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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the present study was to determine the prevalence of and the host factors for asymptomatic pyuria (ASP) in women with type 2 diabetes. The study included 179 type 2 diabetic women and consecutive 455 non-diabetic women attending as out-patients in 1996. Patients with symptoms of a urinary tract infection were excluded. ASP was defined as the presence of more than 10 leukocytes/high-power field in a random urine sample. Diabetic women more often had ASP than non-diabetic women (27.9 vs. 15.8%, P<0.001). The prevalence of ASP was significantly increased in patients with a duration of diabetes exceeding 15 years (0 approximately 4 years; 20.3%, 5 approximately 9 years; 24.3%, 10 approximately 14 years; 23.8%, and > or =15 years; 46.3%). No differences were evident in HbA(1C) between diabetic patients without ASP and those with ASP. Diabetic women with ASP more often had diabetic retinopathy, neuropathy, nephropathy, cerebrovascular disease, ischemic heart disease, and hyperlipidemia than those without ASP. However, no statistically significant differences were evident in the prevalence of hypertension, constipation, or dementia. As the degree of neuropathy increases, it is accompanied by an increasing prevalence of ASP (none, 21.4%; blunt tendon reflexes, 24.5%; symptomatic, 50.0%; and gangrene, 66.6%). The prevalence of ASP was significantly increased in the patients with proliferative diabetic retinopathy (none, 23.2%; background, 29.4%; pre-proliferative, 18.2%; and proliferative, 50.0%). As the degree of nephropathy increases, it is accompanied by an increasing prevalence of ASP (none, 20.0%; microalbuminuria, 31.9%; macroalbuminuria, 37.0%; and renal failure, 60.0%). Thus, the prevalence of ASP is increased in women with diabetes and increased with longer duration of diabetes but was not affected by glucose control. The incidence of ASP increases significantly as diabetic microangiopathy becomes severer.
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PMID:Asymptomatic pyuria in diabetic women. 1159 24

We performed a retrospective study of serum factors associated with neovascular glaucoma that can occur following vitrectomy for proliferative diabetic retinopathy. The medical records of 183 patients (241 eyes) who received vitrectomy between August 1996 and August 2000 were studied retrospectively and subsequently analyzed by linear logistic regression analysis and multiple logistic regression tests. Neovascular glaucoma developed at an average of 2.7 months in 31 of 241 eyes (14.1%). The overall anatomical success rate of retinal attachment was 82.5% (199 eyes in 241 eyes), although it decreased to 45.1% (14 eyes in 31 eyes) in eyes with neovascular glaucoma. Serum cholesterol (P = 0.041) and fibrinogen levels (P = 0.020) were significantly associated with the development of neovascular glaucoma. However, no significant association could be found concerning hypertension, diabetic retinopathy or hypercholesterolemia (P > 0.05). We suggest that serum creatinine, cholesterol and fibrinogen levels can be used to predict the development of neovascular glaucoma in vitrectomized eyes with diabetic retinopathy and can further provide a more active approach to preventing the development of this condition.
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PMID:Serum factors associated with neovascular glaucoma following vitrectomy for proliferative diabetic retinopathy. 1181 87

Diabetic retinopathy is the most prevalent microvascular complication of diabetes mellitus and affects the majority of patients who have suffered diabetes for at least 20 years. Due to the lack of specific symptoms screening of patients is required for early retinal lesions to be detected. Chronic hyperglycemia plays a predominant role in the pathogenesis of the disease. A common denominator of hyperglycemic vascular injury is the increased production of mitochondrial reactive oxygen species, leading to the activation of protein kinase C, of the aldose reductase pathway, and to the increased formation of advanced glycation end products, with the well-described deleterious effects on the microvasculature. Moreover, hypertension and factors such as puberty and pregnancy can worsen retinopathy. Effective screening and therapy can prevent blindness. A distinction is made between proliferative and non-proliferative diabetic retinopathy and diabetic macula oedema. The professional associations of ophthalmologists and internists have drawn up guidelines for the necessary examinations, for therapy and the appropriate intervals between check-ups. Laser photocoagulation can halt further loss of vision, in particular in cases of proliferative diabetic retinopathy and diabetic macula oedema. Vitrectomy is an operative procedure that can bring about a functional improvement even for patients in advanced stages.
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PMID:[Epidemiology, pathogenesis and therapy of diabetic retinopathy and maculopathy]. 1201 60

