Your SlideShare is downloading. ×
Classific diabetes
Classific diabetes
Classific diabetes
Classific diabetes
Classific diabetes
Classific diabetes
Classific diabetes
Classific diabetes
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×
Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply

Classific diabetes

505

Published on

Published in: Health & Medicine
0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total Views
505
On Slideshare
0
From Embeds
0
Number of Embeds
0
Actions
Shares
0
Downloads
4
Comments
0
Likes
0
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide

Transcript

  • 1. NEW CLASSIFICATION AND NEW DIAGNOSTIC CRITERIA OF DIABETES MELLITUS 269Continuing Medical Education NEW CLASSIFICATION AND NEW DIAGNOSTIC CRITERIA OF DIABETES MELLITUS R. RottiersINTRODUCTION associated with long-term damage, dysfunction, and fail- ure of various organs, especially the eyes, kidneys, The last 20 years the classification of diabetes nerves, heart, and blood vessels.mellitus and the tests used for its diagnosis were based Several pathogenic processes are involved in theon the recommendations of the National Diabetes Data development of diabetes. These range from autoimmuneGroup of the USA and the second World Health Organi- destruction of the ß-cells of the pancreas with conse-zation Expert Committee on Diabetes Mellitus in 1979, quent insulin deficiency to abnormalities that result inresp. 1980 (1,2). Apart from some minor modifications resistance to insulin action. The basis of the abnormali-by the WHO in 1985 little had been changed until the ties in carbohydrate, fat, and protein metabolism in dia-report by an American Diabetes Association Expert betes is deficient action of insulin on target tissues. De-Committee was launched in 1997, soon followed by a ficient insulin action results from inadequate insulincomplimentary report of a WHO Consultation in 1998 secretion and/or diminished tissue responses to insulin(3,4). at one or more points in the complex pathways of hor- These adaptations were needed due to the consider- mone action. Impairment of insulin secretion and de-able new knowledge regarding the aetiology of differ- fects in insulin action frequently coexist in the sameent forms of diabetes as well as the ever increasing in- patient, and it is often unclear which abnormality, if ei-formation on the predictive value of different blood glu- ther alone, is the primary cause of the hyperglycae-cose values for the complications of diabetes. mia (3). The previous classification of the disease was based, The vast majority of cases of diabetes fall into twoin large part, on the type of pharmacological treatment broad aetiopathogenic categories. In one category (typeused in its management. The new one uses a system 1 diabetes), the cause is an absolute deficiency of insu-based on disease aetiology where possible. lin secretion. Individuals at increased risk of develop- The purpose of this review is to summarize the actu- ment of this type of diabetes can often be identified byally accepted definition, classification and diagnostic cri- serological evidence of an autoimmune pathologic proc-teria of diabetes mellitus. ess occurring in the pancreatic islets and by genetic markers. In the other, much more prevalent category (type 2 diabetes), the cause is a combination of resist-Definition of diabetes mellitus ance to insulin action and an inadequate compensatory insulin secretory response. In the latter category, a de- Diabetes mellitus - as stated by the ADA - is a group gree of hyperglycaemia sufficient to cause pathologicof metabolic diseases characterized by hyperglycaemia and functional changes in various target tissues, but with-resulting from defects in insulin secretion, insulin ac- out clinical symptoms, may be present for a long periodtion, or both. The chronic hyperglycaemia of diabetes is of time before diabetes is detected. During this asymp- tomatic period, it is possible to demonstrate an abnor-––––––––––––––– mality in carbohydrate metabolism by measurement of Address for correspondence : plasma glucose in the fasting state or after a challenge Department of Endocrinology, University Hospital Gent with an oral glucose load. Acta Clinica Belgica, 2003; 58-5
