BARCELONA – Not all type 2 diabetes is the same, and pathophysiologic differences among diabetes subtypes mean that different type 2 patients need different treatment.
"Several specific causes of hyperglycemia are hidden behind the clinical diagnosis of type 2 diabetes," Dr. Henning Beck-Nielsen said at the annual meeting of the European Association for the Study of Diabetes.
"Patients with type 2 diabetes can be divided into three basic pathophysiologic phenotypes: classic type 2 diabetes, insulinopenic type 2 diabetes, and hyperinsulinemic type 2 diabetes." He and his associates identified these and other, less common subtypes by systematically studying more than 1,000 Danish patients newly diagnosed with type 2 diabetes who were entered into a national registry that now totals 40,000 patients.
"We recommend that clinicians measure both GAD [glutamic acid decarboxylase] antibodies and fasting C-peptide in newly diagnosed patients with type 2 diabetes to properly classify the phenotypes," said Dr. Beck-Nielsen, professor and head of the endocrinology research unit at Odense (Denmark) University Hospital. "Measuring C-peptide gives a lot of information."
Patients with the insulinopenic form of type 2 diabetes should receive insulin treatment, those with the hyperinsulinemic form should ideally be treated with a sensitizer drug, while patients with a combination of both defects – classic type 2 diabetes – should be treated according to current recommendations (Diabetes Care 2012;35:1364-79), he said in an interview.
Dr. Beck-Nielsen and his associates studied the first 1,048 Danish patients newly diagnosed with type 2 diabetes by a general practitioner or in an outpatient clinic and enrolled in the Danish Centre for Strategic Research in Type 2 Diabetes (DD2) study. The patients averaged 61 years old, and slightly more than half were men.
Initial analysis identified 918 (87%) of the patients with true type 2 diabetes. Another 6% had steroid-associated diabetes; 4% had diabetes secondary to pancreatitis; 3% were positive for GAD antibodies showing they had latent autoimmune diabetes of adulthood (LADA); and a small number of patients had rare disorders.
Among the 918 with true type 2 diabetes, the Odense researchers used data collected on fasting levels of C-peptide and plasma glucose to make a homeostasis model assessment (HOMA2) and derive from it information on insulin sensitivity and beta-cell activity.
Roughly half the patients had classic type 2 diabetes, about a third had the hyperinsulinemic form, and fewer than a quarter had the insulinopenic form (but not type 1 diabetes or LADA). These clusterings appeared independent of age and sex, but patients with classic type 2 diabetes or the hyperinsulinemic form had a greater prevalence of metabolic syndrome and increased waist circumference.
Patients with insulinopenic type 2 diabetes had an average body mass index of 26.9 kg/m2, were sensitive to insulin, and had a relatively low prevalence of cardiovascular disease, compared with the other two types. Cardiovascular disease prevalence was highest among the hyperinsulinemic patients, who were generally obese and had a 25% cardiovascular disease prevalence compared with a 13% rate in those with insulinopenic diabetes, and an 18% rate in those with classic type 2 diabetes.
Dr. Beck-Nielsen said that he has received research support from Novo Nordisk.
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