Diabetic retinopathy: can we modify its course?
Article Abstract:
Diabetes mellitus is a condition in which the insulin-producing pancreatic beta cells become dysfunctional, resulting in excessively low levels of insulin in the blood. Because a primary effect of insulin is to promote the metabolism of sugars such as glucose, insulin-deficient diabetics have high levels of glucose in the blood (hyperglycemia). Although this condition is controlled somewhat with injections of exogenous insulin, blood sugar regulation is not perfect, and large swings in glucose levels can occur, with intermittent hyperglycemia. High blood glucose levels are known to effect parts of the body, including the retina, which is the neurosensory transmitter of visual perception (part of the eye). The presumed mechanism of diabetes-induced retinopathy is hyperglycemia, which can damage the small blood vessels (capillaries) of the retina. This can, in some cases, induce the formation of new capillaries (proliferation) to re-establish the blood supply to the portions of the retina receiving blood from the damaged capillaries. These vessels can also leak (hemorrhage), and this self-perpetuating cycle results in relatively large amounts of coagulated blood blocking light from reaching the retina. In severe cases, this process can lead to blindness. It is estimated that 60 to 65 percent of diabetic patients will develop proliferative retinopathy after 15 to 20 years of diabetes, and that all diabetics will suffer some form of retinopathy after this period of time. Currently, the only therapy that has been shown to be effective in altering the course of retinopathy is panretinal laser photocoagulation, in which a laser beam is used to stop hemorrhage from the retinal capillaries. A surgical technique for removing coagulated blood from the retina (vitrectomy) yields temporary improvement. The development of alternative therapies for diabetic retinopathy will depend on a greater understanding of the course of the disease at the molecular level. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1991
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Diabetic nephropathy: can the natural history be modified?
Article Abstract:
When the insulin-secreting pancreatic beta cell becomes dysfunctional, the resulting condition is characterized by excessively low levels of insulin in the blood; the condition is known as insulin-dependent diabetes mellitus (IDDM). Because a primary effect of insulin is to promote the metabolism of sugars such as glucose, insulin-deficient diabetics have high levels of glucose in the blood (hyperglycemia). About 30 percent of the patients suffering from IDDM die of kidney failure, or require kidney transplantation or dialysis (a method for removing toxins from the blood). Unlike some other complications associated with IDDM, in which the risk rises progressively with increasing disease duration, there seems to be a critical window for developing kidney failure. If it has not occurred within 15 to 20 years of diabetes onset, it is unlikely to occur. The factors that distinguish the susceptible subset of diabetic patients from those who retain normal kidney function remain unknown. Until those factors can be identified and controlled, the most effective therapeutic strategy available is to control conditions that are known to exacerbate kidney disease in general. These include hypertension (high blood pressure), high levels of protein in the diet, and hyperglycemia. A particularly promising approach seems to be the use of antihypertensive drugs belonging to the class known as angiotensin converting enzyme inhibitors; these drugs appear to not only lower blood pressure, but have beneficial effects on the blood supply to the kidney itself. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1991
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Autonomic influence on cardiovascular performance in diabetic subjects
Article Abstract:
The cardiac function of diabetic patients who are advised or desire to begin exercise programs should be assessed since poor function of the heart muscle, coronary artery disease and cardiac autonomic neuropathy (diminished or dysfunction of the nerves that supply the heart) are associated with diabetes. One third of all diabetics have impaired function of the left ventricle, the heart's main pumping chamber, despite the fact that they are asymptomatic for heart disease. Recent studies reported that diabetics with ineffective nerve activity in their hearts have increased risk of cardiac arrest and abnormal heart rhythms. Twenty-five diabetic patients, who had no symptoms and no indications of oxygen deprivation in the heart muscle, were evaluated for the possibility of autonomic neuropathy with an RR test (used to diagnose cardiac autonomic neuropathy). Diabetic patients were divided into two groups - those with normal and those with abnormal RR variations - and were compared to each other and to a group of healthy adults who had normal RR variations. During bicycle exercise testing the diabetic patients who had abnormal RR variation exercised at a lower level and had less cardiac output (less blood pumped by the heart to the body) than the other diabetics and healthy adults. This was due to decreased cardiac autonomic nerve activity. Using the RR test may help physicians to identify asymptomatic diabetic patients who may require special consideration when exercise programs are considered.
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1989
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