Diagnostic Tool for the treatment of diabetes in adults or children

Diagnostic Tool for the treatment of diabetes in adults or children

Identify a research or evidence-based article that focuses comprehensively on a specific intervention or new diagnostic tool for the treatment of diabetes in adults or children.

In a paper of 750-1,000 words, summarize the main idea of the research findings for a specific patient population. Research must include clinical findings that are current, thorough, and relevant to diabetes and the nursing practice.

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Diagnostic Tool for the treatment of diabetes in adults or children

The Pathophysiologic Basis for Diabetes Treatment: Evolving Perspectives , Presented by Lawrence Blonde, MD, FACP, FACE

The Growing Epidemic of Type 2 Diabetes

The last decade has seen a dramatic increase in the prevalence of obesity[1] which, in turn, has led to an associated increase in the prevalence of many obesity-related diseases, including diabetes. In fact, the increased prevalence of diabetes mirrors the increase in obesity during this period, helping diabetes to reach virtually epidemic proportions.

There now are 20.8 million Americans with diabetes, 20.6 million of whom are adults. This represents just under 10% of all adults in the United States. Among people 60 years of age and older — the fastest-growing age segment of our society — an alarming 21% have diabetes.[2] Type 2 diabetes is also being increasingly diagnosed in children and adolescents, at least in part as the result of an increase in obesity in that age group as well.

Diabetes is the number one cause of adult blindness, the number one cause of end-stage kidney disease, and the number one cause of nontraumatic amputation in this country. Diabetes also increases the prevalence of coronary heart disease and stroke by 2- to 4-fold. Largely related to these complications, direct medical and indirect expenditures attributable to diabetes in 2002 were estimated at $132 billion.[3]

Pathophysiology and Natural History of Type 2 Diabetes

Most people who develop type 2 diabetes develop insulin resistance many years earlier. Initially, enhanced insulin production can compensate for the insulin resistance so that the person maintains normal fasting and postprandial glucoses. However, as insulin levels fall, there is first an increase in postprandial glucose levels followed by fasting hyperglycemia.[4]

Risk for microvascular complications of diabetes — the eye disease, the kidney disease — generally is associated with hyperglycemia sufficient to diagnosis type 2 diabetes. Macrovascular complication risks actually begin in the prediabetes stage, usually associated with insulin resistance. Moreover, many people have type 2 diabetes for 5 to 10 years before the diagnosis is made, so that a significant percentage of them already have complications at the time of diagnosis.[5,6]

The American Diabetes Association (ADA) identifies fasting plasma glucose (FPG) of less than 100 mg/dL as normal. A normal glucose value 2 hours after ingesting a 75-g glucose challenge is less than 140 mg/dL. Diabetes is defined as an FPG of 126 mg/dL or greater, or a 2-hour post-glucose challenge result of 200 mg/dL or greater. Fasting and/or post-glucose challenge values above normal but not diagnostic of diabetes are termed impaired fasting glucose (IFG) or impaired glucose tolerance (IGT), respectively.[3]

People with IFG, IGT, or both are said to have prediabetes. Prior to developing type 2 diabetes, most people have a prediabetes phase, and most people with prediabetes will progress to type 2 diabetes within about 10 years. However, even those who do not will have an increased risk of atherosclerosis.

Studies have indicated that type 2 diabetes can be delayed or even prevented. In the Diabetes Prevention Program study, approximately 3200 people with IGT were randomized into 3 groups. They either received a placebo, metformin, or a lifestyle intervention that had modest goals including losing at least 7% of body weight and exercising 30 minutes a day, 5 days a week, at the equivalent intensity of brisk walking. Compared with placebo, even this modest lifestyle modification was associated with a 58% reduction in the progression from prediabetes to diabetes.[7] So we know that we can at least delay, if not prevent, the progression from prediabetes to diabetes. Therefore, at-risk individuals should be screened during healthcare visits to identify those with pre-diabetes. This approach will also uncover a significant number of people with undiagnosed diabetes so they can receive needed treatment.

Insulin Resistance Syndrome and Metabolic Syndrome

  • Most people with prediabetes also have what has been called the insulin resistance syndrome. This syndrome includes glucose abnormalities, high insulin levels, insulin resistance, dyslipidemia, hypertension, central obesity, and other characteristics, and is associated with increased risk for development of atherosclerosis as well as diabetes.
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  • Most of those with the insulin resistance syndrome have what the National Cholesterol Education Program (NCEP) has called the “metabolic syndrome.” NCEP has identified defining levels for 5 risk factors, including abdominal obesity, increased triglycerides, low high-density lipoprotein (HDL) cholesterol levels, a blood pressure of 130/85 mm Hg or greater, and a glucose level of 100 mg/dL or greater. If a person has 3 or more of those risk factors, they have the metabolic syndrome.

