1. Diabetes and the Lab Eric L. Johnson, M.D. Assistant Medical Director
Altru Diabetes Center
Altru Health System
Associate Professor
Department of Family and Community Medicine
University of North Dakota
School of Medicine and Health Sciences
Grand Forks, ND

2. Objectives
Review common evidence based laboratory measures in the screening, diagnosis and management of diabetes and related conditions
Discuss future directions and practice of laboratory measures in the screening, diagnosis and management of diabetes and related conditions

3. Disclosures Speaker’s Bureau- Novo Nordisk, Medtronic
Advisory Panel- Novo Nordisk, Sanofi
PI or Sub PI on numerous multicenter medication trials at Altru Health System Research Site

4. What We Will Do Diabetes overview and definitions
Discuss screening for diabetes with common laboratory methods
Discuss relationship of blood glucose to complications of diabetes
Short review of other relevant diabetes labs
Discuss future and novel directions in lab testing in diabetes
Case studies

5. U.S. Prevalence of Diabetes
Diagnosed: 29 million people—9.3% of population
90%+ have Type 2
Undiagnosed: 8 million people
83 million people have pre-diabetes
CDC

6. Diabetes In The U.S. 9.3% of all Americans
12.3% of adults age 20 and older
26% of adults age 65 and older
About 2 million diagnoses yearly
Could be 33% by 2050
Prediabetes
37% of adults age 20 and older
51% of Americans 65 and older
CDC

7. Diabetes Complications
Eye disease/blindness ~28.5% of adults over 40 with diabetes have some form of retinopathy (on the rise in U.S. with more cases of type 2 diabetes)
Heart Disease (common)
Stroke (common)
Kidney disease
Nerve damage
Liver disease
Amputation
Infection
Dementia

8. Estimated Prevalence and Cost of Diabetes in North Dakota
~6.7% of adults (~40,000 people)
Medical cost of diabetes: $209,700,000
Indirect Cost: $99,140,000
Total Cost: $308,800,000

9. Estimated Prevalence and Cost of Diabetes in Minnesota
~6% (~300,000 people)
Medical cost of diabetes: $1,750,000,000
Indirect Cost: $929,000,000
Total Cost: $2,679,000,000

10. Diabetes and All-Cause Mortality
Diabetes deaths annually in the U.S. ~233,000
Meta-analysis 97 studies 820,900 people
HR 1.8 death from any cause
HR 1.25 death from cancer
HR 2.32 death from vascular disease
HR death from any other cause
HR=hazard ratio
Emerging Risk Factors Collaboration. N Engl J Med 2011, 364(9):

11. Risks for Complications in Diabetes
Abnormal blood sugar
Abnormal cholesterol
Abnormal blood pressure
Sedentary lifestyle
Smoking 11

12. Diabetes Mellitus Type 1: Usually younger, insulin at diagnosis
Type 2: Usually older, often oral agents at diagnosis
Type “1.5” (Latent Autoimmune) mixed features ~10% of type 2
Gestational: Diabetes of Pregnancy

13. Type 1 Diabetes Mellitus
Autoimmune Disease- destruction of betacells (insulin producers) in pancreas
Lab work up can include antibody testing
(GAD 65, IAA, IA2, sometimes HLA)
Lab work can include C-peptide (part of insulin precursor)- low or zero in T1DM
Insulin can also be measured directly

14. Model of the pathogenesis and natural history of type 1 diabetes.
Model of the pathogenesis and natural history of type 1 diabetes. The modern model expands and updates the traditional model by inclusion of information gained through an improved understanding of the roles for genetics, immunology, and environment in the natural history of T1D. (Adapted from Atkinson and Eisenbarth 2001; with permission.)‏
Atkinson M A Cold Spring Harb Perspect Med 2012;2:a007641
©2012 by Cold Spring Harbor Laboratory Press

15. Type 2 Diabetes Not autoimmune No antibodies
Insulin resistance causes eventual betacell “burnout”
Insulin resistance may be secondary to obesity, family history, smoking, sedentary lifestyle, some medications
Eventually will be insulin deficient to the point that they will need insulin

16. Natural History of Type 2 Diabetes
Uncontrolled Hyperglycemia
Obesity
IFG*
Diabetes
350 –
Fasting Glucose
Postmeal Glucose
300 –
250 –
Glucose (mg/dL)
200 –
150 –
100 –
50 –
250 –
Insulin Resistance
200 –
Relative Function (%)
150 –
100 –
-Cell Failure
-cell Function
50 –
0 –
-10 -5 5 10 15 20 25 30
Years of Diabetes
*IFG=impaired fasting glucose.
Copyright® 2000 International Diabetes Center, Minneapolis, USA. All rights reserved. Adapted with permission.

