Diabetes Mellitus

  • Diagnosis
  • Screening
  • Monitoring
  • Background
  • Pediatrics
  • Lab Tests
  • References
  • Related Topics
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Indications for Testing

  • Known risk factors for type 2 diabetes mellitus (DM)
    • Obesity (BMI ≥25 kg/m2 or ≥23 kg/m2 in Asian Americans)
    • Family history of type 2 DM in first- or second-degree relative
    • At risk race/ethnicity – Native American, African American, Latino, Asian American, Pacific Islander
    • Signs of insulin resistance or conditions associated with insulin resistance (eg, acanthosis nigricans, hypertension, dyslipidemiaPCOS, low birthweight)
    • Maternal history of DM or gestational diabetes mellitus (GDM) during pregnancy
  • No known risk factors for type 2 DM
    • Start screening at age ≥45 years

Criteria for Diagnosis

Laboratory Testing

  • Initial testing – HbA1c, FPG, 2-hr OGTT, or random PG are the preferred tests to diagnose diabetes in nonpregnant adults (see Criteria for Diagnosis)
    • If tests are normal, repeat at minimum of 3 year intervals (ADA, 2016)
    • No test is preferred over another for diagnosis (ADA, 2016)

Differential Diagnosis

  • Type 2 DM
  • Type 1 DM (ketoacidosis)
  • GDM
    • Infection
    • Acute surgical abdomen
      • Appendicitis
      • Cholecystitis/cholelithiasis
      • Pregnancy-related abdominal problem
        • Intrauterine infection
    • Thyroid disease

Adults (one of the following criteria)

Pregnant women (gestational DM)

  • All pregnant females 24-28 weeks gestation should be screened for gestational DM (GDM) (ADA, 2015; ACOG, 2013; AACE/ACE, 2015)
    • Screen if GDM identified 6-12 weeks postpartum using OGTT according to nonpregnant criteria (ADA, 2016)
    • Test for DM every 1-3 years thereafter (ADA, 2016)

Physical Examination

Laboratory Testing

  • Dyslipidemia
    • Lipid panel (fasting)
      • Premise of testing
        • Patients with DM have an increased incidence of lipid abnormalities, creating risk for CVD
        • Lipid-lowering therapies have been demonstrated to reduce macrovascular disease; therefore, identification of dyslipidemia is important
      • Target goals (ADA, 2016)
      • Recommendations for Statin and Combination Treatment in People with Diabetes (ADA, 2016)


        Risk Factors

        Recommended Statin Intensity*

        <40 years



        ASCVD risk factor(s)** Moderate or high
        ASCVD High

        40-75 years



        ASCVD risk factors High
        ASCVD High
        ACS and LDL cholesterol >50 mg/dL (1.3 mmol/L) in patients who cannot tolerate high-dose statins Moderate plus ezetimibe

