic retinopathy were in CII. We also studied the urinary daily excretion rate of alpha 1-microglobulin (alpha 1 m), a low molecular weight protein, which is a useful indicator of tubular function. alpha 1 m was markedly increased only in CII patients (CI vs. CII vs. CIII: 6.2 +/- 1.2 vs. 13.7 +/- 2.1 vs. 7.3 +/- 0.9 mg/day, ANOVA, P < 0.01). In conclusion, we confirm that there is heterogeneity in renal structure in NIDDM patients with MA. This heterogeneity is not due to renal diseases other than diabetes. Increased alpha 1 m and proliferative retinopathy are useful indicators of the subgroup of MA NIDDM patients with typical diabetic glomerulopathy. It is suggested that diabetic microangiopathy explains the simultaneous occurrence of typical diabetic glomerulopathy, proliferative retinopathy and tubular dysfunction in a subgroup of NIDDM patients with MA.
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PMID:Renal structure and function in non-insulin dependent diabetic patients with microalbuminuria. 940 19

Morphologic study of 38 specimens of epiretinal membranes obtained during transciliary vitrectomy in 26 patients with type I diabetes mellitus and 12 with type II diabetes with proliferative diabetic retinopathy of different stages was carried out. In proliferative diabetic retinopathy, new vessels grow mainly along the posterior (retinal) surface of the posterior hyaloid membrane. Sometimes, if there are defects in the posterior hyaloid membrane, proliferative tissue stratifies it and appears on the anterior (hyaloid) surface. We observed no growth of new vessels outside the posterior hyaloid membrane. The impossibility of clinical and mechanical separation of the posterior hyaloid membrane and tumor tissue permits us to regard the stages of proliferative process in diabetic retinopathy as stages in the alteration of the posterior hyaloid membrane proper. Five variants in the structure of proliferative tissue can be distinguished in diabetic retinopathy; we consider that these variants are stages in its development: 1) glial--with predominance of cell-free or hypocellular glial tissue; 2) glial vascular--with growth of thin-wall vessels into glial tissue; 3) glial vascular fibrous--with growth of porous fibrovascular membrane in glial tissue; 4) fibrovascular--with predominance of fibrovascular tissue; and 5) fibrous (cicatricial) hypocellular compact connective tissue with just few vessels or none at all. Reduction of new vessels, involution of proliferative tissue, and development of traction detachment of the retina are associated with the beginning of fibrous proliferation.
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PMID:[Posterior hyaloid membrane as structural base of growth of neovascular tissue in proliferative diabetic retinopathy]. 972 Mar 91

Several haemostatic abnormalities are associated with proliferative diabetic retinopathy. While abnormalities in plasma fibrinolytic activity have been described in diabetic retinopathy, platelets (a rich source of plasminogen activator inhibitor type 1, PAI-1) have received little attention. As a result, little is known about the fibrinolytic potential of circulating whole blood in diabetic retinopathy. The concentrations of tissue-type plasminogen activator (t-PA) and of its fast-acting inhibitor. PAI-1 were measured in plasma from eight patients with type 1 diabetes complicated by proliferative retinopathy, and from eight patients with type 1 diabetes and background or no retinopathy, matched for age, sex and duration of diabetes. The concentration of PAI-1 in platelets was also measured. The ratio of t-PTA to PAI-1 in plasma was significantly higher in patients with proliferative retinopathy than in those without (0.66 vs. 0.37, p < 0.02). The average quantity of PAI-1 per platelet was significantly lower in the group with proliferative retinopathy (0.33 vs. 0.50 ng/10(6) platelets, p < 0.02). These data suggest that among patients with type 1 diabetes, total circulating fibrinolytic potential is higher in those with proliferative retinopathy.
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PMID:Circulating tissue-type plasminogen activator and plasminogen activator inhibitor type 1 in proliferative diabetic retinopathy: a pilot study. 1066 20