    People with the metabolic syndrome are likely to have insulin resistance and be at increased risk to develop diabetes, atherosclerosis, and all of their accompanying morbidities.[8]

    When the NCEP first described the metabolic syndrome in 2001, it was found that almost a quarter of the adult population surveyed and approximately 45% of the subpopulation 60 years of age and older had the metabolic syndrome.[9] A recent update from the NCEP found that now almost 35% of the total adult population has the metabolic syndrome.[10]

    The ADA and the European Association for the Study of Diabetes issued a joint statement calling for a reappraisal of the metabolic syndrome. The statement suggested that the basis for inclusion or exclusion of risk factors in the definition is not clear, and that the rationale for the thresholds is ill defined.

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  • The paper also made several clinical recommendations regarding management of people with metabolic syndrome.[11] The NCEP, in turn, produced a paper outlining their recommendations for the diagnosis and management of the metabolic syndrome.[12] These 2 statements actually agree on many points. Moreover, the 2 organizations have recently published a paper titled “Preventing Cardiovascular Disease and Diabetes: A call to action from the American Diabetes Association and the American Heart Association.” In the conclusion of this paper, they state, “Despite many unresolved scientific issues, a number of cardiometabolic risk factors have been clearly shown to be closely related to diabetes and CVD [cardiovascular disease]: fasting/postprandial hyperglycemia, overweight/obesity, elevated systolic and diastolic blood pressure, and dyslipidemia. Although pharmacologic therapy is often indicated when overt disease is detected, in the early stages of these conditions, lifestyle modification with attention to weight loss and physical activity may well be sufficient.”[13]
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  • Despite its shortcomings, many medical thought leaders and clinicians agree that people with the metabolic syndrome are at increased risk for both diabetes and CVD. Lakka and colleagues used data from the Kuopio Ischaemic Heart Disease Risk Factor study, a population-based, prospective, cohort study of 1209 Finnish men aged 42 to 60 years at baseline (1984-1989) who were initially without CVD, cancer, or diabetes. Follow-up continued through December 1998. They found that CVD and all-cause mortality were increased in men with the metabolic syndrome, even in the absence of baseline CVD and diabetes.[14]
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Factors Contributing to Insulin Resistance

  • Insulin resistance is a key component of the pathophysiology of most cases of type 2 diabetes. While inheritance plays a role, not much is known about the underlying genetic contributors to insulin resistance. However, many contributing environmental factors have been identified.

    Increased visceral or abdominal adipose tissue is a major contributor to insulin resistance. Visceral fat is not simply an inert lipid storage repository, but rather a secretory organ manufacturing and releasing a variety of hormones as well as autocrine and paracrine substances, including inflammatory modulators that increase the risk for a variety of abnormalities.[15] Excess quantities of most of these substances can decrease insulin sensitivity and/or lead to other adverse effects. An exception is adiponectin, which is actually decreased with insulin resistance.

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Insulin Resistance and Type 2 Diabetes

  • While most people with type 2 diabetes have insulin resistance, insulin resistance alone will not produce diabetes. If beta-cell function is normal, one can compensate for insulin resistance by increasing insulin secretion. While this may be associated with findings of the insulin resistance syndrome, it prevents progression to prediabetes or diabetes. In contrast, all type 2 patients have at least a relative defect in the ability to secrete insulin from their beta cells. This results from decrements in both beta-cell function and mass. For example, in the United Kingdom Prospective Diabetes Study (UKPDS), newly diagnosed people with diabetes had, on average, only about 50% of normal beta-cell function.[6,16] As people were followed over the subsequent years of the UKPDS, there was a further progressive fall in beta-cell insulin-secretory function. By extrapolating backward, the researchers estimated that this beta-cell defect had begun 5 to 10 years before the diagnosis of diabetes.
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Studies of Beta-cell Mass

Autopsy studies comparing the volume of beta cells in nondiabetic individuals with that of people with diabetes found a 41% decrease in beta-cell mass among people with type 2 diabetes, regardless of whether individuals were lean or obese.[17] Another cadaver study that compared the islet-cell mass with the total mass of the pancreas revealed decreased islet-cell mass in individuals with type 2 diabetes compared with controls. Furthermore, glucose stimulation of isolated islet cells in vitro demonstrated that insulin release was decreased in cells from the patients with type 2 diabetes.[18] Progressive loss of beta-cell mass and beta-cell function, therefore, is an important therapeutic target in the management of people with type 2 diabetes.

