Kits
Anti-GAD
Kits
Description
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 environmental
agents. 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.
During the preclinical phase, this autoimmune
process is marked by circulating autoantibodies to
beta cell antigens. These autoantibodies, such as
anti-insulin (IAA), anti-glutamic acid decarboxylase
(GAD) and anti-tyrosine phosphatase ICA 512 (IA2),
are present years before the onset of type 1 diabetes
and prior to clinical symptoms.
GAD, the enzyme that catalyzes the conversion of
glutamate to GABA, has been identified in two
isoforms, molecular weight 65.000 (GAD65) and
67.000 (GAD67). Although GAD autoantibodies are
found in type 1 diabetes and in the rare neurological
disorder Stiff-man syndrome (SMS), the GAD
autoantibodies profile in the two diseases differs.
Autoantibodies of SMS patients recognize a
combination of linear and conformational epitopes of
GAD while GAD65 autoantibodies in patients with
type 1 diabetes are predominantly directed to the
conformational epitopes. GAD65 autoantibodies
(GAD65 Abs) are present in 70-80% of newly
diagnosed patients with type 1 diabetes.
The combination of the autoantibodies to GAD65 and
IA2 is highly relevant for risk assessment of type 1
diabetes in children and adolescence.
These tests in combination are more sensitive and
predictive than ICA in risk groups, e.g. relatives of
patients with type 1 diabetes.
GAD65 Abs also occur in a subset of adults with type
2 diabetes. These patients can have pronounced
hyperglycemia, and after therapy with oral
hypoglycemic agents for several months to years they
may become insulin dependent. Therefore, these
patients are thought to have a slowly progressive form
of type 1 diabetes, often called latent diabetes or latent
autoimmune diabetes in adults (LADA).
The presence of GAD65 Abs in sera of such patients is
a sensitive and specific marker for future insulin
dependency.
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 environmental
agents. 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.
During the preclinical phase, this autoimmune
process is marked by circulating autoantibodies to
beta cell antigens. These autoantibodies, such as
anti-insulin (IAA), anti-glutamic acid decarboxylase
(GAD) and anti-tyrosine phosphatase ICA 512 (IA2),
are present years before the onset of type 1 diabetes
and prior to clinical symptoms.
GAD, the enzyme that catalyzes the conversion of
glutamate to GABA, has been identified in two
isoforms, molecular weight 65.000 (GAD65) and
67.000 (GAD67). Although GAD autoantibodies are
found in type 1 diabetes and in the rare neurological
disorder Stiff-man syndrome (SMS), the GAD
autoantibodies profile in the two diseases differs.
Autoantibodies of SMS patients recognize a
combination of linear and conformational epitopes of
GAD while GAD65 autoantibodies in patients with
type 1 diabetes are predominantly directed to the
conformational epitopes. GAD65 autoantibodies
(GAD65 Abs) are present in 70-80% of newly
diagnosed patients with type 1 diabetes.
The combination of the autoantibodies to GAD65 and
IA2 is highly relevant for risk assessment of type 1
diabetes in children and adolescence.
These tests in combination are more sensitive and
predictive than ICA in risk groups, e.g. relatives of
patients with type 1 diabetes.
GAD65 Abs also occur in a subset of adults with type
2 diabetes. These patients can have pronounced
hyperglycemia, and after therapy with oral
hypoglycemic agents for several months to years they
may become insulin dependent. Therefore, these
patients are thought to have a slowly progressive form
of type 1 diabetes, often called latent diabetes or latent
autoimmune diabetes in adults (LADA).
The presence of GAD65 Abs in sera of such patients is
a sensitive and specific marker for future insulin
dependency.