  • 2. 270 NEW CLASSIFICATION AND NEW DIAGNOSTIC CRITERIA OF DIABETES MELLITUS We will not go into the well known symptoms and 2. The terms type 1 and type 2 diabetes are retained,the different acute as well as long-term complications with Arabic numerals being used rather than romanof diabetes. numerals. The Arabic numerals are recommended in part because the roman numeral II can easily be con- fused by the public as the number 11. The class, orClassification of diabetes mellitus and other form, named type 1 diabetes encompasses the vastcategories of glucose regulation majority of cases that are primarily due to pancreatic islet ß-cell destruction and that are prone to ketoaci- In the former classification diabetes was divided in dosis. Most type 1 diabetes is characterized by thefive distinct types: insulin-dependent (IDDM, type 1), presence of islet cell (ICA), GAD, IA-2, or insulinnon-insulin-dependent (NIDDM, type 2), gestational antibodies (5). There is a genetic predispositiondiabetes mellitus (GDM), malnutrition-related diabetes, (HLA-associations) to autoimmune destruction ofand other types. In addition the 1979 classification in- ß-cells, and it is also related to environmental fac-cluded the category of impaired glucose tolerance (IGT), tors that are still poorly defined. Immune-mediatedin which plasma glucose levels during an oral glucose diabetes commonly occurs in childhood and adoles-tolerance test (OGTT) were above normal but below cence, but it can occur at any age, even in the 8th andthose defined as diabetes. The mean features of the 9th decades of life. While most patients become verychanges in the new ADA/WHO classification (Table 1) soon dependent on insulin, others, particularly adults,are as follows: may retain residual ß-cell function sufficient to pre-1. The terms insulin-dependent diabetes and vent ketoacidosis for many years. Recently this type non-insulin-dependent diabetes and their acronyms, of diabetes with a slow progression is referred to as IDDM and NIDDM, are eliminated. These terms latent auto-immune diabetes of the adult (LADA), have been confusing and have frequently resulted in especially characterized by the presence of classifying the patient based on treatment rather than GAD-antibodies (6). Many individuals with this aetiology. LADA-subcategory of type 1 diabetes - at diagnosisTABLE 1. Aetiological classification of disorders of glycemia (4).Type 1 (beta-cell destruction, usually leading to absolute insulin deficiency) Autoimmune IdiopathicType 2 (may range from predominantly insulin resistance with relative insulin deficiency to a predominantlysecretory defect with or without insulin resistance)Other specific types Genetic defects of beta-cell function Genetic defects in insulin action Diseases of the exocrine pancreas Endocrinopathies Drug- or chemical-induced Infections Uncommon forms of immune-mediated diabetes Other genetic syndromes sometimes associated with diabetesGestational diabetesActa Clinica Belgica, 2003; 58-5
  • 3. NEW CLASSIFICATION AND NEW DIAGNOSTIC CRITERIA OF DIABETES MELLITUS 271 wrongly mimicking a type 2 DM-phenotype - even- specific types: A. Genetic defects of ß-cell function tually become dependent on insulin for survival and (see Table 1). This is due to the identification of the are at risk for ketoacidosis. Although type 1 patients gene defects of these different MODY-phenotypes. are rarely obese when they present with this type of Most patients with type 2 diabetes are obese, and diabetes, the presence of obesity is not incompatible obesity itself causes some degree of insulin resist- with the diagnosis. These patients may also be more ance. Patients who are not obese by traditional weight prone to the development of other autoimmune dis- criteria may have an increased percentage of body orders such as Graves’ disease, Hashimoto’s thyroidi- fat distributed predominantly in the abdominal re- tis and Addison’s disease (7). gion. For that reason the distinction between type 2 Some forms of type 1 diabetes have no known a (non-obese) and type 2 b (obese) - made in the 1979 aetiologies. Some of them have permanent classification - has been eliminated. Ketoacidosis sel- insulinopenia and are prone to ketoacidosis, but have