Test ID: INAB Insulin Antibodies, Serum
Reporting Name
Insulin Abs, SUseful For
Predicting the future development of type 1 diabetes in asymptomatic children, adolescents, and young adults, when used in conjunction with family history, HLA-typing, and other autoantibodies, including GD65S / Glutamic Acid Decarboxylase (GAD65) Antibody Assay, Serum and islet cell antigen 2 (IA-2) antibodies
Differential diagnosis of type 1 versus type 2 diabetes
Evaluating diabetics with insulin resistance in patients with established diabetes (type 1 or type 2)
Investigation of hypoglycemia in nondiabetic subjects
Clinical Information
The onset of autoimmune diabetes mellitus (type 1 diabetes mellitus) is preceded (and accompanied) by the appearance of autoantibodies to a variety of pancreatic islet cell antigens in serum, including insulin. The level of these autoantibodies is generally low and may even fall during follow-up. In genetically predisposed, but disease-free, individuals (first degree relatives of patients with type 1 diabetes or individuals with permissive HLA alleles), detection of multiple islet cell autoantibodies is a strong predictor for subsequent development of type I diabetes.
Once type 1 diabetes has become fully manifest, insulin autoantibody levels usually fall to low or undetectable levels. However, after insulin therapy is initiated, autoantibody production may recur as a memory response. Insulin autoantibody production is more common when therapeutic insulin of animal origin is used (rarely used in contemporary practice). Larger therapeutic doses may be required because of antibody-induced insulin resistance.
Insulin antibodies may be found in nondiabetic individuals complaining of hypoglycemic attacks. In this setting their presence can be an indicator of "factitious hypoglycemia" due to the surreptitious injection of insulin, rather than to a clinical problem (eg, insulinoma). However, insulin autoantibodies in nondiabetic subjects can occasionally develop without exposure to exogenous insulin and may rarely become a cause of episodic hypoglycemia. Anti-idiotypic autoantibodies against insulin autoantibodies have been demonstrated in some cases. Interaction of these antibodies with insulin autoantibodies could displace bound insulin from the insulin autoantibodies, resulting in hypoglycemia.
In addition to IgG and IgM insulin autoantibodies, IgE antibodies (identified by the fluorescence enzyme immunoassay) may occur. IgE insulin autoantibodies result in immediate hypersensitivity reactions, such as urticaria, but do not lead to insulin resistance or hypoglycemia as can be seen with the IgG antibodies. This test only determines the presence of IgG and IgM antibodies, not IgE antibodies.
In conjunction with family history, HLA-typing and measurement of other islet cell autoantibodies (glutamic acid decarboxylase [GAD65] antibody and islet cell antigen 2 antibody [IA-2]), insulin autoantibody testing helps predict the future development of type I diabetes in asymptomatic children, adolescents, and young adults. Inclusion of a recently described fourth autoantibody (zinc transporter 8, ZnT8) further enhances the prediction of type 1 diabetes occurrence and its distinction from type 2 diabetes.
Interpretation
Seropositivity (≥0.03 nmol/L) in a patient never treated with insulin is consistent with predisposition to type 1 diabetes. Seropositivity is not as informative of type 2 diabetes status as other islet cell antibodies in patients who are receiving (or have received) insulin therapy because this antibody can arise secondary to therapy. It is thought that high levels of insulin autoantibodies might contribute to insulin resistance.
A family history of type 1 diabetes, other organ-specific autoimmunity and a diabetes-permissive HLA phenotype strengthens the prediction of type 1 diabetes development. The detection of multiple islet cell antibodies is indicative of the likely development of future type 1 diabetes.
In patients presenting with hypoglycemia, the presence of insulin autoantibodies may indicate surreptitious insulin administration or, rarely, insulin autoantibody-related hypoglycemia. The differential diagnosis cannot be made on the basis of insulin autoantibody detection alone. C-peptide and insulin measurements are always required in addition to insulin autoantibody measurements in the diagnosis of hypoglycemia.
Report Available
3 to 9 daysDay(s) Performed
Sunday, Wednesday
Clinical Reference
1. Schernthaner G: Immunogenicity and allergenic potential of animal and human insulins. Diabetes Care 1993;3:155-165
2. Lernmark A: Type 1 diabetes. Clin Chem 1999;45:1331-1338
3. Eisenbarth GS, Jeffery J: The natural history of type 1A diabetes. Arq Bras Endocrinol Metabol 2008 Mar;52(2):146-155
Method Name
Radioimmunoassay (RIA)
Specimen Type
SerumSpecimen Required
Collection Container/Tube:
Preferred: Red top
Acceptable: Serum gel
Submission Container/Tube: Plastic vial
Specimen Volume: 1.5 mL
Collection Instructions: Centrifuge and aliquot serum into a plastic vial.
Specimen Minimum Volume
1 mL
Specimen Stability Information
Specimen Type | Temperature | Time | Special Container |
---|---|---|---|
Serum | Refrigerated (preferred) | 28 days | |
Frozen | 28 days | ||
Ambient | 72 hours |
Reference Values
≤0.02 nmol/L
Reference values apply to all ages.
Test Classification
This test was developed, and its performance characteristics determined by Mayo Clinic in a manner consistent with CLIA requirements. This test has not been cleared or approved by the US Food and Drug Administration.CPT Code Information
86337
LOINC Code Information
Test ID | Test Order Name | Order LOINC Value |
---|---|---|
INAB | Insulin Abs, S | 60463-7 |
Result ID | Test Result Name | Result LOINC Value |
---|---|---|
8666 | Insulin Abs, S | 60463-7 |
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