HbA1c in relation to incident diabetes and diabetes-related complications in non-diabetic adults at baseline.

AIMS: We compared the utility of glycated hemoglobin (HbA1c) and oral glucose tolerance (oGTT) in non-diabetic patients for identifying incident diabetes; all-cause mortality; cardiovascular disease (CVD) mortality; CVD, coronary heart disease (CHD), and ischemic stroke events; and diabetes microvascular complications. METHODS: Data from a New Zealand community setting were prospectively linked to hospitalization, mortality, pharmaceutical and laboratory test results data. After applying exclusion criteria (prior laboratory diagnosis or history of drug treatment for diabetes or hospitalization for diabetes or CVD event), there were 31,148 adults who had an HbA1c and 2-h 75g oGTT. HbA1c was measured by ion-exchange high-performance liquid chromatography, and glucose using a commercial enzymatic method. We compared glycemic measures and outcomes using multivariable Cox proportional hazards regression. RESULTS: The median follow-up time was 4years (range 0 to 13). The mean age was 57·6years and 53·0% were male. After adjusting for other glycemic measures (fasting glucose, 2-h glucose and/or HbA1c where relevant) in addition to age, sex, ethnicity and smoking habit, the hazard ratios for incident diabetes and diabetes complications of retinopathy and nephropathy were highest for 2-h glucose levels, followed by HbA1c and lastly by fasting glucose. However, all-cause mortality and CHD were significantly associated with HbA1c concentrations only, and ischemic stroke and CVD events with 2-h glucose only. Circulatory complications showed a stronger association with HbA1c. CONCLUSION: Apart from neuropathy, HbA1c showed stronger associations with outcomes compared to fasting glucose and provides a convenient alternative to an oGTT.

The distribution and frequency of blood lipid testing by sociodemographic status among adults in Auckland, New Zealand.

INTRODUCTION: National cardiovascular disease (CVD) guidelines recommend that adults have cholesterol levels monitored regularly. However, little is known about the extent and equity of cholesterol testing in New Zealand. AIM: To investigate the distribution and frequency of blood lipid testing by sociodemographic status in Auckland, New Zealand. METHODS: We anonymously linked five national health datasets (primary care enrolment, laboratory tests, pharmaceuticals, hospitalisations and mortality) to identify adults aged ≥25 years without CVD or diabetes who had their lipids tested in 2006-2010, by age, gender, ethnicity and area of residence and deprivation. Multivariate logistic regression was used to estimate the likelihood of testing associated with these factors. RESULTS: Of the 627 907 eligible adults, 66.3% had at least one test between 2006 and 2010. Annual testing increased from 24.7% in 2006 to 35.1% in 2010. Testing increased with age similarly for men and women. Indian people were 87% more likely than New Zealand European and Others (NZEO) to be tested, Pacific people 8% more likely, but rates for Maori were similar to NZEO. There was marked variation within the region, with residents of the most deprived areas less likely to be tested than residents in least deprived areas. DISCUSSION: Understanding differences within and between population groups supports the development of targeted strategies for better service utilisation. While lipid testing has increased, sociodemographic variations persist by place of residence, and deprivation. Of the high CVD risk populations, lipid testing for Maori and Pacific is not being conducted according to need.

Availability of troponin testing for cardiac patients in New Zealand 2002 to 2011: implications for patient care.

AIMS: For patients presenting with an acute coronary syndrome (ACS), troponin T or I levels are crucial for the diagnosis of myocardial infarction (MI). We investigated troponin tests, analyser types and thresholds used in New Zealand (NZ) from 2002 to 2011. METHODS: We reviewed troponin tests available at hospitals in NZ which admitted ACS patients and those who had troponin testing in 2002 (n=41), 2007 (n=43) and 2011 (n=43). We also contacted community laboratories and manufacturers. RESULTS: In 2010-11 there were nine different troponin analysers in 43 hospitals provided by five companies. Troponin T assays were used in 58% of the hospitals and 42% used troponin I as their first-line method. Quoted cutpoints have become more aligned since 2002 and 2007, but are still different from laboratory cutpoints using point of care methods. CONCLUSIONS: There are differences in troponin tests available across NZ. Test thresholds and units vary, even for the same test, and available diagnostic information cannot always be used to identify a troponin rise and fall. Care is needed when comparing results from different methods and when point of care instruments are used. A coordinated national approach to the development of new biochemical tests, such as troponins, may result in better use of resources and better patient care.

