Glucose Intolerance Clinical Presentation

  • Author: Samuel T Olatunbosun, MD, FACP; Chief Editor: George T Griffing, MD   more...
 
Updated: Feb 2, 2012
 

History

There are varying and similar presentations between patients with type 1 diabetes mellitus, type 2 diabetes mellitus, gestational diabetes, prediabetes, and glucose intolerance.

Type 1 diabetes mellitus

The warning symptoms of type 1 diabetes include polyuria, polydipsia, and polyphagia due to hyperglycemia. Patients may present with the unexplained weight loss and easy fatigability that result from reduced glucose use and increased catabolism.

Irritability, drowsiness, and loss of consciousness may occur, especially as ketoacidosis develops. The temporal profile is consequent to progression of the metabolic derangement, which is characterized by dehydration, electrolyte abnormalities, osmolality, and acid-base disturbances. After presentation with ketoacidosis, a patient may briefly revert to normoglycemia without requiring therapy (ie, the honeymoon remission).

Type 2 diabetes mellitus

Patients with type 2 diabetes may have any of the symptoms described under type 1 diabetes, but often these persons are asymptomatic. Hyperosmolar nonketotic coma, which may complicate type 2 diabetes mellitus, is characterized by severe dehydration secondary to osmotic diuresis from hyperglycemia. Ketoacidosis, although uncommon, may also occur in type 2 diabetes.

For more information, see Hyperosmolar Coma.

Antecedent history in patients with type 2 diabetes includes frequent or recurrent infections, poor wound healing, blurring of vision, and numbness or tingling sensations in the extremities.

Gestational diabetes mellitus

Gestational diabetes is typically detected during routine screening of pregnant women for glucose intolerance. Any degree of glucose intolerance with onset or recognition during gestation places a patient in the category of gestational diabetes mellitus.

Prediabetes

The categories of impaired glucose tolerance (IGT) and impaired fasting glucose have been officially termed prediabetes, because they are risk factors for future diabetes and for cardiovascular disease.[30, 31]

Patients with impaired glucose homeostasis are generally asymptomatic. Features of related risk factors for cardiovascular disease may be present, even with a mild degree of hyperglycemia. They include a history of hypertension, obesity, dyslipidemia, and/or macrovascular disease, such as stroke, coronary disease, or peripheral vascular disease.

In most cases of IGT and impaired fasting glucose, the presence of 1 or more cardiovascular risk factors indicates the need for a screening test for disorders of glucose tolerance.

Glucose intolerance

Diagnosis of glucose intolerance may coincide with various patient conditions that may be complicated by glucose intolerance, such as liver cirrhosis, end-stage renal disease, and some rare genetic disorders.

Next

Physical Examination

Overt hyperglycemia that has progressed to diabetes, if left untreated, may result in signs of dehydration. Hypotension and other features of hemodynamic decompensation occur with worsening hyperglycemia. Other clinical features, such as Kussmaul respiration and altered level of consciousness due to metabolic derangement, are commonly observed during acute deterioration. Evidence of a precipitating factor, such as fever from an infectious process, may be present and should always be sought.

In routine evaluation of patients with glucose intolerance, weight, height, waist, and hip measurements are recommended. The aim is to determine the body mass index (BMI), the risk level, and the presence of truncal obesity. In type 2 diabetes, 60-90% of the patients are obese. A patient may have central adiposity in spite of a normal BMI. Skin-fold thickness measurement may also be useful in determining regional fat distribution, although it is not often accurate or reproducible.

Peripheral stigmata of lipid abnormalities and atherosclerosis, such as premature arcus cornealis, xanthelasma, eruptive (skin) xanthomata, tendon xanthomata, and lipemia retinalis, may be found in some patients.

Blood pressure measurement is important, because hypertension is a frequent component of the dysmetabolic syndrome. Hypertension is 1.5 to 2 times more common in individuals with diabetes than in matched individuals without diabetes. Approximately 40% of individuals with hypertension have impaired glucose tolerance.

A thorough evaluation of the various systems and organs is pertinent. An eye examination is important; ocular manifestations, such as pupillary abnormalities, cataract, refractory errors, retinopathy, and other changes, may be found in patients with diabetes. These manifestations result mainly from chronic, uncontrolled hyperglycemia.

