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New Onset Diabetes (new + onset_diabetes)
Selected AbstractsCardiovascular drugs as antidiabetic agents: evidence for the prevention of type 2 diabetesDIABETES OBESITY & METABOLISM, Issue 7 2008D. P. Macfarlane Given the long-term health consequences and increasing incidence of type 2 diabetes, there is great interest to potentially prevent or delay its onset. Primary prevention studies have demonstrated that intensive exercise and weight reduction, and to a lesser extent certain antidiabetic agents, can reduce new onset diabetes in at-risk individuals. Results from post hoc analyses and secondary end-point outcomes of large randomized controlled trials of cardiovascular drugs suggest that these may also have beneficial effects, reducing the incidence of new onset diabetes in addition to their proven cardiovascular benefits. Multiple meta-analyses confirm that drugs primarily acting on the renin,angiotensin system (RAS) reduce the incidence of diabetes in the populations studied, perhaps via improved insulin sensitivity and/or effects on pancreatic beta cells. However, results from the recent Diabetes REduction Approaches with Medication study specifically failed to show a significant reduction in the incidence of diabetes with ramipril in individuals with abnormal glucose tolerance at baseline. There is only limited evidence that statins improve glucose tolerance, and although beta-blockers tend to have detrimental effects on glucose tolerance, newer agents with vasodilatory properties may confer benefits. With current guidelines, the use of cardiovascular drugs modifying the RAS will increase in at-risk individuals, but at present, they cannot be recommended to prevent diabetes. [source] Cardioprotection with beta-blockers: myths, facts and Pascal's wagerJOURNAL OF INTERNAL MEDICINE, Issue 3 2009F. H. Messerli Abstract. Beta-blockers were documented to reduce reinfarction rate more than 3 decades ago and subsequently touted as being cardioprotective for a broad spectrum of cardiovascular indications such as hypertension, diabetes, angina, atrial fibrillation as well as perioperatively in patients undergoing surgery. However, despite lowering blood pressure, beta-blockers have never shown to reduce morbidity and mortality in uncomplicated hypertension. Also, beta-blockers do not prevent heart failure in hypertension any better than any other antihypertensive drug class. Beta-blockers have been shown to increase the risk on new onset diabetes. When compared with nondiuretic antihypertensive drugs, beta-blockers increase all-cause mortality by 8% and stroke by 30% in patients with new onset diabetes. Beta-blockers are useful for rate control in patients with chronic atrial fibrillation but do not help restore sinus rhythm or have antifibrillatory effects in the atria. Beta-blockers provide symptomatic relief in patients with chronic stable angina but do not reduce the risk of myocardial infarction. Adverse effects of beta-blockers are common including fatigue, dizziness, depression and sexual dysfunction. However, beta-blockers remain a cornerstone in the management of patients having suffered a myocardial infarction and for patients with heart failure. Thus, recent evidence argues against universal cardioprotective properties of beta-blockers but attest to their usefulness for specific cardiovascular indications. [source] Review article: hepatitis C virus infection and type-2 diabetes mellitus in renal diseases and transplantationALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2005F. Fabrizi Summary A link between hepatitis C virus infection and development of diabetes mellitus has been suggested by many investigators; however, this remains controversial. The mechanisms underlying the association between hepatitis C virus and diabetes mellitus are unclear but a great majority of clinical surveys have found a significant and independent relationship between hepatitis C virus and diabetes mellitus after renal transplantation and orthotopic liver transplantation. We have systematically reviewed the scientific literature to explore the association between hepatitis C virus and diabetes mellitus in end-stage renal disease; in addition, data on patients undergoing orthotopic liver transplantation were also analysed. The unadjusted odds ratio for developing post-transplant diabetes mellitus in hepatitis C virus-infected renal transplant recipients ranged between 1.58 and 16.5 across the published studies. The rate of anti-hepatitis C virus antibody in serum was higher among dialysis patients having diabetes mellitus (odds ratio 9.9; 95% confidence interval 2.663,32.924). Patients with type-2 