In order to elucidate the relationships between posterior ocular structures, 48 samples of epiretinal membranes were examined, which were obtained during transcilliary vitrectomy for proliferative diabetic retinopathy of different stages (29 patients with type I diabetes mellitus and 19 with type 2). The findings of morphological analysis and preoperative ophthalmoscopy (color photographs) demonstrated clinical and morphological correlations of stages of proliferative diabetic retinopathy. Impossibility of differential diagnosis between posterohyaloid membrane and newly formed tissue by clinical methods and impossibility of their mechanical intraoperative separation allow us to regard the stages of proliferative process as stages in changes of the posterohyaloid membrane proper. The posterohyaloid membrane is detected clinically and morphologically only in the presence of pathological changes, including diabetic retinopathy. We detected the following clinical histological correlations of proliferative process stages in diabetic retinopathy: 1) glial; 2) glio-vascular; 3) glio-vascular-fibrous; 4) fibrovascular; 5) fibrous (cicatricial). The histology of stages of proliferative diabetic retinopathy and correlation of histological findings with the clinical (ophthalmoscopic) picture of the process are described in detail. Recommendations on the treatment of each of these stages are offered.
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PMID:[Pathological basis for clinical stages of the proliferative process in diabetic retinopathy]. 1209 28

A total number of 100 patients were examined over a period of one year to find out any correlation between diabetic maculopathy and diabetic nephropathy. Twenty-two belonged to insulin dependent diabetes mellitus group and 78 patients were in the non-insulin dependent diabetes mellitus group who were suffering from diabetes over a period of 0-25 years and more. Another group comprising 6 patients were chosen from these 100 patients who were suffering from nephropathy diagnosed clinically and on pathological investigations. Background and proliferative--both types of diabetic retinopathy were found with increased incidence with the persistence of the disease in both types of diabetes mellitus. Nine patients had diabetic maculopathy, out of which 6 patients (66.66%) were suffering from diabetic nephropathy. Proliferative diabetic retinopathy is more common in insulin dependent diabetes mellitus than in non-insulin dependent diabetes mellitus of more than 25 years of duration. Maculopathy is more common in non-insulin dependent diabetes mellitus and there is strong correlation between diabetic maculopathy and diabetic nephropathy.
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PMID:Association of diabetic maculopathy with diabetic nephropathy--a study. 1600 29

The knowing of the ocular consequences of diabetes is essential for the evaluation of the risk factors for the cataract surgery. The clinical study was made on a total number of 19 diabetic patients (3 with insulin dependent diabetes and the rest with noninsulin dependent diabetes), which were operated for cataract from september 2001 till march 2002. Preoperatory preparation presumed a good metabolic control of diabetes and a very carefully examination of the retina. The surgical technique was the extracapsular cataract extraction, followed by the implantation of a posterior chamber IOL, respectively phacoemulsification with the implantation of a foldable lens. The presence of a proliferative diabetic retinopathy, of a rubeosis iridis, of the neovascularization of the angle, or the preexistence of the vitreoretinal surgery (vitrectomy) were the main factors which dictated the anatomical and functional postoperatory prognosis. In conclusion, evenly the diabetic patient is a highly risk patient, the adequate preoperator preparation, the right treatment and a carefully follow-up could assure the success of the surgery in those cases.
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PMID:[Particular aspects of treatment in diabetic eye cataract]. 1272 95

Selective loss of retinal pericytes is the earliest histopathological hallmark in diabetic retinopathy. Various structural and functional abnormalities in diabetic retinas are the consequent of the loss of pericytes. Therefore, elucidating the molecular mechanisms for pericyte loss and targeting this characteristics change in early diabetic retinopathy may help to slow the development and progression of sight-threatening retinopathy in diabetes. Protein kinase C (PKC) inhibition has been used in therapeutic trials intended to reduce the incidence of proliferative diabetic retinopathy. However, we speculate that it is likely to do more harm than good in diabetic retinopathy because PKC inhibition augments pro-apoptotic effects of high glucose on cultured retinal pericytes. In the DCCT-Epidemiology of Diabetes Interventions and Complications Research, the reduction in the risk of progressive retinopathy resulting from intensive therapy in patients with type 1 diabetes persisted for at least four years, despite increasing hyperglycemia. These clinical studies strongly suggest that so-called "hyperglycemic memory" causes vascular damage in diabetic retinopathy. Glucose react non-enzymatically with the amino groups of proteins to initiate a complex series of rearrangement and dehydration reactions to produce a class of irreversibly cross-linked, fluorescent moieties, termed advanced glycation end products (AGEs). The formation and accumulation of AGEs progress at an extremely accelerated rate in diabetic retinas, and these products have been implicated in the pathogenesis of loss of pericytes in diabetic retinopathy. The nature of AGEs is most compatible with the theory of 'hyperglycemic memory' as well. We hypothesize here that PKC inhibition is likely to do harm in diabetic retinopathy, while inhibition of AGE formation might be a promising therapeutic strategy for treatment of this devastating complication.
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PMID:Inhibition of protein kinase C might be harmful to diabetic retinopathy. 1519 66

