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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension occurs in approximately 30% of patients with type 1 diabetes and from 50 to 80% of patients with type 2 diabetes. Although the pathogenesis of hypertension is distinct in each type, hypertension markedly enhances the already high risk of cardiovascular and renal disease in types 1 and 2 and implications for treatment are similar in both. The threshold for blood pressure treatment in diabetic patients is generally agreed to be 140/90 mm/hg with a target BP of < 130/80. So-called "lifestyle modifications" play an important role in therapy, particularly in type 2 patients, by decreasing blood pressure and improving other risk factors for cardiovascular disease. Indeed non-pharmacologic interventions have been demonstrated to prevent the development of type 2 diabetes in patients at high risk to develop the disease. Aggressive anti-hypertensive drug treatment is warranted given the high risk associated with the combination of diabetes and hypertension and the demonstrated effectiveness of anti-hypertensive treatment in reducing cardiovascular morbidity and mortality in this group of patients. ACE inhibitors and ARBs are the cornerstones of pharmacologic management, in no small part because of the renoprotective effects of these agents in antagonizing the development and progression of diabetic renal disease. Multiple agents, including diuretics, will usually be required to attain target blood pressure levels.
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PMID:Diabetes and hypertension: pathogenesis, prevention and treatment. 1570 16

A patient with a history of type II diabetes mellitus (DM), end stage renal disease (ESRD), and congestive heart failure (CHF) developed necrotizing fasciitis caused by Serratia marcescens after scraping his leg on rocks in a river while fishing. Aggressive management with surgical debridement, antibiotics, and pressure support was unsuccessful.
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PMID:A fatal case of necrotizing fasciitis caused by Serratia marcescens. 1586 38

Aggressive treatment of hypertension is effective in reducing both microvascular and macrovascular complications in type 2 diabetes, with target BP < 130/80 mmHg being recommended. Angiotensin-converting enzyme inhibitors were found to be more effective than the other traditional agents in reducing the onset of clinical proteinuria in individuals with both type 1 and type 2 diabetes and incipient nephropathy. However, small trials on patients with type 2 diabetes and overt nephropathy failed to demonstrate a specific renoprotective role for this class of drugs. The aim of the Program for Irbesartan Mortality and Morbidity Evaluation was to ascertain whether angiotensin II receptor blockers are effective in both preventing the development of clinical proteinuria and delaying the progression of nephropathy in type 2 diabetes. The Irbesartan in Patients with Type 2 Diabetes and Microalbuminuria (IRMA) Study showed that, as compared with conventional therapy, irbesartan is better at preventing the development of clinical proteinuria and at restoring normoalbuminuria for comparable BP control in patients with incipient nephropathy. The Irbesartan Diabetic Nephropathy Trial showed that irbesartan is more effective than traditional antihypertensive therapies in reducing the progression toward ESRD in patients with type 2 diabetes and overt nephropathy regardless of changes in BP. Moreover, secondary analysis of the Irbesartan Diabetic Nephropathy Trial showed that the achieved systolic pressure as well as baseline and current proteinuria significantly predict renal outcomes. In conclusion, the results of the Program for Irbesartan Mortality and Morbidity Evaluation demonstrate that irbesartan significantly prevents the development of clinical proteinuria in individuals with microalbuminuria and delays the progression of nephropathy in individuals with proteinuria. Moreover, the renoprotective effects of irbesartan go beyond its effect on BP.
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PMID:Prevention and treatment of diabetic nephropathy: the program for irbesartan mortality and morbidity evaluation. 1593 34

