title: Clinical and metabolic characteristics of patients with latent autoimmune diabetes in adults (LADA): absence of rapid beta-cell loss in patients with tight metabolic control.
abstract: OBJECTIVE
  The present study compared the clinical and metabolic characteristics of latent autoimmune diabetes in adults (LADA) with type 2 diabetes, as well as the residual beta-cell function and progression to insulin treatment, over a 2-year follow-up period, of antibody (Ab)-positive and Ab-negative patients who achieved tight glycaemic control (HbA(1c) 7.0+/-0.8% and 6.5+/-0.9%, respectively, at the time of entry into the study).
  
  
  RESULTS
  Glutamic acid decarboxylase antibodies (GADA) and/or islet cell antibodies (ICA) were detected in 10% of patients presenting with non-insulin-dependent diabetes. Around half of Ab-positive patients required insulin treatment during the follow-up. Ab-positive patients displayed lower stimulated C-peptide levels both at entry and during the follow-up compared with Ab-negative patients, although no significant decline in C-peptide levels was observed in either subgroup over two years. Nevertheless, Ab-positive patients progressed more frequently to insulin treatment, and stimulated C-peptide tended to decrease in LADA patients who subsequently required insulin, whereas it remained stable in those who were non-insulin-dependent. In those who progressed, the trend towards C-peptide decline persisted even after starting insulin treatment.
  
  
  CONCLUSIONS
  LADA patients demonstrate lower residual beta-cell function than do type 2 diabetes patients. However, those who achieve tight metabolic control do not present with a rapid decline in beta-cell function. Further studies are needed to determine the optimal treatment strategy in such patients.
authors.affiliation: Clinique d'endocrinologie, maladies métaboliques et nutrition, institut du thorax, hôpital Laennec, boulevard Jacques-Monod, Nantes cedex 1, France. lucy.chaillous@wanadoo.fr
authors.forename: L
authors.initials: L
authors.lastname: Chaillous
authors.forename: B
authors.initials: B
authors.lastname: Bouhanick
authors.forename: V
authors.initials: V
authors.lastname: Kerlan
authors.forename: E
authors.initials: E
authors.lastname: Mathieu
authors.forename: P
authors.initials: P
authors.lastname: Lecomte
authors.forename: P-H
authors.initials: PH
authors.lastname: Ducluzeau
authors.forename: M
authors.initials: M
authors.lastname: Delamaire
authors.forename: E
authors.initials: E
authors.lastname: Sonnet
authors.forename: D
authors.initials: D
authors.lastname: Maugendre
authors.forename: R
authors.initials: R
authors.lastname: Maréchaud
authors.forename: V
authors.initials: V
authors.lastname: Rohmer
authors.forename: P
authors.initials: P
authors.lastname: Saï
authors.forename: B
authors.initials: B
authors.lastname: Charbonnel
mesh_terms: D000328:Adult; D017668:Age of Onset; D000368:Aged; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism*; D015992:Body Mass Index; D002096:C-Peptide / Q000097:blood; D003430:Cross-Sectional Studies; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology*; D018450:Disease Progression; D005260:Female; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007328:Insulin / Q000627:therapeutic use*; D050417:Insulin-Secreting Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D002096:C-Peptide; D007004:Hypoglycemic Agents; D007328:Insulin