insulin dependent diabetes mellitus (type 1 diabetes)

Last edited 12/2018 and last reviewed 07/2021

Type 1 diabetes mellitus (T1D) or previously known as insulin dependent diabetes (IDDM), is a condition characterised by persistent hyperglycaemia due to absolute insulin deficiency caused by autoimmune destruction of the insulin-producing beta cells of the pancreas (1).

Nearly 90% of T1D patients have one or more islet autoantibodies such as insulin (IAA), glutamic acid decarboxylase (GADA), insulinoma-associated autoantigen 2 (IA-2), and zinc transporter 8 (ZnT8A) (2)

  • studies of first-degree relatives of patients with T1D have reported that the persistent presence of two or more autoantibodies is an almost certain predictor of clinical hyperglycemia and diabetes.
    • the rate of progression is dependent on the age at first detection of antibody, number of antibodies, antibody specificity, and antibody titer (3)
  • in some parts of the world (in Africa and Asia), a significant proportion of patients are negative for autoantibodies and this type of T1D is termed “idiopathic” (type 1b) (1)

Historically, T1D was considered as a disorder in children and adolescents. However this opinion has changed over the past decade and people with T1D may present at any age (2)

  • differential diagnosis of diabetes in children, adolescents and young adults has become a challenging task due to the emergence of type 2 diabetes mellitus (T2D), and the increasing prevalence of obesity in the general population, which minimizes the value of body mass index as a distinguishing feature between T1D and T2D (3).

The Juvenile Diabetes Research Foundation, American Diabetes Association and the Endocrine Society have identified three stages of “early” T1D:

  • stage 1 - individual has evidence of autoimmunity but is normoglycemic
  • stage 2 - there is evidence of glucose intolerance
  • stage 3 - characterized by symptomatic hyperglycemia

Note: “Pre-Stage 1” has also been described which includes individuals with a genetic predisposition to islet-cell autoimmunity in whom autoantibodies are as yet undetectable (1).