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Diagnosis, Prognosis, and Treatment of Impaired Glucose Tolerance and Impaired Fasting Glucose

Summary (continued)

Discussion

Diagnosis

An accurate diagnosis of DM is required because the consequences for the individual are considerable and lifelong. The diagnosis of IFG or IGT is used as a risk indicator for future DM and/or CVD. The problem with these arbitrary classifications is that test reproducibility is poor, and this encourages repeat testing that adds to the uncertainty and confusion of the diagnosis when results are different.

Reproducibility of IGT and IFG

The observed reproducibility for both IGT and IFG classification in these studies was roughly 50 percent. The kappa coefficients for the IGT category were quite low and indicate overall fair agreement. The potential factors contributing to the variation and poor reproducibility were not assessed for this review.

The probability that a significant change has occurred in serial measurements can be estimated by calculating the reference change value (RCV). For FPG, the RCV = 2^½ * 1.96 * (1.42 + 6.32)^½ or 17.9 percent. For 2-hr PG, the RCV = 2^½ * 1.96 * (1.42 + 16.62)^½ or 46.4 percent. The difference between two fasting glucose values would therefore need to be greater than 17.9 percent to be significantly different. A lower RCV would increase the sensitivity to change, or reduce the variation noise, and could be achieved if the analytical and/or the biological variation are lowered.

In the best case scenario, the lowest biological variability reported for fasting glucose was an FPG CVI of 4.8 percent.⁸⁴ If this value is used along with an intra-laboratory imprecision of 1 percent and no bias, the RCV can be reduced to 13.6 percent. This is the very best or lowest amount of variation possible for a fasting plasma glucose measurement.

Comparison of IFG and IGT diagnosis

This review also compared among studies the proportion of participants classified as IGT (2-hr PG), IGT (FPG and 2-hr PG), I-IGT, IFG, I-IFG, and IGT/IFG. Comparisons among these categories were statistically significant except for I-IGT versus IFG and I-IFG versus IGT/IFG. This exemplifies the importance of clearly distinguishing categories as this can affect the proportion of study subjects and the conclusions from prognosis and treatment data.

The reproducibility for both IGT and IFG categorization is poor by both observed and kappa analysis. Because of the large variability in glucose measurement, the absolute FPG and 2-hr PG measurements may be more informative than categorization into IFG and IGT, respectively. Comparison of IGT and IFG categories shows a wide degree of variation among populations.

The prevalence of IGT is greater than for IFG in almost all studies. High-risk populations have an equal or greater proportion of IFG compared to IGT diagnoses. Statistically, the proportion of study participants classified as IGT by 2-hr PG alone is greater than if the diagnostic criteria of both 2-hr PG and FPG are used. This will affect the conclusions of prognosis and possibly treatment data in population studies using only the 2-hr PG concentration (WHO epidemiological criteria).

Prognosis

This review provides further evidence of the relevance of the OGTT as a diagnostic test. Despite the many shortcomings of the OGTT reviewed here, it detects a very high-risk group for future DM and may either need to be more accessible to clinicians or replaced by a simpler test that provides comparable predictive information. The OGTT also detects a group at risk for CVD; and if IGT is causally related to CVD, the AR estimates suggest that its treatment may reduce CVD risk by as much as 20 percent to 40 percent.

These studies highlight the relevance of fasting and postchallenge glucometabolic abnormalities to clinically relevant outcomes. Intervention studies have already shown that DM can be prevented in these individuals with some interventions.

Risk for progression to DM

The results of this systematic review clearly show that IGT, IFG, I-IGT, I-IFG, and combined IGT/IFG are strong risk factors for future DM. The combined group has the strongest risk factor, and this observation is not surprising given the fact that the diagnostic threshold for DM is just a farther point along the dysglycemic spectrum than the threshold for either IFG or IGT.

Nevertheless, these large risk estimates clearly do suggest that any clinical approach directed at preventing DM should include a policy of detecting IFG or IGT. They do not support suggestions that measures of glucose are not necessary to detect individuals at risk for future DM. However, such a policy may be useful to reduce the number of individuals who require a glucose test.