dom occurs spontaneously in this type of diabetes; no evidence of autoimmunity. Most of them are of when seen, it usually arises in association with the African or Asian origin. These cases are classified as stress of another illness such as infection. The risk type 1 idiopathic. of developing this form of diabetes increases with3. The class type 2 diabetes includes the most preva- age, obesity and lack of physical activity. It occurs lent form of diabetes, which results from insulin re- more frequently in women with prior GDM and in sistance with an insulin secretory defect (8). Whereas individuals with hypertension or dyslipidemia. patients with this form of diabetes may have insulin 4. The class malnutrition-related diabetes mellitus has levels that appear normal or elevated, the high blood been eliminated. While it appears that malnutrition glucose levels in these diabetic patients would be may influence the expression of other types of dia- expected to result in even higher insulin values had betes, the evidence that diabetes can be directly their ß-cell function been normal. Thus, insulin se- caused by protein deficiency is not convincing (9). cretion is defective and insufficient to compensate Fibrocalculous pancreatopathy (formerly a subtype for the insulin resistance. On the other hand, some of malnutrition-related diabetes) has been reclassi- individuals have essentially normal insulin action but fied as a disease of the exocrine pancreas. markedly impaired insulin secretion. This situation 5. The class ‘Other specific types’ of diabetes has grown is more frequent in nonobese subjects. Its frequency constantly. It means that a specific aetiology has been varies in different racial/ethnic subgroups. It is often determined for every subgroup and form included associated with strong familial, likely genetic, pre- here. Most of them are exceptional but worth of be- disposition, much more than what is seen in type 1 ing searched for when atypical signs are present at diabetes. However the genetics of this form of dia- diagnosis of a new case. Due to the long list we will betes are complex and not clearly defined. At least not discuss them here. initially, and often throughout their lifetime, these 6. Gestational diabetes mellitus (GDM) is retained. individuals do not need insulin treatment to survive. GDM is defined as any degree of glucose intoler- There are probably many different causes of this form ance with onset or first recognition during pregnancy. of diabetes, and it is likely that the proportion of pa- The definition applies regardless of whether insulin tients in this category will decrease in the future as or only diet modification is used for treatment or of identification of specific pathogenic processes and whether the condition persists after pregnancy. It does genetic defects permits better differentiation among not exclude the possibility that unrecognized glucose them and a more definitive subclassification. Al- intolerance may have antedated or begun concomi- though the specific aetiologies of this form of diabe- tantly with the pregnancy. Six weeks or more after tes are not known, autoimmune destruction of ß-cells pregnancy ends, the woman should be reclassified does not occur here and patients do not have the other into one of the following categories: 1) diabetes, 2) causes of diabetes listed in category III of Table 1. IFG, 3) IGT, or 4) normoglycaemia (see further). In As an example of such a reclassification one can the majority of cases of GDM, glucose regulation mention the MODY-type (maturity-onset diabetes of will return to normal after delivery. GDM compli- the young) previously included in the type 2 cates ~2.1% of all pregnancies in the U.S.A. Clini- diabetes-group. This form has been removed here and cal recognition of GDM is important in order to pre- is now part of the third group of diabetes, i.e. Other vent the GDM-associated perinatal morbidity and Acta Clinica Belgica, 2003; 58-5
