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At least 145 records · Page 8Linked to original sources
PubMed2004

Health promotion and health education about diabetes mellitus.

Diabetes mellitus, especially if poorly controlled, is a major contributory cause for blindness, heart attacks, amputations, strokes, kidney failure and impotence. The prevalence of diabetes is increasing globally. Fortunately there is compelling evidence from clinical trials that lifestyle modifications and education can minimise the risk of diabetes, and new treatments can reduce the burden of morbidity and mortality. We now have modified insulin, infusion pumps, dialysis, kidney and pancreas transplants, and effective therapies for reducing lipids and blood pressure. However, important as these advances are, diabetes and its complications can be prevented, or delayed, by modifying risk factors. Persons with diabetes must understand their disease and be empowered to avoid obesity, smoking and unhealthy diets, and encouraged to exercise, and control blood glucose. Good health education, health promotion and access to professional care are essential for persons with diabetes mellitus. Valuable health information is available from Diabetes UK and the Internet.

Diabetes Complications↗
PubMed2006

An uncommon case of diabetic mastopathy in type II non-insulin dependent diabetes mellitus.

Diabetic mastopathy is an uncommon tumor-like proliferation of fibrous tissue of the breast that usually occurs in a patient who has suffered from type I diabetes mellitus of long duration. Here we report a rare case of diabetic mastopathy that occurred in type II non-insulin dependent diabetes mellitus. This patient was a 63-year-old postmenopausal woman. Mammography, ultrasonography and MR imaging could not distinguish it from breast cancer. Although the core needle biopsy specimen showed fibrosis without evidence of malignancy, excisional biopsy was performed. Histological findings demonstrated typical diabetic mastopathy with keloid-like fibrosis, perivascular lymphocytic infiltration, and lymphocytic lobulitis without evidence of malignancy. These lymphocytes were composed predominantly of B-cells. Five months after surgical biopsy, a nodular formation approximately 4 cm in diameter recurred adjacent to the resected end of the biopsy.

Biopsy, Needle↗
PubMed1997

Vascular homeostasis, adhesion molecules, and macrovascular disease in non-insulin-dependent diabetes mellitus.

Diabetes mellitus is characterized by fasting hyperglycaemia and the development of chronic vascular complications. While microvascular disease has been strongly related to glycaemic control, the major cause of mortality in diabetes is due to macrovascular disease affecting the cardiac and cerebrovascular circulations, which appear to have a more complex pathogenesis. Diabetes is associated with a 3-5-fold increase in death from myocardial infarction and similar figures pertain to stroke. The processes involved in atherothrombotic disease are complex and include variation in lipid metabolism, vascular responses, cell/cell interactions, and in the fluid and cellular phases of coagulation and fibrinolysis. The complex interactions between all of these processes are crucially altered by the metabolic milieu that characterizes diabetes mellitus, tipping the delicate balance towards atheroma formation, platelet aggregation and thrombus formation. This article will review these mechanisms and the effects of diabetes in the pathogenesis of vascular disease.

Blood Vessels↗
PubMed1991

Impact of blood pressure and antihypertensive treatment on incipient and overt nephropathy, retinopathy, and endothelial permeability in diabetes mellitus.

Diabetic nephropathy is the main cause of the increased morbidity and mortality in insulin-dependent diabetes mellitus (IDDM) patients. Elevated blood pressure accelerates and effective blood pressure reduction with beta-blockers and/or angiotensin-converting enzyme (ACE) inhibitors delays the progression of nephropathy and reduces albuminuria. All previous reports dealing with the natural history of diabetic nephropathy demonstrated a cumulative death rate between 50 and 77% 10 yr after onset of nephropathy. Effective antihypertensive treatment reduced the cumulative death rate to 15-20% 10 yr after onset of nephropathy. Recent randomized control studies indicate that ACE inhibition may delay and even prevent the development of diabetic nephropathy in normotensive IDDM patients with persistent microalbuminuria. Several cross-sectional and prospective studies suggest an association between elevated blood pressure and the development and progression of diabetic retinopathy. Furthermore, carotid insufficiency or other causes of unilaterally or bilaterally reduced retinal blood flow (pressure) diminish the development of diabetic retinopathy. Diabetic retinopathy is characterized by abnormal leakage of fluorescein through the blood-retinal barrier, an abnormality that can be reversed during antihypertensive treatment. It is well documented that elevated blood pressure, poor metabolic control, and diabetic microangiopathy independently enhance the endothelial leakage of plasma proteins in diabetes mellitus. A link between capillary hypertension, increased extravasation of plasma proteins, and the development and progression of diabetic microangiopathy has been suggested. Blood pressure reduction diminishes the extravasation of plasma proteins. The above results strongly support the case for early and effective treatment of arterial blood pressure elevation in diabetes.

