18416
Evaluation of Methods for Diagnosing Diabetes Mellitus Due to Hyperglycemia or Insulin Secretion
Alireza Masoudi 1
1 Department of laboratory sciences, faculty of allied medical sciences, medical university of Qom, Iran
Abstract
Diabetes is a group of metabolic diseases characterized by hyperglycemia due to impaired insulin secretion, insulin function, or both. Chronic hyperglycemia in diabetes is associated with long-term damage, dysfunction, and failure of various organs, especially the eyes, kidneys, nerves, heart, and blood vessels. Numerous pathogenic processes are involved in the development of diabetes. These processes range from autoimmune degradation of pancreatic beta cells and subsequent insulin deficiency to abnormalities that lead to insulin resistance. The basis of problems in the metabolism of carbohydrates, fats, and proteins in diabetes is a defect in the function of insulin in the target tissues. Insulin dysfunction results from insufficient insulin secretion or failure to respond to insulin at one or more points in complex hormonal pathways. Impaired insulin secretion and problems with insulin function often occur simultaneously in a patient, and it is not clear which abnormality is the main cause of hyperglycemia. Symptoms of severe hyperglycemia include hyperemia, binge drinking, weight loss, and sometimes overeating and blurred vision. Growth disorders and susceptibility to certain infections may also be present with chronic hyperglycemia. The acute and life- threatening consequences of uncontrolled diabetes are hyperglycemia with ketoacidosis or non- ketonic hyperosmolar syndrome. In this article, we diagnose and classify diabetes mellitus.
Keywords: diabetes mellitus, metabolic, hyperglycemia, insulin
Preface
Classification of diabetes mellitus and other glucose control groups:
Attributing a type of diabetes to one person depends on the circumstances at the time of diagnosis, and many people with diabetes simply do not fit into one group.
For example, a person with gestational diabetes mellitus (GDM) may also be hyperglycemic after childbirth and may actually be diagnosed with type 2 diabetes. Or a person who develops diabetes due to high doses of exogenous steroids may become normoglycemic when the glucocorticoid is stopped, but then may develop diabetes a few years later and after recurrent periods of pancreatitis. Another example is a person who is being treated with thiazides and develops diabetes years later. Because thiazides themselves rarely cause hyperglycemia, such people are more likely to have type 2 diabetes, which is exacerbated by medication. Therefore, for the clinician and the patient, identifying a specific type of diabetes is less important than understanding the pathogenesis of hyperglycemia and its effective treatment.
level
Types
normoglycemia Hyperglycemia
Normal regulation of glucose
Possibility of glucose tolerance or possibility of fasting
Diabetes mellitus No need
for insulin
Needful of insulin
Needful of insulin for being alive
Type 1
Type 2
Other special
Gestational
Figure 1: Glycemic Disorders: Etiological Types and Stages. Even after ketoacidosis, these patients can return to normoglycemia quickly without the need for continuous treatment (ie, "honeymoon" improvement); In rare cases, patients in these groups (such as Vacor poisoning, gestational type 1 diabetes) may need insulin to survive.
Type 1 diabetes (destruction of beta cells, which usually leads to a lack of insulin)
Immune-mediated diabetes: This form of diabetes, which accounts for only 5 to 10 percent of all diabetes, was formerly referred to as insulin-dependent diabetes, type 1 diabetes, or juvenile diabetes. It results from the autoimmune degradation of pancreatic beta cells by cellular immunity. Beta cell immunodeficiency markers include autoantibodies against islet cells, autoantibodies against insulin, autoantibodies against GAD (GAD65), and autoantibodies against tyrosine phosphatase IA-2 and IA-2β. One and usually more of these autoantibodies are present in 85 to 90% of people when fasting hyperglycemia is detected. The disease is also strongly associated with HLA, is associated with DQA and DQB genes, and is influenced by DRB genes. These HLA-DR / DQ alleles can be predisposing or protective.