Despite the beneficial effects of good glycaemic control, loss of vision because of diabetic retinopathy (DR) still occurs. Recent studies have suggested that hypertension is a risk factor for the development and progression of DR and that blood pressure reduction can delay the progression of retinopathy. The renin-angiotensin system is activated by chronic hyperglycaemia, and the vitreous fluid level of angiotensin II (AII) is elevated in patients with proliferative diabetic retinopathy and diabetic macular oedema. AII increases vascular permeability and promotes neovascularization. It has been suggested that an autocrine-paracrine relationship may exist between AII and vascular endothelial growth factor in the ocular tissues. Accordingly, angiotensin-converting enzyme inhibitors or AII Type 1 (AT1) receptor blockers may be useful therapeutic agents for preventing the progression of DR.
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PMID:Pathogenesis of diabetic retinopathy and the renin-angiotensin system. 1462 51

Diabetic retinopathy, a retinal microangiopathy, is the leading cause of blindness for persons aged 20 to 65 years in the United States. Routine screening and early treatment are cost-effective and have been shown to help preserve sight. Primary care physicians play a key role in treatment of systemic factors that lead to poor outcomes and referral to an ophthalmologist or a retinal specialist for screening and local treatment. This article, the first of two on retinal vascular disease, provides a review of nonproliferative and proliferative diabetic retinopathy. The second article, which will appear in an upcoming issue of POSTGRADUATE MEDICINE, discusses retinal vascular disease in hypertension.
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PMID:Diabetic retinopathy. Control of systemic factors preserves vision. 1527 89

In a previous article (July 2004, page 57), Dr Colucciello reviewed nonproliferative and proliferative diabetic retinopathy. In this article, he discusses retinal vascular disease associated with hypertension, which is especially likely to occur in persons with vasculopathic risk factors. Retinal vein occlusion, retinal arterial macroaneurysm, retinal artery occlusion, and carotid artery disease are predictive of progressive systemic vascular disease. Modification of risk factors and prompt identification of retinal vascular disease optimize vision outcomes and preserve quality of life.
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PMID:Retinal vascular disease in hypertension. Risk factor modification optimizes vision outcomes. 1620 1

Pigment epithelium-derived factor (PEDF) is a natural extracellular component of the retina with neuronal differentiating activity. Decreased levels of PEDF in the mammalian eye have been shown to participate in proliferative diabetic retinopathy. In addition, we have recently found in in vitro experiments that PEDF protected against pericyte apoptosis, the earliest histopathological hallmark of diabetic retinopathy. These observations suggest that the loss of PEDF in the mammalian eye plays an important role in the development and progression of diabetic retinopathy. However, the functional role of endothelial cell (EC)-derived PEDF in pericyte survival and the regulation of PEDF gene expression remain to be elucidated. In this study, we examined the effects of anti-PEDF antibody (Ab) on the viable cell number of cocultured pericytes with microvascular ECs. We further studied the effects of angiotensin II (Ang II) on PEDF gene expression in ECs. Anti-PEDF Ab significantly inhibited the growth-stimulating effects of cocultured ECs on pericytes. Furthermore, Ang II significantly decreased PEDF mRNA levels in ECs, which was completely reversed by an Ang II type 1 receptor blocker, telmisartan. Our present results suggest that PEDF is an EC-derived mitogen or survival factor for retinal pericytes. Suppression by Ang II of the EC-derived PEDF may be involved in exacerbation of diabetic retinopathy in patients with hypertension.
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PMID:Pigment epithelium-derived factor is a pericyte mitogen secreted by microvascular endothelial cells: possible participation of angiotensin II-elicited PEDF downregulation in diabetic retinopathy. 1644 May 85