        >75 years



        ASCVD risk factors Moderate or high
        ASCVD High
        ACS and LDL cholesterol >50 mg/dL (1.3 mmol/L) in patients who cannot tolerate high-dose statins Moderate plus ezetimibe
      • Laboratory testing recommendations
        • Initial evaluation every 5 years in DM for those not taking statins
        • Lipid profile at initiation of statins and periodically thereafter
        • Treat aggressively with statins based on initial risk assessment (ACC/AHA, 2013)
          • No target goals set by ACC/AHA
  • Antiplatelet agents (ADA, 2016)
    • Premise of testing
      • Patients with DM are at increased risk for stroke and heart attack
      • Consider acetylsalicylic acid in those with >10% 10-yr cardiovascular risk
    • Laboratory testing recommendations
      • None
  • Hepatic function
    • Premise of testing
      • Patients with DM are at risk for steatohepatitis
    • Laboratory testing recommendations
      • Liver function tests –  AST, ALT, alkaline phosphatase, and bilirubin
      • Initial evaluation and annually thereafter if values are normal on initial testing
  • Renal function (ADA, 2016)
    • Creatinine and estimated glomerular filtration rates (eGFR)
      • Premise of testing
        • Many drugs require adjusted dosing based on creatinine, creatinine clearance or eGFR and DM may affect renal function in the course of the disease
        • Absolute creatinine values do not reflect glomerular filtration rates in many patients
          • Diabetic nephropathy diminishes creatinine clearance
          • Renal function thereby diminishes clearance and glomerular filtration rate
        • Creatinine and eGFR are broad measures of renal function
      • Laboratory testing recommendations
        • Serum creatinine and eGFR at least annually
          • For the following patients
            • Type 1 DM ≥ 5 years
            • All patients with type 2 DM
            • All patients with hypertension
          • More frequent monitoring necessary for abnormal eGFRs (ADA, 2016)
          • KIDGO guidelines are useful for deciding intervals for abnormal values (KIDGO, 2011)
    • Albuminuria
      • Premise of testing
        • Diabetic nephropathy occurs in 20-40% of patients with DM and is the single leading cause of end-stage renal disease – adding angiotensin converting enzyme (ACE) inhibitors reduces progression
        • Persistent albuminuria (range 30-299 mg/24 hours and concentrations ≥300 mg/24 hours) signifies the earliest stage of diabetic nephropathy
      • Target goal
        • <30 mg/24 hour urine (ADA, 2016; AACE/ACE, 2015)
      • Laboratory testing recommendations
        • Spot urine or 24-hour urine for microalbumin annually
          • For the following patients
            • Type 1 DM ≥ 5 years
            • All patients with type 2 DM
            • All patients with hypertension
  • Thyroid function (ADA, 2016)
    • TSH, autoimmune antibodies
      • Premise of testing
      • Laboratory testing recommendations
        • Initial evaluation using TSH/antibody testing (for type 1 DM) and, if normal, TSH every 3 years thereafter (ADA, 2016)
  • Celiac testing (ADA, 2016)
    • tTG or DPG
    • Premise of testing
      • Other autoimmune diseases occurs more frequently in children with type 1 DM
    • Laboratory testing recommendations
      • At initial diagnosis
      • If symptoms develop after diagnosis

Diabetes mellitus (DM) is a group of metabolic diseases resulting from defects in insulin secretion and/or insulin resistance that can lead to significant morbidity and mortality in affected patients.

Classification of Diabetes Mellitus

  • Type 1 DM – 90-95% in pediatric population; absolute insulin deficiency due to autoimmune destruction of islet cells
  • Type 2 DM – most are teenagers or older; insulin resistance with or without insulin deficiency
  • Gestational diabetes mellitus (GDM) – exclusive to pregnant females
  • Other types of DM due to other causes (eg, cystic fibrosis, drug-induced, monogenetic)

Type 1 Diabetes Mellitus

  • See Pediatrics tab

Type 2 Diabetes Mellitus

Gestational Diabetes Mellitus

Type 1 Diabetes Mellitus

Clinical Background


  • Prevalence
    • Varies by nationality – common in Northern European populations; uncommon in Chinese, Indian populations
    • 1/400-600 children and adolescents
  • Age
    • Majority diagnosed before or during adolescence
    • Peaks at 5-7 years and adolescence
  • Sex – M>F (slightly)
  • Inheritance
    • Interplay between genetic susceptibility and environmental factors
      • HLA class II haplotypes most common (DRB-DQ2, DR4-DQ8)
      • Stages (Scientific statement JDF, Endocrine Society ADA, Insel, 2015)
        • Stage 1 – autoimmunity +/normoglycemia/presymptomatic type 1 DM
        • Stage 2 – autoimmunity +/dysglycemia/presymptomatic type 1 DM
        • Stage 3 – autoimmunity +/dysglycemia/symptomatic type 1 DM


  • Autoimmune mediated destruction of insulin-producing β-cells of the islets of Langerhans in the pancreas with diminished or absent circulating insulin
  • Absolute insulin deficiency of type 1 DM is a result of the following
    • Chronic inflammatory response mediated against the islet cells
    • Cell-mediated destruction of islet cells accompanied by production of islet cell antibodies
      • Autoantibodies – order of appearance appears related to HLA-DQ genotype
        • Islet cell antibodies (ICA)
          • May be detected years prior to clinical symptoms
        • Glutamic acid decarboxylase (GAD)
        • Insulinoma antigen 2 (IA-2)
        • Insulin autoantibodies (IAA)
        • Zinc transporter 8 (ZnT8)
      • Presence of two or more of these antibodies is a major criteria for stage 1 DM (presymptomatic stage)
      • Number of autoantibodies appears to correlate with risk of type 1 DM development (Insel, 2015)

Clinical Presentation

  • Polydipsia, polyuria, polyphagia
  • Nonspecific symptoms
    • Fatigue
    • Nausea, emesis
    • Weight loss
    • Blurred vision
  • Length of time from clinical presentation to diagnosis is typically a few weeks
  • Complications