In this form of diabetes, the rate of beta cell destruction is so varied that it is rapid in some people (mostly infants and children) and slow in others (mostly adults). Some patients, especially children and adolescents, may have ketoacidosis as the first manifestation of the disease. Others have mild fasting hyperglycemia, which can quickly turn into severe hyperglycemia or ketoacidosis in the presence of infection or other stress. Some, especially adults, may have enough beta cell function for years to prevent ketoacidosis; Such people eventually become insulin dependent for survival and are at risk for ketoacidosis. In this late stage of the disease, insulin secretion will be low or absent, manifested by low or undetectable amounts of plasma peptide-C. Immune-mediated diabetes usually occurs in childhood and adolescence, but can occur at any age, even in the eighth or ninth decade of
18418 life.
Autoimmune degradation of beta cells has several genetic causes and is also related to environmental factors that are not yet well defined. Although patients are rarely obese when they present with this type of diabetes, the presence of obesity does not contradict the diagnosis. These patients are also prone to other autoimmune disorders such as Graves' disease, Hashimoto's thyroiditis, Addison's disease, vitiligo, celiac disease, autoimmune hepatitis, myasthenia gravis, and pernicious anemia.
Idiopathic diabetes: Some forms of type 1 diabetes have no known etiology. Some of these patients have persistent insulinopenia and are prone to ketoacidosis, but have no evidence of autoimmunity. Although only a small number of patients with type 1 diabetes fall into this group, those who end up in this group are often African or Asian. People with this form of diabetes suffer from cyclic ketoacidosis and show varying degrees of insulin deficiency between periods. This type of diabetes is highly inherited, lacks immunological evidence for beta cell autoimmunity, and is not associated with HLA. The complete need for insulin replacement therapy in these patients may sometimes be present and sometimes not.
Type 2 diabetes (range from insulin resistance with relative insulin deficiency to impaired insulin secretion with insulin resistance)
This type of diabetes, which accounts for 90 to 95 percent of all cases of diabetes, formerly known as non-insulin dependent diabetes, type 2 diabetes, or adult-onset diabetes, includes people who are insulin resistant and usually have insulin deficiency. Have relative (instead of complete). These people do not need insulin therapy to survive, at least initially, and often throughout their lives. There are probably many different causes for this type of diabetes.
Although the specific etiologies are not known, autoimmune degradation of beta cells does not occur, and patients have no other cause for diabetes as listed above or below.
Most patients with this type of diabetes are obese, and obesity itself causes some degree of insulin resistance. Patients who are not obese by traditional weight standards are more likely to have a high percentage of fat that is more distributed in the abdomen. Ketoacidosis rarely occurs spontaneously in this type of diabetes; And when seen, it usually occurs in connection with stress, another illness such as infection. This type of diabetes usually goes undiagnosed for years because the hyperglycemia develops gradually and in the more early stages is often not so severe that the patient notices any of the classic symptoms of diabetes. However, such patients are at risk for problems with large and small arteries. While patients with this form of diabetes may have insulin levels that appear normal or high, higher blood glucose levels in these diabetics are expected to lead to higher insulin levels if their beta cells function normally.
Therefore, insulin secretion is difficult in these patients and is not sufficient to compensate for insulin resistance. Insulin resistance may improve with weight loss or hyperglycemic drug therapy, but rarely remains normal. The risk of starting this type of diabetes increases with age, obesity, and lack of physical activity. It is more common in women with previous GDM, and in people with high blood pressure or dyslipidemia, and its occurrence varies under different racial groups. It is often associated with genetic predisposition, and this association is greater than with autoimmune type 1 diabetes. However, the genetics of this type of diabetes are complex and not well understood
Other specific types of diabetes:
Beta cell genetic defects: Several types of diabetes are associated with monogenetic defects in beta cell function. These types of diabetes are usually characterized by the development of hyperglycemia at a young age (usually before the age of 25). These are called juvenile-onset puberty (MODY) and are characterized by impaired insulin secretion with minimal or even no insulin dysfunction. Inherited by the dominant autosomal pattern. Abnormalities at six genetic loci on different chromosomes have been identified to date.