Exogenous recombinant human erythropoietin (rHuEPO) is a beneficial therapeutic agent for correction of anemia in both chronic kidney disease (CKD) and end-stage renal disease (ESRD) patients. Transfusion requirements in ESRD patients are reduced significantly and anemia management is much improved. Despite widespread use and near-universal exposure of ESRD patients to the drug, rHuEPO remains an effective and safe product. However, a number of nonhematologic complications are described with rHuEPO therapy. Most notable is hypertension, whereas the connection between seizure and enhanced thrombosis is less clear. A possible complication recently described is exacerbation of proliferative diabetic retinopathy. Finally, other less common adverse effects, although rare in most patients, should be recognized as such by physicians who prescribe rHuEPO.
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PMID:Nonhematologic complications of erythropoietin therapy. 1689 4

People with diabetes have an increased risk of developing microvascular complications, diabetic retinopathy, diabetic nephropathy and diabetic neuropathy, which, if undetected or left untreated, can have a devastating impact on quality of life and place a significant burden on health care costs. In addition, diabetic microvascular complications can reduce life expectancy. The strongest risk factors are glycaemic control and diabetes duration; however, other modifiable risk factors such as hypertension, hyperlipidaemia and smoking, and unmodifiable risk factors including age at onset of diabetes and genetic factors may all play a part. Along with the presence of external risk factors, some associations have also been noted between diabetic microvascular complications themselves. There is evidence that diabetic retinopathy in association with increased blood pressure is an important risk factor for diabetic nephropathy progression. Significant correlations have also been shown between the presence of diabetic peripheral neuropathy and the presence of background or proliferative diabetic retinopathy. Clinical trials are currently in progress looking at a number of approaches to designing treatments to prevent the adverse effects of hyperglycaemia. It is essential however, that risk factors associated with the progression and development of diabetic microvascular complications are detected and treated at an early stage in order to further reduce morbidity and mortality. Considering all three complications as interrelated may well facilitate early detection of microvascular disease. Despite good long-term glycaemic and blood pressure control, diabetes remains a major cause of blindness, renal failure and amputations. As the incidence of diabetes continues to rise, the burden of diabetic microvascular complications will increase in future, hence the need for early detection. Considering the microvascular complications of diabetes as related, and enquiring proactively about complications, may well facilitate early detection of microvascular disease.
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PMID:Diabetic microvascular complications: can patients at risk be identified? A review. 1707 42

The diabetes epidemic continues unabated, leading to an increasing number of acute and chronic complications, including sight-threatening proliferative diabetic retinopathy. Currently, there is no accepted pharmaceutical therapy for diabetic retinopathy besides nearnormal glycemia, treatment of hypertension, and dyslipidemia. For an effective treatment of retinopathy, one would recommend a concept leading to the downregulation of endogenous angiogenic stimulators and the upregulation of endogenous angiogenic inhibitors, resulting in a restoration of the balance in angiogenic control. The naturally occurring growth hormone inhibitor, somatostatin, has been suggested as candidate for developing novel therapies. Somatostatin may exert its antiangiogenic effects, both through antagonism of the growth hormone axis and through direct antiproliferative and apoptotic effects on endothelial cells. Therefore, the use of long-acting somatostatin analogues will lead to an upregulation of antiangiogenic signaling. Use of long-acting somatostatin analogues in diabetic retinopathy would be an important extension of the initial concept that somatostatin is a regulator of growth hormone secretion only. Currently available analogues have already allowed to modulate the expression of diabetic retinopathy at various disease stages. Somatostatin analogues remain the only nondestructive therapeutic alternative to patients with proliferative diabetic retinopathy who have failed to respond to panretinal photocoagulation.
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PMID:Use of long-acting somatostatin analogue treatment in diabetic retinopathy. 1724 82


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