Topics

An update on the evidence, and implications for the medical community

The current public debate about same-sex marriage raises a number of significant issues for medical professionals and researchers in Australia. Misinformation is circulating in the public domain that children and adolescents with same-sex parents are at risk of poorer health and wellbeing than other children. An increased public health risk exists as a result of homophobic campaign messages for the entire lesbian, gay, bisexual, transgender, intersex and queer (LGBTIQ+) community, including a mental health risk for same-sex couples, their children, and young people who identify as LGBTIQ+.

1 Murdoch Childrens Research Institute, Melbourne, VIC
2 University of Melbourne, Melbourne, VIC
3 Royal Children's Hospital, Melbourne, VIC
4 Victorian Clinical Genetics Services, Melbourne, VIC
5 Children's Hospital at Westmead, Sydney, NSW
6 Liggins Institute, University of Auckland, Auckland, NZ

Correspondence: frank.oberklaid@rch.org.au

* Joint first authors

Competing interests:

No relevant disclosures.

1. Columbia Law School. What does the scholarly research say about the wellbeing of children with gay or lesbian parents? http://whatweknow.law.columbia.edu/topics/lgbt-equality/what-does-the-scholarly-research-say-about-the-wellbeing-of-children-with-gay-or-lesbian-parents (accessed Sept 2017).
2. Manning WD, Fettro MN, Lamidi E. Child well-being in same-sex parent families: review of research prepared for American Sociological Association Amicus Brief. Popul Res Policy Rev 2014; 33: 485-502.
3. Dempsey D. Same-sex parented families in Australia. Melbourne: Australian Institute of Family Studies, 2013. https://aifs.gov.au/cfca/publications/same-sex-parented-families-australia (accessed Sept 2017).
4. Qu L, Knight K, Higgins D. Same-sex couple families in Australia 2016. Melbourne: Australian Institute of Family Studies, 2016. https://aifs.gov.au/publications/same-sex-couple-families-australia (accessed Sept 2017).
5. Biblarz TJ, Stacey J. How does the gender of parents matter? J Marriage Fam 2010; 72: 3-22.
6. Carlson MJ, Corcoran ME. Family structure and children’s behavioral and cognitive outcomes. J Marriage Fam 2001; 63: 779-792.
7. Golombok S. Parenting: what really matters. London: Routledge, 2000.
8. Short E, Riggs DW, Perlesz A, et al. Lesbian, gay, bisexual and transgender (LGBT) parented families. Melbourne: The Australian Psychological Society, 2007.
9. Tasker F. Lesbian mothers, gay fathers, and their children: a review. J Dev Behav Pediatr 2005; 26: 224-240.
10. Wise S. Family structure, child outcomes and environmental mediators: an overview of the Development in Diverse Families Study. Melbourne: Australian Institute of Family Studies, 2003. https://aifs.gov.au/publications/family-structure-child-outcomes-and-environmental-mediators (accessed Sept 2017).
11. Crowl A, Ahn S, Baker J. A meta-analysis of developmental outcomes for children of same-sex and heterosexual parents. J GLBT Fam Stud 2008; 4: 385-407.
12. Miller BG, Kors S, Macfie J. No differences? Meta-analytic comparisons of psychological adjustment in children of gay fathers and heterosexual parents. Psychol Sex Orientat Gend Divers 2017; 4: 14-22.
13. Regnerus M. How different are the adult children of parents who have same-sex relationships? Findings from the New Family Structures Study. Soc Sci Res 2012; 41: 752-770.
14. Amato PR. The well-being of children with gay and lesbian parents. Soc Sci Res 2012; 41: 771-774.
15. Cheng S, Powell B. Measurement, methods, and divergent patterns: reassessing the effects of same-sex parents. Soc Sci Res 2015; 52: 615-626.
16. Crouch SR, McNair R, Waters E. Impact of family structure and socio-demographic characteristics on child health and wellbeing in same-sex parent families: a cross-sectional survey. J Paediatr Child Health 2016; 52: 499-505.
17. Crouch SR, Waters E, McNair R, et al. Parent-reported measures of child health and wellbeing in same-sex parent families: a cross-sectional survey. BMC Public Health 2014; 14: 635.
18. Crouch SR, Waters E, McNair R, et al. ACHESS–The Australian study of child health in same-sex families: background research, design and methodology. BMC Public Health 2012; 12: 646.
19. Bos HM, Gartrell NK, van Balen F, et al. Children in planned lesbian families: a cross-cultural comparison between the United States and the Netherlands. Am J Orthopsychiatry 2008; 78: 211-219.
20. Sanders EK, Chalk HM. Predictors of psychological outcomes in nonheterosexual individuals. Psi Chi J Psychol Res 2016; 21: 100-110.
21. Shapiro DN, Peterson C, Stewart AJ. Legal and social contexts and mental health among lesbian and heterosexual mothers. J Fam Psychol 2009; 23: 255-262.
22. Frost DM, Fingerhut AW. Daily exposure to negative campaign messages decreases same-sex couples’ psychological and relational well-being. Group Process Intergroup Relat 2016; 19: 477-492.
23. Hatzenbuehler ML, McLaughlin KA, Keyes KM, Hasin DS. The impact of institutional discrimination on psychiatric disorders in lesbian, gay, and bisexual populations: a prospective study. Am J Public Health 2010; 100: 452-459.
24. Morris S. Snapshot of mental health and suicide prevention statistics for LGBTI people and communities, Sydney: National LGBTI Health Alliance, 2016. http://lgbtihealth.org.au/resources/snapshot-mental-health-suicide-prevention-statistics-lgbti-people (accessed Sept 2017).
25. Daraganova G. Self-harm and suicidal behaviour of young people aged 14-15 years old. The Longitudinal Study of Australian Children annual statistical report 2016. Melbourne: Australian Institute of Family Studies, 2017. https://aifs.gov.au/publications/self-harm-and-suicidal-behaviour-young-people-aged-14-15-years-old (accessed Sept 2017).
26. Strauss P, Cook A, Winter S, et al. Trans Pathways: the mental health experiences and care pathways of trans young people. Summary of results. Perth: Telethon Kids Institute, 2017. https://www.telethonkids.org.au/our-research/brain-and-behaviour/mental-health-and-youth/youth-mental-health/trans-pathways (accessed Sept 2017).
27. Almeida J, Johnson RM, Corliss HL, et al. Emotional distress among LGBT youth: the influence of perceived discrimination based on sexual orientation. J Youth Adolesc 2009; 38: 1001-1014.
28. Raifman J, Moscoe E, Austin SB, McConnell M. Difference-in-differences analysis of the association between state same-sex marriage policies and adolescent suicide attempts. JAMA Pediatr 2017; 171: 350-356.

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Narrative review

Reducing antibiotic prescribing in Australian general practice: time for a national strategy

Christopher B Del Mar, Anna Mae Scott, Paul P Glasziou, Tammy Hoffmann, Mieke L van Driel, Elaine Beller, Susan M Phillips and Jonathan Dartnell

Med J Aust 2017; 207 (9): . || doi: 10.5694/mja17.00574
Published online: 23 October 2017

Topics

Pharmaceutical preparations

Respiratory tract diseases

General medicine

Summary

In Australia, the antibiotic resistance crisis may be partly alleviated by reducing antibiotic use in general practice, which has relatively high prescribing rates — antibiotics are mostly prescribed for acute respiratory infections, for which they provide only minor benefits.
Current surveillance is inadequate for monitoring community antibiotic resistance rates, prescribing rates by indication, and serious complications of acute respiratory infections (which antibiotic use earlier in the infection may have averted), making target setting difficult.
Categories of interventions that may support general practitioners to reduce prescribing antibiotics are: regulatory (eg, changing the default to “no repeats” in electronic prescribing, changing the packaging of antibiotics to facilitate tailored amounts of antibiotics for the right indication and restricting access to prescribing selected antibiotics to conserve them), externally administered (eg, academic detailing and audit and feedback on total antibiotic use for individual GPs), interventions that GPs can individually implement (eg, delayed prescribing, shared decision making, public declarations in the practice about conserving antibiotics, and self-administered audit), supporting GPs’ access to near-patient diagnostic testing, and public awareness campaigns.
Many unanswered clinical research questions remain, including research into optimal implementation methods.
Reducing antibiotic use in Australian general practice will require a range of approaches (with various intervention categories), a sustained effort over many years and a commitment of appropriate resources and support.

1 Centre for Research in Evidence-Based Practice, Bond University, Gold Coast, QLD
2 University of Queensland, Brisbane, QLD
3 Therapeutic Guidelines, Melbourne, VIC
4 NPS MedicineWise, Sydney, NSW

Correspondence: CDelMar@bond.edu.au

Acknowledgements:

We received funds from the National Health and Medical Research Council for the Centre for Research Excellence in Minimising Antibiotics in Acute Respiratory Infections in Primary Care.

Competing interests:

We have been commissioned by the Australian Commission for Safety and Quality and Health Care and Bupa to provide expertise and to design patient decision aids.

