IAA

Type 1 diabetes, also known as Insulin-dependent
diabetes mellitus (IDDM), results from a chronic
autoimmune destruction of the Insulin secreting
pancreatic beta cells, probably initiated by exposure of
genetically susceptible host to an environmental agent.
Autoimmune destruction of beta cells is thought to be
completely asymptomatic until 80-90% of the cells are
lost. This process may take years to complete and may
occur at any time in all ages.
The presence of Insulin autoantibodies (IAA) in patients
never treated with Insulin, as opposed to Insulin
antibodies (IAb), is an evidence of an ongoing
destruction process of pancreatic beta cells in type 1
diabetes.
IAA are particularly important when determining type 1
diabetes risk since their prevalence is significantly
elevated in subjects developing the disease in childhood
and moreover, they are often the first autoantibodies to
be detected before onset of the disease. The
prevalence of IAA is inversely correlated with the age of
diagnosis.
In type 1 diabetics with recent onset of the disease in
the age younger than 5 years IAA can be determined on
over 90 % of the patients, whereas in type 1 diabetics
over 20 years the prevalence of IAA is greater than 20
%.
The IAA measurement, together with that of antibodies
to glutamic acid decarboxylase (GAD65 Ab), protein
tyrosine phosphatase-like antigen IA2 and Islet cells
antigens (ICA) forms the basis of current strategies for
predicting future onset of type 1 diabetes.
In addition to autoantibodies to human Insulin,
antibodies induced by Insulin treatment can be
frequently found. Such antibodies occur at much higher
concentration and are mainly directed against denatured
(incorrectly folded) fraction of applied Insulin.
This may lead to formation of antigen-antibodycomplexes
and by this reducing of the activity of the
injected Insulin. Measurements are necessary to obtain
an optimal disease management when applying Insulin.