摘要:

Purpose of reviewThe prevalence of cardiovascular disease is markedly increased in patients with type 2 diabetes and to a somewhat lesser extent impaired glucose tolerance (IGT). This has generally been attributed to the concurrent presence of cardiovascular disease risk factors, including dyslipidemia, hypertension, coagulation abnormalities, and insulin resistance (i.e., the metabolic syndrome). This article reviews the current literature on cardiovascular disease in patients with diabetes, and in particular, the notion that treatment should be initiated as early as possible, indeed even prior to the onset of diabetes, to prevent this complication.Recent findingsThe recently reported Steno-2 Trial on multifactorial intervention and cardiovascular disease in type 2 diabetic patients with microalbuminuria demonstrated a 50% decrease in the incidence of cardiovascular events. However, morbidity and mortality rates were still high, suggesting the need either for additional therapies or for earlier treatment, or both. The potential of earlier treatment was evaluated in the Diabetes Prevention Program Trial (DPP) in which the effects of lifestyle modification with diet and exercise and pharmacologic therapy were assessed in patients with IGT. Cardiovascular endpoints have not yet been reported; however, it was clearly shown that progression to type 2 diabetes was diminished by nearly 60% when patients were treated with diet and exercise and by 31% when metformin was used. Similar results with lifestyle modification were also obtained in the Finnish Diabetes Prevention Study.The metabolic syndrome antedates and may be causal for type 2 diabetes, IGT, and cardiovascular disease in many patients, and hypothetically it could be an even more effective target for prevention. Recent studies suggest that the metabolic syndrome may be related to dysregulation of a malonyl CoA-AMP–activated protein kinase (AMPK) fuel sensing mechanism that allows lipid to accumulate in muscle, liver, and other sites. Therapeutically, this is an attractive notion, since AMPK is activated by exercise, metformin, thiazolidinediones, and the fat cell–derived hormone adiponectin, all of which appear to diminish tissue lipid accumulation, increase insulin sensitivity, and decrease coronary heart disease.SummaryNumerous studies suggest that treatment directed at the metabolic syndrome, which often antedates type 2 diabetes and IGT should be considered as a means of preventing both these disorders and the cardiovascular disease with which they are often associated. Available evidence suggests that diet, exercise, and other treatments that activate AMPK could be useful in diminishing cardiovascular disease risk in these individuals, as well as retarding the development of diabetes.

ISSN:1068-3097    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of the reviewMortality from cardiovascular complications is largely responsible for the guarded prognosis of patients with diabetes mellitus. One important event that contributes to these cardiovascular complications is endothelial dysfunction, an early, yet reversible feature of diabetes. Endothelial function is closely associated with nitric oxide biology and signaling and is particularly sensitive to oxidative stress that is associated with diabetes mellitus. The purpose of this brief review, therefore, is to highlight recent findings concerning the mechanisms of diabetic endothelial dysfunction with a particular focus on oxidative stress.Recent findingsSeveral sources of superoxide have been identified in diabetes including NADPH oxidases, mitochondria, and endothelial nitric oxide synthase that cause endothelial dysfunction through peroxynitrite formation. In addition, tyrosine nitration of the prostacyclin synthase by peroxynitrite leads to decreased prostacyclin formation and is a novel mechanism of oxidative stress impairing endothelial function independent of nitric oxide bioavailability. Although unrelated to oxidative stress, exciting evidence points to a role for endothelial progenitor cells with regard to their decreased availability and impaired function in diabetes that may play a role in shaping future investigative strategies.SummaryThus, increasing evidence over the past few years has implicated oxidative stress as a central feature of impaired endothelial function in diabetes. These recent findings should help to identify strategies to improve endothelial function in diabetes and, perhaps, reduce the vascular the complications of this disease.

ISSN:1068-3097    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewDyslipidemia may contribute to the accelerated atherosclerosis of diabetes and the microvascular complications of nephropathy and retinopathy. In type 1 diabetes, the standard lipid profile is relatively normal, but lipoproteins may be abnormal in other aspects such as size, composition including nonenzymatic glycation and alterations in related enzymes, and function. These quantitative and qualitative alterations of lipoproteins may be influenced by both genetic and acquired factors. To provide the reader with an update of this ongoing area of research, we review the literature relevant to lipoprotein abnormalities in type 1 diabetes that was published between March 1, 2002 and February 28, 2003.Recent findingsA dyslipoproteinemia that resembles that usually associated with insulin resistance is revealed by lipoprotein subclass analysis by nuclear magnetic resonance. Further studies support there being abnormal composition and function of low-density lipoprotein and high-density lipoprotein in diabetes, such as nonenzymatic glycation and altered enzyme activities. New studies provide evidence linking some lipoprotein-related genotypes in type 1 diabetes to abnormal lipoproteins, and in some cases, to complication susceptibility.SummaryNew tools, including novel assays and surrogate measures of vascular disease, have been used to increase knowledge of potential mediators of vascular damage and to suggest rational novel interventions to reduce the burden of the chronic vascular complications of type 1 diabetes. Further clinical and basic science research in the area is warranted to guide clinical practice.