 Type 2 Diabetes Mellitus

  • See Clinical Background section


Indications for Testing

Criteria for Diagnosis

  • Refer to Diagnosis section

Laboratory Testing

  • HbA1c fasting plasma glucose, 2-hour oral glucose tolerance test (OGTT), and random glucose are the preferred tests to diagnose diabetes in children (ADA,2014)
    • Random glucose measures have greater variability and less reproducibility in children
  • Insulin antibody testing
    • Refer to “Indications for Insulin Antibody Testing” table in in Diagnosis section


  • HbA1c
    • Premise of testing
      • Glycation of hemoglobin is non-linear over time and occurs over the whole lifespan of the red blood cell (~120 days)
      • Correlates with risk of long-term complications and with DM control over previous 2-3 months
    • Target goal (ADA, 2016)
      • <7.5% for all pediatric groups
    • Laboratory testing recommendations
      • 2 measurements per year for patients meeting target goal (ADA, 2016)
      • 3 month testing for those not meeting goals
      • If patient is not hypoglycemic, goal should be <7%
      • Blood glucose goals should be modified in children with frequent hypoglycemia or hypoglycemia unawareness
      • More frequent monitoring in patients with HbA1c ≥7.5%
        • Not more often than every 3 months (ADA, 2016; AACE/ACE, 2015)
      • False lowering – hemolytic anemias, sickle cell disease, acute blood loss
      • False elevation – splenectomy, iron deficiency anemia, hyperbilirubinemia, hypertriglyceridemia, uremia
  • Hypoglycemia
    • Not infrequent when children are using insulin
      • Diligence required for younger children
Tests generally appear in the order most useful for common clinical situations. Click on number for test-specific information in the ARUP Laboratory Test Directory.

Hemoglobin A1c 0070426
Method: Quantitative High Performance Liquid Chromatography/Boronate Affinity


Unstable hemoglobins or hemolytic anemia may yield falsely low results

Iron deficiency anemia may yield falsely high results

Glucose, Plasma or Serum 0020024
Method: Quantitative Enzymatic

Glucose Tolerance Test 0020542
Method: Quantitative Enzymatic

Glucose Screen, Pregnancy 0020047
Method: Quantitative Enzymatic

Lipid Panel 0020421
Method: Quantitative Enzymatic

Microalbumin, Urine 0050203
Method: Quantitative Immunoturbidimetry

Glomerular Filtration Rate, Estimated 0020725
Method: Quantitative Enzymatic

Hepatic Function Panel 0020416
Method: Quantitative Enzymatic/Quantitative Spectrophotometry

Thyroid Stimulating Hormone with reflex to Free Thyroxine 2006108
Method: Quantitative Electrochemiluminescent Immunoassay

Thyroid Stimulating Immunoglobulin 0099430
Method: Quantitative Bioassay/Quantitative Chemiluminescent Immunoassay


Blocking antibodies specific to TSHR may decrease TSI antibody concentrations; net response is most likely physiologic

TSH serum concentration ≥6 mU/L may cause a false-positive result

Thyroid Stimulating Hormone Receptor Antibody (TRAb) 2002734
Method: Quantitative Electrochemiluminescent Immunoassay

Fructosamine 0099012
Method: Quantitative Spectrophotometry


Variations in concentrations of serum proteins can affect results

High concentration of ascorbic acid interferes with the assay

1,5 Anhydroglucitol Quantitative, Serum or Plasma 0081335
Method: Quantitative Enzymatic


Do not use in poorly controlled disease because test is not sensitive

In patients with poorly controlled DM 1,5-AG is less sensitive to modest changes in glycemic control due to continuous glycosuria

Decreased in individuals with renal glucose thresholds that are markedly different from 180 mg/dL (eg, chronic renal failure, pregnancy, dialysis) and in those undergoing steroid therapy

Alpha-glucosidase inhibitors can decrease 1,5-AG by interfering with intestinal absorption

LipoFit by NMR 2013716
Method: Quantitative Nuclear Magnetic Resonance Spectroscopy/ Quantitative Enzymatic/ Detergent Solubilization

LipoFit by NMR, Particle Count Only 2013715
Method: Quantitative Nuclear Magnetic Resonance Spectroscopy


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References from the ARUP Institute for Clinical and Experimental Pathology®

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Medical Reviewers

Last Update: May 2017