  • 4. 272 NEW CLASSIFICATION AND NEW DIAGNOSTIC CRITERIA OF DIABETES MELLITUS mortality. The incidence of birth defects is not af- Diagnostic criteria for diabetes mellitus fected by GDM for it presents during the second half of pregnancy. Deterioration of glucose tolerance oc- The new classification of diabetes - presented by the curs normally during pregnancy, particularly in the ADA - has been accompanied by revised criteria for the 3rd trimester. Previous recommendations have been diagnosis of diabetes (Table 2). that screening for GDM be performed in all preg- The new diagnostic criteria strongly suggest that the nancies. However, there are certain factors that place diagnosis of diabetes be made on the basis of fasting women at lower risk for the development of glucose blood glucose (FPG) only. The ADA also recommends intolerance during pregnancy, and it is likely not cost- that estimates of diabetes prevalence and incidence for effective to screen such patients. This low-risk group epidemiological studies should be based on a FPG ≥ comprises women who are <25 years of age and of 126 mg/dI. The OGTT should not be used for epide- normal body weight, have no family history (i.e. miological research, because it is an imprecise test with first-degree relative) of diabetes, and are not mem- poor reproducibility. Moreover, this recommendation is ber of an ethnic/racial group with a high prevalence made in the interest of standardization and also to fa- of diabetes (Hispanic, Asian, African-American, cilitate field work, particularly where the OGTT may Native American). Pregnant women who fulfill all be difficult to perform and where the cost and demands of these criteria need not be screened for GDM. Thus, on participants’ time may be excessive. The WHO agrees selective rather than universal screening for glucose with the new definitions, but suggests continued use of intolerance in pregnancy is now recommended. the OGTT for patients with blood glucose levels in the7. Assigning a type of diabetes to an individual often “uncertain” range (i.e. between the levels that establish depends on the circumstances present at the time of or exclude diabetes). diagnosis and many diabetic individuals do not eas- If a diagnosis of diabetes is made, the clinician must ily fit into a single class. For example, a person with feel confident that the diagnosis is fully established since GDM may continue to be hyperglycaemic after de- the consequences for the individual are considerable and livery and may be determined to have, in fact, type 1 lifelong. The requirements for diagnostic confirmation diabetes. for a person presenting with severe symptoms and gross8. The name impaired glucose tolerance (IGT) has been hyperglycaemia differ from those for the asymptomatic retained but is seen as a stage, not as a class. The person with blood glucose levels found to be just above analogous intermediate stage of fasting glucose is the cut-off value. Severe hyperglycaemia detected un- named impaired fasting glucose (IFG). They refer to der conditions of acute infective, traumatic, circulatory a metabolic stage intermediate between normal glu- or other stress may be transitory and should not in itself cose homeostasis and diabetes. They can be observed be regarded as diagnostic of diabetes. For the asympto- as intermediate stages in any of the disease processes matic person, at least one additional plasma/blood glu- listed in Table 1. cose test result with a value in the diabetic range is es- sential, either fasting, from a random (casual) sample, or from the OGTT.TABLE 2. Criteria for the diagnosis of diabetes mellitus (3).1. Symptoms of diabetes plus casual plasma glucose concentration of ≥ 200 mg/dl (11.1 mmol/l). Casual is defined as any time of day without regard to time since last meal. The classic symptoms of diabetes include polyuria, polydipsia, and unexplained weight loss. or2. FPG ≥ 126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h. or3. 2-h PG ≥ 200 mg/dl (11.1 mmol/l) during an OGTT. The test should be performed as described by WHO (29), using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.Acta Clinica Belgica, 2003; 58-5