Cardiovascular disease (especially coronary heart disease ) is the most common complication and cause of death in patients with type 2 diabetes. CHD prevention should be the major focus in preventive care of diabetes patients. There is a solid evidence base from which to recommend aggressive control of elevated blood pressure and lipids to reduce CHD events in diabetes. Aggressive glycemic control alone will not reduce CHD events, but will prevent diabetes-specific microvascular complications. Blood pressure should be treated to a goal of at least 130/80 mm Hg, and possibly lower, using angiotensin-converting enzyme inhibitors, thiazide diuretics, or beta blockers as first-line agents. Low-density lipoprotein cholesterol should be treated with a statin to reduce the level by 30% to 40%, regardless of pretreatment level, to a goal of less than 100 mg/dL for most patients or a goal of less than 70 mg/dL in diabetes patients with CHD. Patients with high-density lipoprotein levels less than 40 mg/dL may benefit from fibrate therapy. Cigarette smoking should be actively discouraged, and prophylactic aspirin therapy should be prescribed for most patients. A regular program of physical activity and weight control should be prescribed to improve insulin sensitivity. Use of thiazolidinediones may be considered early in the course of hypoglycemic therapy, but additional research is needed to define the role of insulin sensitization as a primary means to reduce CHD risk in type 2 diabetes.
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PMID:Prevention of coronary heart disease in diabetes. 1600 57

Serotonin (5-HT) is a neuromodulator that regulates many aspects of animal behavior, including mood, aggression, sex drive, and sleep. In vertebrates, most of the behavioral effects of 5-HT appear to be mediated by G-protein-coupled receptors (GPCRs). Here, we show that SER-1 is the 5-HT GPCR responsible for the stimulatory effects of exogenous 5-HT in two sexually dimorphic behaviors of Caenorhabditis elegans, egg laying and male ventral tail curling. Loss of ser-1 function leads to decreased egg laying in hermaphrodites and defects in the turning step of mating behavior in males. ser-1 is expressed in muscles that are postsynaptic to serotonergic neurons and are known to be required for these behaviors. Analysis of the ser-1 mutant also reveals an inhibitory effect of 5-HT on egg laying that is normally masked by SER-1-dependent stimulation. This inhibition of egg laying requires MOD-1, a 5-HT-gated chloride channel. Loss of mod-1 function in males also produces defects in ventral tail curling and enhances the turning defects in ser-1 mutant males. Sustained elevations in 5-HT levels result in behavioral adaptation to both the stimulatory and inhibitory actions of the neurotransmitter, indicating that both SER-1 and MOD-1 signaling can be modulated. Removal of wild-type animals from high levels of exogenous 5-HT produces a SER-1-dependent withdrawal response in which egg laying is significantly decreased. These studies provide insight into the role of 5-HT in behavior and the regulation of 5-HT(2) receptor function.
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PMID:The G-protein-coupled serotonin receptor SER-1 regulates egg laying and male mating behaviors in Caenorhabditis elegans. 1629 40

Necrotizing fasciitis is a soft-tissue infection characterized by extensive necrosis of subcutaneous fat, neurovascular structures, and fascia. In general, fascial necrosis precedes muscle and skin involvement, hence its namesake. Initially, this uncommon and rapidly progressive disease process can present as a form of cellulitis or superficial abscess. However, the high morbidity and mortality rates associated with necrotizing fasciitis suggest a more serious, ominous condition. A delay in diagnosis can result in progressive advancement highlighted by widespread infection, multiple-organ involvement, and, ultimately, death. We present a case of limb salvage in a 52-year-old patient with type 2 diabetes mellitus and progressive fascial necrosis. A detailed review of the literature is presented, and current treatment modalities are described. Aggressive surgical debridement, comprehensive medical management of the sepsis and comorbidities, and timely closure of the resultant wound or wounds are essential for a successful outcome.
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PMID:Necrotizing fasciitis in a patient with type 2 diabetes mellitus. 1641 86

Patients with type 2 diabetes mellitus are at high risk for cardiovascular events and heart failure. The major serious complication of this disorder is large vessel atherosclerosis leading to myocardial infarction and stroke. Aggressive target setting for modifiable cardiovascular risk factors such as dyslipidemia, hypertension, and a procoagulant state, and judicious choice of efficacious therapies have been shown to produce significant reductions in cardiovascular events. The effectiveness of percutaneous coronary intervention (PCI) in diabetes is discussed, and the factors that may influence outcomes are explored. A major unresolved question is the potential role of tight glucose control for reducing macrovascular complications in patients with diabetes. With the increased attention being given to cardiovascular risk factor reduction, the opportunity exists to substantially decrease the largest causes of mortality in diabetic patients. This article reviews the current and emerging therapeutic strategies for these purposes from the cardiologists' point of view.
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PMID:[Type 2 diabetes mellitus and cardiovascular diseases: evaluation, treatment and prevention strategies]. 1650 21