A neurologic examination is also necessary, because muscle wasting, sensory abnormalities, and other features of neuropathy are characteristic of many patients with diabetes who have chronic complications.

Related diseases

Specific phenotypic characteristics are found in certain conditions, especially the genetic syndromes.

In addition to glucose intolerance, patients with type A insulin resistance (absent or dysfunctional insulin receptor) may have certain clinical features such as (1) acanthosis nigricans, which is hyperpigmentation and skin thickening of flexural areas, or (2) features of hyperandrogenism, some variants of which may be characterized by thin or muscular body habitus or acral enlargement (pseudoacromegaly).

Due to autoantibodies to the insulin receptor, this resistance commonly manifests as symptomatic diabetes mellitus; ketoacidosis is unusual. Other genetic syndromes associated with insulin resistance include leprechaunism (abnormal facies, growth retardation) and lipodystrophic states (diverse phenotypic manifestations).

Other patients may have physical findings that are characteristic of certain internal organ diseases, in which glucose intolerance is only part of the spectrum of metabolic derangement that complicates these conditions. In cirrhosis, the liver may be normal, enlarged, or shrunken, depending on the disease stage. Other clinical features of portal hypertension and liver cell failure are often present. In cases of uremia, the various systemic changes, with the wide range of external manifestations that occur in the late phases of renal failure, are generally evident.

Previous
Proceed to Differential Diagnoses
 
 
Contributor Information and Disclosures
Author

Samuel T Olatunbosun, MD, FACP  Endocrinology Department, Wilford Hall Medical Center, 59th Medical Wing, Lackland Air Force Base

Samuel T Olatunbosun, MD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians-American Society of Internal Medicine, and American Diabetes Association

Disclosure: Nothing to disclose.

Coauthor(s)

Samuel Dagogo-Jack, MD, MBBS, MSc, FRCP  Professor of Medicine, Program Director, Division of Endocrinology, Diabetes and Metabolism, University of Tennessee Health Science Center

Samuel Dagogo-Jack, MD, MBBS, MSc, FRCP is a member of the following medical societies: American College of Physicians, American Diabetes Association, American Federation for Medical Research, Endocrine Society, and Royal College of Physicians

Disclosure: Eli Lilly None Speaking and teaching; GlaxoSmithKline None Speaking and teaching; Merck None Speaking and teaching

Specialty Editor Board

David S Schade, MD  Chief, Division of Endocrinology and Metabolism, Professor, Department of Internal Medicine, University of New Mexico School of Medicine and Health Sciences Center

David S Schade, MD is a member of the following medical societies: American College of Physicians, American Diabetes Association, American Federation for Medical Research, Endocrine Society, New Mexico Medical Society, New York Academy of Sciences, and Society for Experimental Biology and Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Don S Schalch, MD  Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, University of Wisconsin Hospitals and Clinics

Don S Schalch, MD is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, Central Society for Clinical Research, and Endocrine Society

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD  Professor of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

References

  1. [Guideline] American Diabetes Association. Standards of medical care in diabetes--2011. Diabetes Care. Jan 2011;34 Suppl 1:S11-61. [Medline]. [Full Text].

  2. Buchanan TA, Xiang AH. Gestational diabetes mellitus. J Clin Invest. Mar 2005;115(3):485-91. [Medline]. [Full Text].

  3. Cooper DH, Krainik AJ, Lubner SJ, et al, eds. The Washington Manual of Medical Therapeutics. Philadelphia, Pa: Lippincott Williams & Wilkins; 2007.

  4. Fauci AS, Braunwald E, Kasper DL, et al, eds. Harrison's Principles of Internal Medicine. 17th ed. New York, NY: McGraw-Hill; 2008.

  5. Corpeleijn E, Mensink M, Kooi ME, Roekaerts PM, Saris WH, Blaak EE. Impaired skeletal muscle substrate oxidation in glucose-intolerant men improves after weight loss. Obesity (Silver Spring). May 2008;16(5):1025-32. [Medline].

