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

Microalbuminuria is a predictor of excess cardiovascular morbidity and mortality in both hypertensive and diabetic subjects. The reasons for this are multifactorial and relate to metabolic and haemodynamic problems seen in this population. In diabetic patients, microalbuminuria correlates more with glycosylated haemoglobin than with the duration of diabetes. The pathogensis of microalbuminuria includes alterations in glomerular shunting of albumin, increased intraglomerular pressure and increased amounts of certain growth factors that alter cell permeability. The urine Micral test is an easy way to screen for the presence of microalbuminuria. The increase in microalbuminuria over time can be documented by annual quantitation using a radioimmunoassay technology. Aggressive control of BP is vitally important in order to preserve renal function. Antihypertensive agents that lower both intraglomerular pressure and volume are preferable, since they consistently attenuate both the increase in microalbuminuria and structural changes within the glomerulus. In addition to BP control, other measures known to reduce the rise in microalbuminuria include a reduced dietary protein intake and good long-term blood glucose control. Unfortunately, there is no definitive study, in humans, that conclusively demonstrates a preservation of renal function directly relates to an attenuated rise in microalbuminuria. Thus, while microalbuminuria is clearly a risk factor for development of diabetic nephropathy and an indicator of hypertensive renal disease, its reduction has not demonstrated functional or structural benefit in humans. This is in large part due to the inpracticality of such a trial because of the duration needed to see an effect. Interestingly, a beneficial effect on renal survival has been shown with albuminuria reduction independent of BP reduction.
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PMID:Microalbuminuria and progressive renal disease. 785 23

Lower-extremity ischemia can lead to impaired healing of saphenous vein excision sites in patients with significant peripheral vascular disease (PVD). Five patients who required infrainguinal revascularization for wound necrosis of the harvest site after coronary artery bypass grafting are described. The male/female ratio was 2:3 with a mean age of 67 (range 45-87) years. The most commonly associated problems were insulin-dependent diabetes mellitus (80%) and congestive heart failure (60%). The saphenous vein was harvested from the thigh and leg in three patients and exclusively from the leg in the others. Manifestations of ischemia ranged from persistent ulceration to complete wound disruption threatening limb loss. Impaired healing was isolated to infragenicular wounds in all patients. Pedal pulses were not detected in any of the affected extremities. Determination of the ankle/brachial pressure indices (ABI) revealed values of < 0.5 in three affected limbs. Non-compressible vessels resulted in falsely raised ABI of > 1.0 in the remaining two limbs; however, Doppler waveform analysis in these patients demonstrated significant PVD. Aggressive wound care and antibiotic therapy were continued for mean of 9 weeks before operative intervention. Infrainguinal reconstruction included femoropopliteal (two), femorotibial (two) and popliteal-tibial bypass (one). Autologous arm and saphenous veins in addition to expanded polytetrafluoroethylene grafts were used effectively. Limb salvage and wound healing were achieved in 100% of the patients without untoward sequelae. It is concluded that unrecognized PVD in patients undergoing coronary artery bypass grafting can lead to significant morbidity. Patients at risk may be identified with a combination of history, physical examination and non-invasive testing.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vein harvest ischemia: a peripheral vascular complication of coronary artery bypass grafting. 795 53

The purpose of this paper is to describe the management of a previously undiagnosed non-insulin-dependent diabetic patient with a severe burn injury. The hyperglycaemia and glucose intolerance following burn injury was complicated by the hyperglycaemia of diabetes mellitus. Intravenous insulin infusion monitored by hourly glucose levels was required to manage this hyperglycaemia. During day 11 postburn injury, this patient required 2104 units of insulin to control his hyperglycaemia. Aggressive detection and management of infections complemented by early debridement and coverage of the burn wound were other important considerations in the management of this patient. The diagnosis of non-insulin-dependent diabetes mellitus (NIDDM) was made after the patient recovered from his burn injury. His rehabilitation programme has included primary prevention strategies for NIDDM that focus on health-improving behaviours such as improved diet, exercise, and weight control.
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PMID:Non-insulin-dependent diabetes mellitus: diagnostic and therapeutic challenges in the severely burned patient--a case report. 805 48