A polymorphism (D20S32e) close to the human melanocortin receptor 3 is associated with insulin resistance but not the metabolic syndrome.

Insulin resistance (IR) is postulated to underlie diabetes, the metabolic syndrome (MS) and cardiovascular disease (CVD). The D20S32e marker close to the melanocortin receptor-3 (hMC3-R) has been shown to be associated with IR in a large New Zealand Maori kindred, a population at high risk for MS and CVD. Here we examine the potential association of the D20S32e marker with the MS in this 60 member Maori kindred. There was a significant association between the D20S32e "B" allele and the fasting insulin component under both polygenic (beta=-5.3077; p=0.008) and common sibship effect (beta=-4.2161; p=0.03) models. No significant association between the same allele of D20S32e and the MS was observed after adjusting for age under a polygenic (p=0.103) or sibling (p=0.09) correlation model. We conclude that in this Maori kindred, the D20S32e polymorphism is significantly associated with insulin resistance but not with MS. Our data supports the hypothesis that multiple gene variants are necessary for the development of the MS.

Metabolic characteristics of patients with apparently normal fasting plasma glucose.

AIMS: To describe the prevalence of dysglycaemia in patients with fasting glucose <6.1 mmol/L. METHODS: Consecutive patients referred for OGTT between July 2002 and December 2003 to eight Diagnostic Medical Laboratory depots in the Auckland region of New Zealand were invited to participate. In addition to a standard OGTT, patients' BMI was calculated and HbA1c, fructosamine, lipids, and insulin concentrations were measured. Patients were grouped according to fasting glucose of <5.5 mmol/L=normal, 5.5-6.0 mmol/L="high fives", 6.1-6.9 mmol/L="old" impaired fasting glucose, and greater than and equal to 7 mmol//L=diabetes. RESULTS: 310 patients were studied. 111 patients had a fasting glucose of <5.5 mmol/L, and of these, 23 had IGT and 2 diabetes on OGTT; 85 patients had a fasting glucose 5.5-6.0 mmol/L, and 18 of these had IGT and 11 diabetes on OGTT; 75 patients had a fasting glucose of 6.1-6.9 mmol/L, and of these, 33 had IGT and 21 diabetes on OGTT; 39 patients had a fasting glucose greater than and equal to 7 mmol/L and 38 were confirmed diabetic on OGTT. CONCLUSION: This study suggests that the upper limit of normal fasting glucose be lowered to <5.5 mmol/L in line with Australian and American Diabetes Society guidelines.

Melanocortin-3 receptor gene variants in a Maori kindred with obesity and early onset type 2 diabetes.

Genetic studies suggest a diabetes susceptibility locus on human chromosome 20, near the melanocortin receptor-3 (MC3-R) gene. We examined the MC3-R as a candidate gene for type 2 diabetes in 12 members of a large Maori kindred with multiple affected members. The coding region of the MC3-R gene was sequenced for both diabetic and non-diabetic individuals. Two separate single base pair substitutions were found in the MC3-R coding sequence and these resulted in amino acid changes, Lysine6Threonine and Isoleucine81Valine. Neither of these MC3-R variants tracked with the presence of diabetes. Furthermore, the variant and wild type MC3-R showed similar functional coupling to adenylyl cyclase. A polymorphic marker (D20S32e) close to the human MC3-R (hMC3-R) coding sequence was investigated in a 60-member pedigree for association with diabetes and other metabolic parameters. There was an association between D20S32e genotype and fasting insulin (P=0.0085) and the insulin resistance index, HOMA-R (P=0.0042). An association was also found between genotype and HDL levels during oral glucose tolerance testing (P=0.0037). These associations were independent of BMI, age, gender and diabetes. Our data do not support a role for variations in the coding region of the hMC3-R in the development of type 2 diabetes in this Maori kindred, but suggest that a locus on chromosome 20 q, close to D20S32e, may contribute to both insulin secretion and action in the Maori kindred.