  6. DeFronzo RA. Pathogenesis of type 2 diabetes mellitus. Med Clin North Am. Jul 2004;88(4):787-835, ix. [Medline].

  7. Dagogo-Jack S, Santiago JV. Pathophysiology of type 2 diabetes and modes of action of therapeutic interventions. Arch Intern Med. Sep 8 1997;157(16):1802-17. [Medline].

  8. Sjöström L. Analysis of the XENDOS study (Xenical in the Prevention of Diabetes in Obese Subjects). Endocr Pract. Jan-Feb 2006;12 Suppl 1:31-3. [Medline].

  9. Li CL, Chen SY, Lan C, Pan WH, Chou HC, Bai YB, et al. The effects of physical activity, body mass index (BMI) and waist circumference (WC) on glucose intolerance in older people: A nationwide study from Taiwan. Arch Gerontol Geriatr. Mar 3 2010;[Medline].

  10. Ko GT, So WY, Tong P, Ma RC, Kong AP, Ozaki R, et al. Hypoadiponectinaemia enhances waist circumference as a predictor of glucose intolerance and clustering of risk factors in Chinese men. Diabetes Metab. Jun 2010;36(3):192-7. [Medline].

  11. Vella A, Camilleri M, Rizza RA. The gastrointestinal tract and glucose tolerance. Curr Opin Clin Nutr Metab Care. Jul 2004;7(4):479-84. [Medline].

  12. Joy SV, Rodgers PT, Scates AC. Incretin mimetics as emerging treatments for type 2 diabetes. Ann Pharmacother. Jan 2005;39(1):110-8. [Medline].

  13. Ahrén B. [New strategy in type 2 diabetes tested in clinical trials. Glucagon-like peptide 1 (GLP-1) affects basic caused of the disease]. Lakartidningen. Feb 21-27 2005;102(8):545-9. [Medline].

  14. Bock G, Dalla Man C, Campioni M, Chittilapilly E, Basu R, Toffolo G, et al. Pathogenesis of pre-diabetes: mechanisms of fasting and postprandial hyperglycemia in people with impaired fasting glucose and/or impaired glucose tolerance. Diabetes. Dec 2006;55(12):3536-49. [Medline]. [Full Text].

  15. Cowie CC, Rust KF, Byrd-Holt DD, et al. Prevalence of diabetes and impaired fasting glucose in adults in the U.S. population: National Health And Nutrition Examination Survey 1999-2002. Diabetes Care. Jun 2006;29(6):1263-8. [Medline]. [Full Text].

  16. Harris MI, Flegal KM, Cowie CC, Eberhardt MS, Goldstein DE, Little RR, et al. Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in U.S. adults. The Third National Health and Nutrition Examination Survey, 1988-1994. Diabetes Care. Apr 1998;21(4):518-24. [Medline]. [Full Text].

  17. King H, Rewers M. Global estimates for prevalence of diabetes mellitus and impaired glucose tolerance in adults. WHO Ad Hoc Diabetes Reporting Group. Diabetes Care. Jan 1993;16(1):157-77. [Medline].

  18. Diabetes mellitus. Report of a WHO Study Group. World Health Organ Tech Rep Ser. 1985;727:1-113. [Medline].

  19. Gerich JE. Postprandial hyperglycemia and cardiovascular disease. Endocr Pract. Jan-Feb 2006;12 Suppl 1:47-51. [Medline].

  20. [Best Evidence] Nissen SE, Wolski K. Effect of rosiglitazone on the risk of myocardial infarction and death from cardiovascular causes. N Engl J Med. Jun 14 2007;356(24):2457-71. [Medline]. [Full Text].

  21. Reaven GM. Insulin resistance and its consequences: non-insulin-dependent diabetes mellitus and coronary heart disease. In: Leroith D, ed. Diabetes Mellitus: A Fundamental and Clinical Text. Philadelphia, Pa: Lippincott-Raven; 1996:509-19.

  22. Tai ES, Goh SY, Lee JJ, Wong MS, Heng D, Hughes K, et al. Lowering the criterion for impaired fasting glucose: impact on disease prevalence and associated risk of diabetes and ischemic heart disease. Diabetes Care. Jul 2004;27(7):1728-34. [Medline]. [Full Text].