ISSN:1068-3097    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewDiabetes results in the development of diabetic cardiomyopathy, a primary cardiac disease characterized pathologically by cardiomyocyte hypertrophy and apoptosis, and hemodynamically by impaired cardiac relaxation progressing to overt contractile failure. Despite the overwhelming incidence of diabetes, diabetic cardiomyopathy still remains a poorly understood disorder for which no established cause or specific treatment exists.Recent findingsRecent data in animal models of diabetes, as well as studies examining the role of metabolism in regulating myocardial phenotype, suggest that derangements in glucose metabolism and lipid transport may directly alter cardiac structure and function. In this review, we discuss the potential mechanisms underlying the development of diabetic cardiomyopathy.SummaryRecent findings will allow for greater insight into the pathogenesis of diabetic cardiomyopathy and allow for the development of novel therapeutic targets.

ISSN:1068-3097    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewThis article reviews the recent literature concerning peripheral vascular disease (PVD) in diabetic patients and how to treat it.Recent findingsMost of the literature published between March 2002 and February 2003 on this subject discusses the importance of medical therapies for control of diabetes and other comorbidities, as well as endovascular management of critical limb ischemia.SummaryDiabetes confers a high incidence of cardiovascular complications, including those associated with PVD. PVD occurs at a younger age, does not spare women, and progresses more rapidly and severely in diabetic patients. PVD-related ulcerations leading to infection, poor healing, gangrene, and resultant amputations are an increasing problem for diabetic patients, despite our best efforts.

ISSN:1068-3097    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Prolactinoma is the most common hormone-secreting pituitary adenoma. The approach to prolactinomas has changed in the past 25 years, thanks to treatment with dopamine agonists, which is characterized by a potent prolactin inhibitory effect, a tumor-shrinking effect, and a good tolerability. Cabergoline is a new dopamine agonist with a natural long duration of action and selectivity for the D2receptor. The authors discuss the criteria for stopping treatment with cabergoline in prolactinomas. According to their experience, they withdraw cabergoline treatment in prolactinomas after normalization of serum prolactin levels and tumor disappearance or no further reduction of tumor size on MRI during the last 12 months of follow-up.

ISSN:1068-3097    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

The rare condition of acromegaly requires vigorous therapy to relieve symptoms, control comorbidities and to restore life expectancy to normal. In most individuals, transsphenoidal surgery is the appropriate, initial treatment; although, the majority of patients have macroadenomas and are not cured by surgery. The role of radiotherapy in patients not cured by surgery is controversial and evolving. However, even when administered, radiotherapy can take several years to achieve control of the GH/IGF-I axis; thus, patients require medical therapy.Currently, most patients receive somatostatin analogs; but unfortunately, GH and IGF-I levels remain elevated in a significant minority. The GH receptor antagonist pegvisomant is capable of normalizing serum IGF-I in 97% of patients and thus offers the prospect of achieving biochemical control in virtually every patient. However, pegvisomant does not lower circulating GH levels and makes no attempt to restrain tumor growth. This review contrasts the relative merits of the two classes of drug and attempts to define their places in the acromegaly treatment algorithm.

ISSN:1068-3097    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewAlthough clinicians often rely on experience and anecdote to diagnose Cushing syndrome and its subtypes, clinical decision-making is increasingly influenced by hierarchical evidence-based criteria.Spectrum effectrefers to the variability of diagnostic test performance across different populations. The objective of this review is to discuss spectrum effect in the evaluation of Cushing syndrome and to alert the clinician and clinical investigator to a phenomenon that commonly affects diagnostic tests.Recent findingsMost of the diagnostic tests used for Cushing syndrome have been developed and tested in highly specialized referral centers following rigid diagnostic test protocols that may not be accurately reproduced when the tests are applied in medical practice within the community. Because of an increasing concern to raise awareness of this issue, thorough evaluation of the performance of diagnostic tests is advocated. To avoid spectrum effect, investigators should include a heterogeneous group of patients and perform subgroup analyses by stratifying on the characteristic defining the subgroup.SummaryFailure to identify and address the spectrum effect ultimately may erroneously confirm or exclude the diagnosis of Cushing syndrome and its subtypes.

ISSN:1068-3097    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewGrowth hormone deficiency is no longer just a condition of childhood. The significant derangements in many metabolic parameters and the potential serious consequences of untreated growth hormone deficiency in adulthood, including increased cardiovascular mortality, have raised awareness of growth hormone as a hormone that influences much more than growth, and growth hormone deficiency as a condition that disrupts much more than height. Consequently, the standard pediatric approach to treatment of growth hormone deficiency, which focuses myopically on linear growth and ends at attainment of adult height, needs to be reexamined. This review addresses key issues surrounding the transition of the patient with growth hormone deficiency from the end of childhood to the beginning of adulthood.Recent findingsA number of factors are predictive of persistence of growth hormone deficiency after childhood, including the etiology and age at onset of childhood growth hormone deficiency, number of additional pituitary hormone deficits, reflecting severity of pituitary dysfunction, and serum concentrations of insulin-like growth factor I and insulin-like growth factor binding protein-3. There are many negative consequences of discontinuation of growth hormone at attainment of final height, and patients with severe growth hormone deficiency should probably continue therapy uninterrupted through the transition phase. Patients in this phase of development require higher growth hormone doses than adults, and responses to growth hormone therapy are significantly influenced by gender.SummaryThe transition phase represents a newly defined developmental stage that serves to complete the aspects of physical and metabolic development that remain immature after attainment of adult height. As such, the physiology and pathology of this group of patients differ from those in childhood or in adulthood. Assessment and treatment of patients in this phase of life should acknowledge that these patients are not just “older children” or “younger adults,” but that they are a unique and separate group with distinct and different needs.

ISSN:1068-3097    

出版商:OVID    

年代:2003

数据来源: OVID

ISSN:1068-3097    

出版商:OVID    

年代:2003

数据来源: OVID