Dyslipidemia is an important component of the metabolic syndrome. Dyslipidemia in the metabolic syndrome is characterized by hypertriglyceridemia, low serum levels of high density lipoprotein cholesterol (HDL-C) and an increase in the serum fraction of small dense low density lipoprotein cholesterol (LDL-C) particles. Serum LDL-C elevation is frequently present, but is not a criterion of the metabolic syndrome. A Medline search was conducted using the terms metabolic syndrome, dyslipidemia, hypertriglyceridemia and HDL cholesterol. The metabolic syndrome is a common and important risk factor for cardiovascular disease and progression to type 2 diabetes mellitus. Dyslipidemia is present in most patients with the metabolic syndrome and is treatable with therapeutic lifestyle changes and pharmacotherapy. Aggressive management of atherogenic dyslipidemia is justified by the very high cardiovascular risk associated with this disorder. Atherogenic dyslipidemia is frequently present in patients with the metabolic syndrome and requires aggressive treatment due to the very high risk for cardiovascular disease and progression to type 2 diabetes mellitus.
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PMID:Dyslipidemia in the metabolic syndrome: clinical implications and management. 1677 53

Olanzapine is a novel antipsychotic, approved for the acute and maintenance treatment of schizophrenia and bipolar I disorder. Despite the publicity regarding reported adverse events with the novel antipsychotics, such as weight gain and Type II diabetes mellitus, olanzapine remains a useful and important medicine. It is a selective monoaminergic antagonist with high-affinity binding to a number of receptors thought to be implicated in some psychotic and mood symptoms. The complex pharmacology of olanzapine has lead to studies exploring its use in treating substance abuse, aggression/violence, borderline personality disorder, schizotypal personality disorder, obsessive-compulsive disorder and as a neuroprotective agent in schizophrenia. As the pharmacology of olanzapine and other novel antipsychotics becomes better understood, future effective treatment strategies are likely to match an individual's genetic makeup and receptor profiles to the most compatible agent.
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PMID:Olanzapine: a 5-year perspective. 1678 5

Sleep has important homeostatic functions, and sleep deprivation is a stressor that has consequences for the brain, as well as many body systems. Whether sleep deprivation is due to anxiety, depression, or a hectic lifestyle, there are consequences of chronic sleep deprivation that impair brain functions and contribute to allostatic load throughout the body. Allostatic load refers to the cumulative wear and tear on body systems caused by too much stress and/or inefficient management of the systems that promote adaptation through allostasis. Chronic sleep deprivation in young healthy volunteers has been reported to increase appetite and energy expenditure, increase levels of proinflammatory cytokines, decrease parasympathetic and increase sympathetic tone, increase blood pressure, increase evening cortisol levels, as well as elevate insulin and blood glucose. Repeated stress in animal models causes brain regions involved in memory and emotions, such as hippocampus, amygdala, and prefrontal cortex, to undergo structural remodeling with the result that memory is impaired and anxiety and aggression are increased. Structural and functional magnetic resonance imaging studies in depression and Cushing's disease, as well as anxiety disorders, provide evidence that the human brain may be similarly affected. Moreover, brain regions such as the hippocampus are sensitive to glucose and insulin, and both type 1 and type 2 diabetes mellitus are associated with cognitive impairment and (for type 2 diabetes mellitus) increased risk for Alzheimer's disease. Animal models of chronic sleep deprivation indicate that memory is impaired along with depletion of glycogen stores and increases in oxidative stress and free radical production. Taken together, these changes in brain and body are further evidence that sleep deprivation is a chronic stressor and that the resulting allostatic load can contribute to cognitive problems, which can, in turn, further exacerbate pathways that lead to disease.
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PMID:Sleep deprivation as a neurobiologic and physiologic stressor: Allostasis and allostatic load. 1697 22


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