Type 1 diabetes is usually thought of as a disorder of onset in childhood, adolescence or early adulthood. However, in recent years, aided by the availability of serological tests for islet cell autoimmunity, its presentation in older adults has become well recognised, particularly in people of European descent. In this age group, the disease is often of slow onset and commonly mistaken for type 2 diabetes.[1]

Type 1 diabetes is rare in Pāsifika children living in the Pacific Islands, but does occur in the New Zealand-born offspring of migrants.[2, 3] In adults of Pāsifika descent, type 2 diabetes is very common, primarily because of high levels of obesity, and it becomes even more prevalent after migration to westernised countries, such as Australia and New Zealand. To our knowledge, adult-onset type 1 diabetes in first-generation Pāsifika migrants has not been recognised previously. We describe six such patients, all of whom were originally diagnosed with type 2 diabetes.

Details of the patients are given in the Table 1. One patient (no. 4) was diagnosed with diabetes before and one (no. 1) shortly after migration; the other four were diagnosed 9–33 years after migration. Only one (no. 6) had any known European ancestry. The interval between diagnosis of diabetes and starting insulin treatment was 0–3 years. Type 1 diabetes was confirmed by the finding of serum antibodies to glutamic acid decarboxylase and undetectable or low fasting C-peptide levels (an indicator of endogenous insulin production). The interval between diagnosis of diabetes and recognition that it was type 1 (rather than type 2) ranged from 2 to 19 years.

Table 1. Clinical and biochemical findings in six Pāsifika migrants to New Zealand with adult-onset type 1 diabetes
NumberGender – originAge (years) atStart of insulin (year)BMI (kg/m2)Hypertension-dyslipidaemiaAnti-GAD (U/L)Fasting C-peptide (pmol/L)Insulin requirements (u/kg)
  1. †Normal <15 U/L. ‡Normal 370–1470 pmol/L. BMI, body mass index; GAD, antibodies to glutamic acid decarboxylase.


The clinical clues that led to the correct diagnosis were severe symptoms and rapid progression to needing insulin (two patients), labile blood sugars with hypoglycaemic episodes (three), diabetic ketoacidosis (one), the presence of other autoimmune disease (two) and a child in the family having type 1 diabetes (one). Insulin requirements for glycaemic control were relatively low (0.35–0.67 u/kg body weight). Factors that may have misled clinicians into continuing to believe that these patients had type 2 diabetes included the high mean body mass index (BMI) of 31 kg/m2 (only one had a BMI < 25 kg/m2) and that most had features of the metabolic syndrome (dyslipidaemia and/or hypertension).

Type 1 diabetes is strongly associated with certain polymorphisms of the class II human leucocyte antigen (HLA) genes encoding DR and DQ, proteins that are involved in the regulation of immune responses. Genotyping of DQA1/DQB1 and DRB1 was performed using Luminex bead technology (One Lambda Inc., Los Angeles, CA, USA). Haplotypes were assigned based on known HLA-DQ–DR associations in Polynesians.[4] In European subjects, five alleles have been particularly associated with susceptibility to late-onset type 1 diabetes,[5] two of which were found in five of our patients: DRB1*0901-DQA1*0301-DQB1*0303 (three subjects) and DRB1*0403-DQA1*0301-DQB1*0302 (two subjects).

We conclude that type 1 diabetes can occur in adults of Pāsifika descent, on a similar HLA background to that seen in European subjects. Consideration of all aspects of the phenotype aids accurate diagnosis, and this in turn should have a significant impact on treatment.


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  2. References
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