Multiple low doses of streptozotocin (mid sz 40 mg/kg/day, five consecutive days) induce autoimmune diabetes in mice. The aim of the present work was to study beta-cell function in mice injected with splenocytes from mid-sz diabetic mice. Mononuclear splenocytes (MS) from control or diabetic donors were injected into syngeneic C57BL/6J healthy mice (5 x 10(7) MS, ip). MS from diabetic donors did not produce basal hyperglycemia, but they induced abnormal ip glucose tolerance in recipient mice. These "diabetic" MS were also preferentially trapped by the recipient's pancreas. Perifused pancreas from mice injected with MS from mid sz-diabetic donors showed a diminished first and second phase of glucose-induced insulin secretion after 15 days of the cell injection. At this time, pancreatic insulin content among MS recipients did not differ from that found in controls or diabetic donors. Diabetic MS treated with Mitomycin C prior to transfer did not inhibit insulin secretion in recipient mice. Injection of MS from mice made diabetic by a single high sz dose (200 mg/kg) did not induce any alterations of the insulin secretion in recipients. There is enough evidence when using athymic and euthymic (BALB/c nu/nu and +/nu) mice to suggest that proliferation of the injected splenocytes enhanced the progression to the diabetic state, and that both donor and recipient T lymphocytes played an important part in this progression. The results suggest that injection of MS from mid sz-diabetic mice interfere with glucose-stimulated insulin secretion in recipient mice and provide a basis for the study of the mechanisms involved in the onset and modulation of autoimmune pancreatic aggression.
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PMID:Beta-cell function in mice injected with mononuclear splenocytes from multiple-dose streptozotocin diabetic mice. 818 65

Fifty consecutive heel ulcers were managed in three groups by debridement, split-thickness skin graft (STSG), bypass procedures, and orthotics. Group I consisted of 24 ulcers in patients with diabetes (DM) and peripheral vascular disease (PVD), 14 patients in Group II with DM only, and 12 patients with PVD only (Group III). Healing occurred in 56.5%, 64.3%, and 83.3%, respectively. An average of 2.2 procedures were performed per patient. Follow-up periods were for a minimum of two years or until amputation. Time for complete healing and the number of amputations performed were similar in all groups. Of the diabetics (combined from Groups I and II), a subgroup of 27% required partial excision of the os calcis to facilitate closure. After saline dressing changes, STSG was accomplished over thin granulation tissue. Forty percent of this subgroup healed, 30% remained open, and 30% were amputated. Aggressive management, soft-tissue coverage, and orthotic use can lead to a functional weight-bearing extremity.
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PMID:Salvage of the diabetic foot with exposed os calcis. 822 53

Atherosclerosis is the principal cause of diabetic morbidity and mortality. Diabetic dyslipidemia, obesity, and hypertension are significant contributing factors in the acceleration of the atherosclerotic process. Regardless of the type of diabetes, increased levels of very-low-density lipoprotein triglyceride, modified levels of low-density lipoprotein cholesterol, and decreased levels of high-density lipoprotein (HDL) cholesterol are the main lipoprotein abnormalities in diabetic patients. These abnormalities can be improved in part by glycemic control, but additional intervention may be needed. Diet and exercise are important elements in the management of dyslipidemia, but lipid-lowering drugs (especially fibrates and HMG-CoA reductase inhibitors) also may be necessary for the control of diabetic dyslipidemia. Based on these findings, the American Diabetes Association Consensus Panel and the revised treatment guidelines of the National Cholesterol Education Program recommend treatment of hypertriglyceridemia/low HDL cholesterol as a risk factor of coronary heart disease in diabetic and nondiabetic individuals alike. Aggressive treatment is recommended, therefore, particularly in diabetic patients and in all patients with existing vascular disease.
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PMID:Prevention of atherosclerosis in diabetes: emphasis on treatment for the abnormal lipoprotein metabolism of diabetes. 826 43