diabetes-related glomerulonephritis had the highest anti-hepatitis C virus prevalence [19.5% (24/123) vs. 3.2% (73/2247); P < 0.001] in a large cohort of Japanese patients who underwent renal biopsy. The link between hepatitis C virus and diabetes mellitus may explain, in part, the detrimental role of hepatitis C virus on patient and graft survival after orthotopic liver transplantation and/or renal transplantation. Preliminary evidence suggests that anti-viral therapies prior to renal transplantation and novel immunosuppressive regimens may lower the occurrence of diabetes mellitus in hepatitis C virus-infected patients after renal transplantation. Clinical trials are under way to assess if the hepatitis C virus-linked predisposition to new onset diabetes mellitus after renal transplantation may be reduced by newer immunosuppressive medications. [source] Diuretics: A modern day treatment option? (Review Article)NEPHROLOGY, Issue 5 2006MARTIN GALLAGHER SUMMARY: The choice of drugs to initiate therapy for the management of hypertension remains contentious and diuretics are central to this controversy. Because most of the major trials involve complex treatment algorithms and allow diverse background treatments, one of the greatest challenges lies in separating out true class-specific effects , for example, separating true class-specific effects of diuretics from those of beta blockers. Despite these difficulties, the evidence confirms that diuretics are at least as effective as the newer first line groups in preventing cardiovascular events. The main area of doubt lies in relation to the risk of renal outcomes and of metabolic outcomes, such as new onset diabetes , where the evidence suggests that drugs that inhibit the renin-angiotensin system may be more protective than all other drug classes. These issues are reflected in the most recent international guidelines, all of which include diuretics among the first-line drugs for the treatment of hypertension, although they do differ on the role of diuretics in the initiation of therapy. Diuretics remain important for treating hypertension, especially in combination with other drug classes. The particular place of diuretics in the rank order of drugs must be tailored to suit the clinical situation in the individual patient. This will vary from a preferred option, as in black patients or elderly patients with systolic hypertension, to a second-line option in patients at high risk of developing new onset diabetes. [source] Fasting c-peptide and insulin-like growth factor-binding protein-1 levels help to distinguish childhood type 1 and type 2 diabetes at diagnosisPEDIATRIC DIABETES, Issue 2 2007Lorraine E Levitt Katz Background:, Children with new onset diabetes (n = 175) were evaluated over 12-months. Patients were presumptively diagnosed with type 2 diabetes mellitus (T2DM) (n = 26) based on obesity, a relative with T2DM, the ability to wean from insulin, and absence of glutamic acid decarboxylase-65 (GAD-65) antibodies. We hypothesized that markers of insulinization at diagnosis, including fasting C-peptide and insulin-like growth factor-binding protein (IGFBP)-1, in addition to initial CO2 levels and urine ketones, would help in distinguishing type 1 diabetes mellitus (T1DM) from T2DM. Results:, Children with T1DM (84 male, 65 female) had a mean age of 8.7 ± 4.3 yr and a racial background of 78% white, 19% black, and 3% other. In contrast, children with T2DM (13 female, 13 male) had a mean age of 14.2 ± 3.1 yr with a racial background of 58% black, 27% white, and 15% other. Fasting C-peptide level was 0.38 ± 0.37 ng/mL in T1DM vs. 2.66 ± 2.14 ng/mL in T2DM; a C-peptide of 0.85 ng/mL had 83% sensitivity in distinguishing T1DM from T2DM. Fasting IGFBP-1 level was 38.1 ± 39.1 ng/mL (T1DM) vs. 3.6 ± 4.5 ng/mL (T2DM); a value of 3.6 ng/dL could distinguish the two types of diabetes with 93% sensitivity. Urinary ketones were found in 79% of children with T1DM compared with 56% of those with T2DM, and the magnitude was associated with type of diabetes. Initial CO2 level for T1DM was 17.9 ± 6.9 mmol/L vs. 22.7 ± 5.7 mmol/L for T2DM; a value of 21.5 mmol/L could distinguish the two types of diabetes with 83% sensitivity. Conclusions:, In addition to obesity, family history of T2DM, and absence of GAD-65 antibodies, children with new-onset T2DM may be distinguished from those with T1DM by a combination of biochemical parameters (C-peptide, IGFBP-1, CO2, and urine ketones). [source] Allograft diabetic nephropathy may progress to end-stage renal diseasePEDIATRIC TRANSPLANTATION, Issue 4 2004Moro O. Salifu Abstract:, Mesangial expansion and glomerular basement membrane thickening characteristic of diabetic nephropathy