17. Decreased Incretin Effect
The Ominous Octet
Islet b-cell
Impaired
Insulin Secretion
Decreased Incretin Effect
Increased
Lipolysis
Islet a-cell
Increased
Glucagon Secretion
Insulin and appetite interact in the brain when neurotransmitters in the hypothalamus signal satiety in response to increased insulin.
Adding brain and neurotransmitter dysfunction to the pathogenic picture of type 2 diabetes gives us the ominous octet.
Increased Glucose
Reabsorption
Neurotransmitter
Dysfunction
Increased
HGP
Decreased Glucose
Uptake
DeFronzo Diabetes 2008 17

18. Type 1.5 Latent Autoimmune Diabetes
Usually look like Type 2 at onset
Rapidly progress to a Type 1 presentation after a few weeks or months
A “slow smoldering” autoimmune response
Usually end up treating like a type 1

19. Type 1 Diabetes Diagnosis
Usually symptomatic, weight loss, polyuria, polydipsia, polyphagia, fatigue, ill-appearning
Usually very hyperglycemic (>250)
Always positive for urine ketones (and serum ketones)

20. Type 2 Diagnosis Usually more subtle
Fatigue is often presenting complaint
Many discovered incidentally
Ketosis present in about 20%, usually with another associated problem (illness, infection, heart attack, stroke)

21. Diabetes Risk and Prevention
Type 1- mostly unknown, some familial
Type 2- obesity, smoking, sedentary lifestyle, familial
Prevention:
Type 1- none known
Type 2- lifestyle management (likely applies to GDM as well)

22. Diabetes Guideline Management
2 main sets of guidelines utilized in U.S.
American Diabetes Association (ADA)
American Association of Clinical Endocrinology (AACE)
Lots of overlap, AACE considered
“more intense”

23. Diabetes Guideline Management
Evidence based
Well accepted
Clinically relevant
Can be incorporated into clinical practice
Emphasize comprehensive risk management
Ties together “numbers” with risk

24. Key Laboratory Testing in Diabetes Diagnosis
Fasting plasma glucose
2 hour post-prandial glucose
Casual (random) glucose
A1C
Oral glucose tolerance test (OGTT)- usually 2 hours
Insulin antibody and/or GAD antibody and sometimes HLA typing
Sometimes C-peptide

25. Other Lab Testing in Diabetes
Serum creatinine
Creatinine Clearance (GFR)
Electrolytes
Liver function tests (fatty liver disease-common in Type 2)
Urine for microalbumin or gross protein (dipstick)
24 hour urine collection-protein
Lipid profiles (usually done fasting)
Thyroid (often TSH, can be antibodies, T4, T3)
Tissue Transglutamase IgA and IgG
Vitamin D
Vitamin B12

26. Diabetes Complications and Lab Testing
Lab testing is useful for screening, prevention, prediction, and management of many diabetes complications

27. Screening and Diagnosis of Diabetes

28. Diabetes Diagnosis Normal <100 <140 <5.7
Category FPG (mg/dL) h 75gOGTT A1C
Normal < < <5.7
Prediabetes
Diabetes >126** > >6.5
Or patients with classic hyperglycemic symptoms with plasma glucose >200
** On 2 separate occasions
Diagnostic criteria for diabetes have changed.
Impaired fasting glucose (IFG) is a new term, defined as fasting plasma glucose between 110 and 125 mg/dL.
Diabetes is diagnosed at a serum glucose level of >126 mg/dL on at least two occasions.
For low risk individuals over the age of 45 years, the ADA recommends routine screening every 3 years with fasting glucose. OGTT are not recommended for screening.
Diabetes Care 36:Supplement 1, 2013
2011

29. Why Is >100 Abnormal?
Evidence that more diabetes related eye disease begins at this number
Evidence that other diabetes related complications may begin at this number, including cardiovascular disease

30. A1C Definition
Glucose is bound non-enzymatically to the hemoglobin molecule
Directly proportional to the time-integrated mean BG concentration during the preceding 2 to 3 months
An ‘average’ of Glucose values over 2-3 months
Usually done every 3-6 months clinically
Henry: Clinical Diagnosis by Laboratory Methods, 2005 
Rakel: Conn's Current Therapy 2006, 58th ed., 2006