Hypertension and diabetes appear to increase coronary heart disease risk in part by causing an abnormality in lipid metabolism. Most affected are patients with familial dyslipidemic hypertension (FDH) and noninsulin-dependent diabetes mellitus (NIDDM). The lipid disorders most often encountered in these patients are increased levels of triglycerides, very low-density lipoprotein (VLDL) cholesterol, and small, dense low-density lipoprotein (LDL) cholesterol, and low levels of high-density lipoprotein (HDL) cholesterol. These abnormalities appear to result from increased hepatic secretion of VLDL particles due to increased concentrations of free fatty acids and glucose, reduced VLDL clearance due to reduced activity of lipoprotein lipase, and reduced LDL clearance due to glycosylation of ligand proteins. Treatment of the dyslipidemia associated with FDH should follow the guidelines from the National Cholesterol Education Program. Treatment in men and women with NIDDM should be considered when LDL cholesterol levels are 130 mg/dl or above, triglyceride levels are 200 mg/dl or above, or non-HDL cholesterol levels are 160 mg/dl or greater. Aggressive lifestyle changes should be initiated first, including weight loss in obese patients, control of glucose levels in those with NIDDM, avoidance of antihypertensive drugs that may worsen lipid levels in patients with FDH, and eating a diet restricting saturated fat and cholesterol. Addition of lipid-altering drugs should be considered if such changes do not achieve effective lipid control. The agent should be tailored to the patient's lipid profile, in general by using bile acid resins, niacin, or reductase inhibitors to lower LDL cholesterol and gemfibrozil or niacin to lower triglycerides. Niacin should be avoided in patients with NIDDM.
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PMID:Understanding and treating dyslipidemia associated with noninsulin-dependent diabetes mellitus and hypertension. 836 60

Odontogenic infections rarely lead to involvement of the lateral and retropharyngeal spaces. When this does occur, the microbiology of the infection is similar to the typical odontogenic infection, ie, Streptococcus and oral anaerobes including Peptostreptococcus, Bacteroides, and Fusobacterium. There is an increased incidence of Fusobacterium seen in the more severe infections, as well as a higher incidence of Streptococcus milleri. Many patients who have deep cervical infections also have some compromise in their host defense mechanism, such as diabetes. The signs and symptoms of deep cervical space infections are similar to those of the severe submandibular space infection, but also includes sialorrhea, respiratory distress, odynophagia, and dysphagia. Lateral soft-tissue radiographs of the neck are useful in assisting with the diagnosis of retropharyngeal infections, and CT scans can provide definitive information regarding lateral pharyngeal space involvement. Treatment includes the use of high-dose intravenous bacteriocidal antibiotics. The recommended antibiotics are penicillin-metronidazole, ampicillin-sulbactam, or clindamycin. Certain cephalosporins may also be useful in selected patients. Early surgical intervention is also indicated. Aggressive incision and drainage of all of the involved spaces is necessary to assure early resolution of the infection. Continual airway monitoring and the establishment of surgical airways is the final portion of the treatment triad.
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PMID:Contemporary management of deep infections of the neck. 844 62

We report 3 cases of gangrene of the penis seen at our institution after penile prosthesis implantation. All 3 patients had insulin-dependent diabetes mellitus. Amputation was required in 2 patients. Aggressive debridement in conjunction with hyperbaric oxygen prevented amputation in the third patient.
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PMID:Gangrene of the penis after implantation of penile prosthesis: case reports, treatment recommendations and review of the literature. 851 Feb 51

A better knowledge of the pathogenesis of type 1 diabetes (IDDM) may open the road to the prevention of the diseases. Primary prevention is meant to identify susceptible subjects, either soon after birth or before the immunological aggression of beta cells. The practical approach in this respect is very difficult because multiple obstacles must be overcome. Secondary prevention involves subjects who already show immunological or metabolic alterations, as the presence of ICA, antiinsulin antibodies, GAD antibodies and a defect of the first phase of insulin secretion. Most authors attach great interest to trials with insulin and nicotinamide. Insulin seems to reduce antigen expression when beta cells are damaged. Nicotinamide exerts a protection toward diabetes in animals, and, as scavanger of free radicals, facilitates beta cell regeneration. Research is going on, all over the world, and special multicenter trials are in progress both in the USA and Europe.
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PMID:[Prevention of juvenile diabetes (type 1): reality or fiction?]. 856 82


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