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International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #4: Classification of Diabetes Mellitus and Other Categories of Glucose Intolerance Part 4 of 6

DeFronzoCoverAntipsychotic agents

There is accumulating evidence supporting an association of certain psychiatric conditions with type 2 diabetes which can be attributed to side-effects of treatment and a high baseline risk of diabetes in this patient group [48]. Diabetes can be induced by the use of atypical antipsychotics including clozapine, olanzapine, risperidone, quetiapine, ziprasidone, and aripiprazole. These drugs have a direct effect of raising blood glucose and also lead to weight gain, [48] which subsequently may increase blood glucose levels.

Clozapine and olanzapine have been associated with a higher risk of diabetes than other antipsychotic agents in several studies [48]. These drugs have been associated with new-onset diabetes, exacerbation of pre-existing diabetes, and presentations with complications such as ketoacidosis.The data on risperidone and quetiapine in the studies mentioned earlier show inconsistent findings [48].

Atypical antipsychotics may have an independent effect on insulin sensitivity. Studies comparing insulin sensitivity in patients taking clozapine, olanzapine, or risperidone showed that those in clozapine and olanzapine groups had significantly decreased insulin sensitivity compared to risperidone groups. While there is generally less long-term data on aripiprazole and ziprasidone, a comparison of olanzapine and aripiprazole use in schizophrenic patients showed an increase in glucose in the olanzapine group [48].

Anti-HIV agents

Diabetes is fourfold more common in HIV-infected men exposed to highly active antiretroviral therapy (HAART) than HIV-negative men. Although most of the diabetes observed in this group is type 2 there has been a recent report of autoimmune diabetes and the development of anti-GAD antibodies after immune system recovery post HAART therapy [49], which suggests that type 1 diabetes can also arise in this group from treatment.

HAART is based on the use of a class of drugs known as protease inhibitors (PIs) and include atazanavir, darunavir, saquinavir, and ritonavir. PIs have been shown to increase insulin resistance and reduce insulin secretion, by interfering with GLUT-4 mediated glucose transport. PIs interfere with cellular retinoic acid-binding protein type 1 which interacts with peroxisomal proliferator-activated gamma (PPARγ) receptor. Inhibition of PPARγ promotes adipocyte inflammation, release of free fatty acids and insulin resistance [49]. Hyperglycemia resolves in almost all patients when PIs are discontinued [49] and all PIs do not have the same metabolic effects, with some drugs having a worse adverse effect than others.

Apart from HAART, another class of anti-HIV drugs associated with diabetes are the nucleoside analogs (reverse transcriptase inhibitors) (NRTIs) [50] especially when used for long periods of time [51]. The risk of diabetes is highest with stavudine, but the risk is also significant with zidovudine and didanosine. Proposed mechanisms include insulin resistance, lipodystrophy, and mitochondrial dysfunction [51]. It is postulated that PIs confer acute metabolic risks, while NRTIs confer cumulative risks of diabetes in predisposed, exposed persons. The use of both classes of drugs may be additive for diabetes risk [51].

Glucocorticoids

Glucocorticoids are the most common cause of drug-induced diabetes. They are used in the treatment of many medical conditions but are mostly prescribed for their anti-inflammatory effects [52]. They act through multiple pathways at the cellular and molecular levels, suppressing the cascades that would otherwise result in inflammation and promoting pathways that produce anti-inflammatory protein [53]. The mechanism by which glucocorticoids cause diabetes is thought to be mainly via insulin resistance, but there is also some evidence of effects on insulin secretion [54].

The effect of glucocorticoids is mainly on nonfasting glucose rather than fasting glucose levels [52], but there is uncertainty as to whether this reflects a relationship with clock time (perhaps linked to dosing times), or to a predominant effect on postprandial blood glucose levels.

Infections

Certain viruses have been associated with β-cell destruction. Diabetes occurs in some patients with congenital rubella [55]. Coxsackie B, cytomegalovirus, and other viruses (e.g. adenovirus and mumps) have been implicated in inducing diabetes [56–58].