1. World Health Organization. Antimicrobial resistance: global report on surveillance, 2014. Geneva: WHO; 2014. http://www.who.int/drugresistance/documents/surveillancereport/en (accessed May 2017).
2. O’Neill J, Chair. Antimicrobial resistance: tackling a crisis for the health and wealth of nations. London: HM Government (UK) and Wellcome Trust; 2014. http://amr-review.org/sites/default/files/AMR%20Review%20Paper%20-%20Tackling%20a%20crisis%20for%20the%20health%20and%20wealth%20of%20nations_1.pdf (accessed Sept 2017).
3. Australian Commission on Safety and Quality in Health Care. AURA 2016: first Australian report on antimicrobial use and resistance in human health. Sydney: ACSQHC; 2016. https: //www.safetyandquality.gov.au/publications/aura-2016-first-australian-report-on-antimicroibal-use-and-resistance-in-human-health (accessed Apr 2017).
4. Høg BB, Korsgaard H, Sönksen UW, editors. DANMAP 2015 — use of antimicrobial agents and occurrence of antimicrobial resistance in bacteria from food animals, food and humans in Denmark. Danish Integrated Antimicrobial Resistance Monitoring and Research Programme; 2015. http://www.danmap.org/∼/media/Projekt%20sites/Danmap/DANMAP%20reports/DANMAP%20%202015/DANMAP%202015.ashx (accessed May 2017).
5. Tyrstrup M, Beckman A, Mölstad S, et al. Reduction in antibiotic prescribing for respiratory tract infections in Swedish primary care- a retrospective study of electronic patient records. BMC Infect Dis 2016; 16: 709.
6. Costelloe C, Metcalfe C, Lovering A, et al. Effect of antibiotic prescribing in primary care on antimicrobial resistance in individual patients: systematic review and meta-analysis. BMJ 2010; 340: c2096.
7. Fletcher-Lartey S, Yee M, Gaarslev C, Khan R. Why do general practitioners prescribe antibiotics for upper respiratory tract infections to meet patient expectations: a mixed methods study. BMJ Open 2016; 6: e012244.
8. Craig JC, Williams GJ, Jones M, et al. The accuracy of clinical symptoms and signs for the diagnosis of serious bacterial infection in young febrile children: prospective cohort study of 15 781 febrile illnesses. BMJ 2010; 340.
9. Butler CC, Rollnick S, Pill R, et al. Understanding the culture of prescribing: qualitative study of general practitioners’ and patients’ perceptions of antibiotics for sore throats. BMJ 1998; 317: 637-642.
10. Hoffmann TC, Del Mar C. Clinicians’ expectations of the benefits and harms of treatments, screening, and tests: A systematic review. JAMA Int Med 2017; 177: 407-419.
11. Coombs G, Pearson J, Nimmo G, Christiansen K. Molecular epidemiology of MRSA in the Australian community; AGAR SAP10 Conference; Brisbane 2012 http://www.agargroup.org/publications (accessed Sept 2017).
12. Del Mar C. Managing sore throat: a literature review. I. Making the diagnosis. Med J Aust 1992; 156: 572-575.
13. Britt H. Bettering the evaluation and care of health (BEACH); media statement: closure of BEACH program after 18 years [website]. Sydney: University of Sydney; 2016. http://sydney.edu.au/medicine/fmrc/media/BEACH-closure-2016-04.php (accessed May 2017).
14. Dallas A, Magin P, Morgan S, et al. Antibiotic prescribing for respiratory infections: a cross-sectional analysis of the ReCEnT study exploring the habits of early-career doctors in primary care. Fam Pract 2015; 32: 49-55.
15. NPS MedicineWise. Using MedicineInsight data: Australia’s first large-scale general practice data program [website]. Sydney: NPS MedicineWise; 2016. https://www.nps.org.au/medicine-insight/using-medicineinsight-data (accessed June 2017).
16. McCullough AR, Pollack AJ, Plejdrup Hansen M, et al. Antibiotics for acute respiratory infections in general practice: comparison of prescribing rates with guideline recommendations. Med J Aust 2017; 207: 65-69. <MJA full text>
17. Cheng AC, Turnidge J, Collignon P, et al. Control of fluoroquinolone resistance through successful regulation, Australia. Emerg Infect Dis 2012; 18: 1453-1460.
18. McGuire TM, Smith J, Del Mar C. The match between common antibiotics packaging and guidelines for their use in Australia. Aust N Z J Public Health 2015; https://doi.org/10.1111/1753-6405.12385.
19. eTG complete Melbourne Antibiotics 2017 Therapeutic Guidelines Limited Antibiotic version 15. http://www.tg.org.au/index.php?sectionid=41 (accessed June 2017).
20. Ivers N, Jamtvedt G, Flottorp S, et al. Audit and feedback: effects on professional practice and healthcare outcomes. Cochrane Database Syst Rev 2012; (6): CD000259.
21. Hallsworth M, Chadborn T, Sallis A, et al. Provision of social norm feedback to high prescribers of antibiotics in general practice: a pragmatic national randomised controlled trial. Lancet 2016; 387: 1743-1752.
22. Spurling GK, Del Mar CB, Dooley L, et al. Delayed antibiotics for respiratory infections. Cochrane Database Syst Rev 2013; (4): CD004417. (Update in press 2017).
23. Little P, Stuart B, Smith S, et al. Antibiotic prescription strategies and adverse outcome for uncomplicated lower respiratory tract infections: prospective cough complication cohort (3C) study. BMJ 2017; 357.
24. Coxeter P, Del Mar Chris B, McGregor L, et al. Interventions to facilitate shared decision making to address antibiotic use for acute respiratory infections in primary care. Cochrane Database Syst Rev 2015; (11): CD010907.
25. Hoffmann TC, Légaré F, Simmons MB, Shared decision making: what do clinicians need to know and why should they bother? Med J Aust 2014; 201: 35-39. <MJA full text>
26. Trevena L, Shepherd HL, Bonner C, et al. Shared Decision Making in Australia in 2017. Zeitschrift für Evidenz, Fortbildung und Qualität im Gesundheitswesen 2017; 123-124: 17-20.
27. Hoffmann TC, Del Mar CB. Effect of decision aids for acute respiratory infections on the use of antibiotics in general practice: a cluster randomised controlled trial. Trial ID no. ACTRN12616000644460. Australian New Zealand Clinical Trials Registry; 2016. https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=370698&isReview=true (accessed Aug 2017).
28. Meeker D, Knight TK, Friedberg MW, et al. Nudging guideline-concordant antibiotic prescribing: a randomized clinical trial. JAMA Inter Med 2014; 174: 425-431.
29. NPS MedicineWise. Management of specific respiratory tract infections: clinical e-audit. Sydney: NPS MedicineWise; 2017. https://www.nps.org.au/cpd/activities/management-of-specific-respiratory-tract-infections?p=GPs (accessed May 2017).
30. Huang Y, Chen R, Wu T, et al. Association between point-of-care CRP testing and antibiotic prescribing in respiratory tract infections: a systematic review and meta-analysis of primary care studies. Br J Gen Pract 2013; 63: e787-e794.
31. Cals JW, Butler CC, Hopstaken RM, et al. Effect of point of care testing for C reactive protein and training in communication skills on antibiotic use in lower respiratory tract infections: cluster randomised trial. BMJ 2009; 338: b1374.
32. Delaney BC, Hyde CJ, McManus RJ, et al. Systematic review of near patient test evaluations in primary care. BMJ 1999; 319: 824-827.
33. MacReady N. French campaign reduces antibiotic prescriptions. Lancet Infect Dis 2009 9: 469.
34. Wright J. Thousands of GPs rapped for high antibiotic prescribing. Australian Doctor (Sydney) 2017; 27 June. https://www.australiandoctor.com.au/news/latest-news/thousands-of-gps-rapped-for-high-antibiotic-prescr (accessed Aug 2017).
35. Hoffmann TC, Montori VM, Del Mar C. The connection between evidence-based medicine and shared decision making. JAMA 2014; 312: 1295-1296.
36. Coxeter PD, Del Mar CB, Hoffmann TC. Preparing parents to make an informed choice about antibiotic use for common acute respiratory infections in children: a randomised trial of brief decision aids in a hypothetical scenario. The Patient 2017; 10: 463-474.
37. Howie JG, Richardson IM, Gill G, Durno D. Respiratory illness and antibiotic use in general practice. J R Coll Gen Pract 1971; 21: 657-663.
38. NPS MedicineWise. Respiratory tract infections: manage your symptoms. Sydney: NPS MedicineWise; 2016. https://activities.nps.org.au/nps-order-form/Resources/NPS-MedicineWise-RTI-Action-Plan.pdf (accessed June 2017).
39. Coxeter PD, Del Mar CB, Hoffmann TC. Parents’ expectations and experiences of antibiotics for acute respiratory infections in primary care. Ann Fam Med 2017; 15: 149-154.
40. Sabuncu E, David J, Bernède-Bauduin C, et al. Significant reduction of antibiotic use in the community after a nationwide campaign in France, 2002-2007. PLoS Med 2009; 6: e1000084.
41. Bleidorn J, Gagyor I, Kochen M, et al. Symptomatic treatment (ibuprofen) or antibiotics (ciprofloxacin) for uncomplicated urinary tract infection? Results of a randomized controlled pilot trial. BMC Med 2010; 8: 30.
42. Gagyor I, Bleidorn J, Kochen MM, et al. Ibuprofen versus fosfomycin for uncomplicated urinary tract infection in women: randomised controlled trial. BMJ 2015; 351: h6544.
43. Thomas M, Del Mar C, Glasziou P. How effective are treatments other than antibiotics for acute sore throat? Br J Gen Pract 2000; 50: 817-820.
44. Hayward G, Thompson MJ, Henegan CJ, et al. Corticosteroids for relief of pain in sore throat: a systematic review and meta-analysis. BMJ 2009; 339: 2976.
45. Lim CJ, Kwong MW, Stuart RL, et al. Antibiotic prescribing practice in residential aged care facilities — health care providers’ perspectives. Med J Aust 2014; 201: 98-102. <MJA full text>
46. Public Health Agency of Sweden and National Veterinary Institute. Use of antimicrobials and occurrence of antimicrobial resistance in Sweden. UppaL, Sweden: SWEDRES/SVARM; 2013. http://www.sva.se/globalassets/redesign2011/pdf/om_sva/publikationer/swedres_svarm2013.pdf (accessed June 2017).
47. Australian Department of Health. Investing $5.9 million to tackle antimicrobial resistance [media release]. 26 May 2017. http://www.health.gov.au/internet/ministers/publishing.nsf/Content/health-mediarel-yr2017-hunt054.htm (accessed June 2017).