The most common type is related to mutations on chromosome 12 in a hepatic transcription factor called nuclear hepatocyte factor (HNF) -1α. The second type is associated with mutations in the glucokinase gene on the 7p chromosome and leads to defective glucokinase molecules. Glucokinase converts glucose to glucose-6-phosphate, which in turn stimulates the metabolism of insulin by beta cells. Thus, glucokinase acts as a "glucose sensor" for beta cells. Due to defects in the glucokinase gene, an increase in plasma glucose levels is necessary for normal insulin levels. The less
common forms are caused by mutations in other transcription factors, including HNF-4α, HNF-1β, promoter factor (IPF0-α, and NeuroD1).
Spot mutations have been found in mitochondrial DNA that are linked to diabetes and deafness. The most common mutation occurs at position 3,243 in the leucine tRNA gene, leading to the transfer of A to G. A similar problem occurs in MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis, and pseudo-stroke);
However, diabetes is not part of this syndrome, which indicates different phenotypic expressions of this genetic problem.
Genetic abnormalities that lead to the inability to convert pre-insulin to insulin have been identified in a small number of families, and are inherited with an autosomal dominant pattern. Glucose intolerance is mild. Similarly, the production of mutant insulin molecules with impaired receptor binding has been identified in several families and has an autosomal inheritance, with glucose metabolism being only slightly impaired or even normal.
Genetic defects in insulin function: There are unusual causes for diabetes that result from genetically determined insulin function abnormalities. Metabolic abnormalities associated with insulin receptor mutations may range from moderate hyperinsulinemia and hyperglycemia to severe diabetes. Some people with these mutations may have acanthosis nigricans. Women may become menopausal and have enlarged ovaries and cysts. In the past, this syndrome was called type 1 insulin resistance. Leprechaunism and Rabson-Mendenhall syndromes are two pediatric syndromes that have mutations in the insulin receptor gene with subsequent changes in insulin receptor function and high insulin resistance. The first has certain aspects of the face and is usually fatal in children, while the second is associated with abnormalities of the teeth and nails and pineal hyperplasia.
Changes in the structure and activity of insulin receptors are not evident in patients with insulin-resistant lipoatrophic diabetes. Therefore, it is assumed that the problems must be in the conduction paths after the receiver.
Exocrine pancreatic diseases: Any process that spreads damage to the pancreas can lead to diabetes. Acquired processes include pancreatitis, trauma, infection, pancreatectomy, and pancreatic carcinoma. With the exception of cancer, the damage to the pancreas must be extensive for diabetes; Adrenocarcinomas that affect only a small portion of the pancreas have also been linked to diabetes. This indicates a mechanism other than a simple decrease in beta cell mass. Cystic fibrosis and hemochromatosis also damage beta cells and
18420 disrupt insulin secretion if they are large enough. Fibrocalculosis pancreatopathy
may be associated with abdominal pain that spreads to the lower back and calcification of the pancreas that is detected on radiology. Pancreatic fibrosis and calcium stones were found in the exocrine cavity at autopsy.
Endocrinopathies: Several hormones (eg, growth hormone, cortisol, glucagon, epinephrine) are antagonists of insulin function. Large amounts of these hormones (eg acromegaly, Cushing's syndrome, glucagonoma, pheochromocytoma, respectively) can cause diabetes. This condition is more common in people with previous impairment of insulin secretion, and hyperglycemia usually resolves when too much hormone is gone.
Hypokalemia induced by somatostatinoma and aldosteronoma can cause diabetes, at least in part, by inhibiting insulin secretion. Hyperglycemia usually resolves after successful tumor resection.
Drug-induced diabetes or chemicals:
Many drugs can interfere with insulin secretion. These drugs may not cause diabetes on their own, but they may induce diabetes in people with insulin resistance. In such cases, the classification is unclear, as the relative importance of beta cell dysfunction and insulin resistance is unknown. Certain toxins such as Vacor (a rat toxin) and intravenous pentamidine can permanently destroy pancreatic beta cells. Fortunately, such drug reactions are rare. There are also many drugs and hormones that can interfere with insulin activity. Examples include nicotinic acid and glucocorticoids. Patients receiving interferon-α have been reported to have diabetes associated with islet cell antibodies and, in some cases, severe insulin deficiency. The list in Table 1 does not cover all cases, but it does list the most commonly identified drugs, hormones, or toxin-induced forms of diabetes.