Risk for CVD outcomes

The reviewed studies provide confirmation that IFG or IGT are risk factors for fatal and nonfatal CVD and are consistent with other studies that were excluded because whole blood or capillary samples were used to assay glucose levels. Moreover, the suggestion that IGT is a greater risk factor for CVD than IFG is supported by this systematic review but is based on the findings of a single study.⁸⁵ This is not surprising given the fact that IGT is detected in response to stressing the physiology with a nonphysiological glucose load, thus exposing a degree of metabolic dysregulation that would not be apparent on the basis of fasting glucose levels alone.

Treatment

Prevention of DM: lifestyle interventions

This systematic review clearly demonstrates that DM can be prevented or delayed with lifestyle modification. All but one of the five studies that evaluated a combined diet and exercise program found significant benefits, with a pooled relative risk of 54 percent for progression to diabetes. The only trial to show no effect of a combined diet and exercise intervention was of short duration (6-month followup). Interventions with diet or exercise alone showed mixed results between studies. Efforts to modify dietary intake and activity levels in individuals at increased risk for developing DM are clearly warranted.

Prevention of DM: pharmacotherapeutic interventions

Only four trials to date have evaluated the effect of pharmacotherapeutic interventions on the risk for developing DM in individuals with IGT. Two of these studies, one involving acarbose and one involving metformin, demonstrated reduced rates of progression to DM with a relative risk reduction of about 25 percent. Given this relative paucity of information, recommendation of pharmacological intervention for the prevention of DM would seem premature at this time.

Pediatric Population

Despite the paucity of population-based studies, several cohort studies in high-risk groups suggest that IGT is a significant and potentially growing problem in the pediatric population. Indeed, larger proportions of children may have IGT than is currently recognized. It is critical to acquire an understanding of the precursors of type 2 DM development in children and youth. However, few conclusions can be made based on the current pediatric literature. Further investigation of prevalence in children and adolescents is necessary to clarify the magnitude of the problem.

Diagnosis

The reproducibility of the diagnosis of IGT with OGTT testing and the clinical significance of IFG versus IGT have not been widely examined in the pediatric literature. Although young age has been implicated as a predictor of poor reproducibility of OGTT results in adults, suggesting that reproducibility may be worse in adolescents and children, this was not the experience in one small pediatric study (n=10).⁷⁷

Clearly, further investigation of the reliability of diagnostic criteria for IFG and IGT is warranted. Furthermore, given the importance of the prevention of type 2 DM, it may be advantageous to identify children who have disturbed glucose metabolism (insulin resistance and/or beta cell dysfunction) before they develop IFG or IGT.

Prognosis

An understanding of how disturbed glucose metabolism progresses to IGT and to type 2 DM is key to the primary prevention of DM. Currently, details of this progression are completely lacking in the pediatric population.

Prevalence data for type 2 DM suggest prognosis may vary with age, pubertal status, and ethnicity. Family history of DM, exposure to a diabetic environment in utero, fitness and physical activity, fat distribution, and characteristics of nutritional intake may also influence the prognosis of IFG and IGT. Longitudinal studies are required to examine mid- and long-term outcomes of IGT and the determinants of outcome in multiple ethnic groups and across a broad age range.

Investigation of other metabolic outcomes in children and adolescents with IFG and IGT would further improve our understanding of disturbance in health in this population. Better understanding of the prognosis of IGT in children and adolescents will clarify the need for intervention and contribute to optimal intervention study design.

Treatment

A single study has described the pharmacological treatment of IGT, and no randomly controlled lifestyle intervention has been reported in the pediatric age group. Given the increasing rates of IFG/IGT, research on the optimal approach to the management of these children should be a research priority. This research should compare lifestyle intervention and pharmacotherapy and identify optimal methodologies for young populations and their families. Although glycemic status is a key outcome variable, other metabolic and psychosocial outcomes should also be examined.