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Position statement summary

Cardiac Society of Australia and New Zealand position statement executive summary: coronary artery calcium scoring

Christian R Hamilton-Craig, Clara K Chow, John F Younger, V M Jelinek, Jonathan Chan and Gary YH Liew

Med J Aust 2017; 207 (8): . || doi: 10.5694/mja16.01134
Published online: 16 October 2017

Topics

Cardiovascular diseases

Diagnostic techniques and procedures

Summary

Introduction

This article summarises the Cardiac Society of Australia and New Zealand position statement on coronary artery calcium (CAC) scoring. CAC scoring is a non-invasive method for quantifying coronary artery calcification using computed tomography. It is a marker of atherosclerotic plaque burden and the strongest independent predictor of future myocardial infarction and mortality. CAC scoring provides incremental risk information beyond traditional risk calculators such as the Framingham Risk Score. Its use for risk stratification is confined to primary prevention of cardiovascular events, and can be considered as individualised coronary risk scoring for intermediate risk patients, allowing reclassification to low or high risk based on the score. Medical practitioners should carefully counsel patients before CAC testing, which should only be undertaken if an alteration in therapy, including embarking on pharmacotherapy, is being considered based on the test result.

Main recommendations

CAC scoring should primarily be performed on individuals without coronary disease aged 45–75 years (absolute 5-year cardiovascular risk of 10–15%) who are asymptomatic.
CAC scoring is also reasonable in lower risk groups (absolute 5-year cardiovascular risk, < 10%) where risk scores traditionally underestimate risk (eg, family history of premature CVD) and in patients with diabetes aged 40–60 years.
We recommend aspirin and a high efficacy statin in high risk patients, defined as those with a CAC score ≥ 400, or a CAC score of 100–399 and above the 75th percentile for age and sex.
It is reasonable to treat patients with CAC scores ≥ 100 with aspirin and a statin.
It is reasonable not to treat asymptomatic patients with a CAC score of zero.

Changes in management as a result of this statement

Cardiovascular risk is reclassified according to CAC score.
High risk patients are treated with a high efficacy statin and aspirin.
Very low risk patients (ie, CAC score of zero) do not benefit from treatment.

1 Heart and Lung Institute, The Prince Charles Hospital, Brisbane, QLD
2 Centre for Advanced Imaging, University of Queensland, Brisbane, QLD
3 The George Institute for Global Health, Sydney, NSW
4 Westmead Hospital, Sydney, NSW
5 Royal Brisbane and Women's Hospital, Brisbane, QLD
6 St Vincent's Hospital, Melbourne, VIC
7 Cardiovascular Research Centre, Australian Catholic University, Melbourne, VIC
8 Griffith University, Gold Coast, QLD
9 Gold Coast Heart Centre, Gold Coast, QLD
10 University of Adelaide, Adelaide, SA
11 Epworth HealthCare, Melbourne, VIC

Correspondence: c.hamiltoncraig@uq.edu.au

Competing interests:

No relevant disclosures.

1. Detrano R, Guerci AD, Carr JJ, et al. Coronary calcium as a predictor of coronary events in four racial or ethnic groups. N Engl J Med 2008; 358: 1336-1345.
2. Wang Z, Hoy WE. Is the Framingham coronary heart disease absolute risk function applicable to Aboriginal people? Med J Aust 2005; 182: 66-69. <MJA full text>
3. Greenland P, LaBree L, Azen SP, et al. Coronary artery calcium score combined with Framingham score for risk prediction in asymptomatic individuals. JAMA 2004; 291: 210-215.
4. Budoff MJ, Shaw LJ, Liu ST, et al. Long-term prognosis associated with coronary calcification: observations from a registry of 25,253 patients. J Am Coll Cardiol 2007; 49: 1860-1870.
5. LaMonte MJ, FitzGerald SJ, Church TS, et al. Coronary artery calcium score and coronary heart disease events in a large cohort of asymptomatic men and women. Am J Epidemiol 2005; 162: 421-429.
6. Yeboah J, Young R, McClelland RL, et al. Utility of nontraditional risk markers in atherosclerotic cardiovascular disease risk assessment. J Am Coll Cardiol 2016; 67: 139-147.
7. McClelland RL, Jorgensen NW, Budoff M, et al. 10-year coronary heart disease risk prediction using coronary artery calcium and traditional risk factors: derivation in the MESA (Multi-Ethnic Study of Atherosclerosis) with validation in the HNR (Heinz Nixdorf Recall) study and the DHS (Dallas Heart Study). J Am Coll Cardiol 2015; 66: 1643-1653.
8. Hecht H, Blaha MJ, Berman DS, et al. Clinical indications for coronary artery calcium scoring in asymptomatic patients: expert consensus statement from the SCCT. J Cardiovasc Comput Tomogr 2017; 11: 157-168.
9. Sarwar A, Shaw LJ, Shapiro MD, et al. Diagnostic and prognostic value of absence of coronary artery calcification. JACC Cardiovasc Imaging 2009; 2: 675-688.
10. Blaha M, Budoff MJ, Shaw LJ, et al. Absence of coronary artery calcification and all-cause mortality. JACC Cardiovasc Imaging 2009; 2: 692-700.
11. Shareghi S, Ahmadi N, Young E, et al. Prognostic significance of zero coronary calcium scores on cardiac computed tomography. J Cardiovasc Comput Tomogr 2007; 1: 155-159.
12. Blaha MJ, Cainzos-Achirica M, Greenland P, et al. Role of coronary artery calcium score of zero and other negative risk markers for cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis (MESA). Circulation 2016; 133: 849-858.
13. Valenti V, Ó Hartaigh B, Heo R, et al. A 15-year warranty period for asymptomatic individuals without coronary artery calcium: a prospective follow-up of 9,715 individuals. JACC Cardiovasc Imaging 2015; 8: 900-909.
14. Greenland P, Bonow RO, Brundage BH, et al. ACCF/AHA 2007 clinical expert consensus document on coronary artery calcium scoring by computed tomography in global cardiovascular risk assessment and in evaluation of patients with chest pain. J Am Coll Cardiol 2007; 49: 378-402.
15. Stone NJ, Robinson JG, Lichtenstein AH, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014; 63(25 Pt B): 2889-2934.
16. Arad Y, Spadaro LA, Roth M, et al. Treatment of asymptomatic adults with elevated coronary calcium scores with atorvastatin, vitamin C, and vitamin E: the St. Francis Heart Study Randomized Clinical Trial. J Am Coll Cardiol 2005; 46: 166-172.
17. Blaha MJ, Silverman MG, Budoff MJ. Is there a role for coronary artery calcium scoring for management of asymptomatic patients at risk for coronary artery disease? Clinical risk scores are not sufficient to define primary prevention treatment strategies among asymptomatic patients. Circ Cardiovasc Imaging 2014; 7: 398-408; discussion.
18. Antithrombotic Trialists’ Collaboration; Baigent C, Blackwell L, et al. Aspirin in the primary and secondary prevention of vascular disease: collaborative meta-analysis of individual participant data from randomised trials. Lancet 2009; 373: 1849-1860.
19. Berger JS, Roncaglioni MC, Avanzini F, et al. Aspirin for the primary prevention of cardiovascular events in women and men: a sex-specific meta-analysis of randomized controlled trials. JAMA 2006; 295: 306-313.
20. Seshasai SR, Wijesuriya S, Sivakumaran R, et al. Effect of aspirin on vascular and nonvascular outcomes: meta-analysis of randomized controlled trials. Arch Intern Med 2012; 172: 209-216.
21. Miedema MD, Duprez DA, Misialek JR, et al. Use of coronary artery calcium testing to guide aspirin utilization for primary prevention: estimates from the multi-ethnic study of atherosclerosis. Circ Cardiovasc Qual Outcomes 2014; 7: 453-460.
22. Min JK, Lin FY, Gidseg DS, et al. Determinants of coronary calcium conversion among patients with a normal coronary calcium scan: what is the “warranty period” for remaining normal? J Am Coll Cardiol 2010; 55: 1110-1117.
23. Raggi P, Callister TQ, Shaw LJ. Progression of coronary artery calcium and risk of first myocardial infarction in patients receiving cholesterol-lowering therapy. Arterioscler Thromb Vasc Biol 2004; 24: 1272-1277.
24. Budoff MJ, Hokanson JE, Nasir K, et al. Progression of coronary artery calcium predicts all-cause mortality. JACC Cardiovasc Imaging 2010; 3: 1229-1236.

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Narrative review

Atopic dermatitis: the new frontier

Victoria R Harris and Alan J Cooper

Med J Aust 2017; 207 (8): . || doi: 10.5694/mja17.00463
Published online: 16 October 2017

Topics

Immune system diseases

Pharmaceutical preparations

Skin and connective tissue diseases

Summary

Atopic dermatitis (AD) is the most common inflammatory skin condition in adults and children.
AD is a chronic disease that has a considerable negative impact on the quality of life of patients and their families.
Most cases of AD may be effectively treated with topical therapies that are directed at decreasing cutaneous inflammation and alleviating pruritus. These therapies include emollients, antihistamines, topical corticosteroids, topical calcineurin inhibitors and antimicrobial and antiseptic measures; more refractory cases may require additional oral immunosuppression (eg, cyclosporine, azathioprine, methotrexate and mycophenolate).
Improved understanding of the immune pathogenesis of AD, including the role of T helper cells and the inflammatory pathways involved, has led to breakthrough translational clinical research and treatment.
New targeted immunotherapies, such as inhibitors of interleukin (IL)-4, IL-13, IL-31, Janus associated kinase and phosphodiesterase, have had promising results from phase 2 and 3 trials for patients with moderate to severe AD.