  23. Tam WH, Ma RC, Yang X, Li AM, Ko GT, Kong AP, et al. Glucose intolerance and cardiometabolic risk in adolescents exposed to maternal gestational diabetes: a 15-year follow-up study. Diabetes Care. Jun 2010;33(6):1382-4. [Medline]. [Full Text].

  24. Franks PW, Hanson RL, Knowler WC, Sievers ML, Bennett PH, Looker HC. Childhood obesity, other cardiovascular risk factors, and premature death. N Engl J Med. Feb 11 2010;362(6):485-93. [Medline].

  25. Kakad R, Anwar A, Dyer P, Webber J, Dale J. Fasting plasma glucose is not sufficient to detect ongoing glucose intolerance after pregnancy complicated by gestational diabetes. Exp Clin Endocrinol Diabetes. Apr 2010;118(4):234-6. [Medline].

  26. Alberti KG. Impaired glucose tolerance: what are the clinical implications?. Diabetes Res Clin Pract. Jul 1998;40 Suppl:S3-8. [Medline].

  27. Blake DR, Meigs JB, Muller DC, Najjar SS, Andres R, Nathan DM. Impaired glucose tolerance, but not impaired fasting glucose, is associated with increased levels of coronary heart disease risk factors: results from the Baltimore Longitudinal Study on Aging. Diabetes. Aug 2004;53(8):2095-100. [Medline].

  28. Festa A, D'Agostino R Jr, Hanley AJ, Karter AJ, Saad MF, Haffner SM. Differences in insulin resistance in nondiabetic subjects with isolated impaired glucose tolerance or isolated impaired fasting glucose. Diabetes. Jun 2004;53(6):1549-55. [Medline].

  29. Olatunbosun ST. Diagnosis and follow-up of subjects with impaired glucose tolerance: how reliable is OGTT? Report from a Nigerian survey. Diabetes Res Clin Pract. Aug 1998;41(2):147-8. [Medline].

  30. Faerch K, Vaag A, Holst JJ, Glümer C, Pedersen O, Borch-Johnsen K. Impaired fasting glycaemia vs impaired glucose tolerance: similar impairment of pancreatic alpha and beta cell function but differential roles of incretin hormones and insulin action. Diabetologia. May 2008;51(5):853-61. [Medline].

  31. Nathan DM, Davidson MB, DeFronzo RA, Heine RJ, Henry RR, Pratley R, et al. Impaired fasting glucose and impaired glucose tolerance: implications for care. Diabetes Care. Mar 2007;30(3):753-9. [Medline].

  32. Bersoux S, Cook CB, Wu Q, et al. Hemoglobin a1c testing alone does not sufficiently identify patients with prediabetes. Am J Clin Pathol. May 2011;135(5):674-7. [Medline].

  33. Einhorn D, Reaven GM, Cobin RH, Ford E, Ganda OP, Handelsman Y, et al. American College of Endocrinology position statement on the insulin resistance syndrome. Endocr Pract. May-Jun 2003;9(3):237-52. [Medline].

  34. Flier JS. Syndromes of insulin resistance. In: Becker KL, ed. Principles and Practice of Endocrinology and Metabolism. 2nd ed. Philadelphia, Pa: Lippincott; 1249-59.

  35. American Diabetes Association. Standards of medical care in diabetes--2008. Diabetes Care. Jan 2008;31 Suppl 1:S12-54. [Medline].

  36. Pham DQ, Nogid A, Plakogiannis R. Sitagliptin: a novel agent for the management of type 2 diabetes mellitus. Am J Health Syst Pharm. Mar 15 2008;65(6):521-31. [Medline].

  37. Mest HJ, Mentlein R. Dipeptidyl peptidase inhibitors as new drugs for the treatment of type 2 diabetes. Diabetologia. Apr 2005;48(4):616-20. [Medline].

  38. Ahrén B, Schmitz O. GLP-1 receptor agonists and DPP-4 inhibitors in the treatment of type 2 diabetes. Horm Metab Res. Nov-Dec 2004;36(11-12):867-76. [Medline].

  39. van Raalte DH, van Genugten RE, Linssen MM, Ouwens DM, Diamant M. Glucagon-like peptide-1 receptor agonist treatment prevents glucocorticoid-induced glucose intolerance and islet-cell dysfunction in humans. Diabetes Care. Feb 2011;34(2):412-7. [Medline]. [Full Text].