  • 5. NEW CLASSIFICATION AND NEW DIAGNOSTIC CRITERIA OF DIABETES MELLITUS 273 If such samples fail to confirm the diagnosis of dia- 2 h. Pregnant women who meet WHO criteria for dia-betes mellitus, it will usually be advisable to maintain betes mellitus or IGT (Table 4) are classified as havingsurveillance with periodic re-testing until the diagnos- gestational diabetes mellitus. After the pregnancy ends,tic situation becomes clear. In these circumstances, the the woman should be reclassified as having either dia-clinician should take into consideration such additional betes mellitus, or IGT, or normal glucose tolerance basedfactors as family history, age, adiposity, and concomi- on the results of a 75 g OGTT six weeks or more aftertant disorders, before deciding on a diagnostic or thera- delivery. The different criteria of ADA and WHO dopeutic course of action. It should be reiterated that the not promote an efficient use of the OGTT for screeningdiagnosis of diabetes in an asymptomatic subject should of vulnerable pregnant women.never be made on the basis of a single blood glucosevalue. An alternative to the single blood glucose esti-mation or OGTT has long been sought to simplify the Clinical staging of diabetes mellitus and otherdiagnosis of diabetes. Glycated haemoglobin, reflect- categories of glucose toleranceing average glycaemia over a period of weeks, wasthought to provide such a test. Although in certain cases In all types of diabetes the degree of hyperglycae-it gives equal or almost equal sensitivity and specificity mia may change over time, depending on the extent ofto glucose measurement, it is not available in many parts the underlying disease process. The severity of the meta-of the world, and is not sufficiently standardized for its bolic abnormality can progress, regress, or stay the same.use to be recommended at this time. If an OGTT is per- Thus, the degree of hyperglycaemia reflects the sever-formed, it is sufficient to measure the blood glucose ity of the underlying process and its treatment more thanvalues while fasting and at 2 h after a 75 g oral glucose the nature of the process itself.load. For children the oral glucose load is related to bodyweight: 1.75 g /kg. The diagnostic criteria in children - Diabetes mellitus:are the same as for adults (3,4). Diabetes mellitus, regardless of underlying cause, is subdivided into: insulin requiring for survival (corre-Diagnosis of gestational diabetes sponding to the former clinical class of IDDM), e.g. C-peptide deficient; insulin requiring for control, i.e. The criteria for abnormal glucose tolerance in preg- metabolic control, rather than for survival, e.g. somenancy, which are widely used in the U.S.A., were pro- endogenous insulin secretion but insufficient to achieveposed by O’Sullivan and Mahan in 1964 (10). These normoglycaemia without added exogenous insulin; andcriteria, revised by the NDDG in 1979, have been not insulin requiring, i.e. those who may be controlledadopted by the ADA, but are at variance with WHO cri- satisfactorily by non-pharmacological methods or drugsteria. Most American obstetricians use a screening test other than insulin. Together the latter two subdivisionsconsisting of a 50 g oral glucose load followed by a constitute the former class of NIDDM (4).plasma glucose determination 1 h later. Screening shouldbe performed - in high-risk women (cfr supra) - between24 and 28 weeks of gestation, and the patient need not TABLE 3. Diagnosis of GDM with a 100 g or 75 gbe fasting. A value of ≥ 140 mg/dl 1 h after the 50 g load glucose load (10).indicates the need for a full diagnostic, 100 g, 3-h OGTTperformed in the fasting state. This two-step process - a mg/dl mmol/l50 g screening test and, if that is positive, a 100 g or 100-g Glucose loadalternatively a 75 g diagnostic test - is the testing scheme Fasting 95 5.3in current use not only in the U.S.A., but also in many 1-h 180 10.0parts of Europe (Table 3). 2-h 155 8.6 Instead, in order to determine if gestational diabetes 3-h 140 7.8is present in pregnant women, the WHO recommends a 75-g Glucose loadstandard OGTT be performed after overnight fasting Fasting 95 5.3(8-14 h) by giving 75 g anhydrous glucose in 250-300 1-h 180 10.0ml water. Plasma glucose is measured fasting and after 2-h 155 8.6 Acta Clinica Belgica, 2003; 58-5
