Review of the NZ schedule: what tests should be supported?

Review of the NZ schedule: what tests should be supported?

ABSTRACTS in the early years of life. In addition, once established, obesity appears to be vigorously defended.4 References 1. Stunkard AJ, Harris J...

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ABSTRACTS

in the early years of life. In addition, once established, obesity appears to be vigorously defended.4 References

1. Stunkard AJ, Harris JR, Pedersen NL, et al. The body-mass index of twins who have been reared apart. N Engl J Med 1990; 322: 1483–7. 2. Bouchard C, Tremblay A, Despre´s JP, et al. The response to long-term overfeeding in identical twins. N Engl J Med 1990; 322: 1477–82. 3. Stunkard AJ, Sørensen TI, Hanis C, et al. An adoption study of human obesity. N Engl J Med 1986; 314: 193–8. 4. Sumithran P, Prendergast LA, Delbridge E, et al. Long-term persistence of hormonal adaptations to weight loss. N Engl J Med 2011; 365: 1597–604.

PHARMACOLOGICAL AND NON-PHARMACOLOGICAL GLP-1 RECEPTOR STIMULANTS Jerry R. Greenfield1,2,3 1Department of Diabetes and Endocrinology, St Vincent’s Hospital, Darlinghurst, 2Diabetes and Obesity Research Program, Garvan Institute of Medical Research, Darlinghurst, and 3Department of Medicine, UNSW, Kensington, NSW, Australia Type 2 diabetes is characterised by insulin resistance and impaired insulin secretion. Both defects are detectable prior to the diagnosis of diabetes. The incretin system, comprising glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP), has been the target of pharmacological therapies that stimulate insulin release. Macronutrients in the distal small intestine and colon result in release of GLP-1 from intestinal L-cells and GIP from intestinal K-cells. GLP-1 is rapidly degraded (within minutes) by dipeptidyl peptidase-4 (DPP-4). GLP-1 increases insulin secretion in a glucose-dependent manner. It also causes gastric deceleration and induces satiety. Most, but not all, studies demonstrate that type 2 diabetes is characterised by GLP-1 deficiency and resistance to GIP action. Exenatide and liraglutide are GLP-1 receptor agonists that are resistant to degradation by DPP-4. Both medications have been associated with improvements in insulin secretion and glycaemic control, and significant weight loss. Recent data demonstrate that metformin and acarbose also increase GLP-1 secretion from intestinal L-cells. Amino acids, particularly glutamine, have also been shown to have GLP-1-secretagoge effects. Finally, bariatric procedures, particularly bypass and ileal interposition procedures induce GLP-1 secretion in obese subjects. HARMONISATION OF TEST PROFILES AND RETESTING INTERVALS IN THE UK W. Stuart A. Smellie Department of Biochemistry, University Hospital of North Durham, Durham, England The UK is not alone in endeavouring to harmonise test profiles and retesting intervals. Many routine profiles date back to the time of continuous flow analysers when reagent costs were negligible. However, since the switch to discrete analysers many years ago, routine core test reagents now cost around £0.07 Sterling or

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AU$0.10 each, a small sum, but large when numbers are taken into account. Different test profiles also lead to confusion. Rationalising test profiles and introducing recommended default minimum retesting intervals offers an opportunity to reduce costs and standardise approaches. This talk describes work to establish UK consensus suggestions to harmonise routine chemistry profiles,1 and minimum retesting intervals.2 For profiles, some profile content was straightforward whilst some were more difficult. Some also require far wider debate, such as the measurement of serum protein to calculate ‘globulins’ in reality mostly a screening test for monoclonal gammopathy. A shift to diagnosis-based testing would allow a tailored approach, which could harmonise practices, and requesting. References 1. Smellie WSA. Time to harmonise common laboratory test profiles. BMJ 2012; 344: e1169. 2. Lang T. National Minimum Re-testing Interval Project. http://www.acb.org. uk/docs/default-source/guidelines/acb-mri-recommendations-a4-computer. pdf?sfvrsn=2 (accessed 23/09/2013).

REVIEW OF THE NZ SCHEDULE: WHAT TESTS SHOULD BE SUPPORTED? Cam Kyle Diagnostic Medlab, Auckland, New Zealand In 2011 the New Zealand DHB Funding/Planning managers group commissioned a project reviewing laboratory test requesting practice to determine appropriate test referral criteria and exclusions, and which tests should be publically funded. The intent was to develop a National Laboratory Schedule providing more uniform test access and requesting patterns according to best practice principles. Initial terms of reference were to develop a master test list, then develop relevant referral criteria and exclusions. Particular attention was to be given to ‘tests that create issues in terms of volumes and referral appropriateness’. A Laboratory Schedule Review group was formed, with representation including DHB funding managers, pathologists, and laboratory managers. Subspecialty groups of pathologists were also convened to review tests in their discipline and provide recommendations. All tests in clinical pathology disciplines have now been classified as either Tier 1 (‘open access’) or Tier 2 (‘specialist tests where the referrer needs appropriate vocational registration or credentialing to order the test’). As per the Terms of Reference, the biochemistry group focused on developing requesting guidelines or referral criteria for those tests where volumes have increased dramatically. Examples of individual biochemistry tests will be given. The report of the working group has been adopted in late 2013 as a non-binding policy guide for DHBs across New Zealand. It is expected that referral guidelines and/or criteria for more tests will be developed in future. Progress on test coding and electronic ordering will also enable future use of this system at point of test request.

Copyright © Royal College of pathologists of Australasia. Unauthorized reproduction of this article is prohibited.

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PATHOLOGY 2014 ABSTRACT SUPPLEMENT

Pathology (2014), 46(S1)

Copyright © Royal College of pathologists of Australasia. Unauthorized reproduction of this article is prohibited.