Uncommon but specific forms of immune-mediated diabetes mellitus

Diabetes may be associated with several immunologic diseases with a pathogenesis or etiology different from that which leads to the type 1 diabetes process. Postprandial hyperglycemia of a severity sufficient to fulfill the criteria for diabetes has been reported in rare individuals who spontaneously develop insulin autoantibodies. However, these individuals generally present with symptoms of hypoglycemia rather than hyperglycemia [59]. The “stiff man syndrome” is an autoimmune disorder of the central nervous system, characterized by stiffness of the axial muscles with painful spasms. Affected people usually have high titers of anti-GAD and approximately one third to one half will develop type 1 diabetes [60].

Anti-insulin receptor antibodies can cause diabetes by binding to the insulin receptor thereby reducing the binding of insulin to target tissues [61]. However, these antibodies can also act as an insulin agonist after binding to the receptor and can thereby cause hypoglycemia [62]. Anti-insulin receptor antibodies are occasionally found in patients with systemic lupus erythematosus and other autoimmune diseases [63].

Other genetic syndromes associated with diabetes

Many genetic syndromes are accompanied by an increased incidence of diabetes mellitus. These include the chromosomal abnormalities of Down syndrome, Klinefelter syndrome, and Turner syndrome. These and other similar disorders are listed in Table 1.4.

ITDMTable1.4

Diabetes is commonly observed in cystic fibrosis patients. While it shares features of type 1 and type 2 diabetes, cystic fibrosis-related diabetes (CFRD) is a distinct clinical entity. It is primarily caused by insulin insufficiency, although fluctuating levels of insulin resistance related to acute and chronic illness and medications such as bronchodilators and glucocorticoids also play a role [64]. Since blood glucose levels within the IGT range appear to have an adverse effect on lung function, it has been suggested that diagnostic criteria for CFRD should be lower than that for other forms of diabetes, but data are currently inadequate to make this change [64]. CFRD is not associated with atherosclerotic vascular disease, despite the fact that individuals with cystic fibrosis nowadays can have a lifespan well into the 50s and 60s.

There are several distinct clinically defined subgroups of diabetes where an etiology has not yet been defined. In recognition of this, during the most recent WHO consultation, it was recommended that a category of “unclassified” or “nonclassical phenotype” be available.

References:

