GLUTAMIC ACID DECARBOXYLASE AB

Code
900.1716
Name
GLUTAMIC ACID DECARBOXYLASE AB
Category
None
Department
Send-Out
Start Date
Expiration Date
Synonyms
GAD, GAD Antibody, GAD65 Antibody
CPT Codes
83520
Site
SBMF
Reference Test
28276
ATLAS Test Code

Specimen Information

Type

Gold, SST

Volume

1.0 ml

Transport Info

Centrifuge and immediately transfer serum to separate plastic tube
Frozen

Fasting Required?
False
Patient Instructions

Reference Range

Less than 5 U/mL

Methodology

Enzyme-Linked Immunosorbent Assay (ELISA)

Clinical Significance

Glutamic acid decarboxylase (GAD) is the enzyme responsible for the synthesis of neurotransmitter gamma-aminobutyric acid in neurons and pancreatic beta cells. It is represented by two isoforms, GAD65 and GAD67, which are the products of two different genes. GAD65 is the dominant autoantigen in stiff-person syndrome (SPS) and insulin-dependent diabetes mellitus (IDDM).

In SPS, the immune system makes antibodies against GAD65. GAD65 plays an important role in the production of gamma-aminobutyric acid (GABA), a neurotransmitter that inhibits certain activity in the spinal cord and brain.

Type I diabetes, IDDM, accounts for approximately 15% of the diabetic population. IDDM is generally seen in children and young adults, but it can strike at any age. Insulin deficiency results in autoimmune destruction of insulin producing pancreatic beta cells. Clinical onset of diabetes does not occur until 80-90% of these cells are destroyed. Prior to clinical onset, type1 diabetes can be characterized by lymphocytic infiltration of the islet cells and various circulating autoantibodies. Measuring these autoantibodies as disease markers at the pre-diabetic stage affords an opportunity to predict and prevent the clinical onset of the disease.

GAD65 antibodies have been found in 70-90% of pre-diabetic and Type 1 diabetic patients. It is the most sensitive single marker for identifying individuals at risk of developing diabetes. GAD65 is more prevalent in older children and late-onset Type 1 diabetes and the marker has been shown to be detected ten years prior to disease onset.

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