No radioactive isotopes should be administered 24 hours prior to specimen collection

Gold serum separator (SST) tube

Immediatley following collection, mix sample by gently inverting 5 times

1. Allow sample to clot for a minimum of 30 minutes
2. Spin within two (2) hours of sample collection
3. Transfer serum to a Screw-cap polypropylene frozen transport vial/tube - 4mL (LabCorp), labelled as serum
4. Freeze

Screw-cap polypropylene frozen transport vial/tube - 4mL (LabCorp)

Red serum vial/tube, 5 mL

1. Allow sample to clot 
2. Spin within two (2) hours of sample collection
3. Transfer serum to a Screw-cap polypropylene frozen transport vial/tube - 4mL (LabCorp), labelled as serum
4. Freeze

Frozen (preferred) - 2 years

Freeze/thaw cycles - stable x 6

Refrigerated - 3 days

Ambient - 2 days

Radioactive isotopes administered 24 hours prior to venipuncture

Insulin-I125 binding capacity

uU/mL

Type 1 diabetes, commonly referred to as insulin-dependent diabetes (IDDM), is caused by pancreatic beta-cell destruction that leads to an absolute insulin deficiency. The clinical onset of diabetes does not occur until 80% to 90% of these cells have been destroyed. Prior to clinical onset, type 1 diabetes is often characterized by circulating autoantibodies against a variety of islet cell antigens, including glutamic acid decarboxylase (GAD), tyrosine phosphatase (IA(2)), and insulin.  The autoimmune destruction of the insulin-producing pancreatic beta cells is thought to be the primary cause of type 1 diabetes. The presence of these autoantibodies provides early evidence of autoimmunedisease activity, and their measurement can be useful in assisting the physician with the prediction, diagnosis, and management of patients with diabetes. Insulin is the only beta-cell specific autoantigen thus far identified. Antibodies to insulin are found predominantly, though not exclusively, in young children developing type 1 diabetes. In insulin-naive (untreated) patients, the prevalence of antibodies to insulin is almost 100% in very young individuals and almost absent in adult onset of type 1 diabetes. Because the risk of diabetes is increased with the presence of each additional autoantibody marker, the positive predictive value of insulin antibody measurement is increased when measured in conjunction with antibodies to GAD and IA-2.