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In 1992 the entrance channel through the tidal inlet to Tauranga Harbour, which is located along the Bay of Plenty littoral drift system, was deepened from 10 m to 14 m. The deepened channel has become a sediment trap for littoral drift bypassing and tidal current driven sediment transport through the inlet. Since 1992, there has been an increase in maintenance dredging requirements at the inlet, because of sand accumulation along the southeastern border of the entrance channel. Previous studies have identified an ebb tide-induced eddy operating on the eastern side of the ebb-jet as it exits the tidal gorge. In this article, the eddy system has been simulated with a validated two-dimensional hydrodynamic model, detailing time-varying current patterns over the ebb-tidal delta. Particular emphasis is placed on defining the trajectory of the eddy and evaluating its influence on the observed sedimentation patterns. The model results indicate the formation of opposing eddies on either side of the entrance channel, both of which are transient in nature. The centre of the eastern eddy propagates seaward along the downdrift margin of the entrance channel as the ebb-jet lengthens. Bathymetric survey residuals between 2004 and 2006 confirm significant accumulations of sediment along this downdrift margin. The evidence is consistent that the eddy system exerts a directional control over transport of sediments entrained by waves over the ebb-tidal delta. [ABSTRACT FROM AUTHOR]

When screening for carnitine uptake disorder (CUD), the New Zealand (NZ) newborn screening (NBS) service identified infants as screen-positive if they had initial and repeat free carnitine (C0) levels of less than 5.0 μmol/L. Since 2006, the NBS service has identified two infants with biochemical and genetic features consistent with neonatal CUD and nine mothers with features consistent with maternal CUD. A review of the literature suggests that these nine women reflect less than half the true prevalence and that CUD is relatively common. However, the NZ results (two infants) suggest a very low sensitivity and positive predictive value of NBS. While patients presenting with significant disease due to CUD are well described, the majority of adults with CUD are asymptomatic. Nonetheless, treatment with high-dose oral L-carnitine is recommended. Compliance with oral L-carnitine is likely to be poor long term. This may represent a specific risk as treatment could repress the usual compensatory mechanisms seen in CUD, such that a sudden discontinuation of treatment may be dangerous. L-carnitine is metabolized to trimethylamine-N-oxide (TMAO) and treated patients have extremely high plasma TMAO levels. TMAO is an independent risk factor for atherosclerosis and, thus, caution should be exercised regarding long-term treatment with high-dose carnitine of asymptomatic patients who may have a biochemical profile without disease. Due to these concerns, the NZ Newborn Metabolic Screening Programme (NMSP) initiated a review via a series of advisory and governance committees and decided to discontinue screening for CUD., (© 2018 SSIEM.)

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.

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.

Aim: To investigate the differences in the baseline cardiovascular disease (CVD) risk profiles of Pacific peoples and Europeans assessed in routine primary care practice by PREDICT, a web-based clinical decision support programme for assessing and managing CVD risk., Methods: PREDICT has been implemented in primary care practices from nine consenting PHOs in Auckland and Northland. Between 2002 and January 2009, over 70,000 CVD risk assessments were conducted. These analyses compare CVD risk factors for Pacific and European patients., Results: Baseline risk assessments were completed for 39,835 Europeans and 10,301 Pacific peoples aged 35-74 years. Over 85% of the Pacific cohort was comprised of the four main Pacific ethnic groups in New Zealand (Samoan, Tongan, Cook Island Maori and Niuean). Fijians (n=1341) were excluded from the analyses because of a likely misclassification error with Indian Fijians. On average, Pacific peoples in the PREDICT cohort were 4 years younger at the time of risk assessment than Europeans, and were overrepresented in areas of high socioeconomic deprivation. At risk assessment, Pacific men were 1.5 times as likely to be current smokers as European men, whereas similar or lower proportions of Pacific women smoked compared with European women. Pacific peoples were approximately three times more likely to have diabetes as Europeans. Pacific peoples had higher diastolic blood pressures and Pacific women had higher total cholesterol/HDL ratios. Both Pacific men and women had a significantly higher predicted risk of CVD in the next 5 years than Europeans, based on the Framingham risk score., Conclusions: The PREDICT programme has already generated the largest cohort of Pacific peoples ever to be studied in New Zealand. This comparative analysis of patients who have been screened highlights significant disparities in CVD risk factors for Pacific peoples particularly for diabetes in both sexes and for smoking in men. Targeting these modifiable risk factors will be important in addressing the widening inequalities in CVD outcomes between Pacific peoples and Europeans.

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.

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.