31. A1C ~ “Average Glucose” A1C eAG % mg/dL mmol/L 6 126 7.0 6.5 140 7.8
Formula: 28.7 x A1C eAG
calculator at professional.diabetes.org/eAG
American Diabetes Association

32. A1C Technical Issues “Mismatch” with Fingerstick
Genetic variants that alter value (i.e., HbS, HbE, HbC, and HbD)
Acquired conditions that alter value (i.e., kidney disease, anemias, conditions affecting erthrocyte turnover, pregnancy)

33. A1C Lab Measurement Over 100 ways to measure A1C
Most common methods are antibodies (immunoassays) or cation-exchange chromatography
National Glycohemoglobin Standardization Program (NGSP) has been instrumental in standardizing A1C testing among laboratories

34. A1C Advantages For Diagnosing Diabetes
Convenience- doesn’t require fasting or a 2 hour test
May capture those who don’t yet have abnormal fasting plasma glucose
Reflects chronicity and duration of abnormal glucose values
Short-term Factors that affect fasting glucose don’t affect A1C

35. Fasting Glucose for Diabetes Diagnosis: Advantages 
Glucose assay easily automated 
Widely available 
Inexpensive 
Single sample

36. Fasting Glucose for Diabetes Diagnosis: Disadvantages
• Patient must fast ≥8 h 
• Large biological variability 
• Diurnal variation 
• Sample not stable 
• Numerous factors alter glucose concentrations, e.g., stress, acute illness 
• No harmonization of glucose testing
Need 2 values for diagnosis 

37. Fasting Glucose for Diabetes Diagnosis: Disadvantages
• Concentration varies with source of the sample (venous, capillary, or arterial blood) 
• Concentration in whole blood is different from that in plasma 
• Guidelines recommend plasma, but many laboratories measure serum glucose 
• FPG less tightly linked to diabetes complications (than A1C) 
• Reflects glucose homeostasis at a single point in time

38. 2 hour Glucose Testing Advantages
2 hour post challenge or post prandial may be the most sensitive marker of glucose intolerance
2 hour is most predictive of cardiovascular disease and mortality
ADA and WHO actually prefer 2 hour

39. 2 Hour Glucose Testing Disadvantages
Lacks reproducibility 
Extensive patient preparation 
Time-consuming and inconvenient
Unpalatable 
Expensive 
Influenced by numerous medications
Subject to the same limitations as FPG

40. Type 2 Diabetes Screening in Children/Adolescents
Overweight
-BMI >85th percentile
-weight for height >85th percentile
-weight >120% of ideal for height
Plus risk factors similar to adults

41. Gestational Diabetes Occurs in 2-9% of pregnancies
~135,000 cases in U.S. annually
Increasing numbers- obesity, but many probably have prexisting diabetes or prediabetes
Lifestyle management
Insulin
(usually preferred, better efficacy)
or sulfonylureas (in very select cases)
Am J Obstet Gynecol 192:1768–1776, 2005
Diabetes Care 31(S1) 2008
Diabetes Care 25: , 2002

42. Gestational Diabetes and Type 2 Diabetes Risk
Gestational Diabetes should be considered a pre-diabetes condition
Women with gestational diabetes have a 7-fold future risk of type 2 diabetes vs.women with normoglycemic pregnancy
35-60% go on to have DM
Lancet, 2009, 373(9677):

43. Gestational Diabetes (GDM) Screening
Screen for type 2 diabetes first prenatal visit if risk factors
Not known to have diabetes, screen for GDM at 24 –28 weeks of gestation
Controversy exists: ACOG (supported by NIH), ADA
Diabetes Care 34:Supplement 1, 2011 Lancet, 2009, 373(9677):

44. Gestational Diabetes (GDM) ADA
Overnight fast, 75g OGTT
Fasting >92 mg/dl
1 h >180 mg/dl
2 h >153 mg/dl
Thought to identify more patients with glucose intolerance
Diabetes Care 35:Supplement 1, 2012
Diabetes Care 2010; 33: 676–682

45. Gestational Diabetes (GDM) ACOG
2 Step approach
1 hour 50gm OGT (screening) >130
Then proceed to 3 hour OGTT
Thought to identify those who actually need to be treated