Royal North Shore Hospital, Sydney, NSW

Correspondence: Victoria.harris@health.nsw.gov.au

Competing interests:

No relevant disclosures.

1. Hanifin JM, Reed ML. A population-based survey of eczema prevalence in the United States. Dermatitis 2007; 18: 82-91.
2. Harrop J, Chinn S, Verlato G, et al. Eczema, atopy and allergen exposure in adults: a population-based study. Clin Exp Allergy 2007; 37: 526-535.
3. Simpson E, Thomas B, Eckert L, et al. Patient burden of moderate to severe atopic dermatitis (AD): insights from a phase 2b clinical trial of dupilumab in adults. J Am Acad Dermatol 2016; 74: 491-498.
4. Wollenberg A, Orange A, Deleuran M, et al. ETFAD/EADV Eczema task force 2015 position paper on diagnosis and treatment of atopic dermatitis in adult and paediatric patients. J Eur Acad Dermatol Venereol 2016; 30: 729-747.
5. Gittler JK, Shemer A, Suarez-Farinnas M, et al. Progressive activation of T(H)2/T(H)22 cytokines and selective epidermal proteins characterises acute and chronic dermatitis. J Allergy Clin Immunol 2012; 130: 1344-1354.
6. Weidinger S, Novak N. Atopic dermatitis. Lancet 2016; 387: 1109-1122.
7. Palmer C, Irvine AD, Terron-Kwiatkowski A. Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis. Nat Genet 2006; 38: 441-446.
8. Rupnik H, Rijavec M, Korosec P. Filaggrin loss-of-function mutations are not associated with atopic dermatitis that develops in late childhood or adulthood. Br J Dermatol 2015; 172: 455-462.
9. Narkajima S, Kitoh A, Egawa G, et al. IL17A as an inducer for Th2 immune responses in murine atopic dermatitis models. J Invest Dermatol 2014; 134: 122-130.
10. Malajian D, Guttman-Yassky E. New pathogenic and therapeutic paradigms in atopic dermatitis. Cytokine 2015; 73: 311-318.
11. Hamilton JD, Ungar B, Guttman-Yassky E. Drug evaluation review: dupilumab in atopic dermatitis. Immunotherapy 2015; 7: 1043-1058.
12. Lias P, Wakefield J. Therapeutic implications of a barrier-based pathogenesis of atopic dermatitis. Clin Rev Allergy Immunol 2011; 41: 282-295.
13. Biedermann T. Dissecting the role of infections in atopic dermatitis. Acta Derm Venereol 2006; 86: 99-109.
14. Niebuhr M, et al. Staphylococcal exotoxins are strong inducers of IL22: a potential role in atopic dermatitis. J Allergy Clin Immunol 2010; 126: 1176-1183 e4
15. Deckers IA, McLean S, Linssen S, et al. Investigating international time trends in the incidence and prevalence of atopic eczema 1990–2010: a systematic review of epidemiological studies. PLoS One 2012; 7: e39803.
16. Kantor R, Silverberg JI. Environmental risk factors and their role in the management of atopic dermatitis. Expert Rev Clin Immunol 2017; 13: 15-26.
17. Thaci D, Simpson EL, Beck LA, et al. Efficacy and safety of dupilumab in adults with moderate-to-severe atopic dermatitis inadequately controlled by topical treatments: a randomised, placebo-controlled, dose-ranging phase 2b trial. Lancet 2016; 387: 40-52.
18. Simpson E, Chalmers J, Hanifin J. Emollient enhancement of the skin barrier from birth offers effective atopic dermatitis prevention. J Allergy Clin Immunol 2014; 134: 818-823.
19. Ong PY, Ohtake T, Brandt C, et al. Endogenous antimicrobial peptides and skin infections in atopic dermatitis. N Engl J Med 2002; 347: 1151-1160.
20. Francis N, Ridd M, Thomas-Jones E, et al. Oral and topical antibiotics for clinically infected eczema in children: a pragmatic randomized controlled trial in ambulatory care. Ann Fam Med 2017; 15: 124-130.
21. Huang J, Abrams M, Tlougan B, et al. Treatment of Staphylococcus aureus colonization in atopic dermatitis decreases disease severity. Paediatrics 2009; 123: e808-e814.
22. Eichenfield LF, Wynnis TL, Berger TG. Guidelines for the care and management of atopic dermatitis. J Am Acad Dermatol 2014; 71: 116-132.
23. Schmitt J, von Koletzki L, Svensson A, Apfelbacher C. Efficacy and tolerability of proactive treatment with topical corticosteroids and calcineurin inhibitors for atopic eczema: systematic review and meta-analysis of randomized controlled trials. Br J Dermatol 2011; 164: 415-428.
24. Smith SD, Stephens AM, Werren JC, Fischer GO. Treatment failure in atopic dermatitis as a result of parental health belief. Med J Aust 2013; 199: 467-469. <MJA full text>
25. Hong E, Smith SD, Fischer G. Evaluation of the atrophogenic potential of topical corticosteroids in paediatric dermatology patients. Pediatr Dermatol 2011; 28: 393-396.
26. Mooney E, Rademaker M, Dailey R, et al. Adverse effects of topical corticosteroids in paediatric eczema: Australasian consensus statement. Australas J Dermatol 2015; 56: 241-251.
27. Smith SD, Farrugia LL, Harris V, et al. Evaluation of the influence of family and friends, and the Internet on patient perceptions of long-term topical corticosteroid use. J Dermatolog Treat 2017; doi: 10.1080/09546634.2017.1306017 [Epub ahead of print].
28. Smith S, Hong E, Fearns S, et al. Corticosteroid phobia and other confounders in the treatment of childhood atopic dermatitis explored using parent focus groups. Australas J Dermatol 2010: 51: 168-174.
29. Smith S, Harris V, Lee A, et al. General practitioners’ knowledge about use of topical corticosteroids in paediatric atopic dermatitis in Australia. Aust Fam Physician 2017; 46: 335-340.
30. Eichenfield LF, Lucky AW, Boguniewicz M, et al. Safety and efficacy of pimecrolimus (ASM 981) cream 1% in the treatment of mild and moderate atopic dermatitis in children and adolescents. J Am Acad Dermatol 2002; 46: 495-504.
31. Breuer K, Werfel T, Kapp A. Safety and efficacy of topical calcineurin inhibitors in the treatment of childhood atopic dermatitis. Am J Clin Dermatol 2005; 6: 65-77.
32. Hanifin JM. Phosphodiesterase and immune dysfunction in atopic dermatitis. J Dermatol Sci 1990; 1: 1-6.
33. Hanifin JM, Chan SC, Cheng JB, et al. Type 4 phosphodiesterase inhibitors have clinical and in vitro anti-inflammatory effects in atopic dermatitis. J Invest Dermatol 1996; 107: 51-56.
34. Paller A, Tom W, Lebwohl M, et al. Efficacy and safety of crisaborole ointment, a novel, nonsteroidal phosphodiesterase 4 (PDE4) inhibitor for the topical treatment of atopic dermatitis (AD) in children and adults. J Am Acad Dermatol 2016; 75: 494-503.
35. Bissonnette R, Papp KA, Poulin Y. Topical tofacitinib for atopic dermatitis: a phase IIa randomized trial. Br J Dermatol 2016; 175: 902-911.
36. Rubel D. Biologics beyond psoriasis [unpublished presentation]. 50th Annual Scientific Meeting of the Australasian College of Dermatologist; Sydney (Australia), 6-9 May 2017.
37. Silva SH, Guedes ACM, Gontijo B, et al. Influence of narrow-band UVB phototherapy on cutaneous microbiota of children with atopic dermatitis. J Eur Acad Dermatol Venereol 2006; 20: 1114-1120.
38. Meagher LJ, Wines N, Cooper A. Atopic dermatitis: review of immunopathogenesis and advances in immunosuppressive therapy. Australas J Dermatol 2002; 43: 247-254.
39. Salek MS, Finlay AY, Luscombe DK. Cyclosporin greatly improves the quality of life of adults with severe atopic dermatitis. A randomized, double-blind, placebo-controlled trial. Br J Dermatol 1993; 129: 422-430.
40. Granlund H, Erkko P, Remitz A, et al. Comparison of cyclosporin and UVAB phototherapy for intermittent one-year treatment of atopic dermatitis. Acta Derm Venereol 2001; 81: 22-27.
41. Goujon C, Bérard F, Dahel K. Methotrexate for the treatment of adult atopic dermatitis. Eur J Dermatol 2006; 16: 155-158.
42. Meggitt SJ, Reynolds NJ. Azathioprine for atopic dermatitis. Clin Exp Dermatol 2001; 26: 369-375.
43. Yee J, Orchard D. Monitoring requirements for oral azathioprine, methotrexate and cyclosporine in a paediatric dermatology clinic and literature review. Australas J Dermatol 2016; doi: 10.1111/ajd.12526 [Epub ahead of print].
44. Kim DH, Park KY, Kim BY, et al. Anti-immunoglobulin E in the treatment of refractory atopic dermatitis. Clin Exp Dermatol 2013; 38: 496-500.
45. Noda S, Krueger J, Guttman-Yassky E. The translational revolution and use of biologics in patients with inflammatory skin diseases. J Allergy Clin Immunol 2015; 135: 324-336.
46. Ezzat MHM, Hasan ZE, Shaheen KYA. Serum measurement of inteleukin-31 (IL-31) in paediatric atopic dermatitis: elevated levels correlate with severity scoring. J Eur Acad Dermatol Venereol 2011; 25: 334-339.
47. Levy L, Urban J, King B, et al. Treatment of recalcitrant atopic dermatitis with the oral Janus Kinase Inhibitor tofacinib citrate. J Am Acad Dermatol 2015; 73: 395-399.
48. Beck L, Thaci D, Hamilton JD, et al. Dupilumab treatment in adults with moderate to severe atopic dermatitis. N Engl J Med 2014; 371: 130-139.
49. Neis MM, Peters B, Dreuw A, et al. Enhanced expression levels of IL-31 correlate with IL-4 and IL-13 in atopic and allergic contact dermatitis. J Allergy Clin Immunol 2006; 118: 930-937.
50. Thaci D, Simpson E, Bieber T, et al. Efficacy and safety of dupilumab in adults with moderate-to-severe atopic dermatitis inadequately controlled by topical treatments: a randomised, placebo-controlled, dose-ranging phase 2b trial. Lancet 2016; 387: 40-52.
51. Corren J, Lemanske RF, Hanania NA, et al. Lebrikizumab treatment in adults with asthma. N Engl J Med 2011; 365: 1088-1098.
52. Lebwohl M, Strober B, Menter A. Phase 3 studies comparing brodalumab with ustekinumab in psoriasis. N Engl J Med 2015; 373: 1318-1328.
53. Weiss D, Schaschinger M, Ristl R, et al. Ustekinumab treatment in severe atopic dermatitis: down-regulation of T-helper 2/22 expression. J Am Acad Dermatol 2017; 76: 91-97e3.
54. Samorano LP, Hanfin JM, Simpson El, et al. Inadequate response to ustekinumab in atopic dermatitis – a report of two patients. J Eur Acad Dermatol Venereol 2016; 30: 522-523.
55. Ruzicka T, Hanifin JM, Furue M, et al. Anti-interleukin-31 receptor A antibody for atopic dermatitis. N Engl J Med 2017; 376: 826-835.
56. Fleischmann R, Kremer J, Cush J. Placebo-controlled trial of tofacitinib monotherapy in rheumatoid arthritis. N Engl J Med 2012; 367: 495-507.
57. Volf E, Au S, Dumont N, et al. A phase 2, open-label, investigator-initiated study to evaluate the safety and efficacy of apremilast in subjects with recalcitrant allergic contact or atopic dermatitis. J Drugs Dermatol 2012; 11: 341.