Antihypertensive Agents↗
PubMedDate not supplied

Molecular changes in proximal tubule function in diabetes mellitus.

Diabetic kidney disease is initially associated with hypertension and increased urinary albumin excretion. The hypertension is mediated by enhanced volume expansion due to enhanced salt and water retention by the kidney. The increased urinary albumin is not only due to increased glomerular leak, but also to a decrease in albumin reabsorption by the proximal tubule. The precise molecular mechanisms underlying these two phenomena and whether there is any link between the increase in Na(+) retention and proteinuria remain unresolved. There is significant evidence to suggest that increased Na(+) retention by the proximal tubule Na(+)/H(+) exchanger isoform 3 (NHE3) can play a role in some forms of hypertension. Increased NHE3 activity in models of diabetes mellitus may explain, in part, the enhanced salt retention observed in patients with diabetic kidney disease. The NHE3 also plays a role in receptor-mediated albumin uptake in the proximal tubule. The uptake of albumin requires the assembly of a macromolecular complex that is thought to include the megalin/cubulin receptor, NHE3, the vacuolar type H(+)-ATPase (v-H(+)-ATPase), the Cl(-) channel ClC-5 and interactions with the actin cytoskeleton. The NHE3 seems to exist in two functionally distinct membrane domains, one involved with Na(+) reabsorption and the other involved in albumin uptake. The present review focuses on the evidence derived from in vivo studies, as well as complementary studies in cell culture models, for a dual role of NHE3 in both Na(+) retention and albumin uptake. We suggest a possible mechanism by which disruption of the proximal tubule albumin uptake mechanism in diabetes mellitus may lead to both increased Na(+) retention and proteinuria.

Animals↗
PubMed1989

Subclinical hyponatremia, hyperkalemia and hypomagnesemia in patients with poorly controlled diabetes mellitus.

Diabetes mellitus is associated with disturbances in electrolyte metabolism. We studied 68 patients with insulin-requiring diabetes mellitus followed up in the Home Monitoring Clinic in order to assess the relationship between electrolyte disturbances and severity of diabetes. There is a significant correlation of serum sodium (r = -0.323, P less than 0.01), potassium (r = 0.416, P less than 0.001), magnesium (r = -0.292, P less than 0.02) with fasting glucose. Thus, in patients with high fasting blood glucose, sodium and magnesium tend to be lower while potassium is higher. Among the three parameters, only serum magnesium significantly correlates with the level of hemoglobin A1 (r = -0.356, P less than 0.001) and thus may be related to the long-term control of diabetes. On the other hand, the hyponatremia and hyperkalemia are more likely to be related to short-term metabolic control as reflected by fasting blood glucose. To conclude, minor changes in electrolytes have been found in a group of 68 Chinese patients receiving insulin. There is a remote possibility that these electrolyte changes may influence the chemical events responsible for long-term diabetic complications.

Blood Glucose↗
PubMedDate not supplied

[Acute postoperative mononeuropathy in a patient with type II diabetes mellitus].

Diabetes mellitus is an endocrinologic illness that affects multiple systems. One of then is the nervous system. It has been attempted to establish a relationship between metabolic abnormalities associated with diabetes and the degree of nervous system affectation. We present a case of mononeuritis involving the left peroneal nerve which occurred suddenly during the postoperative phase of a thoracoplasty in a patient with type II diabetes mellitus. The clinical picture was associated with a hyperglycemic nonketotic decompensation. We analyze the precipitating factors and their possible prevention.

Diabetes Mellitus, Type 2↗
PubMed1990

Renal disease in noninsulin-dependent diabetes mellitus.