  1. World Health Organization (WHO): Diabetes Mellitus. Report of a WHO Expert Committee. Technical Report Series 310. Geneva: WHO, 1965.
  2. National Diabetes Data Group: Classification and diagnosis of diabetes mellitus and other categories of glucose intolerance. Diabetes 1979;28:1039–1057.
  3. World Health Organization: WHO Expert Committee on Diabetes Mellitus. Second report. Technical Report Series 646. Geneva: WHO, 1980.
  4. World Health Organization: Diabetes mellitus. Report of a WHO Study Group. Technical Report Series 727. Geneva: WHO, 1985, p. 727.
  5. American Diabetes Association (ADA): Diagnosis and classification of diabetes mellitius. Diabetes Care 2011;34(S1):S62–69.
  6. Kuzuya T, Matsuda A: Classification of diabetes on the basis of etiologies versus degree of insulin deficiency. Diabetes Care 1997;20:219–220.
  7. World Health Organization: Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications. Part 1: Diagnosis and Classification of Diabetes Mellitus.Geneva:WHO, 1999. Report No.WHO/NCD/NCS/99.2.
  8. Tuomi T, Groop L, Zimmet P, et al.: Antibodies to glutamic acid decarboxylase reveal latent autoimmune diabetes mellitus in adults with a non-insulin dependent onset of disease. Diabetes 1993;42:359–362.
  9. Atkinson M, Maclaren N: The pathogenesis of insulin-dependent diabetes mellitus. New England Journal of Medicine 1994;331:1428–1436.
  10. McLarty D, Atharde I, Bottazzo G, et al.: Islet cell antibodies are not specifically associated with insulin-dependent diabetes in Tanzanian Africans. Diabetes Research and Clinical Practice 1990;9:219–224.
  11. Ahrén B, Corrigan C: Intermittant need for insulin in a subgroup of diabetic patients in Tanzania. Diabetic Medicine 1984;2:262–264.
  12. Billings LK, Florez JC: The genetics of type 2 diabetes: what have we learned from GWAS? Annals of the New York Academy of Sciences 2010;1212:59–77.
  13. Kissebah A, Vydelingum N, Murray R, et al.: Relation of body fat distribution to metabolic complications of obesity. Journal of Clinical Endocrinology & Metabolism 1982;54:254–260.
  14. Harris MI, Klein R, Welborn TA, Knuiman MW: Onset of NIDDM occurs at least 4–7 yr before clinical diagnosis. Diabetes Care 1992; 15:815–819.
  15. Gill GV, Mbanya JC, Ramaiya KL, Tesfaye S: A sub-Saharan African perspective of diabetes. Diabetologia 2009;52:8–16.
  16. Sobngwi E, Mauvais-Jarvis F, Vexiau P, et al.: Diabetes in Africans. Part 2: Ketosis-prone atypical diabetes mellitus. Diabetes & Metabolism 2002;28:5–12.
  17. Banerji M, Chaiken R, Huey H, et al.: GAD antibody negative NIDDM in adult black subjects with diabetic ketoacidosis and increased frequency of HLA DR3 and DR4. Flatbush diabetes. Diabetes 1994;13:741–745.
  18. Meigs JB, Shrader P, Sullivan LM, et al.: Genotype score in addition to common risk factors for prediction of type 2 diabetes. New England Journal of Medicine 2008;359:2208–2219.
  19. Hattersley A, Bruining J, Shield J, et al.: ISPAD Clinical Practice Consensus Guidelines 2006–2007. The diagnosis and management of monogenic diabetes in children. Pediatric Diabetes 2006;7:352–360.
  20. Vionnet N, Stoffel M, Takeda J, et al.: Nonsense mutation in the glucokinase gene causes early-onset non-insulin-dependent diabetes mellitus. Nature 1992;356:721–722.
  21. Murphy R, Ellard S, Hattersley AT: Clinical implications of a molecular genetic classification of monogenic beta-cell diabetes. Nature Clinical Practice Endocrinology and Metabolism 2008;4:200–213.
  22. Spyer G, Macleod KM, Shepherd M, et al.: Pregnancy outcome in patients with raised blood glucose due to a heterozygous glucokinase gene mutation. Diabetic Medicine 2009;26:14–18.
  23. Stride A, Vaxillaire M, Tuomi T, et al.: The genetic abnormality in the beta cell determines the response to an oral glucose load. Diabetologia 2002;45:427–435.