46. ACOG 3 hour OGTT Fasting >95 1 hour >180 2 hours >155
2 or more of the above values
Can follow 1 hour screen, or as initial diagnostic test

47. GDM Screening
A1C not ideal for GDM screening, but may be good for type 2 screening
Fructosamine not good for screening
Occasionally, it’s not GDM or pre-existing type 2- may be a new type 1
Most clinics use ACOG
Gynecol Obstet Invest 2011;71:
Diabetes Care 34:Supplement 1, 2011 Lancet, 2009, 373(9677):

48. GDM Complications Macrosomia Fractures Shoulder dystocia
Nerve palsies (Erb’s C5-6)
Pregnancy outcomes can be very poor with HTN/nephropathy
Neonatal hypoglycemia
Gabbe, Obstetrics: Normal and Problem Pregnancies 2002

49. Gestational Diabetes:Outcomes
Hyperglycemia and Adverse Pregnancy Outcomes (HAPO) Study 28,000 women
Good GDM management improves outcomes
NEJM (358) 2008
Diabetes Care 2012

50. Blood Glucose/A1C and Relationship to Complications

51. A1C
Many questions about A1C in recent years with relationship to complications
Let’s try to sort it out…..

52. Diabetes Complications
Macrovascular Complications (Large Vessel)
Cardiovascular disease
Coronary Heart disease (CHD)
Stroke
Peripheral arterial disease (PAD)/amputation
Primarily related to Blood Pressure, Lipids, and post-prandial blood sugar

53. Diabetes Complications
Microvascular Complications (Small Vessel)
Eye disease (retinopathy)
Kidney disease (nephropathy)
Nerve disease (neuropathy)
Primarily related to A1C and fasting blood sugar

54. Diabetes Complications
Other complications
Liver disease (NAFLD, NASH)
All cause mortality risk

55. Diabetes and All-Cause Mortality
Diabetes also associated with death from:
Pneumonia and other infectious diseases
Mental disorders
Nonhepatic digestive diseases
External causes and intentional self-harm
Nervous-system disorders
COPD
Emerging Risk Factors Collaboration. N Engl J Med 2011, 364(9):

56. Avoiding Diabetes Complications
Blood glucose control A1C <7%
Treat lipid profiles with appropriate statin doses vs risk factors/age
Treat blood pressure to target <140/<90
For most non-pregnant adults

57. Recommended statin intensity*
Anti-Lipid Therapy
Age
Risk factors
Recommended statin intensity*
<40 years
None
ASCVD risk factor(s)†
Moderate or high
ASCVD
High
40–75 years
Moderate
ASCVD risk factors
ACS and LDL >50 mg/dL who cannot tolerate high-dose statin
Moderate plus ezetimibe
>75 years
ACS and LDL >50 mg/dL who cannot tolerate high dose statin
*In addition to lifestyle therapy.
†ASCVD risk factors include LDL cholesterol ≥ 100 mg/dL (2.6 mmol/L), high blood pressure, smoking, overweight or obesity,
and family history of premature ASCVD.
ACS, acute coronary syndrome.

58. Targets for Glycemic (blood sugar) Control In Most Non-Pregnant Adults
ADA
AACE
A1c (%)
<7*
≤6.5
Fasting (preprandial) plasma glucose
mg/dL
<110 mg/dL
Postprandial (after meal) plasma glucose
<180 mg/dL
<140 mg/dL
R36/p34/P1/L15
Both the ADA and the AACE recommend tight glucose control for persons with diabetes, although their definitions vary.
Despite the findings of two large-scale trials, the DCCT and UKPDS, a universally agreed-upon set of glucose management goals has yet to be defined. While almost every diabetes management guideline includes the hallmark variables of A1c and fasting plasma glucose, there are slight variations in specific target values. The American Diabetes Association (ADA) currently recommends a target A1c of <7%, while the American Association of Clinical Endocrinologists (AACE) suggests aiming for a value of 6.5% or lower. The ADA proposes a target range for fasting plasma glucose levels between 90 and 130 mg/dL, while the AACE recommends levels below 110 mg/dL. Postprandial plasma glucose recommendations put forth by the two organizations are <180 and <140 mg/dL, respectively.
In addition to these standard variables, there are other important aspects of diabetes management that deserve consideration. Other important issues identified in the two landmark trials, both medically and from a quality of life perspective, include reducing the frequency of hyperglycemic excursions, minimizing the risk of hypoglycemia, especially nocturnal, and minimizing weight gain. Addressing these issues could have an impact on patient motivation and/or treatment compliance, increasing the chance of attaining A1c and plasma glucose goals.
References:
American Diabetes Association. Standards of medical care in diabetes – Diabetes Care. 2006;29(suppl 1):S4-S42. Implementation Conference for ACE Outpatient Diabetes Mellitus Consensus Conference Recommendations: Position Statement at ImplementationPositionStatement.pdf. Accessed January 6, 2006.
R5/pS10/T6
R2/p3/P2
*<6 for certain individuals
American Diabetes Association. Diabetes Care. 2012;35(suppl 1)
Implementation Conference for ACE Outpatient Diabetes Mellitus Consensus Conference Recommendations: Position Statement at Accessed January 6, 2006.
AACE Diabetes Guidelines – 2002 Update. Endocr Pract. 2002;8(suppl 1):40-82. 58