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Conclusions

Analysis from this systematic evidence review suggests the following:

Diagnosis—The reproducibility for both IGT and IFG categorization is poor. Therefore the absolute FPG and 2-hr PG measurement may be more informative than categorization into IFG and IGT respectively. The distribution of study participants in the IGT category varies significantly with the diagnostic criteria used. This will affect findings in epidemiological studies evaluating prognosis and treatment.
Prognosis—Many studies consistently show that both IFG and IGT are strong risk factors for the development of DM. Fewer studies also show that they are risk factors for future CVD and all-cause mortality.
Treatment—There is evidence that combined diet and exercise, as well as drug therapy (metformin, acarbose), may be effective at preventing progression to DM in IGT subjects.
Pediatric population—IGT is relatively common in childhood, particularly in children who are overweight. Further clarification of population-based prevalence and investigation to improve understanding of the diagnosis, clinical significance, and optimal management of IFG and IGT in childhood is required.

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Availability of Full Report

The full evidence report from which this summary was taken was prepared for the Agency for Healthcare Research and Quality (AHRQ) by the McMaster Evidence-based Practice Center under Contract No. 290-02-0020. Printed copies may be obtained free of charge from the AHRQ Publications Clearinghouse by calling 800-358-9295. 9295. Requesters should ask for Evidence Report/Technology Assessment No. 128, Diagnosis, Prognosis, and Treatment of Impaired Glucose Tolerance and Impaired Fasting Glucose.

The Evidence Report is also online on the National Library of Medicine Bookshelf, or can be downloaded as a PDF File (8 MB) [PDF Help].

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References

1. Wild S, Roglic G, Green A, et al. Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. Diabetes Care 2004 May;27(5):1047-53.

2. Reference Manager [computer program]. ISI Research Soft. 10. Carlsbad, CA, USA: ISI Research Soft; 2001.

3. Oremus M, Wolfson C, Perrault A, et al. Interrater reliability of the modified Jadad quality scale for systematic reviews of Alzheimer's disease drug trials. Dement Geriatr Cogn Disord 2001 May;12(3):232-6.

4. MacKay M, Scanlan A, Olsen L, et al. Looking for the evidence: a systematic review of prevention strategies addressing sport and recreational injury among children and youth. J Sci Med Sport 2004 Mar;7(1):58-73.

5. Mooy JM, Grootenhuis PA, de Vries H, et al. Intra-individual variation of glucose, specific insulin and proinsulin concentrations measured by two oral glucose tolerance tests in a general Caucasian population: the Hoorn Study. Diabetologia 1996 Mar;39(3):298-305.

6. de Vegt F, Dekker JM, Stehouwer CD, et al. Similar 9-year mortality risks and reproducibility for the World Health Organization and American Diabetes Association glucose tolerance categories: the Hoorn Study. Diabetes Care 2000 Jan;23(1):40-4.

7. Farrer M, Fulcher G, Albers CJ, et al. Patients undergoing coronary artery bypass graft surgery are at high risk of impaired glucose tolerance and diabetes mellitus during the first postoperative year. Metabolism 1995 Aug;44(8):1016-27.

8. Ko GTC, Chan JCN, Woo J, et al. The reproducibility and usefulness of the oral glucose tolerance test in screening for diabetes and other cardiovascular risk factors. Ann Clin Biochem 1998;35(1):62-7.

9. Ko GT, Chan JC, Woo J, et al. Use of the 1997 American Diabetes Association diagnostic criteria for diabetes in a Hong Kong Chinese population. Diabetes Care 1998 Dec;21(12):2094-7.

10. de Vegt F, Dekker JM, Jager A, et al. Relation of impaired fasting and postload glucose with incident type 2 diabetes in a Dutch population: The Hoorn Study. JAMA 2001 Apr 25;285(16):2109-13.

11. Gabir MM, Hanson RL, Dabelea D, et al. The 1997 American Diabetes Association and 1999 World Health Organization criteria for hyperglycemia in the diagnosis and prediction of diabetes. Diabetes Care 2000 Aug;23(8):1108-12.

12. Qiao Q, Nakagami T, Tuomilehto J, et al. Comparison of the fasting and the 2-h glucose criteria for diabetes in different Asian cohorts. Diabetologia 2000 Dec;43(12):1470-5.

13. Kousta E, Lawrence NJ, Penny A, et al. Implications of new diagnostic criteria for abnormal glucose homeostasis in women with previous gestational diabetes. Diabetes Care 1999 Jun;22(6):933-7.

14. Alberti KGMM, Zimmet PZ. Definition, diagnosis and classification of diabetes mellitus and its complications part 1: Diagnosis and classification of diabetes mellitus—Provisional report of a WHO consultation. Diabet Med 1998 Jul;15(7):539-53.