  24. Hattersley A, Bruining J, Shield J, et al.: The diagnosis and management of monogenic diabetes in children and adolescents. Pediatric Diabetes 2009;10(Suppl 12):33–42.
  25. Iafusco D, Stazi MA, Cotichini R, et al.: Permanent diabetes mellitus in the first year of life. Diabetologia 2002;45:798–804.
  26. Ellard S, Flanagan SE, Girard CA, et al.: Permanent neonatal diabetes caused by dominant, recessive, or compound heterozygous SUR1 mutations with opposite functional effects. American Journal of Human Genetics 2007;81:375–382.
  27. Rigoli L, Di Bella C: Wolfram syndrome 1 and Wolfram syndrome 2. Current Opinion in Pediatrics 2012;24:512–517.
  28. Maassen JA, Kadowaki T: Maternally inherited diabetes and deafness: a new diabetes subtype. Diabetologia 1996;39:375–382.
  29. Robbins DC, Shoelson SE, Rubenstein AH, Tager HS: Familial hyperproinsulinemia. Two cohorts secreting indistinguishable type II intermediates of proinsulin conversion. Journal of Clinical Investigation 1984;73:714–719.
  30. Haneda M, Polonsky KS, Bergenstal RM, et al.: Familial hyperinsulinemia due to a structurally abnormal insulin. Definition of an emerging new clinical syndrome. New England Journal of Medicine 1984;310:1288–1294.
  31. Johns DR: Seminars in medicine of the Beth Israel Hospital, Boston. Mitochondrial DNA and disease. New England Journal of Medicine 1995;333:638–644.
  32. Semple RK, Savage DB, Cochran EK, et al.: Genetic syndromes of severe insulin resistance. Endocrine Reviews 2011;32:498–514.
  33. Gullo L, Pezzilli R, Morselli-Labate AM: Diabetes and the risk of pancreatic cancer. New England Journal of Medicine 1994;331: 81–84.
  34. Permert J, Larsson J, Westermark GT, et al.: Islet amyloid polypeptide in patients with pancreatic cancer and diabetes. New England Journal of Medicine 1994;330:313–318.
  35. Utzschneider KM, Kowdley KV: Hereditary hemochromatosis and diabetes mellitus: implications for clinical practice. Nature Reviews Endocrinology 2010;6:26–33.
  36. Yajnik CS, Shelgikar KM, Naik SS, et al.: The ketoacidosis-resistance in fibro-calculous-pancreatic-diabetes. Diabetes Research and Clinical Practice 1992;15:149–156.
  37. Krejs GJ,Orci L,Conlon JM, et al.: Somatostatinoma syndrome. Biochemical, morphologic and clinical features. New England Journal of Medicine 1979;301:285–292.
  38. Pandit MK, Burke J, Gustafson AB, et al.: Drug-induced disorders of glucose tolerance. Annals of Internal Medicine 1993;118: 529–540.
  39. Miller LV, Stokes JD, Silpipat C: Diabetes mellitus and autonomic dysfunction after vacor rodenticide ingestion. Diabetes Care 1978; 1:73–76.
  40. Assan R, Perronne C,Assan D, et al.: Pentamidine-induced derangements of glucose homeostasis. Diabetes Care 1995;18:47–55.
  41. Madziarska K: New-onset posttransplant diabetes mellitus begins in the dialysis period. Journal of Renal Nutrition 2012;22:162–165.
  42. Drachenberg CB, Klassen DK, Weir MR, et al.: Islet cell damage associated with tacrolimus and cyclosporine: morphological features in pancreas allograft biopsies and clinical correlation. Transplantation 1999;68:396–402.
  43. Penfornis A, Kury-Paulin S: Immunosuppressive drug-induced diabetes. Diabetes & Metabolism 2006;32:539–546.
  44. Fabris P, Betterle C, Floreani A, et al.: Development of type 1 diabetes mellitus during interferon alfa therapy for chronic HCV hepatitis. Lancet 1992;340:548.
  45. Sattar N, Preiss D, Murray HM, et al.: Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials. Lancet 2010;375:735–742.
  46. Preiss D, Seshasai SR, Welsh P, et al.: Risk of incident diabetes with intensive-dose compared with moderate-dose statin therapy: a meta-analysis. JAMA 2011;305:2556–2564.
  47. Wang KL, Liu CJ, Chao TF, et al.: Statins, risk of diabetes, and implications on outcomes in the general population. Journal of the American College of Cardiology 2012;60(14):1231–1238.