59. Target A1C and Complications
Guidelines primarily based on DCCT (Type 1) and UKPDS (Type 2) and subsequent studies
Questions regarding A1C and cardiovascular disease in more recent ACCORD, ADVANCE, and VADT studies

60. A1C and Relative Risk of Microvascular Complications: DCCT
Type 1 Diabetes: DCCT
Microvascular Complications
Retinopathy 15
Nephropathy 13
Neuropathy 11
Microalbuminuria 9
Relative Risk 7 5
Slide 12
A1C and Relative Risk of Microvascular Complications: DCCT
Good glycemic control is essential to reduce the risk of diabetic complications
Based on DCCT data, this slide shows that the relative risk for microvascular complications such as diabetic retinopathy, nephropathy, neuropathy, and microalbuminuria increases with increasing levels of A1C1,2
The relative risk of complications is set to “1” for an A1C of 6%
It is important to note that the risk gradient is continuous with no glycemic threshold for developing complications
1. Skyler J. Endocrinol Metab Clin North Am. 1996;25:243
2. DCCT Research Group. N Engl J Med. 1993;329:977 3 1 6 7 8 9 10 11 12
A1C (%)
Adapted with permission from Skyler J. Endocrinol Metab Clin North Am. 1996;25:243
DCCT Research Group. N Engl J Med. 1993;329:977 60

61. Type 2 Diabetes: UKPDS

62. Blood Glucose, A1C, and CVD
ACCORD, ADVANCE,VADT did not show improved CVD outcomes with A1C less than ~6.0%-6.5%
ADVANCE confirmed less microvascular disease (nephropathy) in tightly controlled
Other data suggest post-prandial, variable glucose, difficult to target may contribute to CVD
Lower A1C associated with less microvascular disease (nephropathy, neuropathy, retinopathy)
(UKPDS, DCCT)
N Engl J Med 2008; 358:
N Engl J Med 2008; 358:
N Engl J Med 2009; 360:
Diabetes Care October (10)

63. Blood Glucose, A1C, and CVD
Recent study showed A1C=6 or >8, higher CVD risk
Meta-analysis of Five Trials
UKPDS2, PROactive3, ADVANCE4, ACCORD5, VADT6
Intensive therapy reduced cardiovascular death, but not all cause mortality
Colayco DC et al Diabetes Care. 2011;34(1):77-83
Ray K et al The Lancet. 2009; 373:

64. A1C and Complications
So?
What Now?

65. Because of the ongoing uncertainty regarding whether intensive glycemic control can reduce the increased risk of CVD in people with type2 DM several long term trials were launched to compare effects of intensive versus standard glycemic control on CVD outcomes in relatively high risk participants with established type 2DM.
In 2008 two of the trials were completed the ADVANCE and VADT and ACCORD terminated its glycemic control study.

66. A1C and Complications
Data suggests lower A1C’s earlier in course of diabetes beneficial
Long term poor control may not benefit from more stringent control now, particularly with reference to CVD- Blood Pressure and Lipid Management need to be targeted
Diabetes Care January 2009;32 (1)
Ann Intern Med Apr 19;154(8):554-9.