15. Norman RJ, Masters L, Milner CR, et al. Relative risk of conversion from normoglycaemia to impaired glucose tolerance or non-insulin dependent diabetes mellitus in polycystic ovarian syndrome. Hum Reprod 2001 Sep;16(9):1995-8.

16. Wein P, Beischer N, Harris C, et al. A trial of simple versus intensified dietary modification for prevention of progression to diabetes mellitus in women with impaired glucose tolerance. Aust NZ J Obstet Gynaecol 1999;39(2):162-6.

17. Pettitt DJ, Narayan KM, Hanson RL, et al. Incidence of diabetes mellitus in women following impaired glucose tolerance in pregnancy is lower than following impaired glucose tolerance in the non-pregnant state. Diabetologia 1996 Nov;39(11):1334-7.

18. Goldberg RB, Mellies MJ, Sacks FM, et al. Cardiovascular events and their reduction with pravastatin in diabetic and glucose-intolerant myocardial infarction survivors with average cholesterol levels: subgroup analyses in the cholesterol and recurrent events (CARE) trial. The Care Investigators. Circulation 1998;98(23):2513-9.

19. Larsson H, Lindgarde F, Berglund G, et al. Prediction of diabetes using ADA or WHO criteria in post-menopausal women: a 10-year follow-up study. Diabetologia 2000 Oct;43(10):1224-8.

20. Charles MA, Eschwege E, Thibult N, et al. The role of nonesterified fatty acids in the deterioration of glucose tolerance in Caucasian subjects: results of the Paris Prospective Study. Diabetologia 1997 Sep;40(9):1101-6.

21. Balkau B, Eschwege E, Ducimetiere P, et al. The high risk of death by alcohol related diseases in subjects diagnosed as diabetic and impaired glucose tolerant: the Paris Prospective Study after 15 years of follow-up. J Clin Epidemiol 1991;44(6):465-74.

22. Fontbonne A, Tchobroutsky G, Eschwege E, et al. Coronary heart disease mortality risk: plasma insulin level is a more sensitive marker than hypertension or abnormal glucose tolerance in overweight males. The Paris Prospective Study. Int J Obes 1988;12(6):557-65.

23. Fontbonne AM, Eschwege EM. Insulin and cardiovascular disease. Paris Prospective Study. Diabetes Care 1991 Jun;14(6):461-9.

24. Fontbonne A, Eschwege E. Insulin-resistance, hypertriglyceridaemia and cardiovascular risk: the Paris Prospective Study. Diabete Metab 1991 May;17(1 Pt 2):93-5.

25. Balkau B, Eschwege E, Fontbonne A, et al. Cardiovascular and alcohol-related deaths in abnormal glucose tolerant and diabetic subjects. Diabetologia 1992 Jan;35(1):39-44.

26. Balkau B, Eschwege E, Papoz L, et al. Risk factors for early death in non-insulin dependent diabetes and men with known glucose tolerance status. BMJ 1993 Jul 31;307(6899):295-9.

27. Balkau B, Forhan A, Eschwege E. Two hour plasma glucose is not unequivocally predictive for early death in men with impaired fasting glucose: more results from the Paris Prospective Study. Diabetologia 2002 Sep;45(9):1224-30.

28. Charles MA, Fontbonne A, Thibult N, et al. Risk factors for NIDDM in white population. Paris prospective study. Diabetes 1991 Jul;40(7):796-9.

29. Ammari F, Batieha A, Jaddou PHH, et al. A natural history of impaired glucose tolerance in North Jordan. Practical Diabetes International 1998;15(5):139-40.

30. Puavilai G, Tiewtranon V, Pensuwan S, et al. Impaired glucose tolerance in Thai adults: status of glucose tolerance after 2-year follow up. J Med Assoc Thai 1987 Mar;70 Suppl 2:68-76.

31. Inoue I, Takahashi K, Katayama S, et al. A higher proinsulin response to glucose loading predicts deteriorating fasting plasma glucose and worsening to diabetes in subjects with impaired glucose tolerance. Diabet Med 1996;13(4):330-6.