Infections: Certain viruses are associated with the destruction of beta cells. Diabetes occurs in patients with congenital jaundice, although most of these patients have the characteristic HLA markers and immunity characteristic of type 1 diabetes. In addition, coxsackievirus B, cytomegalovirus, adenovirus, and mumps virus are involved in inducing specific cases of the disease.
Unusual forms of immune-mediated diabetes
In this group, two conditions are known, and the rest are likely to occur. Stiff-man syndrome is an autoimmune disorder of the central nervous system characterized by axial muscle stiffness with painful spasms. Patients usually have high titers of GAD autoantibodies, and about one- third of them develop diabetes.
Insulin receptor antibodies can cause diabetes by binding to the insulin receptor, thereby blocking the binding of insulin to its receptor in the target tissues. However, in some cases, these antibodies can act as insulin agonists after binding to the receptor, thereby causing hypoglycemia. Insulin receptor antibodies are rarely found in patients with systemic lupus erythematosus and other autoimmune diseases. As with other conditions of severe insulin resistance, patients with insulin receptor antibodies often have acanthosis nigricans. In the past, this syndrome was called type B insulin resistance.
Other genetic syndromes sometimes associated with diabetes:
Many genetic syndromes are associated with an increased incidence of diabetes. These include chromosomal abnormalities of Down syndrome, Klinefelter syndrome, and Turner syndrome.
Wolfram syndrome is an autosomal recessive disorder characterized by insulin-deficient diabetes and lack of beta cells at autopsy. Other manifestations include diabetes insipidus, hypogonadism, ocular atrophy, and neural deafness. Other syndromes are listed in Table 1.
Gestational diabetes mellitus
For many years, GDM has been defined as any measure of glucose intolerance that begins or first detects during pregnancy. Although most cases resolve with childbirth, this definition used to determine whether the condition remains stable after pregnancy or not, and did not rule out the possibility that glucose intolerance may have been present or started at the same time as pregnancy. . This definition facilitated a uniform strategy for tracking and classifying GDM, but its limitations have been identified for years. Because the growing epidemic of obesity and diabetes has led to a higher incidence of type 2 diabetes in women, the number of pregnant women with undiagnosed type 2 diabetes has increased.
Following studies in 2009-2008, the International Diabetes Association. The Pregnancy Study Group (IADPSG), an international forum with representatives from several children's and diabetes organizations, including the American Diabetes Association (ADA), recommended that high-risk women, who at the initial prenatal visit use criteria Standards (Table 3) have diabetes, the diagnosis of diabetes is obvious, not pregnancy. About 7% of all pregnancies (ranging from 1% to 14%, depending on the population studied and the diagnostic tests used) have GDM, leading to more than 200,000 cases per year.
Table 1: Etiological classification of diabetes mellitus
I. Type 1 diabetes (destruction of beta cells, usually leading to total insulin deficiency) A. Safety-mediated
B. Idiopathic
II. Type 2 diabetes (may range from overcoming insulin resistance with partial insulin deficiency to overcoming the secretory problem with insulin resistance)
III. Other special types
A. Genetic defects in beta cell function 1. Chromosome 12, HNF-1α (MODY3) 2. Chromosome 7, glucokinase (MODY2) 3. Chromosome 20, HNF-4α (MODY1)
4. Chromosome 13, promoter factor insulin-1 (IPF-1; MODY4) 5. Chromosome 17, HNF-1β (MODY5)
6. Chromosome 2, NeuroD1 (MODY6) 7. Mitochondrial DNA
8. Others
B. Genetic defects in insulin function 1. Type A insulin resistance
18422 2. Leprosy
3. Robson-Menden Hall Syndrome 4. Lipoatrophic diabetes
5. Others
C. Exocrine pancreatic diseases 1. Pancreatitis
2. Trauma / pancreatectomy 3. Neoplasia
4. Cystic fibrosis 5. Hemochromatosis
6. Fibrocalculosis pancreatopathy 7. Others
D. Endocrinopathies 1. Acromegaly
2. Cushing's syndrome 3. Glucagonoma 4. Pheochromocytoma 5. Hyperthyroidism 6. Somatostatinoma 7. Aldosteronoma 8. Others
E. induced by drugs and chemicals 1. Vacour
2. Pentamidine 3. Nicotinic acid 4. Glucocorticoids 5. Thyroid hormone 6. Diazoxide
7. Beta-adrenergic agonists 8. Thiazides
9. Dilantin
10. Gamma-interferon 11. Others
F. Infections 1. Genital ruble 2. Cytomegalovirus 3. Others
G. Unusual forms of immune-mediated diabetes 1. "still-mean" syndrome
2. Insulin receptor antibodies 3. Others
H. Other genetic syndromes that are sometimes associated with diabetes 1. Down Syndrome
2. Clean Filter Syndrome 3. Turner syndrome 4. Wolfram syndrome 5. Friedrich Ataxia 6. Huntington
7. Lawrence-Moon-Biddle Syndrome 8. Myotonic dystrophy
9. Porphyria
10. Prader-Willi syndrome 11. Others
IV. Gestational diabetes mellitus
Patients with any type of diabetes may need insulin therapy at some stage of their disease. Such insulin use alone does not classify patients.