  • 6. 274 NEW CLASSIFICATION AND NEW DIAGNOSTIC CRITERIA OF DIABETES MELLITUS- Impaired glucose tolerance and impaired fasting Change in diagnostic value for fasting plasma/ glycaemia blood glucose concentration As mentioned above, impaired glucose tolerance The major change in the diagnostic criteria for dia-(IGT), rather than being a class as in the previous clas- betes mellitus from the previous NDDG/WHO recom-sification, is categorized as a stage in the natural history mendation is the lowering of the diagnostic value of theof disordered carbohydrate metabolism. A stage of ‘im- fasting plasma glucose concentration to 126 mg/dI (7.0paired fasting glycaemia’ or ‘nondiabetic fasting hyper- mmol/I) and above, from the former level of 140 mg/dIglycaemia’ is also recognized because such subjects, like (7.8 mmol/l) and above. For whole blood the new levelthose with IGT, have increased risks of progressing to is 110 mg/dl (6.1 mmo/l) and above, from the formerdiabetes and macrovascular disease. 120 mg/dI (6.7 mmol/l). The new fasting criterion is Individuals who meet criteria for IGT or IFG (Table chosen to represent a value which in most persons is of4) may be euglycaemic in their daily lives as shown by approximately equal diagnostic significance to that ofnormal or near-normal glycated haemoglobin levels. IFG the 2-h post-load concentration, which is not changed.and IGT are not clinical entities in their own right but This equivalence has been established from severalrather risk factors for future diabetes and cardiovascu- population-based studies. Furthermore, several studieslar disease. IFG and IGT are often associated with the have shown increased risk of microvascular disease ininsulin resistance syndrome (also known as syndrome persons with fasting plasma glucose concentrations ofX or the metabolic syndrome), which consists of insu- 126 mg/dI and over (12), and of macrovascular diseaselin resistance, compensatory hyperinsulinemia to main- in persons with such fasting concentrations, even in thosetain glucose homeostasis, obesity (especially abdomi- with 2-h values of <140 mg/dI (13).nal or visceral obesity), dyslipidemia of thehigh-triglyceride and/or low-HDL type, and hyperten-sion. The insulin resistance syndrome contains many Is a glucose tolerance test important for clini-features that increase cardiovascular risk. Thus, IGT may cal practice?not be directly involved in the pathogenesis of cardio-vascular disease, but rather may serve as an indicator or As mentioned earlier the WHO judged an OGTTmarker of enhanced risk by virtue of its correlation with should be used for patients with blood glucose levels inthe other elements of the metabolic syndrome that are the ‘uncertain’ range. Indeed the shift from using 2-hcardiovascular risk factors (3). values on an OGTT to FPG causes changes in the preva- lence of diabetes mellitus, depending on the population- Normoglycaemia studied. It should be recognized that some of the indi- viduals identified by fasting values may be different from A fasting venous plasma glucose concentration of those identified by the 2h values, and that overall preva-less than 110 mg/dl has been chosen as ‘normal’. Al- lence may be somewhat different, although not alwaysthough this choice is arbitrary, such values are observed (14,15). In one report, the old criteria were more likelyin people with proven normal glucose tolerance, and to diagnose diabetes in lean subjects, while the new cri-values above this are associated with a progressively teria were more likely to identify it in middle-aged obesegreater risk of developing micro- and macrovascular subjects (16). In another review, almost twice as manycomplications (11). Recognition of the pathological subjects were classified as diabetic by the new than theprocess at an early stage may be useful if progression to old fasting criteria (17). Older subjects appear to be mostmore advanced stages can be prevented. Conversely, affected by the new criteria. In a study of 4515 subjectseffective treatments, or occasionally the natural history over the age of 65 years, the prevalence of untreatedof some forms of diabetes mellitus, may result in rever- diabetes with the new fasting criterion versus the oldsion of hyperglycaemia to a state of normoglycaemia. 2-h OGTT criteria was 7.7 versus 14.8 percent, respec- tively (18). Thus, many elderly subjects who would pre- viously have been given a diagnosis of diabetes would currently be classified as non-diabetic.Acta Clinica Belgica, 2003; 58-5