32. Keech A, Colquhoun D, Best J, et al. Secondary prevention of cardiovascular events with long-term pravastatin in patients with diabetes of impaired fasting glucose: Results from the LIPID trial. Diabetes Care 2003;26(10):2713-21.

33. Rubins HB, Robins SJ, Collins D, et al. Diabetes, plasma insulin, and cardiovascular disease: subgroup analysis from the Department of Veterans Affairs high-density lipoprotein intervention trial (VAHIT). Arch Intern Med 2002;162(22):2597-604.

34. Bonora E, Kiechl S, Oberhollenzer F, et al. Impaired glucose tolerance, Type II diabetes mellitus and carotid atherosclerosis: prospective results from the Bruneck Study. Diabetologia 2000 Feb;43(2):156-64.

35. Fisman EZ, Motro M, Tenenbaum A, et al. Impaired fasting glucose concentrations in nondiabetic patients with ischemic heart disease: a marker for a worse prognosis. Am Heart J 2001 Mar;141(3):485-90.

36. Tenenbaum A, Motro M, Fisman EZ, et al. Status of glucose metabolism in patients with heart failure secondary to coronary artery disease. Am J Cardiol 2002;90(5):529-32.

37. Saydah SH, Loria CM, Eberhardt MS, et al. Subclinical states of glucose intolerance and risk of death in the U.S. Diabetes Care 2001 Mar;24(3):447-53.

38. Tominaga M, Eguchi H, Manaka H, et al. Impaired glucose tolerance is a risk factor for cardiovascular disease, but not impaired fasting glucose. The Funagata Diabetes Study. Diabetes Care 1999 Jun;22(6):920-4.

39. Saydah SH, Loria CM, Eberhardt MS, et al. Abnormal glucose tolerance and the risk of cancer death in the United States. Am J Epidemiol 2003 Jun 15;157(12):1092-100.

40. Knowler WC, Barrett-Connor E, Fowler SE, et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 2002;346(6):393-403.

41. Pan XR, Li GW, Hu YH, et al. Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance. The Da Qing IGT and Diabetes Study. Diabetes Care 1997;20(4):537-44.

42. Liao D, Asberry PJ, Shofer JB, et al. Improvement of BMI, body composition, and body fat distribution with lifestyle modification in Japanese Americans with impaired glucose tolerance. Diabetes Care 2002 Sep;25(9):1504-10.

43. Lindstrom J, Eriksson JG, Valle TT, et al. Prevention of diabetes mellitus in subjects with impaired glucose tolerance in the Finnish diabetes prevention study: results from a randomized clinical trial. J Am Soc Nephrol 2003;14(7 Suppl 2):S108-S113.

44. Oldroyd JC, Unwin NC, White M, et al. Randomised controlled trial evaluating the effectiveness of behavioural interventions to modify cardiovascular risk factors in men and women with impaired glucose tolerance: outcomes at 6 months. Diabetes Res Clin Pract 2001;52(1):29-43.

45. Weber-Hamann B, Hentschel F, Kniest A, et al. Hypercortisolemic depression is associated with increased intra-abdominal fat. Psychosomatic-Medicine 2002;64(2):274-7.

46. Chiasson JL, Josse RG, Gomis R, et al. Acarbose for prevention of type 2 diabetes mellitus: the STOP-NIDDM randomised trial. Lancet 2002;359(9323):2072-7.

47. Lehtovirta M, Forsen B, Gullstrom M, et al. Metabolic effects of metformin in patients with impaired glucose tolerance. Diabet Med 2001;18(7):578-83.

48. Li CL, Pan CY, Lu JM, et al. Effect of metformin on patients with impaired glucose tolerance. Diabet Med 1999;16(6):477-81.

49. Vermes E, Ducharme A, Bourassa MG, et al. Enalapril reduces the incidence of diabetes in patients with chronic heart failure: insight from the Studies of Left Ventricular Dysfunction (SOLVD). Circulation 2003 Mar 11;107(9):1291-6.

50. Chiasson JL, Josse RG, Gomis R, et al. Acarbose treatment and the risk of cardiovascular disease and hypertension in patients with impaired glucose tolerance: the STOP-NIDDM trial. JAMA 2003;290(4):486-94.

