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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper discusses psychosocial influences of diabetes mellitus type 1 on children and young patients. A group of 21 patients, age 9 to 14 years with Diabetes mellitus type 1 attended a course in "Autogenic Training" for a period of 11 weeks. From the multidimensional questionnaire for children (PFK 9-14, SETZ U. RAUSCHE 1976) 15 dimensions of personality and 5 second rank factors were extracted at the beginning and at the end of training and 5 months later. Additionally HbA1-scores were assessed at the beginning and at the end at a 2 month and a 5 month-follow-up. At the beginning of the course only on one of the 15 scales a significant difference could be observed between experimental group and age related normal population. After training 5 scales and one second rank factor showed significant changes. Significant reduction was observed in: "need for aggressive forms of dominance behaviour" "feeling of submission with respects to other:", "emotional lability" and "tendency for dependence on adults". A significantly increased score was observed in the scale measuring "self confidence regarding one's own meaning, decisions and planning ability". The second rank faktor "neuroticism" was significantly reduced. Against expectations there was no reduction in HbA1 scores. At the end of training HbA1 scores even had increased significantly. But this might have been related to the high frequency of infections during this course. In subjective ratings of training evaluation most of the course members and their parents described fewer problems with attention, less test-anxiety and less aggression and nervousness. The results of this prospective pilot-study are discussed in terms of the psychodynamic influence on diabetes.
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PMID:[Autogenic training in children and adolescents with type 1 diabetes mellitus]. 920 90

An interaction between high plasma lipoprotein(a) [Lp(a)], unfavorable plasma lipids, and other risk factors may lead to very high risk for premature CAD. Plasma Lp(a), lipids, and other coronary risk factors were examined in 170 cases with early familial CAD and 165 control subjects to test this hypothesis. In univariate analysis, relative odds for CAD were 2.95 (P < .001) for plasma Lp(a) above 40 mg/dL. Nearly all the risk associated with elevated Lp(a) was found to be restricted to persons with historically elevated plasma total cholesterol (6.72 mmol/L [260 mg/dL] or higher) or with a total/HDL cholesterol ratio > 5.8. Nonlipid risk factors were also found to at least multiply the risk associated with Lp(a). When Lp(a) was over 40 mg/dL and plasma total/HDL cholesterol > 5.8, relative odds for CAD were 25 (P = .0001) in multiple logistic regression. If two or more nonlipid risk factors were also present (including hypertension, diabetes, cigarette smoking, high total homocysteine, or low serum bilirubin), relative odds were 122 (P < 1 x 10(-12)). The ability of nonlipid risk factors to increase risk associated with Lp(a) was dependent on at least a mildly elevated total/HDL cholesterol ratio. In conclusion, high Lp(a) was found to greatly increase risk only if the total/HDL cholesterol ratio was at least mildly elevated, an effect exaggerated by other risk factors. Aggressive lipid lowering in those with elevated Lp(a) therefore appears indicated.
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PMID:Lipoprotein(a) interactions with lipid and nonlipid risk factors in early familial coronary artery disease. 940 56

People with type II diabetes have a twofold to fourfold increased risk of dying from the complications of cardiovascular disease. Atherosclerosis and vascular thrombosis are major contributors. The increased risk is present before fasting hyperglycemia is seen. These individuals often have a sedentary life-style, poor physical conditioning, insulin resistance, centripetal obesity, hypertension, dyslipidemia, and a prothrombotic state. Chronic hyperglycemia is then added to these risk markers. Microalbuminuria may precede hyperglycemia in type II diabetes, occurs in 30% to 40% of these individuals after diabetes is established, and is a predictor of cardiovascular events. Early intervention in high-risk individuals may delay or prevent fasting hyperglycemia. An all-inclusive approach that focuses on early risk factor (or marker) identification and management to prevent or delay accelerated atherosclerosis and thrombosis in type II diabetes is an attractive strategy. However, the database to support this strategy is limited. In particular, large-scale prospective trial data are not available to support the concept of intensive glycemic regulation to prevent progression of macrovascular disease in type II diabetes. This is in contrast to the situation regarding microvascular disease of the eyes and kidneys. Recently, indirect data of a correlative nature have emerged, and short- and long-term prospective trials at early and late stages of type II diabetes are now being reported. These studies are analyzed and interpreted in this report. In contrast, the database to support an intensive antiplatelet regimen to prevent vascular thrombotic events in people with type II diabetes is large, and these studies are reviewed. They are of a type and magnitude to allow definite recommendations for aspirin therapy in type II diabetes. Aggressive therapy directed at hypertension, hyperlipidemia, and elevated urinary albumin in people with type II diabetes appears to be indicated. Increased attention to the multifactorial aspects of treatment of the type II diabetic patient is needed. Our present challenge is to translate these findings for patients and primary health care providers so that effective actions may be implemented.
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PMID:Multifactorial aspects of the treatment of the type II diabetic patient. 943 50