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Research

The prevalence of monogenic diabetes in Australia: the Fremantle Diabetes Study Phase II

Timothy ME Davis, Ashley E Makepeace, Sian Ellard, Kevin Colclough, Kirsten Peters, Andrew Hattersley and Wendy A Davis

Med J Aust 2017; 207 (8): . || doi: 10.5694/mja16.01201
Published online: 16 October 2017

Topics

Endocrine system diseases

Statistics, epidemiology and research design

Abstract

Objective: To determine the prevalence of monogenic diabetes in an Australian community.

Design: Longitudinal observational study of a cohort recruited between 2008 and 2011.

Setting: Urban population of 157 000 people (Fremantle, Western Australia).

Participants: 1668 (of 4639 people with diabetes) who consented to participation (36.0% participation).

Main outcome measures: Prevalence of maturity-onset diabetes of the young (MODY) and permanent neonatal diabetes in patients under 35 years of age, from European and non-European ethnic backgrounds, who were at risk of MODY according to United Kingdom risk prediction models, and who were then genotyped for relevant mutations.

Results: Twelve of 148 young participants with European ethnic backgrounds (8%) were identified by the risk prediction model as likely to have MODY; four had a glucokinase gene mutation. Thirteen of 45 with non-European ethnic backgrounds (28%) were identified as likely to have MODY, but none had a relevant mutation (DNA unavailable for one patient). Two patients with European ethnic backgrounds (one likely to have MODY) had neonatal diabetes. The estimated MODY prevalence among participants with diagnosed diabetes was 0.24% (95% confidence interval [CI], 0.08–0.66%), an overall population prevalence of 89 cases per million; the prevalence of permanent neonatal diabetes was 0.12% (95% CI, 0.02–0.48%) and the population prevalence 45 cases per million.

Conclusions: One in 280 Australians diagnosed with diabetes have a monogenic form; most are of European ethnicity. Diagnosing MODY and neonatal diabetes is important because their management (including family screening) and prognosis can differ significantly from those for types 1 and 2 diabetes.

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1 University of Western Australia, Perth, WA
2 Fiona Stanley Hospital, Perth, WA
3 Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, United Kingdom
4 Royal Devon and Exeter NHS Foundation Trust, Exeter, United Kingdom

Correspondence: tim.davis@uwa.edu.au

Acknowledgements:

We are grateful to patients who participated in the Fremantle Diabetes Study Phase II (FDS2), and FDS2 staff for help with collecting and recording clinical information. We thank the biochemistry department at Fremantle Hospital and Health Service for performing laboratory tests. FDS2 has been supported by the National Health and Medical Research Council (NHMRC; project grants 513781 and 1042231). Timothy Davis is supported by an NHMRC Practitioner Fellowship (1058260). The funders had no role in the design and conduct of the study, or in the preparation of the manuscript and the decision to submit it for publication.

Competing interests:

No relevant disclosures.

1. Murphy R, Ellard S, Hattersley AT. Clinical implications of a molecular genetic classification of monogenic beta-cell diabetes. Nat Clin Pract Endocrinol Metab 2008; 4: 200-213.
2. Galler A, Stange T, Muller G, et al. Incidence of childhood diabetes in children aged less than 15 years and its clinical and metabolic characteristics at the time of diagnosis: data from the Childhood Diabetes Registry of Saxony, Germany. Horm Res Paediatr 2010; 74: 285-291.
3. Ledermann HM. Maturity-onset diabetes of the young (MODY) at least ten times more common in Europe than previously assumed? Diabetologia 1995; 38: 1482.
4. Shields BM, Hicks S, Shepherd MH, et al. Maturity-onset diabetes of the young (MODY): how many cases are we missing? Diabetologia 2010; 53: 2504-2508.
5. Karges B, Meissner T, Icks A, et al. Management of diabetes mellitus in infants. Nat Rev Endocrinol 2012; 8: 201-211.
6. Ellard S, Bellanné-Chantelot C, Hattersley AT; European Molecular Genetics Quality Network MODY Group. Best practice guidelines for the molecular genetic diagnosis of maturity-onset diabetes of the young. Diabetologia 2008; 51: 546-553.
7. Shields BM, McDonald TJ, Ellard S, et al. The development and validation of a clinical prediction model to determine the probability of MODY in patients with young-onset diabetes. Diabetologia 2012; 55: 1265-1272.
8. Davis TM, Bruce DG, Davis WA. Cohort profile: the Fremantle Diabetes Study. Int J Epidemiol 2013; 42: 412-421.
9. Australian Bureau of Statistics. Socio-economic indexes for areas. Updated Sept 2013. http://www.abs.gov.au/websitedbs/censushome.nsf/home/seifa (accessed Sept 2015).
10. Ellard S, Lango Allen H, De Franco E, et al. Improved genetic testing for monogenic diabetes using targeted next-generation sequencing. Diabetologia 2013; 56: 1958-1963.
11. Shackleton S, Lloyd DJ, Jackson SN, et al. LMNA, encoding lamin A/C, is mutated in partial lipodystrophy. Nat Genet 2000; 24: 153-156.
12. Heidet L, Decramer S, Pawtowski A, et al. Spectrum of HNF1B mutations in a large cohort of patients who harbor renal diseases. Clin J Am Soc Nephrol 2010; 5: 1079-1090.
13. Harvey JN, Craney L, Kelly D. Estimation of the prevalence of diagnosed diabetes from primary care and secondary care source data: comparison of record linkage with capture-recapture analysis. J Epidemiol Community Health 2002; 56: 18-23.
14. Australian Bureau of Statistics. 4820.0.55.001. Diabetes in Australia: a snapshot, 2007–08. Sept 2011. http://www.abs.gov.au/ausstats/abs@.nsf/mf/4820.0.55.001 (accessed Jan 2017).
15. Sewell MF, Presley LH, Holland SH, Catalano PM. Genetic causes of maturity onset diabetes of the young may be less prevalent in American pregnant women recently diagnosed with diabetes mellitus than in previously studied European populations. J Matern Fetal Neonatal Med 2015; 28: 1113-1115.
16. Harron KL, Feltbower RG, McKinney PA, et al. Rising rates of all types of diabetes in south Asian and non-south Asian children and young people aged 0–29 years in West Yorkshire, UK, 1991–2006. Diabetes Care 2011; 34: 652-654.
17. Al-Sheyab F, Khamaiseh E, Halaweh MA, Khaul RW. Characterization of glucokinase polymorphisms associated with maturity-onset diabetes of the young (MODY2) in Jordanian population. Tsitol Genet 2009; 43: 58-63.
18. Ng MC, Cockburn BN, Lindner TH, et al. Molecular genetics of diabetes mellitus in Chinese subjects: identification of mutations in glucokinase and hepatocyte nuclear factor-1α genes in patients with early-onset type 2 diabetes mellitus/MODY. Diabet Med 1999; 16: 956-963.
19. Misra S, Shields B, Colclough K, et al. South Asian individuals with diabetes who are referred for MODY testing in the UK have a lower mutation pick-up rate than white European people. Diabetologia 2016; 59: 2262-2265.
20. Søvik O, Irgens HU, Molnes J, et al. Monogenic diabetes mellitus in Norway. Norsk Epidemiologi 2013; 23: 55-60.
21. Lindner TH, Cockburn BN, Bell GI. Molecular genetics of MODY in Germany. Diabetologia 1999; 42: 121-123.
22. Moises RS, Reis AF, Morel V, et al. Prevalence of maturity-onset diabetes of the young mutations in Brazilian families with autosomal-dominant early-onset type 2 diabetes. Diabetes Care 2001; 24: 786-788.
23. Chevre JC, Hani EH, Boutin P, et al. Mutation screening in 18 Caucasian families suggest the existence of other MODY genes. Diabetologia 1998; 41: 1017-1023.
24. Giuffrida FM, Reis AF. Genetic and clinical characteristics of maturity-onset diabetes of the young. Diabetes Obes Metab 2005; 7: 318-326.
25. Pearson ER, Starkey BJ, Powell RJ, et al. Genetic cause of hyperglycaemia and response to treatment in diabetes. Lancet 2003; 362: 1275-1281.
26. Grulich-Henn J, Wagner V, Thon A, et al. Entities and frequency of neonatal diabetes: data from the diabetes documentation and quality management system (DPV). Diabet Med 2010; 27: 709-712.

