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Type 1 diabetes
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Table 20-4. Comparison of type 1 and type 2 diabetes.
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Comparison of type 1 and type 2 diabetes mellitus
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 Type 1Type 2
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Onsetusually under 20 years of ageusually over 40 years of age
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Insulin synthesisabsent: immune destruction of β-cellspreserved: combination of impaired β-cell function and insulin
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Plasma insulin concentrationlow or absentlow, normal, or high
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Geneticinheritancenot associated with HLA,
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susceptibilityassociated with HLA antigenspolygenic
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Islet cell antibodies at diagnosisyesno
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Obesityuncommoncommon
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Ketoacidosisyespossible as a result of major stress
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Type 1 diabetes was formerly known as insulin-dependent diabetes, IDDM, or juvenile diabetes, and type 2 diabetes was described as noninsulin-dependent diabetes, NIDDM, or maturity-onset diabetes.
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Table 20-5. Diagnostic criteria for diabetes mellitus and glucose intolerance.
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Diagnosis of diabetes mellitus and glucoseView drug information intolerance
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ConditionDiagnostic criteria (mmol/L)Diagnostic criteria (mg/dL)Comments
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normal fasting plasma glucoseView drug informationbelow 6.1below 110 
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impaired fasting glucoseView drug information (IFG)equal or above 6.1 but below 7.0equal or above 110 but below 126 
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impaired glucoseView drug information tolerance (IGT)plasma glucoseView drug information 2 h after 75 g load 7.8 or above, but below 11.1plasma glucoseView drug information 2 h after 75 g load 140 or above, but below 200diagnosed during OGIT
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diabetes mellitus*   
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criterion 1random plasma glucoseView drug information 11.1 or aboverandom plasma glucoseView drug information 200 or above 
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criterion 2fasting plasma glucoseView drug information 7.0 or abovefasting plasma glucoseView drug information 126 or above 
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criterion 32 h value during OGTT 11.1 or above2 h value during OGTT 200 or above 
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*If one of the criteria is fulfilled, diagnosis is provisional. The diagnosis needs to be confirmed next day using a different criterion.
If accompanied by symptoms (polyuria, polydypsia, unexplained weight loss). These are the criteria proposed by the American Diabetes Association in 1997 (see Further Reading).
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Type 1 diabetes develops in young people, with the peak incidence at approximately 12 years of age. It is caused by autoimmune destruction of pancreatic β-cells. The precipitating cause is still unclear. It could be that a viral infection initiates the autoimmune reaction. Alternatively, a cytokine response to viral infection, or to another insult, could attract monocytes and macrophages that infiltrate and destroy the pancreatic islets. In addition to the inflammatory infiltration of the islets, a proportion of patients have antibodies against β-cell proteins. These are often present before the diagnosis of diabetes. Circulating autoantibodies to insulin itself are also present in some individuals.
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The susceptibility to type 1 diabetes appears to be inherited, however, no 'diabetes gene' has yet been discovered. The best investigated susceptibility gene is located on chromosome 6 in the major histocompatibility complex (MHC) that codes for immune system recognition molecules known as histocompatibility antigens (HLA) (see Chapter 36). Susceptibility to type 1 diabetes is associated with HLA types DR4 and DQw8, whereas DR2 and DQw1.2 appear to suppress the tendency to develop the disease. The sibling of a type 1 diabetic patient has a 10% chance of developing diabetes by the age of 50 years.
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