  48. Guo JJ, Keck PE, Jr,, Corey-Lisle PK, et al.: Risk of diabetes mellitus associated with atypical antipsychotic use among patients with bipolar disorder: a retrospective, population-based, case-control study. Journal of Clinical Psychiatry 2006;67:1055–1061.
  49. Kalra S, Kalra B, Agrawal N, Unnikrishnan A: Understanding diabetes in patients with HIV/AIDS. Diabetology and Metabolic Syndrome 2011;3:2.
  50. De Wit S, Sabin CA, Weber R, et al.: Incidence and risk factors for new-onset diabetes in HIV-infected patients: the Data Collection on Adverse Events of Anti-HIV Drugs (D:A:D) study. Diabetes Care 2008;31:1224–1229.
  51. Fleischman A, Johnsen S, Systrom DM, et al.: Effects of a nucleoside reverse transcriptase inhibitor, stavudine, on glucose disposal and mitochondrial function in muscle of healthy adults. American Journal of Physiology—Endocrinology and Metabolism 2007;292: E1666–1673.
  52. Lansang MC, Hustak LK: Glucocorticoid-induced diabetes and adrenal suppression: how to detect and manage them. Cleveland Clinical Journal of Medicine 2011;78:748–756.
  53. Rhen T, Cidlowski JA: Antiinflammatory action of glucocorticoids–new mechanisms for old drugs. New England Journal of Medicine 2005;353:1711–1723.
  54. van Raalte DH, Nofrate V, Bunck MC, et al.:Acute and 2-week exposure to prednisolone impair different aspects of beta-cell function in healthymen. European Journal of Endocrinology 2010;162:729–735.
  55. Forrest JM, Menser MA, Burgess JA: High frequency of diabetes mellitus in young adults with congenital rubella. Lancet 1971; 2:332–334.
  56. King ML, Bidwell D, Shaikh A, et al.: Coxsackie-B-virus-specific IgM responses in children with insulin-dependent (juvenile-onset; type I) diabetes mellitus. Lancet 1983;1(8339):1397–1399.
  57. Karjalainen J, Knip M, Hyoty H, et al.: Relationship between serum insulin antibodies, islet cell antibodies and Coxsackie-B4 and mumps virus-specific antibodies at the clinical manifestation of Type I (insulin-dependent) diabetes. Diabetologia 1988;31: 146–152.
  58. Pak C, Eun H-M, McArthur R, Yoon J: Association of cytomegalovirus infection with autoimmune type 1 diabetes. Lancet 1988;II:1–4.
  59. Hirata Y, Ishizu H, Ouchi N, et al.: Insulin autoimmunity in a case of spontaneous hypoglycaemia. Journal of the Japan Diabetes Society 1970;13:312–320.
  60. Solimena M, De Camilli P: Autoimmunity to glutamic acid decarboxylase (GAD) in Stiff-Man syndrome and insulin-dependent diabetes mellitus. Trends in Neuroscience 1991;14:452–457.
  61. Flier JS: Lilly Lecture: syndromes of insulin resistance: from patient to gene and back again. Diabetes 1992;41:1207–1219.
  62. Khan C, Baird K, Flier JS, Jarret D: Effects of autoantibodies to the insulin receptor on isolated adipocytes. Studies of insulin binding and insulin action. Journal of Clinical Investigation 1977;60:1094–1106.
  63. Tsokos GC, Gorden P, Antonovych T, et al.: Lupus nephritis and other autoimmune features in patients with diabetes mellitus due to autoantibody to insulin receptors. Annals of Internal Medicine 1985;102:176–181.
  64. Moran A, Brunzell C, Cohen RC, et al.: Clinical care guidelines for cystic fibrosis-related diabetes: a position statement of the American Diabetes Association and a clinical practice guideline of the Cystic Fibrosis Foundation, endorsed by the Pediatric Endocrine Society. Diabetes Care 2010;33:2697–2708.
  65. Azzopardi P, Brown AD, Zimmet P, et al.: Type 2 diabetes in young Indigenous Australians in rural and remote areas: diagnosis, screening, management and prevention. Medical Journal of Australia 2012;197:32–36.
  66. Pozzilli P,Guglielmi C:Double diabetes: a mixture of type 1 and type 2 diabetes in youth. Endocrine Development 2009;14:151–166.
  67. Craig ME, Hattersley A, Donaghue KC: Definition, epidemiology and classification. In:Hanas R,Donaghue KC, Klingensmith G, et al. (eds.) Global IDF/ISPAD Guideline for Diabetes in Childhood and Adolescence. Brussels: International Diabetes Federation, 2011.