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Research

The incidence and multiplicity rates of keratinocyte cancers in Australia

Nirmala Pandeya, Catherine M Olsen and David C Whiteman

Med J Aust 2017; 207 (8): . || doi: 10.5694/mja17.00284
Published online: 16 October 2017

Topics

Skin and connective tissue diseases

Neoplasms

Abstract

Objectives: To assess the incidence and multiplicity of keratinocyte cancers (basal cell carcinoma [BCC] and squamous cell carcinoma [SCC]) excised in Australia, and to examine variations by age, sex, state, and prior skin cancer history.

Design: Analysis of individual-level Medicare data for keratinocyte cancer treatments (identified by eight specific MBS item codes) during 2011–2014. Histological data from the QSkin prospective cohort study were analysed to estimate BCC and SCC incidence.

Setting: A 10% systematic random sample of all people registered with Medicare during 1997–2014.

Participants: People aged at least 20 years in 2011 who made at least one claim for any MBS medical service during 2011–2014 (1 704 193 individuals).

Main outcome measures: Age-standardised incidence rates (ASRs) and standardised incidence ratios (SIRs).

Results: The person-based incidence of keratinocyte cancer excisions in Australia was 1531 per 100 000 person-years; incidence increased with age, and was higher for men than women (SIR, 1.43; 95% CI, 1.42–1.45). Lesion-based incidence was 3154 per 100 000 person-years. The estimated ASRs for BCC and SCC were 770 per 100 000 and 270 per 100 000 person-years respectively. During 2011–2014, 3.9% of Australians had one keratinocyte cancer excised, 2.7% had more than one excised; 74% of skin cancers were excised from patients who had two or more lesions removed. Multiplicity was strongly correlated with age; most male patients over 70 were treated for multiple lesions. Keratinocyte cancer incidence was eight times as high among people with a prior history of excisions as among those without.

Conclusions: The incidence and multiplicity of keratinocyte cancer in Australia are very high, causing a large disease burden that has not previously been quantified.

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QIMR Berghofer Medical Research Institute, Brisbane, QLD

Correspondence: david.whiteman@qimrberghofer.edu.au

Acknowledgements:

We are grateful to Jonathan Davies and Archie De Guzman (QIMR Berghofer IT Department) for their help in obtaining and managing Medicare data and extracting the relevant subset for this analysis. This work is supported by the National Health and Medical Research Council (grant numbers 1073898, 1058522). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests:

No relevant disclosures.

1. Staples MP, Elwood M, Burton RC, et al. Non-melanoma skin cancer in Australia: the 2002 national survey and trends since 1985. Med J Aust 2006; 184: 6-10. <MJA full text>
2. Australian Institute for Health and Welfare. Health system expenditure on cancer and other neoplasms in Australia, 2008–09 (AIHW Cat. No. CAN 78; Cancer Series No. 8). Canberra: AIHW, 2013.
3. Australian Institute for Health and Welfare, Australasian Association of Cancer Registries. Cancer in Australia: an overview 2012 (AIHW Cat. No. CAN 70; Cancer Series No. 74). Canberra: AIHW, 2012.
4. Fransen M, Karahallos A, Sharma N, et al. Non-melanoma skin cancer in Australia. Med J Aust 2012; 197: 565-568. <MJA full text>
5. Olsen CM, Williams PF, Whiteman DC. Turning the tide? Changes in treatment rates for keratinocyte cancers in Australia 2000 through 2011. J Am Acad Dermatol 2014; 71: 21-26.e1.
6. Medicare Australia. Linkable de-identified 10% sample of Medicare Benefits Schedule (MBS) and Pharmaceutical Benefits Schedule (PBS) Australia. 2016. https://researchdata.ands.org.au/linkable-de-identified-schedule-pbs/673945 (accessed July 2017).
7. Olsen CM, Green AC, Neale RE, et al. Cohort profile: the QSkin Sun and Health Study. Int J Epidemiol 2012; 41: 929-929i.
8. Australian Bureau of Statistics. 3101.0. Australian demographic statistics, Mar 2013. Sept 2013. http://www.abs.gov.au/AUSSTATS/abs@.nsf/DetailsPage/3101.0Mar%202013?OpenDocument (accessed Jan 2017).
9. Thompson BS, Olsen CM, Subramaniam P, et al. Medicare claims data reliably identify treatments for basal cell carcinoma and squamous cell carcinoma: a prospective cohort study. Aust N Z J Public Health 2016; 40: 154-158.
10. National Cancer Control Initiative. The 2002 national non-melanoma skin cancer survey. A report by the NCCI Non-melanoma Skin Cancer Working Group. Melbourne: NCCI, 2003. https://canceraustralia.gov.au/publications-and-resources/cancer-australia-publications/2002-national-non-melanoma-skin-cancer-survey (accessed July 2017).
11. Whiteman DC, Thompson BS, Thrift AP, et al. A model to predict the risk of keratinocyte carcinomas. J Invest Dermatol 2016; 136: 1247-1254.
12. Rogers HW, Weinstock MA, Feldman SR, Coldiron BM. Incidence estimate of nonmelanoma skin cancer (keratinocyte carcinomas) in the US population, 2012. JAMA Dermatol 2015; 151: 1081-1086.
13. Lomas A, Leonardi-Bee J, Bath-Hextall F. A systematic review of worldwide incidence of nonmelanoma skin cancer. Br J Dermatol 2012; 166: 1069-1080.

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Editorials

Whither melanoma in Australia?

B Mark Smithers, Jeff Dunn and H Peter Soyer

Med J Aust 2017; 207 (8): . || doi: 10.5694/mja17.00740
Published online: 16 October 2017

Topics

Skin and connective tissue diseases

Neoplasms

To improve melanoma outcomes, the focus on prevention, early detection and new treatment strategies must continue

Over the past 5 years, we have seen a dramatic response to the intense biological research into late-stage, metastatic melanoma, with therapies targeting melanoma metastases and improving an individual’s immune response to the disease. This has led to an improvement in progression-free and overall survival in a group of patients who would have previously been treated with drugs that had little effect. Intense research and clinical trials continue with the aim of identifying patients most likely to respond, as well as exploring new combinations of therapies with this new paradigm for melanoma treatment.

1 University of Queensland, Brisbane, QLD
2 Princess Alexandra Hospital, Brisbane, QLD
3 Institute for Resilient Regions, University of Southern Queensland, Toowoomba, QLD
4 Cancer Council Queensland, Brisbane, QLD
5 Dermatology Research Centre, The University of Queensland Diamantina Institute, Brisbane, QLD

Correspondence: m.smithers@uq.edu.au

Competing interests:

No relevant disclosures.

1. Whiteman DC, Green AC, Olsen CM. The growing burden of invasive melanoma: projections of incidence rates and numbers of new cases in six susceptible populations through 2031. J Invest Dermatol 2016; 136: 1161-1171.
2. Green AC, Baade P, Coory M, et al. Population-based 20-year survival among people diagnosed with thin melanomas in Queensland, Australia. J Clin Oncol 2012; 30: 1462-1467.
3. Davis NC. Cutaneous melanoma: the Queensland experience. Curr Probl Surg 1976; 13: 1-63.
4. Gordon LG, Rowell D. Health system costs of skin cancer and cost-effectiveness of skin cancer prevention and screening: a systematic review. Eur J Cancer Prev 2015; 24: 141-149.
5. Ainger SA, Jagirdar K, Lee KJ, et al. Skin pigmentation genetics for the clinic. Dermatology 2017; 233: 1-15.
6. Janda M, Soyer HP. Greater precision in melanoma prevention. JAMA Dermatol 2017; 153: 18-19.
7. Janda M, Soyer HP. Automated diagnosis of melanoma. Med J Aust 2017; 207: 361-362.
8. Mar VJ, Chamberlain AJ, Kelly JW, et al. Clinical practice guidelines for the diagnosis and management of melanoma: melanomas that lack classical clinical features. Med J Aust 2017; 207: 348-350.
9. Pan Y, Adler NR, Wolfe R, et al. Nodular melanoma is less likely than superficial spreading melanoma to be histologically associated with a naevus. Med J Aust 2017; 207: 333-338.
10. Australian Institute of Health and Welfare. Skin cancer in Australia (AIHW Cat. No. CAN 96) Canberra: AIHW 2016.