Table 2: Diabetes Risk Increase Categories
* For all three tests, the risk is continuous, extending to less than the lower end of the range and rising disproportionately to the ends of the range.
18424
Diabetes Risk Categories:
In 1997 and 2003, a committee specializing in the diagnosis and classification of diabetes mellitus identified an intermediate group of people whose glucose levels did not meet diabetes standards but were higher than normal. These individuals were defined as impaired fasting glucose (IFG) [fasting plasma glucose (FPG), 100 mg / dl (5.6mmol / l) to 125 mg / dl], or impaired glucose tolerance (IGT)] 2-hour test values Oral glucose tolerance (OGTT) equivalent to 140 mg / dl to 199 mg / dl [.
People with IFG or IGT are referred to as prediabetes, which indicates a relatively high risk of developing diabetes in the future. IFG and IGT should not be seen as a clinical problem in themselves, but rather as a risk factor for diabetes as well as cardiovascular disease. They can be considered as intermediate stages in each of the disease processes listed in Table 1. IFG and IGT are associated with obesity (especially abdominal or visceral obesity), dyslipidemia with high triglycerides or low HDL cholesterol, and high blood pressure. Interventions by organizing lifestyles, with the goal of increasing physical activity and losing 5 to 10 percent of body weight, and specific medications have been shown to prevent or delay the development of diabetes in people with IGT; The potential effect of such interventions in reducing mortality or the occurrence of cardiovascular disease has not been demonstrated to date. It should be noted that a report by the ADA Committee of Experts in 2003 reduced the FPG low clearance point for IFG excretion from 110 mg / dl to 100 mg / dl, in part to ensure that the prevalence of IFG was similar to that of IGT. However, the World Health Organization (WHO) and many other diabetes organizations did not adopt this change in the definition of IFG.
Because A1C is used to diagnose diabetes in people with a variety of risk factors, it will also identify people at higher risk for diabetes. When the International Committee of Experts in its 2009 report recommended the use of A1C to diagnose diabetes, it emphasized the set of risks for diabetes by all glycemic criteria and did not formally identify an equivalent intermediate group for A1C. The group also stressed that people with A1C levels above the normal range of the lab but below the clear diagnostic point for diabetes (6 to less than 6.5%) are at a very high risk of developing diabetes. In fact, the incidence of diabetes in people with A1C levels in this range is more than 10 times higher in people with lower levels (4-7). However, the range of 6 to less than 6.5% does not succeed in identifying a significant number of patients with IFG or IGT. Prospective studies show that people within the A1C range of 5.5 to 6 have a cumulative incidence of 5 years of diabetes, ranging from 12 to 25 percent, which is much (3 to 8 times) higher than the incidence in the entire US population. Analyzes of NHANES representative country data show that the A1C value, which most accurately identifies individuals with IFG or IGT, is between 5.5 and 6%. In addition, linear regression analysis of these data shows that among the non-diabetic adult population, FPG of 110 mg / dl is associated with A1C of 5.6%, while FPG of 100 mg / dl is associated with A1C of 5.4%. Finally, evidence from the Diabetes Prevention Program (DPP), in which the average A1C was 5.9%, shows that preventive interventions are effective in groups of people with both A1C levels above and below 5.9%. For these reasons, the most appropriate A1C level above which preventive intervention should be initiated is probably somewhere in the range of 5.5 to 6%.