67. Summarizing Blood Glucose, A1C, and Diabetes Complications
Probably more associated with microvascular complications
Glucose variability, post-prandial glucose
Probably more associated with macrovascular complications
Optimal A1C may be unclear for all patients with CVD risk

68. Optimal A1C Age Co-Morbid Conditions/Complications Length of Diabetes
Resources
Ability to manage complex regimens
Hypoglycemia

69. Goals of Glucose Management
More stringent (<6.5) may be reasonable:
-No significant CVD
-Short duration
-Long life expectancy
Diabetes Care 36:Supplement 1, 2013

70. Goals of Glucose Management
Less stringent (<7.5-8+) may be reasonable:
History of severe hypoglycemia
Limited life expectancy
Advanced complications or comorbid conditions
Longstanding difficult to control diabetes
Diabetes Care 36:Supplement 1, 2013

71. Other Important Labs In Diabetes

72. Lipids and Cardiovascular Complications:
Total cholesterol <200
Triglycerides <150
HDL (“good”) >40 men, >50 women
LDL (“bad”) <100, <70 high risk
These are no longer “targets”, but abnormals represent “at risk”

73. Cardiovascular Complications in Diabetes
Affects about 65% of adults with diabetes
Targeting blood pressure and lipids can reduce risk by about 25-40%
LDL cholesterol is thought to be most tightly associated with CVD risk
This is usually done annually at minimum

74. Kidney Disease Screening
Serum Creatinine - may have age, disease, or muscle mass differences
Creatinine Clearance (or Glomerular Filtration Rate-GFR)- a better measure
CrCl- measure of creatinine filtered in kidneys
GFR- measure of blood filtered in kidneys
National Kidney Foundation Technical Discussion

75. Kidney Disease Screening
Urine for albumin- very predictive of future kidney disease (<30mg is normal on dipstick testing)
Gross proteinuria “trumps” microalbumin
(Proteinuria >300mg)
These tests are usually done annually

76. Chronic Kidney Disease (CKD)
Stage 1: GFR >90 with other evidence of kidney damage (microalbumin- or protein-uria, or abnnormal serum creatinine)
Stage 2: GFR with same qualifiers as Stage 1
Stage 3: GFR 30-59
Stage 4: GFR 15-29
Stage 5: GFR <15

77. Chronic Kidney Disease
Usually a direct result of diabetes and/or concominannt hypertension
May have secondary hyperparathyroidism
Elevated serum Parathyroid hormone (PTH) from hypocalcemia
Abnormalities with phosphorus, Vitamin D

78. Other Tests in Diabetes
Thyroid (TSH) (Type 1)
Celiac (TTG IgA and IgG) (Type 1)
Serum B12 (Type 2)
Vitamin D (25-OH) (Type 2)
LFT’s (often minimal chronic changes with fatty liver disease)

79. Future Directions And Other Lab Testing In Diabetes

80. Continuous Glucose Monitoring Logbook Data

81. Home A1C Testing Limited use
Recall that A1C “turns over” slowly 8-12 weeks
Expensive

82. Other Novel Cardiovascular Inflammatory Markers
Mayo Panel:
High Sensitivity C-reactive Protein (hsCRP)
Homocysteine
Lipoprotein a
Fibrinogen
LDL subfraction/particle size

83. Novel Cardiovascular Risk Assessment
Heart attack and/or stroke and/or peripheral arterial disease at a relatively young age (under age 55 in men, under age 65 in women)
Asymptomatic patients who have a family history of early atherosclerosis
Patients with elevated levels of novel risk factors including C-reactive protein (CRP), fibrinogen, lipoprotein(a) and homocysteine

84. Cases

85. Case #1
12 year old female
Thirst, unintentional weight loss of 15# in 3 weeks
Fasting blood sugar 460
“3+” Ketones in urine
Diagnosis?

86. Case #1 Diagnosis is type 1 diabetes Do we need antibody tests?
Should be tested for thyroid disease (TSH) and celiac disease (TTG IgA and IgG)

87. Case #2
42 y/o hispanic female with hx of GDM 6 years ago, term 10lb 5 oz male infant
Has not been seen for follow-up in years
Obese, noting fatigue
FBS done at annual pap/px is 149
Does this patient have diabetes? What next?

88. Case #2 Diagnosis of diabetes generally requires 2 abnormal values
Patient is at high risk for developing type 2 diabetes
GDM is a pre-diabetes condition
Repeat FBS 3 days later…….

89. Case #2 Repeat FBS 135 Dx: Type 2 diabetes
FBS >126 on 2 separate occasions
A1C 6.3
- Could have done an A1C as a “stand alone” test (>6.5)
Note that different tests don’t “cancel each other out”

90. Summary Diabetes is common
Laboratory markers and tests are very useful for screening and diagnosis of diabetes
Laboratory markers and tests are very useful for management of diabetes and avoidance of complications