Abnormal Insulin and Glucagon Response in Patients With Type 2 Diabetes

Administration of a bolus of intravenous (IV) glucose to a nondiabetic individual results in a biphasic insulin response: there is an immediate first-phase insulin response in the first few minutes, followed by a second-phase, more prolonged response. This first-phase insulin response is absent when a similar IV glucose bolus is administered to someone with type 2 diabetes. This deficiency contributes to the excessive and prolonged glucose rise after a meal in those with diabetes.[19]

In response to a carbohydrate-containing meal, individuals without diabetes not only increase insulin secretion but also simultaneously decrease pancreatic alpha-cell glucagon secretion. The decrease in glucagon is associated with a decrease in hepatic glucose production, and along with the insulin response, results in a very modest increase in postprandial glucose.[20]

In contrast, people with type 2 diabetes have a delayed and diminished insulin response to a carbohydrate meal, and their glucagon secretion is not decreased, and may even be paradoxically increased. These insulin and glucagon abnormalities produce an excessive postprandial glucose excursion. Historically, hyperglycemia in diabetes has been viewed as a failure of insulin-mediated glucose disposal into muscle and adipose tissue. However, these data suggest that hyperglycemia is also the result of excessive appearance of glucose due to unregulated hepatic glucose production. Infusing insulin can improve the insulin but not the glucagon profile. This is why, until recently, it has been difficult to control postprandial glucose levels in patients with diabetes. In fact, more than 30 years ago, Roger Unger presciently stated, “One wonders if the development of a pharmacologic means of suppressing glucagon to appropriate levels would increase the effectiveness of available treatments for diabetes.”[20]

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The Role of Gastric Emptying in Postprandial Hyperglycemia

Another factor contributing to postprandial hyperglycemia is accelerated gastric emptying. The rate of gastric emptying correlates directly with postprandial glucose increments. Many factors, such as the glucose levels themselves, the form of the food ingested, etc, can affect the rate of gastric emptying. However, studies suggest that all other factors being equal, most people with type 1 and type 2 diabetes have accelerated gastric emptying compared to those without diabetes.[21,22]

The Role of Incretins in Glucose Homeostasis

In healthy individuals, an oral glucose load is associated with a greater insulin response than administration of an isoglycemic IV glucose infusion designed to mimic the plasma glucose excursion achieved by the oral glucose load. This enhanced insulin response to oral glucose has been called the incretin effect.[23] Incretin hormones were discovered when researchers tried to understand what caused this enhanced insulin response to oral glucose. These hormones are produced by the gastrointestinal tract in response to incoming nutrients, and have important actions that contribute to glucose homeostasis.

The 2 most important incretins are gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). Type 2 diabetes patients have a resistance to GIP, making it a less attractive therapeutic target. GLP-1 is a 30-amino acid peptide secreted in response to the oral ingestion of nutrients by L cells, primarily in the ileum and colon. There are GLP-1 receptors in islet cells and in the central nervous system, among other places. GLP-1 is metabolized by the enzyme dipeptidyl peptidase-IV (DPP-IV), and the secretion and levels of GLP-1 are decreased in people with type 2 diabetes.

GLP-1 is responsible for a number of actions that help control glucose levels after a meal. It enhances glucose-dependent insulin secretion, inhibits glucagon secretion and therefore hepatic glucose production, and slows gastric emptying. GLP-1 also increases satiety resulting in less food intake. GLP-1 also appears to stimulate insulin gene transcription and insulin synthesis.

In animal studies, GLP-1 has also been shown to increase beta-cell mass by decreasing apoptosis or programmed beta-cell death, and increasing both beta-cell replication and neogenesis, where new beta-cells are formed from pancreatic ductal cells.[24]

  • In a small study of patients with type 2 diabetes, infusion of GLP-1 resulted in an increase in insulin, a decrease in glucagon, and a resultant decrease in glucose. However, as glucose levels approached the normal range, the GLP-1 effects on insulin stimulation and glucagon inhibition declined, indicating glucose dependence of these actions.[25] Glucose-dependent insulin secretion and glucagon inhibition should reduce the risk for hypoglycemia, which would be a therapeutic advantage. Therapies based on this incretin effect are described later on in this activity.

    Unfortunately, GLP-1 is rapidly broken down by the DPP-IV enzyme and, therefore, has a very short half-life in plasma. To use GLP-1 to treat people with type 2 diabetes would require continuous IV infusion, which is not therapeutically attractive.

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Impact of Glucose Level Fluctuations

Diabetes is characterized not just by elevated fasting glucose, but also by elevated postprandial glucoses and enhanced variability of glycemia compared with the nondiabetic state.[26] An A1C of 7.5% can be the result of glucose levels that cluster about 175 mg/dL. However, an A1C of 7.5% can also be the result of glucose levels that vary from as high as 300 mg/dL to the low 50s. Therefore, while the A1C level is useful for assessing overall, average glycemic levels during the previous 2 to 3 months, it does not provide information about fluctuations or peaks in glycemia that may have harmful effects independently.