51. Eriksson J, Tuominen J, Valle T, et al. Aerobic endurance exercise or circuit-type resistance training for individuals with impaired glucose tolerance? Horm Metab Res 1998 Jan;30(1):37-41.

52. Uusitupa MI, Mykkanen L, Siitonen O, et al. Chromium supplementation in impaired glucose tolerance of elderly: effects on blood glucose, plasma insulin, C-peptide and lipid levels. Br J Nutr 1992;68(1):209-16.

53. Nagi DK, Knowler WC, Charles MA, et al. Early and late insulin response as predictors of NIDDM in Pima Indians with impaired glucose tolerance. Diabetologia 1995 Feb;38(2):187-92.

54. Motala AA, Omar MA, Gouws E. High risk of progression to NIDDM in South-African Indians with impaired glucose tolerance. Diabetes 1993 Apr;42(4):556-63.

55. Rosenbloom AL, Hunt SS. Prognosis of impaired glucose tolerance in children with stress hyperglycemia, symptoms of hypoglycemia, or asymptomatic glucosuria. J Pediatr 1982 Sep;101(3):340-4. 56. Solomon MP, Wilson DC, Corey M, et al. Glucose intolerance in children with cystic fibrosis. J Pediatr 2003 Feb;142(2):128-32.

57. Cucinotta D, De Luca F, Gigante A, et al. No changes of insulin sensitivity in cystic fibrosis patients with different degrees of glucose tolerance: an epidemiological and longitudinal study. Eur J Endocrinology 1994 Mar;130(3):253-8.

58. Rakotoambinina B, Delaisi B, Laborde K, et al. Insulin responses to intravenous glucose and the hyperglycemic clamp in cystic fibrosis patients with different degrees of glucose tolerance. Pediatr Res 1994;36(5):667-71.

59. Austin A, Kalhan SC, Orenstein D, et al. Roles of insulin resistance and beta-cell dysfunction in the pathogenesis of glucose intolerance in cystic fibrosis. J Clin Endocrinol Metab 1994;79(1):80-5.

60. Cucinotta D, De Luca F, Arrigo T, et al. First-phase insulin response to intravenous glucose in cystic fibrosis patients with different degrees of glucose tolerance. J Pediatr Endocrinol 1994;7(1):13-7.

61. Peraldo M, Fasulo A, Chiappini E, et al. Evaluation of glucose tolerance and insulin secretion in cystic fibrosis patients. Horm Res 1998;49(2):65-71.

62. Milla CE, Warwick WJ, Moran A. Trends in pulmonary function in patients with cystic fibrosis correlate with the degree of glucose intolerance at baseline. Am J Respir Crit Care Med 2000 Sep;162(3 Pt 1):891-5.

63. Garagorri JM, Rodriguez G, Ros L, et al. Early detection of impaired glucose tolerance in patients with cystic fibrosis and predisposition factors. J Pediatr Endocrinol Metab 2001;14(1):53-60.

64. Arrigo T, Cucinotta D, Conti NS, et al. Longitudinal evaluation of glucose tolerance and insulin secretion in non-diabetic children and adolescents with cystic fibrosis: results of a two-year follow-up. Acta Paediatr 1993 Mar;82(3):249-53.

65. Trivedi N, Mithal A, Gupta SK, et al. Reversible impairment of glucose tolerance in patients with endemic fluorosis. Diabetologia 1993;36(9):826-8.

66. Haeusler G, Frisch H. Growth hormone treatment in Turner's syndrome: Short and long-term effects on metabolic parameters. Clin Endocrinol (Oxf) 1992;36(3):247-54.

67. Schulz B, Witt S, Hildmann W, et al. Islet cell antibodies in individuals at increased risk for IDDM. Exp Clin Endocrinol 1984 Apr;83(2):192-8.

68. Gale EA, European Nicotinamide Diabetes Intervention Trial Group. Intervening before the onset of Type 1 diabetes: baseline data from the European Nicotinamide Diabetes Intervention Trial (ENDIT). Diabetologia 2003 Mar;46(3):339-46.

69. Ratzman K-P, Strese J, Rjasanowski I. Prevalence of islet cell antibodies (ICA) and islet cell surface antibodies (ICSA) in children and adolescents with antecedent mumps infection. Exp Clin Endocrinol 1984;83(2):199-202.