Emphysematous pyelonephritis is a rare, life-threatening complication of upper urinary tract infections, characterized by the presence of gas in renal parenchyma and perirenal space. It occurs in 90% of cases in diabetic patients and E coli is the most common causative germ. The pathogenesis probably involves several factors including enhanced proliferation of microorganisms due to altered immune defences, mixed acid fermentation of glucose leading to gas production, and decreased elimination of the gas because of impaired tissue perfusion. Diagnosis is often delayed because the symptoms may be non-specific, as illustrated by the two cases we report herein. In patients with diabetes and febrile urinary tract infection, obstruction of the urinary tract should first be eliminated by echography. Then, if the infection does not rapidly respond to antimicrobial therapy, a scan should be performed. Aggressive management including correction of hemodynamics, parenteral antimicrobial therapy, and diabetes control with insulin therapy is mandatory, but a surgical procedure (nephrectomy or drainage) is almost always required.
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PMID:[Emphysematous pyelonephritis in diabetics]. 949 90

The primary objectives of claudication treatment are to reduce cardiovascular mortality and improve walking ability. Patients with claudication have 60% mortality over 10 years, with most deaths due to myocardial infarction and stroke. Aggressive risk-factor modification is required in all these patients, particularly smoking cessation, lipid modification, and treatment of hypertension, diabetes and elevated homocysteine levels. Aspirin, ticlopidine and clopidogrel are all effective in reducing the risk of myocardial infarction, stroke and vascular death, and thus antiplatelet therapy should be considered in all claudicants. Patients with disabling claudication should be considered for therapies that relieve claudication pain and improve exercise performance, the most effective being exercise training and smoking cessation. Pentoxifylline, the only approved claudication drug in the United States, has modest efficacy in improving treadmill exercise performance. Other drugs shown to be of some benefit in patients with claudication include propionyl-L-carnitine, cilostazol and possibly prostaglandin derivatives. Several antiplatelet agents and angiogenic growth factors are also being evaluated for the treatment of claudication.
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PMID:Current and future drug therapies for claudication. 954 77

Atherosclerosis kills more patients with diabetes than all other causes combined. Aggressive reversal and treatment of dyslipidemias is the only proven prevention for coronary events in the patient with type 2 diabetes. Glycemic control with diet, oral hypoglycemic agents, and insulin, when necessary, is often only partially effective in normalizing lipid values in type 2 diabetes. Intensive treatment with lipid-regulating agents, particularly HMG-CoA reductase inhibitors, is often necessary to normalize diabetes-associated dyslipidemias. HMG-CoA reductase inhibitors are also the only agents thus far shown in prospective multicenter trials to reduce the risk of coronary events in diabetic patients.
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PMID:Vascular disease and lipids in diabetes. 970 27

Non-obese diabetic (NOD) mice spontaneously develop insulin-dependent diabetes mellitus (IDDM) as a consequence of autoimmune aggression of beta cells of the endocrine pancreas by T cells. T lymphocytes of NOD mice are resistant to apoptosis induced by glucocorticoids, or by starving or DNA-damaging treatments, a feature that was interpreted as being linked to escape of autoreactive T cells from thymic negative selection. c-myc is one of the gene targets of glucocorticoids (GC), its expression being down-regulated by the activated GC-GC receptor complex. We investigated here whether expression of Myc protein, in response to dexamethasone stimulation, was the same in NOD mice and in non-autoimmune strains, namely NON, BALB/c and C57Bl.6. We found a consistent increase in the levels of Myc protein after GC-treatment of lymphocytes of NOD mice, a finding that was in contrast to the down-regulation of c-myc that we observed in lymphocytes from mice not prone to diabetes. We also report that, rather than a absolute resistance to GC-induced cell death, NOD mice display a delayed apoptotic response to GC. We propose that the resistance of NOD mice lymphocytes to GC-induced apoptosis is because of inhibition of the repressive action of GC-GR complexes at the level of c-myc transcription. This deficient action of GC-GR results in increased production of nuclear Myc protein, peculiar to NOD mice cells, following their treatment with GC.
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PMID:Involvement of c-myc in the resistance of non-obese diabetic mice to glucocorticoid-induced apoptosis. 982