Diabetic nephropathy now accounts for approximately one-third of all patients who develop end-stage renal disease. The estimated cost to supply renal replacement therapy for this population now exceeds $750 million. The relatively recent realization that half of these individuals suffer from noninsulin-dependent diabetes mellitus has sparked increased interest in attempts to understand the pathologic processes involved and how they may be similar or different from those alterations seen in insulin-dependent diabetes mellitus. Basic and clinical investigation continues in an attempt to solve the puzzle of pathogenesis, as well as answer questions about the clinical usefulness of microalbuminuria and the appropriate management of hypertension in this population.

Albuminuria↗
PubMed2003

[Contribution of diabetic research to versatile strategies for the treatment of diabetes mellitus].

Diabetes mellitus is a very common life-style-related disease. Both genetic and environmental factors are strongly involved in its etiology and pathogenesis, and patients suffering from this disease are rapidly increasing in number. Since the discoveries of insulin in the 1920s and of antidiabetic sulphonylureas in the 1950s, these agents have been widely used for the treatment of diabetes mellitus. For the use of insulin, however, diabetic patients are imposed to inject insulin daily, and long-term use of sulphonylureas is suggested to impair pancreatic B cell functions. In order to overcome these problems and to achieve the fine control of blood glucose levels, many attempts for novel antidiabetic treatments are currently ongoing, and versatile therapeutic strategies for the treatment are expected to prevent the progression of this disease and resultant diabetic complications that severely affect the individuals' QOL. This paper overviews what diabetic research has done for its treatment and what it will do in the future.

Diabetes Mellitus↗
PubMedDate not supplied

MPO-ANCA-associated pulmonary-renal vasculitis in a patient with diabetes mellitus.

Diabetes mellitus is one of the major causes of chronic renal failure. Typical findings of diabetic nephropathy are early hyperfiltration followed by microalbuminuria and overt proteinuria, resulting in a progressive decrease in glomerular filtration rate. Rapidly progressive glomerulonephritis has rarely been reported in patients with diabetes mellitus. Here, we describe a patient with MPO-ANCA-associated vasculitis, presenting with pulmonary-renal syndrome. Immunosuppressive treatment, including pulse methyl-prednisolone and cyclophosphamide, was administered and the disease was resolved.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed2006

[Molecular diagnosis of diabetes mellitus].

Diabetes mellitus comprises a heterogeneous group of disorders characterized by chronic hyperglycemia. Type 1 and type 2 diabetes result from alterations of various genes, each having partial and additive effects. Thus, the inheritance pattern is rather complex, and environmental factors play an important role in the manifestation and clinical course of the disease. There is no genetic test to diagnose diabetes mellitus type 1 or type 2. However, certain susceptibility genes and genetic variations can be examined for specific scientific questions. Furthermore, defined genetic defects exist of pancreatic beta-cell function (maturity-onset diabetes of the young, mitochondrial diabetes) and insulin action (e.g. insulin resistance syndromes and lipodystrophy syndromes) resembling monogenic disorders. In these cases, genetic tests are crucial for the correct classification of the type of diabetes, genetic counseling, and initiation of the appropriate therapy regimen.

Diabetes Mellitus↗
PubMed2006

[Coronary heart disease in patients with diabetes mellitus].

Diabetes mellitus is a well-recognized risk-factor for coronary artery disease. It is known that diabetic patients have a two-to fourfold increased risk of mortality or morbidity for cardiovascular diseases compared with the general population. Further, many diabetic patients with coronary heart disease have severe diseased coronary arteries: multi-vessel disease and/or severe stenosed vessel(s). In Japan, the prevalence of diabetic patients is rapidly increasing in these days. This article will review the evaluation for risk of coronary heart disease by measuring glucose level, the prognosis of diabetic patients, and the prevention of cardiovascular event in the patients with diabetes mellitus.

Angiotensin II Type 1 Receptor Blockers↗
PubMed1994

[Lipoprotein (a), atherosclerosis, and diabetes mellitus].

Diabetes mellitus is associated with a three to fourfold increased risk for coronary artery disease and diabetic patients frequently have an abnormal plasma lipid profile. Lately, lipoprotein (a) has received attention as an important independent risk factor for cardiovascular disease. This lipoprotein is elevated in patients with type II diabetes mellitus and there may be an association between the metabolic control of these subjects and its levels. In this review the main features of lipoprotein (a) and its relationship to the fibrinolytic system and atherosclerosis are reviewed.