70. Rakotoambinina B, Timsit J, Deschamps I, et al. Insulin responses to intravenous glucose, intravenous arginine and a hyperglycaemic clamp in ICA-positive subjects with different degrees of glucose tolerance. Diabetes Metab 1997 Feb;23(1):43-50.

71. Lorini R, Alibrandi A, Vitali L, et al. Risk of type 1 diabetes development in children with incidental hyperglycemia: A multicenter Italian study. Diabetes Care 2001 Jul;24(7):1210-6.

72. Hanley AJ, McKeown-Eyssen G, Harris SB, et al. Cross-sectional and prospective associations between abdominal adiposity and proinsulin concentration. J Clin Endocrinol Metab 2002 Jan;87(1):77-83.

73. Harris SB, Zinman B, Hanley A, et al. The impact of diabetes on cardiovascular risk factors and outcomes in a native Canadian population. Diabetes Res Clin Pract 2002;55(2):165-73.

74. Zimmet PZ, Collins VR, Dowse GK, et al. Hyperinsulinaemia in youth is a predictor of Type 2 (non-insulin-dependent) diabetes mellitus. Diabetologia 1992;35(6):534-41.

75. Braun B, Zimmermann MB, Kretchmer N, et al. Risk factors for diabetes and cardiovascular disease in young Asutralian Aborigines. Diabetes Care 1996 May;19(5):472-9.

76. Silverman BL, Metzger BE, Cho NH, et al. Impaired glucose tolerance in adolescent offspring of diabetic mothers: relationship to fetal hyperinsulinism. Diabetes Care 1995 May;18(5):611-7.

77. Sinha R, Fisch G, Teague B, et al. Prevalence of impaired glucose tolerance among children and adolescents with marked obesity. N Engl J Med 2002 Mar 14;346(11):802-10.

78. Invitti C, Guzzaloni G, Gilardini L, et al. Prevalence and concomitants of glucose intolerance in European obese children and adolescents. Diabetes Care 2003 Jan;26(1):118-24.

79. Goran MI, Bergman RN, Avila Q, et al. Impaired glucose tolerance and reduced beta-cell function in overweight Latino children with a positive family history for type 2 diabetes. J Clin Endocrinol Metab 2004 Jan;89(1):207-12.

80. Silverman BL, Rizzo TA, Cho NH, et al. Long-term effects of the intrauterine environment. The Northwestern University Diabetes in Pregnancy Center. Diabetes Care 1998 Aug;21 Suppl 2:B142-B149.

81. Fagot-Campagna A, Saaddine JB, Flegal KM, et al. Diabetes, impaired fasting glucose, and elevated HbA1c in U.S. adolescents: the Third National Health and Nutrition Examination Survey. Diabetes Care 2001 May;24(5):834-7.

82. Swai ABM, McLarty DG, Kitange HM, et al. Study in Tanzania of impaired glucose tolerance: Methodological myth? Diabetes 1991;40(4):516-20.

83. Arslanian SA, Lewy V, Danadian K, et al. Metformin therapy in obese adolescents with polycystic ovary syndrome and impaired glucose tolerance: amelioration of exaggerated adrenal response to adrenocorticotropin with reduction of insulinemia/insulin resistance. J Clin Endocrinol Metab 2002 Apr;87(4):1555-9.

84. Widjaja A, Morris RJ, Levy JC, et al. Within- and between-subject variation in commonly measured anthropometric and biochemical variables. Clin Chem 1999;45(4):561-6.

85. Hassan IA, Wickramasinghe YA, Spencer SA. Effect of a change in global metabolic rate on peripheral oxygen consumption in neonates. Archives of Disease in Childhood: Fetal & Neonatal Edition 2003 Mar;88(2):F143-F146

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AHRQ Publication Number No. 05-E026-1
Current as of August 2005

Internet Citation:

Diagnosis, Prognosis, and Treatment of Impaired Glucose Tolerance and Impaired Fasting Glucose. Summary, Evidence Report/Technology Assessment: Number 128. AHRQ Publication Number No. 05-E026-1, August 2005. Agency for Healthcare Research and Quality, Rockville, MD. http://www.ahrq.gov/clinic/epcsums/impglusum.htm