Insulin-dependent diabetes mellitus (IDDM) is not a disease of unbridled destruction. The autoimmune attack on pancreatic beta cells has two distinct stages - insulitis and diabetes - and progression of the former to the latter appears to be highly regulated. Identifying the factors controlling this transition has been difficult because it is a complex process that occurs non-universally and asynchronously. We have overcome these difficulties by coupling a simplified TCR transgenic (tg) model of IDDM and the immunosuppressive drug cyclophosphamide (CY). Young BDC2.5 TCR tg mice show insulitis but not diabetes; CY treatment provoked diabetes in 100% of animals with rapid, highly reproducible kinetics. This allowed a detailed temporal analysis of changes in cellular organization and cytokine gene expression within the lesion. The monokines IL-18, IL-12 and TNF-alpha were pivotal, their induction occurring almost immediately and their coordinate action being required for the onset of aggression. Other cytokines with direct toxicity for beta cells, including IL-1 -beta, IL-6 and IFN-gamma, were subsequently induced; in contrast, there was no cellular or molecular evidence of cell contact-mediated mechanisms of beta cell death.
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PMID:Cellular and molecular changes accompanying the progression from insulitis to diabetes. 993 6

Non-obese diabetic (NOD) mice spontaneously develop autoimmune insulin-dependent diabetes mellitus (IDDM). Infection of the animals with mycobacteria, or immunization with mycobacteria-containing adjuvant, results in permanent protection of NOD mice from diabetes and we have recently reported that the phenomenon is associated with increased numbers of interferon-gamma-producing T cells, possessing increased cytotoxic activity, and also with augmented numbers of activated immunoglobulin M-positive (IgM+) B cells. Here, we have investigated whether protection of NOD mice from IDDM was associated with changes on costimulatory pathways of T and B cells, namely CD28/CTLA-4-B7 and CD40-CD40 ligand (CD40L) and we also further characterized protective T helper (Th) cells with regards to the expression of the differentiation markers CD45RB and CD38. We report that Th cells involved in diabetes vaccination of NOD mice by mycobacterial infection seem to belong to CD45RBlo CD38+ phenotype. The protective effect of Mycobacterium avium infection is also associated with increased CD40L and CTLA-4- expressing Th cells and with the generation of a CD40- IgG+ B cells. Our data are consistent with induction by mycobacterial infection of regulatory CD45RBlo CD38+ Th cells with the ability to trigger deletion or anergy of peripheral self-reactive lymphocytes, with shutting down of IgG+ B-cell response. They also implicate a role for IgG+ B cells in the autoimmune aggression of the endocrine pancreas of NOD mice.
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PMID:A role for CD45RBlow CD38+ T cells and costimulatory pathways of T-cell activation in protection of non-obese diabetic (NOD) mice from diabetes. 1023 47

As the understanding of diabetes continues to improve and treatment methods expand, the clinician can now offer patients with diabetes a greater chance of improved health with fewer complications from diabetes. Aggressive, early treatment of type 2 diabetes, with the goal of achieving a maximum HbA1c of 8% and an ideal of less than 7%, is both health-enhancing and cost-effective. Nonpharmacologic treatments, such as nutrition therapy, exercise, weight loss, and self-management education programs are the most important aspects of care. Pharmacologic therapy should be based on a number of factors and should be individualized for each patient. Treatment options in diabetes will continue to expand as new medications become available and further refinements in treatment decisions occur.
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PMID:Understanding new pharmacologic therapy for type 2 diabetes. 1043 Dec 94


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