  40. Ceriello A, Piconi L, Quagliaro L, et al. Effects of pramlintide on postprandial glucose excursions and measures of oxidative stress in patients with type 1 diabetes. Diabetes Care. Mar 2005;28(3):632-7. [Medline].

  41. Hollander P, Ratner R, Fineman M, Strobel S, Shen L, Maggs D, et al. Addition of pramlintide to insulin therapy lowers HbA1c in conjunction with weight loss in patients with type 2 diabetes approaching glycaemic targets. Diabetes Obes Metab. Nov 2003;5(6):408-14. [Medline].

  42. Ratner RE, Dickey R, Fineman M, Maggs DG, Shen L, Strobel SA, et al. Amylin replacement with pramlintide as an adjunct to insulin therapy improves long-term glycaemic and weight control in Type 1 diabetes mellitus: a 1-year, randomized controlled trial. Diabet Med. Nov 2004;21(11):1204-12. [Medline].

  43. Riddle M, Frias J, Zhang B, Maier H, Brown C, Lutz K, et al. Pramlintide improved glycemic control and reduced weight in patients with type 2 diabetes using basal insulin. Diabetes Care. Nov 2007;30(11):2794-9. [Medline].

  44. Weyer C, Fineman MS, Strobel S, Shen L, Data J, Kolterman OG, et al. Properties of pramlintide and insulin upon mixing. Am J Health Syst Pharm. Apr 15 2005;62(8):816-22. [Medline].

  45. Wysham C, Lush C, Zhang B, Maier H, Wilhelm K. Effect of pramlintide as an adjunct to basal insulin on markers of cardiovascular risk in patients with type 2 diabetes. Curr Med Res Opin. Jan 2008;24(1):79-85. [Medline].

  46. Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care. Jul 1997;20(7):1183-97. [Medline].

  47. Chiasson JL. Acarbose for the prevention of diabetes, hypertension, and cardiovascular disease in subjects with impaired glucose tolerance: the Study to Prevent Non-Insulin-Dependent Diabetes Mellitus (STOP-NIDDM) Trial. Endocr Pract. Jan-Feb 2006;12 Suppl 1:25-30. [Medline].

  48. [Best Evidence] Gillies CL, Abrams KR, Lambert PC, Cooper NJ, Sutton AJ, Hsu RT, et al. Pharmacological and lifestyle interventions to prevent or delay type 2 diabetes in people with impaired glucose tolerance: systematic review and meta-analysis. BMJ. Feb 10 2007;334(7588):299. [Medline]. [Full Text].

  49. Bourn DM, Mann JI, McSkimming BJ, Waldron MA, Wishart JD. Impaired glucose tolerance and NIDDM: does a lifestyle intervention program have an effect?. Diabetes Care. Nov 1994;17(11):1311-9. [Medline].

  50. [Best Evidence] Herman WH, Hoerger TJ, Brandle M, Hicks K, Sorensen S, Zhang P, et al. The cost-effectiveness of lifestyle modification or metformin in preventing type 2 diabetes in adults with impaired glucose tolerance. Ann Intern Med. Mar 1 2005;142(5):323-32. [Medline]. [Full Text].

  51. DeFronzo RA. Pharmacologic therapy for type 2 diabetes mellitus. Ann Intern Med. Aug 17 1999;131(4):281-303. [Medline].

  52. Meneghini LF. Impact of bariatric surgery on type 2 diabetes. Cell Biochem Biophys. 2007;48(2-3):97-102. [Medline].

  53. Hofsø D, Jenssen T, Bollerslev J, Ueland T, Godang K, Stumvoll M, et al. Beta cell function after weight loss: a clinical trial comparing gastric bypass surgery and intensive lifestyle intervention. Eur J Endocrinol. Feb 2011;164(2):231-8. [Medline]. [Full Text].

  54. Du H, van der A DL, van Bakel MM, et al. Glycemic index and glycemic load in relation to food and nutrient intake and metabolic risk factors in a Dutch population. Am J Clin Nutr. Mar 2008;87(3):655-61. [Medline].