  • 7. NEW CLASSIFICATION AND NEW DIAGNOSTIC CRITERIA OF DIABETES MELLITUS 275TABLE 4. Values for diagnosis of diabetes mellitus and other categories of hyperglycaemia (4) Glucose concentration (mmol l-1 (mg dl-1)) Whole blood Plasma Venous Capillary VenousDiabetes Mellitus: Fasting ≥ 6.1 (≥ 110) ≥ 6.1 (≥ 110) ≥ 7.0 (≥ 126) or 2-h post glucose load ≥ 10.0 (≥ 180) ≥ 11.1 (≥ 200) ≥ 11.1 (≥ 200) or bothImpaired Glucose Tolerance (IGT): Fasting concentration (if measured) <6.1 (<110) <6.1 (<110) <7.0 (<126) and 2-h post glucose load ≥ 6.7 (≥ 120) and ≥ 7.8 (≥ 140) and ≥ 7.8 (≥ 140) and < 10.0 (<180) <11.1 (<200) <11.1 (<200)Impaired Fasting Glycaemia (IFG): Fasting ≥ 5.6 (≥ 100) and ≥ 5.6 (≥ 100) and ≥ 6.1 (≥ 110) and <6.1 (<110) <6.1 (<110) <7.0 (<126)2-h (if measured) <6.7 (<120) <7.8 (<140) <7.8 (<140)Value of new versus old criteria as predictors CONCLUSIONof cardiovascular risk The ever increasing number of type 2 diabetic per- It has been shown that the risk for cardiovascular sons worldwide and the high morbidity as well as mor-disease (CVD) is graded across the entire range of hy- tality due to CVD in people with asymptomatic glucoseperglycaemia (19,20). In this regard one must take into intolerance ask for an early and indisputable diagnosis.account the significance of all postprandial glycaemic This is even more important in the light of the encour-peaks occurring during a 24 h period. This arises the aging results from the recent trials to prevent type 2 dia-question if the new criteria, only using the FPG but not betes. Whether this will be true for the early interven-the 2-h OGGT - as a marker of postprandial glycaemia - tion studies in type 1 diabetes has to be awaited upon.will not exclude an important subgroup of high-risk sub- Today, the classification and diagnostic criteria of dia-jects from being detected in an early stage. During the betes mellitus and other categories of glucose intoler-last 4 years data is accumulating that the old criteria ance have been refined in order to help clinicians andwere indeed better predictors of cardiovascular risk and scientists to ameliorate their methods of treatment, andmortality (21-25). In particular, the DECODE-study has especially to start that treatment much earlier in order toshown that the risk of death for impaired fasting glu- prevent the long-term complications. However, somecose was lower than that for impaired glucose tolerance. issues remain uncertain and continuous research will be Nevertheless other authors have brought some argu- needed to further elucidate them.ments showing that the 2-h value on the OGTT addsnothing (26) or very little (27) for identifying CVD riskif the other risk factors are taken into account. Somehave even stated that the OGTT is superfluous (28). Acta Clinica Belgica, 2003; 58-5
  • 8. 276 NEW CLASSIFICATION AND NEW DIAGNOSTIC CRITERIA OF DIABETES MELLITUSREFERENCES 16. DECODE Study Group on behalf of the European Diabetes Epi- demiology Study Group: Will new diagnostic criteria for diabe- tes mellitus change phenotype of patients with diabetes? 1. National Diabetes Data Group: Classification and diagnosis of Reanalysis of European epidemiological data. Br Med J diabetes mellitus and other categories of glucose tolerance. Dia- 1998,317: 371-5. betes 1979,28 :1039-57. 17. Dinneen SF, Maldonado D, Leibson CL et al.: Effects of chang- 2. WHO Expert Committee on Diabetes Mellitus. Second Report. ing diagnostic criteria on the risk of developing diabetes. Dia- Technical Report Series 646. Geneva: WHO, 1980. betes Care 1998,21: 1408. 3. The Expert Committee on the Diagnosis and Classification of 18. Wahl PW, Savage PJ, Psaty BM et al: Diabetes in older adults: Diabetes Mellitus. Report of the Expert Committee on the Diag- Comparison of 1997 American Diabetes Association classifica- nosis and Classification of Diabetes Mellitus. Diabetes Care tion of diabetes with 1985 WHO classification. The Lancet 1997,20: 1183-97. 1998,352: 1012. 