As in the case of the 2-hour FPG and PG, defining the lower limit of an A1C middle group is
somewhat conventional, as the risk of diabetes is with any measure of chain glycemia, extending to normal ranges. To maximize the equity and effectiveness of preventative interventions, such a clean spot for A1C should be the "false negative" costs (failure to identify those with diabetes) versus the "false positive" costs (false positives and then resource payments). Prevent for those who have not been diagnosed with diabetes in any way).
Compared to the fasting glucose clearance point of 100 mg / dl, the A1C clearance point is 5.7% less sensitive but more specific and has a higher positive predictive value to identify people at risk for future diabetes. A large prospective study found that a clean spot of 5.7%, a sensitivity of 66% and a specificity of 88% to detect the occurrence of diabetes in the next 6 years. Receptor performance curve analyzes of country representative data in the United States show that the A1C value is 5.7%, low sensitivity but high specificity for identifying IFP or IGT cases. Other analyzes suggest that A1C (5.7%) is associated with a similar risk of diabetes to high-risk participants. It makes sense to consider the A1C range of 5.7 to 6.4 because it identifies people at high risk for future diabetes and those for whom pre-diabetes correction may be used.
People with an A1C of 5.7 to 6.4 should be aware of the increased risk for diabetes as well as cardiovascular disease and be advised of effective strategies such as weight loss and physical activity to reduce the risk. Like glucose uptake, the risk chain is curvilinear, so that as the A1C rises, the risk of diabetes increases disproportionately.
Therefore, interventions should be intensive and follow-up should be done especially for people with A1C levels above 6%, who should be considered at high risk. Of course, just because a person has a fasting glucose of 98 mg / dl does not indicate a low risk of diabetes;
people with A1C levels below 5.7% may still be at risk, depending on A1C levels and other risk factors, such as obesity and family history. .
Table 2 summarizes the high risk categories for diabetes. Assessing patients at risk should be a combination of examining global risk factors for both diabetes and cardiovascular disease.
Diabetes risk monitoring and counseling should always have a practical dimension in relation to side effects, life expectancy, personal capacity to make lifestyle changes, and overall health goals.
Table 3: Diabetes Diagnosis Criteria
A1C ≥6.5%. The test must be performed in a laboratory that uses an NGSP-approved method standardized for DCCT testing.
Or
FPG ≥ 126 mg / dl. Fasting is defined as not receiving calories for at least 8 hours. * Or
2-hour plasma glucose ≥ 200 mg / dl during OGTT. The test should be performed as described by the World Health Organization, using an amount of glucose containing 75 grams of water- soluble anhydrous glucose. *
Or
11
18420 In patients with classic symptoms of hyperglycemia or hyperglycemic crisis, random plasma glucose ≥ 200 mg / dl.
In the absence of inappropriate hyperglycemia, criteria 1 to 3 should be confirmed by repeated testing.
Diagnostic criteria for diabetes mellitus:
For decades, the diagnosis of diabetes has been based on glucose criteria, whether with FPG or 75-g OGTT. In 1997, the first committee to diagnose and classify diabetes mellitus re- examined diagnostic criteria using the observed association between FPG levels and the presence of retinal problems as a key factor in determining glucose level thresholds. The committee reviewed data from three cross-sectional epidemiological studies that examined retinal problems by deep imaging or direct ophthalmoscopy and assessed glycemia as FPG, 2- hour PG, and A1C. These studies showed glycemic levels, in which less than that, retinopathy was low and in higher amounts, the prevalence of retinopathy increased in a linear pattern. The deciles of the three criteria in which retinopathy began to increase were similar for each criterion in each population. In addition, glycemic values, most of which increased retinopathy, were similar among the populations. These analyzes helped to establish a new diagnostic clear point greater than 126 mg / dl for FPG and confirmed a long-term 2-hour PG value of more than 200 mg / dl.