Arteriosclerosis↗
PubMed2006

Liver disease in patients with diabetes mellitus.

Diabetes mellitus is a growing health concern in our society. In addition to the well-known cardiovascular, renal, and ophthalmologic complications of diabetes, liver-related complications occur commonly and are often underrecognized. The ensuing article will review the relationship between diabetes mellitus and two common liver diseases: chronic hepatitis C and nonalcoholic fatty liver disease. The association with diabetes and cirrhosis, acute liver failure, hepatocellular carcinoma, and outcomes following orthotopic liver transplantation will also be discussed.

Diabetes Complications↗
PubMed1981

[The HLA system and diabetes mellitus].

Diabetes is a heterogeneous disease, and its pathogenesis and etiology are still largely unknown. Recent studies have brought new knowledge showing that HLA antigens and diabetes mellitus are related. It has been found that the relative risk of juvenile onset diabetes requiring insulin treatment is greater for persons who are HLA-A1, A2, B8, BW15, BW40, CW3, DW3, DW4, DRW3 and DRW4 positive. The relative risk of the disease is additive in persons who have two of the above mentioned HLA-B alleles. Some HLA antigens (HLA-B7, DW2, DRW2, A11) are associated with a significantly lower risk of the disease and probably have a "protective" character. Maturity onset diabetes (MOD) and maturity onset diabetes not requiring insulin treatment (MODY) are not related to the HLA system. This means that MOD is completely distinct from JOD with different symptoms, course and etiopathogenesis.

Diabetes Mellitus↗
PubMed1995

Magnesium transport induced ex vivo by a pharmacological dose of insulin is impaired in non-insulin-dependent diabetes mellitus.

Diabetes mellitus may be associated with magnesium depletion, which in turn may contribute to metabolic complications of diabetes including vascular disease and osteoporosis. Intracellular depletion is thought to be due to osmotically induced renal magnesium loss; however, impaired ability of insulin to increase intracellular magnesium during insulin deficiency or insulin resistance could also play a role. Magnesium deficiency per se has also been reported to result in insulin resistance. In order to determine if magnesium transport is altered in non-insulin-dependent diabetes mellitus (NIDDM), we measured intracellular Mg(2+) in circulating lymphocytes obtained from nine normal subjects and seven patients with NIDDM. Ionized intracellular Mg(2+) was determined by fluorescent spectroscopy using Mg-fura-2. A 30 min incubation of insulin with lymphocytes obtained from normal subjects resulted in an increase in Mg(2+) of 8.6 +/- 3.6 percent (mean +/- SEM) at 100 mu U/ml which reached a plateau at approximately 250 mu U/ml (11.0 +/- 1.7 percent). The mean lymphocyte Mg(2+) in the patients (0.198 +/- 0.011 mM) was not significantly lower than normal (0.218 +/- 0.017). Insulin (500 mU/ml) added acutely during the fluorescence reading caused a rapid 31 +/- 3.9 percent rise in intracellular Mg(2+) in the normal subjects, which was significantly greater than the 18 +/- 1.6 percent rise observed in the NIDDM subjects (P < 0.01). The effect of magnesium deficiency was also studied in 3 normal subjects experimentally Mg deficient for 3 weeks. The mean lymphocyte Mg(2+) fell from 0.198 +/- 0.009 mM pre-diet to 0.153 +/- 0.006 mM post-diet. and the insulin-induced rise in Mg(2+) fell from 27.2 percent pre-magnesium depletion to 12.7 percent post-magnesium depletion. These data suggest that insulin resistance and magnesium depletion may result in a vicious cycle of worsening insulin resistance and decrease in intracellular Mg(2+) which may limit the role of magnesium in vital cellular processes.

Adult↗
PubMed1990

Significance of capillary basement membrane changes in diabetes mellitus.

Diabetes mellitus is a disease in which the capillary basement membranes are substantially altered. This diabetic microangiopathy is characterized by a thickening of the basement membrane and changes in its permeability characteristic due to a disturbance in the production and distribution of its functional components. Glucose metabolism and insulin imbalance have been implicated in these basement membrane modifications. The authors describe normal capillary basement membrane architecture and then discuss how pathologic changes caused by diabetes mellitus are related to diabetic foot pathology.

Basement Membrane↗