4. Alberti KGMM, Zimmet PZ for the WHO Consultation: Defini- 19. Balkau B, Shipley M, Jarrett RJ, Pyorala K, Pyorala M, Forhan tion, diagnosis and classification of diabetes mellitus and its A, Eschwege E: High blood glucose concentration is a risk fac- complications. Part 1: Diagnosis and classification of diabetes tor for mortality in middle-aged non-diabetic men: 20-year fol- mellitus. Provisional report of a WHO consultation. Diabetic. low-up in the Whitehall Study, the Paris Prospective Study and Med. 1998,15: 539-53. the Helsinki Policemen Study. Diabetes Care 1998,21: 360-7. 5. Verge CF, Gianani R, Kawasaki E, Yu L, Pietropaolo M, Jackson 20. Coutinho M, Gerstein HC, Wang Y, Yusuf S: The relationship RA et al : Predicting type 1 diabetes in first-degree relatives us- between glucose and incident cardiovascular events: a meta-re- ing a combination of insulin, GAD, and ICA512bdc/IA-2 gression analysis of published data from 20 studies of 95.783 autoantibodies. Diabetes 1996,45: 926-33. individuals followed for 12.4 years. Diabetes Care 1999,22: 233- 6. Humphrey ARG, McCarty DJ, Mackay IR, Rowley MJ, Dwyer 40. T, Zimmet P: Autoantibodies to glutamic acid decarboxylase and 21. Tominaga M, Eguchi H, Manaka H et al: Impaired glucose tol- phenotypic features associated with early insulin treatment in erance is a risk factor for cardiovascular disease, but not im- individuals with adult-onset diabetes mellitus. Diabetic Med. paired fasting glucose. Diabetes Care 1999,22: 920. 1998,15: 113-9. 22. The DECODE study group on behalf of the European Diabetes 7. Betterle C, Zanette F, Pedini B, Presotto F, Rapp LB, Monsciotti Epidemiology Group: Glucose tolerance and mortality: compari- CM et al: Clinical and subclinical organ-specific autoimmune son of WHO and American Diabetes Association diagnostic cri- manifestations in type 1 (insulin-dependent) diabetic patients and teria. The Lancet 1999,354: 617-21. their first-degree relatives. Diabetologia 1983,26: 431-6. 23. Barzilay JI, Spiekerman CF, Wahl PW, et al: Cardiovascular dis- 8. DeFronzo RA, Bonadonna RC, Ferrannini E: Pathogenesis of ease in older adults with glucose disorders: comparison of Ameri- NIDDM. In: Alberti KGMM, Zimmet P, DeFronzo RA, eds. In- can Diabetes Association criteria for diabetes mellitus with WHO ternational Textbook of Diabetes Mellitus, 2nd edn. Chichester: criteria. The Lancet,354: 622-5. Wiley, 1997:635-712. 24. Qiao Q, Pyorala K, Pyorala M et al: Two-hour glucose is a bet- 9. Hoet JJ, Tripathy BB, Rao RH, Yajnik CS: Malnutrition and dia- ter risk predictor for incident coronary heart disease and cardio- betes in the tropics. Diabetes Care 1996,19: 1014-7. vascular mortality than fasting glucose. Eur Heart J 2002,23:10. O’Sullivan JB, Mahan CM: Criteria for the oral glucose toler- 1267. ance test in pregnancy. Diabetes 1964,13 :278. 25. DECODE Study Group: Glucose tolerance and cardiovascular11. Alberti KGMM: The clinical implications of impaired glucose mortality: comparison of fasting and 2-hour diagnostic criteria. tolerance. Diabetic Med 1996,13: 927-37. Arch Intern Med 2001,161: 397-405.12. McCance DR, Hanson RL, Charles MA, Jacobsson LTH, Pettitt 26. Stern MP, Fatehi P, Williams K, Haffner SM: Predicting future DJ, Bennett PH et al : Comparison of tests for glycated haemo- cardiovascular disease: do we need the oral glucose tolerance globin and fasting and two hour plasma glucose concentrations test? Diabetes Care 2002,25: 1851-6. as diagnostic methods for diabetes. Br Med J 1994,308: 1323-8. 27. Meigs JB, Nathan DM, D’Agostino RB, Wilson PWF: Fasting13. Charles MA, Balkau B, Vauzelle-Kervoeden F, Thibault N, and postchallenge glycemia and cardiovascular risk: the Eschwège E: Revision of diagnostic criteria for diabetes (Let- Framingham Offspring Study. Diabetes Care 2002,25: 1845-50. ter). The Lancet 1996,348: 1657-8. 28. Davidson MB:Counterpoint: The oral glucose tolerance test is14. Finch CF, Zimmet PZ, Alberti KGMM: Determining diabetes superfluous. Diabetes Care 2002,25: 49-51. prevalence: a rational basis for the use of fasting plasma glucose 29. World Health Organization: Diabetes Mellitus: Report of a WHO concentrations? Diabetic Med 1990,7 : 603-10. Study Group. Geneva, World Health Organization, 1985 (Tech.15. Ramachandran A, Snehalatha C, Latha E, Vijay V: Evaluation Rep. Ser., n. 727). of the use of fasting plasma glucose as a new diagnostic crite- rion for diabetes in Asian Indian population (Letter). Diabetes Care 1998,21: 666-7.Acta Clinica Belgica, 2003; 58-5

×