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Perspectives

The rationale for action to end new cases of rheumatic heart disease in Australia

Rosemary Wyber, Judith M Katzenellenbogen, Glenn Pearson and Michael Gannon

Med J Aust 2017; 207 (8): . || doi: 10.5694/mja17.00246
Published online: 16 October 2017

Topics

Cardiovascular diseases

Indigenous health

Closing the gap in cardiovascular health

On 25 November 2016, the Australian Medical Association (AMA) launched their annual Report Card on Indigenous Health entitled A call to action to prevent new cases of rheumatic heart disease in Indigenous Australia by 2031.1 In 14 years of AMA report cards, this is the first to focus on a single pathology. The choice of rheumatic heart disease (RHD) is telling: the disease is a striking marker of inequality, a novel lens for considering health systems and a feasible target for definitive disease control.

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1 Telethon Kids Institute, University of Western Australia, Perth, WA
2 Western Australian Centre for Rural Health, University of Western Australia, Perth, WA
3 Australian Medical Association, Canberra, ACT

Correspondence: rosemary.wyber@telethonkids.org.au

Acknowledgements:

The founding members of the END RHD Coalition are the END RHD CRE, the AMA (President Michael Gannon), the National Aboriginal Community Controlled Health Organisation (Chief Executive Officer [CEO] Patricia Turner), RHDAustralia (Director Bart Currie), Aboriginal Medical Services Alliance Northern Territory (CEO John Paterson) and the National Heart Foundation of Australia (CEO John Kelly).

Competing interests:

No relevant disclosures.

1. Australian Medical Association. AMA Report Card on Indigenous Health: a call to action to prevent new cases of rheumatic heart disease in Indigenous Australia by 2031. Canberra: AMA; 2016. https://ama.com.au/system/tdf/documents/2016-AMA-Report-Card-on-Indigenous-Health.pdf?file=1&type=node&id=45394 (accessed Aug 2017).
2. Carapetis J, Beaton A, Cunningham MW, et al. Acute rheumatic fever and rheumatic heart disease. Nat Rev Dis Primers 2016; 2: 15084.
3. Australian Institute of Health and Welfare. Australian Burden of Disease Study: impact and causes of illness and death in Aboriginal and Torres Strait Islander people, 2011. Canberra: AIHW; 2011. http://www.aihw.gov.au/WorkArea/DownloadAsset.aspx?id=60129557109 (accessed Aug 2017).
4. Roberts KV, Maguire GP, Brown A, et al. Rheumatic heart disease in Indigenous children in northern Australia: differences in prevalence and the challenges of screening. Med J Aust 2015; 203: 221. <MJA full text>
5. Australian Bureau of Statistics. 2075.0 — Census of population and housing. 2011 census counts: Aboriginal and Torres Strait Islanders peoples. Canberra: ABS; 2012. http://www.abs.gov.au/ausstats/abs@.nsf/Lookup/2075.0main+features32011 (accessed Aug 2017).
6. Australian Health Ministers’ Advisory Council. Aboriginal and Torres Strait Islander Health Performance Framework 2014 Report. Canberra: Commonwealth of Australia; 2015. https://www.pmc.gov.au/sites/default/files/publications/Aboriginal_and_Torres_Strait_Islander_HPF_2014%20-%20edited%2016%20June2015.pdf (accessed Aug 2017).
7. Australian Institute of Health and Welfare. Rheumatic heart disease and acute rheumatic fever in Australia: 1996–2012 (Cardiovascular Disease Series No.36). Canberra: AIHW; 2013. http://www.aihw.gov.au/WorkArea/DownloadAsset.aspx?id=60129542747 (accessed Aug 2017).
8. Roberts K, Maguire G, Brown A, et al. Echocardiographic screening for rheumatic heart disease in high low risk Australian children. Circulation 2014; 129: 1953-1961.
9. Smith MT, Zurynski Y, Lester-Smith D, et al. Rheumatic fever. identification, management and secondary prevention. Aust Fam Physician 2012; 41: 31-35.
10. McDonald M, Brown A, Noonan S, Carapetis JR. Preventing recurrent rheumatic fever: the role of register based programmes. Heart 2005; 91: 1131-1133.
11. Watkins DA, Mvundura M, Nordet P, Mayosi BM. A cost-effectiveness analysis of a program to control rheumatic fever and rheumatic heart disease in Pinar del Rio, Cuba. PLoS One 2015; 10: e0121363.
12. Baker MG, McDonald A, Zang J, Howden-Chapman P. Infectious diseases attributable to household crowding in New Zealand: a systematic review and burden of disease estimate. Wellington, New Zealand: He Kainga Oranga/Housing and Health Research Programme, University of Otago; 2013. http://www.healthyhousing.org.nz/wp-content/uploads/2010/01/HH-Crowding-ID-Burden-25-May-2013.pdf (accessed Aug 2017).
13. Zühlke LJ, Karthikeyan G. Primary prevention for rheumatic fever: progress, obstacles, and opportunities. Glob Heart 2013; 8: 221-226.
14. Ministry of Health New Zealand. Progress on the Better Public Services rheumatic fever target: Ministry of Health New Zealand, 2017. http://www.health.govt.nz/about-ministry/what-we-do/strategic-direction/better-public-services/previous-bps-target-reduce-rheumatic-fever (accessed Apr 2017).

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Guideline summary

Clinical practice guidelines for the diagnosis and management of melanoma: melanomas that lack classical clinical features

Victoria J Mar, Alex J Chamberlain, John W Kelly, William K Murray and John F Thompson

Med J Aust 2017; 207 (8): . || doi: 10.5694/mja17.00123
Published online: 9 October 2017

Topics

Skin and connective tissue diseases

General medicine

Abstract

Introduction: A Cancer Council Australia multidisciplinary working group is currently revising and updating the 2008 evidence-based clinical practice guidelines for the management of cutaneous melanoma. While there have been many recent improvements in treatment options for metastatic melanoma, early diagnosis remains critical to reducing mortality from the disease. Improved awareness of the atypical presentations of this common malignancy is required to achieve this. A chapter of the new guidelines was therefore developed to aid recognition of atypical melanomas.

Main recommendations: Because thick, life-threatening melanomas may lack the more classical ABCD (asymmetry, border irregularity, colour variegation, diameter > 6 mm) features of melanoma, a thorough history of the lesion with regard to change in morphology and growth over time is essential. Any lesion that is changing in morphology or growing over a period of more than one month should be excised or referred for prompt expert opinion.

Changes in management as a result of the guidelines: These guidelines provide greater emphasis on improved recognition of the atypical presentations of melanoma, in particular nodular, desmoplastic and acral lentiginous subtypes, with particular awareness of hypomelanotic and amelanotic lesions.

1 Victorian Melanoma Service, Alfred Health, Melbourne, VIC
2 Monash University, Melbourne, VIC
3 Peter MacCallum Cancer Centre, Melbourne, VIC
4 Melanoma Institute Australia, Sydney, NSW
5 University of Sydney, Sydney, NSW

Correspondence: victoria.mar@monash.edu

Acknowledgements:

We thank Laura Wuellner, Jutta von Dincklage and Jackie Buck from the Cancer Council Australia Clinical Guidelines Network for their assistance in this work. Development of the new Clinical Practice Guidelines for the Diagnosis and Management of Melanoma was funded by Cancer Council Australia and Melanoma Institute Australia, with additional support from the Skin Cancer College Australasia.

Competing interests:

No relevant disclosures.