recur in diabetic recipients of renal allografts from non-diabetic donors but progression to renal failure is minimally documented. Three female renal allograft recipients (aged 40, 62 and 73 yr), who developed end-stage renal disease (ESRD) due to recurrent diabetic nephropathy (two patients) and de novo diabetes (one patient) are reported. Onset of proteinuria, uncontrolled hypertension, azotemia, renal allograft pathologic findings and the need for hemodialysis were analyzed. None of the kidney donors (one cadaver, two living related) had known diabetes or perturbed glucose metabolism pre-transplantation. The three patients presented had different varieties of diabetes; type 1, type 2 and new onset diabetes after transplantation (NODAT). In each subject, proteinuria was detected by dipstick at a mean of 8.3 yr (range 8,9) post-transplantation and increased to the nephrotic range (3.7,4.8 g/day) inducing hypoalbuminemia and azotemia. A histopathologic diagnosis of allograft diabetic nephropathy was made in a mean of 11.7 yr (range 10,14), based on glomerular basement membrane thickening, nodular and diffuse intercapillary glomerulosclerosis, arteriolosclerosis, and tubular atrophy with marked tubular basement membrane thickening characteristic of advanced diabetic nephropathy. All three patients manifested uremia and resumed hemodialysis. Two patients died from sepsis within 2 months and one patient died 2.5 yr later after resumption of maintenance hemodialysis. We infer that recurrent or de novo diabetic nephropathy in renal allografts follows a clinical decade-long course irrespective of diabetes. Reports of ESRD due to allograft diabetic nephropathy (ADN) have been limited because of shorter survival of diabetic transplant recipients and few kidney biopsies performed in patients with chronic allograft dysfunction. The occurrence of allograft diabetic nephropathy in some, but not all patients, however, suggests that individual genetic variability modulates disease expression. [source] Atypical antipsychotic drugs and diabetesPRACTICAL DIABETES INTERNATIONAL (INCORPORATING CARDIABETES), Issue 9 2003Dr C Livingstone BSc, MBChB, MRCPath Consultant Chemical Pathologist Abstract The atypical antipsychotic drugs have enhanced the quality of life in many patients with schizophrenia. Their main advantage over conventional antipsychotic drugs is their propensity to cause fewer extrapyramidal adverse effects. However, there is increasing evidence that atypical antipsychotic drugs are associated with metabolic adverse effects including weight gain, new onset diabetes (both type 2 diabetes and diabetic ketoacidosis) and hypertriglyceridaemia. These problems are most common with clozapine. We discuss the mechanism of the association and recommendations for screening and monitoring in order that metabolic problems can be detected and treated early. Copyright © 2003 John Wiley & Sons, Ltd. [source] Cigarette smoking is an independent risk factor for type 2 diabetes: a four-year community-based prospective studyCLINICAL ENDOCRINOLOGY, Issue 5 2009Nam H. Cho Summary Objectives, We investigated the association between smoking and its additive effects with insulin resistance and ,-cell function on the incidence of type 2 diabetes in a prospective population-based cohort study. Design and method, A total of 10 038 subjects were recruited from rural and urban areas. All subjects underwent 75 g oral glucose tolerance tests and full biochemical assessments at baseline and during 4-year follow-up period. The final analysis was limited to 4041 men due to the low smoking rates in women. Results, The ex- and heavy current smokers had the highest incidence of diabetes of 12·5% and 11·1% respectively, compared with never-smokers (7·9%) during 4 years. After multivariate adjustment by Cox-proportional hazard model, ex- and current smokers reveal a relative risk of 1·60 (95% CI: 1·07,2·39), 2·06 (1·35,3·16, for <20 cigarettes/day) and 2·41 (1·48,3·93, for ,20 cigarettes/day) respectively compared with never smokers. The risk of new onset diabetes was the highest in those with low homeostasis model assessment for beta cell function (HOMA-,) and high homeostasis model assessment for insulin resistance (HOMA-IR) group in both smokers and never smokers. Conclusions, Smoking is an independent risk factor for type 2 diabetes mellitus and showed synergistic interaction with the status of low insulin secretion and high insulin resistance for developing diabetes. Given the high rates of smoking and growing burden of diabetes in the world, cessation of smoking should be considered as one of the key factors for diabetes prevention and treatment programmes. [source] | ||||||||||