  55. Diamant M, Bunck MC, Heine RJ. [Analogs of glucagon-like peptide-1 (GLP-1): an old concept as a new treatment of patients with diabetes mellitus type 2]. Ned Tijdschr Geneeskd. Sep 25 2004;148(39):1912-7. [Medline].

  56. UK Prospective Diabetes Study (UKPDS) Group. Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). UK Prospective Diabetes Study (UKPDS) Group. Lancet. Sep 12 1998;352(9131):854-65. [Medline].

  57. Henry RR. Thiazolidinediones. Endocrinol Metab Clin North Am. Sep 1997;26(3):553-73. [Medline].

  58. UK Prospective Diabetes Study (UKPDS) Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group. Lancet. Sep 12 1998;352(9131):837-53. [Medline].

  59. Krentz AJ, Bailey CJ. Oral antidiabetic agents: current role in type 2 diabetes mellitus. Drugs. 2005;65(3):385-411. [Medline].

  60. Li CL, Pan CY, Lu JM, Zhu Y, Wang JH, Deng XX, et al. Effect of metformin on patients with impaired glucose tolerance. Diabet Med. Jun 1999;16(6):477-81. [Medline].

  61. McIntosh CH, Demuth HU, Pospisilik JA, Pederson R. Dipeptidyl peptidase IV inhibitors: how do they work as new antidiabetic agents?. Regul Pept. Jun 15 2005;128(2):159-65. [Medline].

  62. Muscelli E, Mari A, Natali A, Astiarraga BD, Camastra S, Frascerra S, et al. Impact of incretin hormones on beta-cell function in subjects with normal or impaired glucose tolerance. Am J Physiol Endocrinol Metab. Dec 2006;291(6):E1144-50. [Medline].

  63. Nauck MA, Meier JJ. Glucagon-like peptide 1 and its derivatives in the treatment of diabetes. Regul Pept. Jun 15 2005;128(2):135-48. [Medline].

  64. Ahrén B, Pacini G. Islet adaptation to insulin resistance: mechanisms and implications for intervention. Diabetes Obes Metab. Jan 2005;7(1):2-8. [Medline].

  65. Hanefeld M, Temelkova-Kurktschiev T, Schaper F, Henkel E, Siegert G, Koehler C. Impaired fasting glucose is not a risk factor for atherosclerosis. Diabet Med. Mar 1999;16(3):212-8. [Medline].

  66. Koska J, DelParigi A, de Courten B, Weyer C, Tataranni PA. Pancreatic polypeptide is involved in the regulation of body weight in pima Indian male subjects. Diabetes. Dec 2004;53(12):3091-6. [Medline].

  67. National Diabetes Data Group. Classification and diagnosis of diabetes mellitus and other categories of glucose intolerance. National Diabetes Data Group. Diabetes. Dec 1979;28(12):1039-57. [Medline].

  68. Newcomer JW. Second-generation (atypical) antipsychotics and metabolic effects: a comprehensive literature review. CNS Drugs. 2005;19 Suppl 1:1-93. [Medline].

  69. Ratner RE. An update on the Diabetes Prevention Program. Endocr Pract. Jan-Feb 2006;12 Suppl 1:20-4. [Medline]. [Full Text].

  70. Reaven GM. Banting lecture 1988. Role of insulin resistance in human disease. Diabetes. Dec 1988;37(12):1595-607. [Medline].

  71. Suzuki H, Fukushima M, Usami M, et al. IGT with fasting hyperglycemia is more strongly associated with microalbuminuria than IGT without fasting hyperglycemia. Diabetes Res Clin Pract. Jun 2004;64(3):213-9. [Medline].

  72. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. The Diabetes Control and Complications Trial Research Group. N Engl J Med. Sep 30 1993;329(14):977-86. [Medline].

  73. Blevins T, Pullman J, Malloy J, Yan P, Taylor K, Schulteis C, et al. DURATION-5: exenatide once weekly resulted in greater improvements in glycemic control compared with exenatide twice daily in patients with type 2 diabetes. J Clin Endocrinol Metab. May 2011;96(5):1301-10. [Medline].

 
Previous
Next
 
Etiologic types and stages of the major disorders of glucose tolerance.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.