Few epidemiological data exist regarding the correlation of anatomic measures of diabetic retinopathy and nephropathy, especially early in the disease processes. The aim of this study was to examine the association of severity of diabetic retinopathy with histological measures of diabetic nephropathy in normoalbuminuric patients with type 1 diabetes. The study included participants (n = 285) in the Renin-Angiotensin System Study (RASS; a multicenter diabetic nephropathy primary prevention trial) who were aged >/=16 years and had 2-20 years of type 1 diabetes with normal baseline renal function measures. Albumin excretion rate (AER), blood pressure, serum creatinine, and glomerular filtration rate (GFR) were measured using standardized protocols. Diabetic retinopathy was determined by masked grading of 30 degrees color stereoscopic fundus photographs of seven standard fields using the Early Treatment Diabetic Retinopathy Study (ETDRS) severity scale. Baseline renal structural parameters, e.g., fraction of the glomerulus occupied by the mesangium or mesangial fractional volume [Vv(Mes/glom)] and glomerular basement membrane width, were assessed by masked electron microscopic morphometric analyses of research percutaneous renal biopsies. No retinopathy was present in 36%, mild nonproliferative diabetic retinopathy in 53%, moderate to severe nonproliferative diabetic retinopathy in 9%, and proliferative diabetic retinopathy in 2% of the cohort. Retinopathy was not related to AER, blood pressure, serum creatinine, or GFR. All renal anatomical end points were associated with increasing severity of diabetic retinopathy, while controlling for other risk factors. These data demonstrate a significant association between diabetic retinopathy and preclinical morphologic changes of diabetic nephropathy in type 1 diabetic patients.
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PMID:The relationship of diabetic retinopathy to preclinical diabetic glomerulopathy lesions in type 1 diabetic patients: the Renin-Angiotensin System Study. 1567 11

During the 1997-2002 period, 48 eyes of 41 patients of the mean age 58 years were operated on because of complications of proliferative diabetic retinopathy. In the cohort of operated patients, the type I diabetes mellitus was determined in 10 (21%) cases, the type II diabetes mellitus in 36 (75%) cases, and in two cases (4%), another type of diabetes was detected. One patient of those two had LADA type diabetes and the second one had secondary diabetes due to chronic pancreatitis. In the early postoperative period, or during first three months postoperatively, after the pars plana vitrectomy, the visual acuity (VA) in 28 (59%) eyes improved, in 16 (33%) eyes remained the same, and in 4 eyes (8%) worsened. VA 1/60 (0.017 or 3/200) and better had 37 (77%) eyes, VA 6/60 (0.1 or 20/200) and better had 17 (37%) eyes, and VA 6/12 and better (0.5 or 20/40) had 3 (6%) eyes only. VA worse than 1/60 (0.017 or 3/200) had 11 (23%) eyes. Authors emphasize the importance of regular and detailed ophthalmologic examinations with early diagnosis of pathological changes and early start of adequate treatment.
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PMID:[Early functional effect of the pars plana vitrectomy in complications of the proliferative diabetic retinopathy]. 1578 55

Individuals with type 1 diabetes have mild performance deficits on a range of neuropsychological tests compared with nondiabetic control subjects. The mechanisms underlying this cognitive deterioration are still poorly understood, but chronic hyperglycemia is now emerging as a potential determinant, possibly through microvascular changes in the brain. In 24 type 1 diabetic patients, we tested at euglycemia and at acute hypoglycemia whether the presence of proliferative diabetic retinopathy, as a marker of microvascular disease, adversely affects the ability of the brain to respond to standardized hypoglycemia, using functional magnetic resonance imaging with a cognitive task. Patients with retinopathy, compared with patients without, showed less deactivation (hence, an increased response) in the anterior cingulate and the orbital frontal gyrus during hypoglycemia compared with euglycemia (P < 0.05). Task performance and reaction time were not significantly different for either group. We conclude that microvascular damage in the brain of patients with retinopathy caused this increased brain response to compensate for functional loss.
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PMID:Microvascular disease in type 1 diabetes alters brain activation: a functional magnetic resonance imaging study. 1644 65


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