  68. Craig ME, Hattersley A, Donaghue KC: Definition, epidemiology and classification of diabetes in children and adolescents. Pediatric Diabetes 2009;10(Suppl 12):3–12.
  69. World Health Organization: Definition and diagnosis of diabetes mellitus and intermediate hyperglycemia. Report of a WHO/IDF consultation. Geneva: WHO, 2006.
  70. Peterson KP, Pavlovich JG, Goldstein D, et al.: What is hemoglobin A1c? An analysis of glycated hemoglobins by electrospray ionization mass spectrometry. Clinical Chemistry 1988;44:1951–1958.
  71. Diabetes Control and Complications Trial Research Group: The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. New England Journal of Medicine 1993;329:977–986.
  72. UKPDS (UK Prospective Diabetes Study 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). Lancet 1998;352:837–853.
  73. Little RR, Rohlfing CL, Sacks DB: Status of hemoglobin A1c measurement and goals for improvement: from chaos to order for improving diabetes care. Clinical Chemistry 2011;57:205–214.
  74. Colagiuri S, Lee CM, Wong TY, et al.: Glycemic thresholds for diabetes-specific retinopathy: implications for diagnostic criteria for diabetes. Diabetes Care 2011;34:145–150.
  75. Khaw KT, Wareham N, Bingham S, et al.: Association of hemoglobin A1c with cardiovascular disease and mortality in adults: the European prospective investigation into cancer in Norfolk. Annals of Internal Medicine 2004;141:413–420.
  76. Stratton IM, Adler AI, Neil HA, et al.: Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. BMJ 2000;321:405–412.
  77. Sacks DB: A1C versus glucose testing: a comparison. Diabetes Care 2011;34:518–523.
  78. World Health Organization: Use of glycated haemoglobin (HbA1c) in the diagnosis of diabetes mellitius. Abbreviated report of a WHO consultation. Geneva: WHO, 2011.
  79. International Expert Committee report on the role of the A1C assay in the diagnosis of diabetes. Diabetes Care 2009;32:1327–1334.
  80. Christensen DL, Witte DR, Kaduka L, et al.: Moving to an A1C-based diagnosis of diabetes has a different impact on prevalence in different ethnic groups. Diabetes Care 2010;33:580–582.
  81. Metzger BE, Lowe LP, Dyer AR, et al.: Hyperglycemia and adverse pregnancy outcomes. New England Journal of Medicine 2008;358: 1991–2002.
  82. Metzger BE, Gabbe SG, Persson B, et al.: International Association of Diabetes and Pregnancy Study Groups recommendations on the diagnosis and classification of hyperglycemia in pregnancy. Diabetes Care 2010;33:676–682.
  83. Santaguida PL, Balion C, Hunt D, et al.: Diagnosis, prognosis, and treatment of impaired glucose tolerance and impaired fasting glucose. Evidence Report/Technology Assessment (Summary) 2005; 1–11.
  84. Unwin N, Shaw J, Zimmet P, Alberti KG: Impaired glucose tolerance and impaired fasting glycaemia: the current status on definition and intervention. Diabetic Medicine 2002;19:708–723.
  85. Shaw JE, Zimmet PZ, Hodge AM, et al.: Impaired fasting glucose: how low should it go? Diabetes Care 2000;23:34–39.
  86. Gabir MM, Hanson RL, Dabelea D, et al.: Plasma glucose and prediction of microvascular disease and mortality: evaluation of 1997 American Diabetes Association and 1999 World Health Organization criteria for diagnosis of diabetes. Diabetes Care 2000;23:1113–1118.
  87. Ford ES, Zhao G, Li C: Pre-diabetes and the risk for cardiovascular disease: a systematic review of the evidence. Journal of the American College of Cardiology 2010;55:1310–1317.
  88. The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus: Follow-up report on the diagnosis of diabetes mellitus. Diabetes Care 2003;26:3160–3167.
  89. American Diabetes Association: Report of the Expert Committee on the diagnosis and classification of diabetes mellitus. Diabetes Care 1997;20:1183–1197.