Early Insulin Treatment in Patients With Latent Autoimmune Diabetes

2014-08-27 03:14:12 | BioPortfolio


Among adult patients diagnosed with type 2 diabetes, about 6% have autoantibodies directed against the insulin producing beta cells in the pancreas. These patients have a progressive beta cell destruction and most of them will be insulin dependent within 3-5 yrs. Patients with this latent autoimmune diabetes in adults (LADA) have a considerable remaining beta cell mass at diagnosis, and are suitable for evaluating new therapies for autoimmune diabetes Animal studies in diabetes prone mice have demonstrated potential positive effects of early insulin treatment, with a lower incidence of diabetes or a delay before diagnosis. The aim of this study was to investigate the effect of early insulin treatment of LADA patients, in respect to residual beta-cell function and metabolic control, compared to a group who were conventionally treated with diet and/or oral hypoglycaemic agents (OHA) and insulin not before it was clinically needed.


All adult newly diagnosed diabetic patients in the certain areas are screened for pancreatic antibodies. Patients clinically classified as Type 2, not insulin requiring at diagnosis and positive for at least one autoantibody are eligible for inclusion. After randomisation to insulin treatment or diet and/or OHA, the patients are followed up with fasting C-peptide every third month. A glucagon test is performed, and stimulated C-peptide and HbA1c, + clinical data and body weight are recorded at baseline and after 12, 24 and 36 months. The final outcome of the study is C-peptide, and change in C-peptide compared to baseline level, and HbA1c, after 36 months.

Study Design

Allocation: Randomized, Intervention Model: Parallel Assignment, Masking: Open Label, Primary Purpose: Treatment


Diabetes, Autoimmune






Lund University Hospital

Results (where available)

View Results


Published on BioPortfolio: 2014-08-27T03:14:12-0400

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Medical and Biotech [MESH] Definitions

A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.

A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).

Diabetes mellitus induced by PREGNANCY but resolved at the end of pregnancy. It does not include previously diagnosed diabetics who become pregnant (PREGNANCY IN DIABETICS). Gestational diabetes usually develops in late pregnancy when insulin antagonistic hormones peaks leading to INSULIN RESISTANCE; GLUCOSE INTOLERANCE; and HYPERGLYCEMIA.

A subtype of DIABETES MELLITUS that is characterized by INSULIN deficiency. It is manifested by the sudden onset of severe HYPERGLYCEMIA, rapid progression to DIABETIC KETOACIDOSIS, and DEATH unless treated with insulin. The disease may occur at any age, but is most common in childhood or adolescence.

A strain of Rattus norvegicus which is a model for spontaneous insulin-dependent diabetes mellitus (DIABETES MELLITUS, INSULIN-DEPENDENT).

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