A1C is a widely used marker of chronic glycemia, reflecting moderate blood glucose levels over a period of more than 2 to 3 months. This test plays an important role in the management of the diabetic patient, as it correlates well with both small vascular problems and to a lesser extent with larger vascular problems, and is widely used as a standard biomarker for glycemic management efficiency. Previous expert committees have not recommended the use of A1C for the diagnosis of diabetes, in part due to the lack of standardization of the test. Of course, A1C tests are now highly standardized so their results can be used in different populations and times. In a recent report, the Quantity of International Experts, after a thorough review of both established and emerging epidemiological evidence, recommended the use of the A1C test to diagnose diabetes, with a threshold of more than 6.5%, and the ADA endorsed the decision. he does. A1C diagnostic clean point of 6.5% is associated with a curvature point for the prevalence of retinopathy, such as diagnostic thresholds for 2-hour FPG and PG. The diagnostic test must be performed using a method approved by the National Glycohemoglobin Standardization Program (NGSP). A1C point-of-care tests are not currently accurate enough for diagnostic purposes.
It makes sense to use a chronic versus acute marker for dysglycemia, especially since A1C is known to clinicians as a marker for glycemic control. In addition, the A1C has several advantages over FPG, including being simpler, because fasting is not necessary, showing more prenatal stability, and having fewer day-to-day changes during periods of stress and illness. Of course, these benefits must be considered at a higher cost, as well as the limited access to A1C testing in certain areas of the developing world, and the incomplete correlation between A1C and moderate glucose in certain individuals. In addition, A1C can be misleading in patients with certain forms of anemia and hemoglobinopathies, which may have a unique racial or geographical distribution. For patients with hemoglobinopathy but with normal red blood cell turnover, such as sickle cell anemia, the A1C test should be used without the intervention of abnormal hemoglobin (updated list is available at www.ngsp.org/prog/index3.html). For
situations with abnormal red blood cell turnover, such as hemolysis anemia and iron deficiency, diabetes mellitus should use broad glucose metrics.
The established glucose test for diabetes is still valid. These criteria include 2 hours of FPG and PG. In addition, patients with severe hyperglycemia, such as those with severe classical hyperglycemia symptoms or hyperglycemic crisis, can be diagnosed with random (or normal) plasma glucose levels greater than 200 mg / dl. In such cases, health care professionals may also perform the A1C test as part of an initial assessment of the severity of diabetes, and in most cases, it will be above the clear point for diabetes. However, in rapidly progressing diabetes, such as the development of type 1 diabetes in some children, A1C may not increase significantly despite quite obvious diabetes.
As the coordination between the 2-hour FPG and PG tests is less than 100%, there is no complete coordination between the A1C and any of the glucose-based tests. Analyzes of NHANES data show that, assuming a case study of undiagnosed cases, the clean spot of A1C is more than 6.5%, one-third less likely to detect undiagnosed diabetes than the clean spot of fasting glucose greater than 126 mg / dl. Slowly Of course, in practice, a large portion of the population with type 2 diabetes is unaware of their condition. Thus, it is possible that the lower sensitivity of A1C at the specified clean point is adjusted to the higher efficiency of the test, and the wider application of the more appropriate test (A1C) may actually increase the number of diagnoses given.
Further research is needed to better identify patients whose glycemic status may be categorized differently by two recent tests (eg, FPG and A1C). Such discrepancies may be due to variation in measurement, change over time, or A1C, FPG, and glucose each assessing different physiological processes. In cases of high A1C but "non-diabetic" FPG, there is a possibility of higher postprandial glucose levels or increased glycemic index when a certain level is hyperglycemic. In contrast (high FPG but lower A1C than the diabetic clear point), there may be an increase in hepatic glucose production or a decrease in glycation.
As with most diagnostic tests, the test result that diagnoses diabetes must be repeated to rule out the possibility of laboratory error, unless the diagnosis is clinically clear, such as a disease with classic symptoms of hyperglycemia or a hyperglycemic crisis. It is best to repeat the same test for confirmation, as compliance is more likely in this case. For example, if the A1C is 7%
and the test result is 6.8%, the diagnosis of diabetes is confirmed. Of course, there are cases where the results of two different tests (eg FPG and A1C) are available to a patient. In such a situation, if the two tests are both above the diagnostic threshold, the diagnosis of diabetes is confirmed.