  • In fact, a number of studies suggest that as glucose levels rise, there is a corresponding increase in oxidative stress, as evidenced by such factors as increased oxidized low-density lipoprotein (LDL) cholesterol, which is more atherogenic. There is also a decreased total radical-trapping antioxidant parameter, which is inversely related to oxidative stress.[27]

    Other studies have related increased glucose levels during glucose tolerance testing to impairments in flow-mediated dilation of the brachial artery (a measure of endothelial function).[28] Therefore, glucose variability and glycemic peaks caused by increasing oxidative stress and endothelial dysfunction could potentially increase the risk for atherosclerosis. In the Verona Diabetes Study, increased glycemic variability was significantly associated with increased cardiovascular mortality.[29]

    There are also effects of glycemic variability and oxidative stress on protein kinase C that could increase the risk for microvascular disease. Additional studies have shown that greater day-to-day variation in glucose can adversely affect quality of life.[30]

    Evidence of the importance of postprandial glucose levels comes from the Diabetes Epidemiology: Collaborative Analysis of Diagnostic Criteria in Europe (DECODE) trial, where the risk of death was better predicted by increased postprandial glucose levels than by increased FPG levels.[31]

    The preceding suggests that postprandial glycemia and glycemic variability may independently contribute to vascular risk in people with diabetes. But postprandial glucose also importantly contributes to A1C levels. Between an A1C of 7.3% and 8.4%, the contribution of FPG and postprandial plasma glucose levels to the A1C appears to be about equal, while at A1Cs above 8.4%, the FPG contribution is greater. However, at A1C levels less than 7.3%, postprandial or postchallenge glucose is the greater contributor to A1C. This suggests that for patients to achieve any goal less than 7.0%, it will be important to control not just FPG but also postprandial glucose.[32]

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Reducing Cardiovascular Disease Risk Through More Aggressive Control

Numerous studies have demonstrated that lowering the A1C in both type 1 and type 2 patients reduces microvascular disease.[33-35] In the Diabetes Control and Complications Trial (DCCT), patients with type 1 diabetes were randomized to either 2 injections of insulin a day, or an intensive therapy consisting of 3 or more daily insulin injections or use of an insulin pump. During the course of this study, the people with more intensive insulin therapy had significantly lower A1C levels and about a 50% decrease in the risk of complications.[33]

The recent report from the DCCT-Epidemiology of Diabetes Interventions and Complications (EDIC) researchers demonstrated that many years after the study, type 1 patients assigned to intensive treatment in the DCCT had a 42% decrease in risk for any cardiovascular outcome and a 57% reduction in the risk for nonfatal myocardial infarction, stroke, or death from CVD, even though there was little difference in the A1C levels of the 2 groups during most of the follow-up period.[36] There are 2 important messages from this study: improving glycemia will reduce the risk for macrovascular disease, and while it is never too late to treat the hyperglycemia of diabetes, the earlier the treatment is begun, the greater the likely benefit because of an apparent metabolic memory of good and bad control.

  • Studies like the DCCT and the UKPDS show that the benefits of improved glycemic control extend down into the normal range.[35,37] Because of this, the American College of Endocrinology (ACE) and the American Association of Clinical Endocrinologists recommend an A1C goal of 6.5% or less. The ADA recommends, in general, an A1C level of less than 7%.[38,39] However, the ADA A1C goal for the individual patient is an A1C as close to normal (less than 6%) as possible without significant hypoglycemia. In addition, there are treatment goals for blood pressure and lipid levels. Most adults with type 2 diabetes who do not have contraindications should be treated with aspirin and, obviously, efforts at smoking cessation should be offered to those who smoke.[38,39]

    Studies have demonstrated that efforts to achieve diabetes management guidelines can be associated with improved outcomes. In the Steno-2 (Steno Diabetes Center, Copenhagen, Denmark) trial, an intensive attempt to achieve A1C, blood pressure, and lipid goals was compared with conventional treatment, and was associated with a 53% reduction in the risk of macrovascular disease and a 60% decrease in microvascular disease risk.[40]

    Despite the evidence that aggressive therapy is beneficial, a recent Centers for Disease Control and Prevention (CDC) report showed that only about one-third of people with diabetes in the year 2000 had an A1C less than 7.0%, only about one-third had blood pressure less than 130/80 mm Hg, and less than one-half had a total cholesterol less than 200 mg/dL. More importantly, only 7% achieved all 3 goals.[41] In addition, a recent nationwide study of 157,000 people with type 2 diabetes found that two-thirds of them had A1C levels exceeding the ACE goal of 6.5% or less.[42] Clearly, there is a lot of room for improvement.

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