On the other hand, when two different tests are available to one person and the results do not match, the test with the result above the clean diagnostic point must be repeated, and the diagnosis is made based on the approved test. That is, if the disease meets the A1C standard for diabetes (two tests above 6.5%) but does not meet the FPG standard (less than 126 mg / dl), or vice versa, the person should be considered to have diabetes. Admittedly, in most cases, the
"non-diabetic" test is probably in the very near range of what is called diabetes.
Because there are pre-analysis and analysis differences for all tests, the second value may be lower than the clean diagnostic point when the test is repeated above the diagnostic threshold.
This is less likely for A1C, somewhat more likely for FPG, and more likely for 2-hour PG. If a laboratory error is ruled out, such patients are likely to have test results close to the threshold
18422 for diagnosis. The doctor will probably follow up with the patient and repeat the tests 3 to 6
months later.
The decision as to which test to use to judge a diabetic patient should be up to the physician, and the availability and feasibility of testing a patient or group of patients should be considered.
Perhaps more important than which diagnostic test to use is to have a diabetes test performed when indicated. There is disappointing evidence that many at-risk patients still receive adequate testing and counseling for the increasingly common disease, or for the cardiovascular risk factors that usually accompany it. they do not. The current diagnostic criteria for diabetes are summarized in Table 3.
Diagnosis of gestational diabetes
GDM is dangerous for both mother and baby. The Hyperglycemia and Pregnancy Outcome (HAPO) study, a large-scale multinational epidemiological study (approximately 25,000 pregnant women), showed that the risk of adverse outcomes for mother, fetus, and infant as a function of maternal glycemia at 24 weeks 28 steadily increased, even within the range previously considered normal for pregnancy. For most problems, there was no danger threshold. These results have led to a re-examination of GDM diagnostic criteria. Following surveys from 2008 to 2009, the IADPSG, an international team with representatives from several children's and diabetes organizations, including the ADA, provided rewritten recommendations for the diagnosis of GDM. The group recommended that all women without diabetes be tested for 75-g OGTT during the 24th to 28th weeks of pregnancy. In addition, the group introduced clear diagnostic points for fasting glucose levels of 1-h and 2-h, and an odd ratio of at least 1.75 was obtained for adverse outcomes compared with women in the HAPO study. Current studies and diagnostic strategies based on the IADPSG statement are listed in Table 4.
These new criteria will significantly increase the prevalence of GDM, firstly because only one abnormal criterion, not two, is sufficient for diagnosis. The ADA believes that there will be a significant increase in the incidence of GDM with these criteria and is sensitive to concerns about the "medicalization" of pregnancies that were previously classified as normal. These changes in diagnostic criteria are due to the alarming increase in obesity and diabetes in the world, and the goal is to optimize pregnancy outcomes for women and their children.
Table 4: Check for GDM detection
Perform 75-g OGTT, by measuring fasting plasma glucose, at 1 and 2 hours, at 24 to 28 weeks of gestation in women who have not previously been diagnosed with diabetes.
OGTT should be done in the morning and after fasting at night for at least 8 hours.
GDM is detected when any of the following plasma glucose levels are obtained:
- Fasting: ≥ 92 mg / dl - 1 hour: ≥ 180 mg / dl - 2 hours: ≥ 153 mg / dl
Conclusion:
Admittedly, there are few data from randomized clinical trials of therapeutic interventions in women that are currently diagnosed with GDM based on just one blood glucose test above the clean spot (contrary to old standards). That at least two abnormal criteria were required). The benefits of these criteria were assessed during pregnancy and for children in an interventional study focusing on women who had milder hyperglycemia than was detected using older diagnostic criteria for GDM. The frequency of follow-up and blood glucose monitoring is not yet known, but it is probably lower than women who were diagnosed with the old criteria. Further studies with appropriate design are needed to determine the optimal rate of monitoring and treatment of women with GDM diagnosed with the new criteria (cases that do not meet the previous definition of GDM). It is important to note that 80 to 90% of women in both mild GDM studies (those with threshold glucose levels recommended here) can be controlled by treatment through lifestyle changes alone.
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