1. Smithson SL, Pan Y, Mar V. Differing trends in thickness and survival between nodular and non-nodular primary cutaneous melanoma in Victoria, Australia. Med J Aust 2015; 203: 20. <MJA full text>
2. Baade PD, English DR, Youl PH, et al. The relationship between melanoma thickness and time to diagnosis in a large population-based study. Arch Dermatol 2006; 142: 1422-1427.
3. Criscione VD, Weinstock MA. Melanoma thickness trends in the United States, 1988-2006. J Invest Dermatol 2010; 130: 793-797.
4. Demierre MF, Chung C, Miller DR, Geller AC. Early detection of thick melanomas in the United States: beware of the nodular subtype. Arch Dermatol 2005; 141: 745-750.
5. Lipsker DM, Hedelin G, Heid E, et al. Striking increase of thin melanomas contrasts with stable incidence of thick melanomas. Arch Dermatol 1999; 135: 1451-1456.
6. Mar V, Roberts H, Wolfe R, et al. Nodular melanoma: a distinct clinical entity and the largest contributor to melanoma deaths in Victoria, Australia. J Am Acad Dermatol 2013; 68: 568-575.
7. Tejera-Vaquerizo A, Mendiola-Fernandez M, Fernandez-Orland A, Herrera-Ceballos E. Thick melanoma: the problem continues. J Eur Acad Dermatol Venereol 2008; 22: 575-579.
8. Baumert J, Schmidt M, Giehl KA, et al. Time trends in tumour thickness vary in subgroups: analysis of 6475 patients by age, tumour site and melanoma subtype. Melanoma Res 2009; 19: 24-30.
9. Bergenmar M, Ringborg U, Mansson Brahme E, Brandberg Y. Nodular histogenetic type – the most significant factor for thick melanoma: implications for prevention. Melanoma Res 1998; 8: 403-411.
10. Chamberlain AJ, Fritschi L, Giles GG, et al. Nodular type and older age as the most significant associations of thick melanoma in Victoria, Australia. Arch Dermatol 2002; 138: 609-614.
11. Kelly JW, Chamberlain AJ, Staples MP, McAvoy B. Nodular melanoma. No longer as simple as ABC. Aust Fam Physician 2003; 32: 706-709.
12. Lin MJ, Mar V, McLean C, et al. Diagnostic accuracy of malignant melanoma according to subtype. Australas J Dermatol 2014; 55: 35-42.
13. Liu WD, Dowling JP, Murray WK, et al. Amelanotic primary cutaneous melanoma – clinical associations and dynamic evolution. Australas J Dermatol 2006; 47(Suppl 1): A1.
14. Menzies SW, Kreusch J, Byth K, et al. Dermoscopic evaluation of amelanotic and hypomelanotic melanoma. Arch Dermatol 2008; 144: 1120-1127.
15. Chamberlain AJ, Fritschi L, Kelly JW. Nodular melanoma: patients’ perceptions of presenting features and implications for earlier detection. J Am Acad Dermatol 2003; 48: 694-701.
16. Phan A, Dalle S, Touzet S, et al. Dermoscopic features of acral lentiginous melanoma in a large series of 110 cases in a white population. Br J Dermatol 2010; 162: 765-771.
17. McCormack CJ, Conyers RK, Scolyer RA, et al. Atypical Spitzoid neoplasms: a review of potential markers of biological behavior including sentinel node biopsy. Melanoma Res 2014; 24: 437-447.
18. Pizzichetta MA, Talamini R, Stanganelli I, et al. Amelanotic/hypomelanotic melanoma: clinical and dermoscopic features. Br J Dermatol 2004; 150: 1117-1124.
19. Menzies SW, Moloney FJ, Byth K, et al. Dermoscopic evaluation of nodular melanoma. JAMA Dermatol 2013; 149: 699-709.
20. Betti R, Martino P, Vergani R, et al. Nodular melanomas: analysis of the casistic and relationship with thick melanomas and diagnostic delay. J Dermatol 2008; 35: 643-650.
21. Richard MA, Grob JJ, Avril MF, et al. Delays in diagnosis and melanoma prognosis (II): the role of doctors. Int J Cancer 2000; 89: 280-285.
22. Richard MA, Grob JJ, Avril MF, et al. Delays in diagnosis and melanoma prognosis (I): the role of patients. Int J Cancer 2000; 89: 271-279.
23. Lin MJ, Mar V, McLean C, Kelly JW. An objective measure of growth rate using partial biopsy specimens of melanomas that were initially misdiagnosed. J Am Acad Dermatol 2014; 71: 691-697.
24. Liu W, Dowling JP, Murray WK, et al. Rate of growth in melanomas: characteristics and associations of rapidly growing melanomas. Arch Dermatol 2006; 142: 1551-1558.
25. Martorell-Calatayud A, Nagore E, Botella-Estrada R, et al. Defining fast-growing melanomas: reappraisal of epidemiological, clinical, and histological features. Melanoma Res 2011; 21: 131-138.
26. Tejera-Vaquerizo A, Barrera-Vigo MV, Lopez-Navarro N, Herrera-Ceballos E. Growth rate as a prognostic factor in localized invasive cutaneous melanoma. J Eur Acad Dermatol Venereol 2010; 24: 147-154.

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Narrative review

Diagnosis and management of irritable bowel syndrome: a guide for the generalist

Ecushla C Linedale and Jane M Andrews

Med J Aust 2017; 207 (7): . || doi: 10.5694/mja17.00457
Published online: 2 October 2017

Topics

Digestive system diseases

General medicine

Summary

Irritable bowel syndrome (IBS) and other functional gastrointestinal disorders (FGIDs) are so prevalent they cannot reasonably have their diagnoses and management based within specialty care. However, delayed diagnosis, lengthy wait times for specialist review, overinvestigation and lack of clear diagnostic communication are common.
The intrusive symptoms of IBS and other FGIDs impair patient functioning and reduce quality of life, and come with significant costs to individual patients and the health care system, which could be reduced with timely diagnosis and effective management.
IBS, in particular, is no longer a diagnosis of exclusion, and there are now effective dietary and psychological therapies that may be accessed without specialist referral.
The faecal calprotectin test is widely available, yet not on the Medical Benefits Schedule, and a normal test result reliably discriminates between people with IBS and patients who warrant specialist referral.

1 University of Adelaide, Adelaide, SA
2 Royal Adelaide Hospital, Adelaide, SA

Correspondence: Jane.Andrews@sa.gov.au

Competing interests:

Jane Andrews has worked as a speaker, consultant and advisory board member for Abbott, AbbVie, Allergan, Celgene, Ferring Pharmaceuticals, Takeda Pharmaceuticals, MSD, Shire, Janssen, Hospira and Pfizer; and has received research funding from Abbott, AbbVie, Ferring Pharmaceuticals, MSD, Shire and Janssen.

1. Cremonini F, Talley NJ. Irritable bowel syndrome: epidemiology, natural history, health care seeking and emerging risk factors. Gastroenterol Clin North Am 2005; 34: 189-204.
2. Halder SL, Locke GR, Schleck CD, et al. Natural history of functional gastrointestinal disorders: a 12-year longitudinal population-based study. Gastroenterology 2007; 133: 799-807.e1.
3. Talley NJ. Functional gastrointestinal disorders as a public health problem. Neurogastroenterol Motil 2008; 20 Suppl 1: 121-129.
4. Spiegel BM. The burden of IBS: looking at metrics. Curr Gastroenterol Rep 2009; 11: 265-269.
5. Enck P, Dubois D, Marquis P. Quality of life in patients with upper gastrointestinal symptoms: results from the Domestic/International Gastroenterology Surveillance Study (DIGEST). Scand J Gastroenterol Suppl 1999; 231: 48-54.
6. Fullerton S. Functional digestive disorders (FDD) in the year 2000—economic impact. Eur J Surg 1998; 164(S12): 62-64.
7. Nellesen D, Yee K, Chawla A, et al. A systematic review of the economic and humanistic burden of illness in irritable bowel syndrome and chronic constipation. J Manag Care Pharm 2013; 19: 755-764.
8. Longstreth GF, Wilson A, Knight K, et al. Irritable bowel syndrome, health care use, and costs: a US managed care perspective. Am J Gastroenterol 2003; 98: 600-607.
9. Rome Foundation. Rome IV collection, 2016. Raleigh: Rome Foundation; 2016. http://theromefoundation.org/rome-iv (accessed July 2017).
10. Locke GR, Zinsmeister AR, Fett SL, et al. Overlap of gastrointestinal symptom complexes in a US community. Neurogastroenterol Motil 2005; 17: 29-34.
11. Chang JY, Locke GR, McNally MA, et al. Impact of functional gastrointestinal disorders on survival in the community. Am J Gastroenterol 2010; 105: 822-832.
12. Knott VE, Holtmann G, Turnbull DA, et al. M1253 patients’ satisfaction with specialist gastroenterologist consultation for irritable bowel syndrome (IBS) and health care utilisation: exploring the role of patient expectations. Gastroenterology 2009; 136: A-382.
13. Longstreth GF, Thompson WG, Chey WD, et al. Functional bowel disorders. Gastroenterology 2006; 130: 1480-1491.
14. Cash BD, Schoenfeld P, Chey WD. The utility of diagnostic tests in irritable bowel syndrome patients: a systematic review. Am J Gastroenterol 2002; 97: 2812-2819.
15. Spiegel BM, Farid M, Esrailian E, et al. Is irritable bowel syndrome a diagnosis of exclusion? A survey of primary care providers, gastroenterologists, and IBS experts. Am J Gastroenterol 2010; 105: 848-858.
16. Hungin AP, Molloy-Bland M, Claes R, et al. Systematic review: the perceptions, diagnosis and management of irritable bowel syndrome in primary care — a Rome Foundation working team report. Aliment Pharmacol Ther 2014; 40: 1133-1145.
17. National Institute for Care and Excellence. Irritable bowel syndrome in adults: quality standard [QS114]. 2016. London: NICE; 2016. https://www.nice.org.uk/guidance/qs114 (accessed Feb 2016).
18. Talley NJ, Boyce PM, Jones M. Predictors of health care seeking for irritable bowel syndrome: a population based study. Gut 1997; 41: 394-398.
19. Levy RL, Korff M, Whitehead WE, et al. Costs of care for irritable bowel syndrome patients in a health maintenance organization. Am J Gastroenterol 2001; 96: 3122-3129.
20. Patel RP, Petitta A, Fogel R, et al. The economic impact of irritable bowel syndrome in a managed care setting. J Clin Gastroenterol 2002; 35: 14-20.
21. Halpert A, Drossman D. Biopsychosocial issues in irritable bowel syndrome. J Clin Gastroenterol 2005; 39: 665.
22. Manning AP, Thompson WG, Heaton KW, Morris AF. Towards positive diagnosis of the irritable bowel. Br Med J 1978; 2: 653-654.
23. Mearin F, Lacy BE. Diagnostic criteria in IBS: useful or not? Neurogastroenterol Motil 2012; 24: 791-801.
24. Spiller R, Camilleri M, Longstreth GF. Do the symptom-based, Rome criteria of irritable bowel syndrome lead to better diagnosis and treatment outcomes? Clin Gastroenterol Hepatol 2010; 8: 129-136.
25. Mikocka-Walus A, Turnbull D, Moulding N, et al. Psychological comorbidity and complexity of gastrointestinal symptoms in clinically diagnosed irritable bowel syndrome patients. J Gastroenterol Hepatol 2008; 23(7 Pt 1): 1137-1143.
26. Lacy BE, Mearin F, Chang L, et al. Bowel disorders. Gastroenterology 2016; 150: 1393-1407.e5.
27. Clinical Insights Steering Committee. Differentiating IBS and IBD, 2013. Melbourne: Crohn’s and Colitis Australia; 2014. https://www.crohnsandcolitis.com.au/site/wp-content/uploads/Differentiating-Between-IBS-and-IBD.pdf (accessed May 2017).
28. Choosing Wisely Australia [website]. Sydney: 2016. http://www.choosingwisely.org.au (accessed Dec 2016).
29. Royal Australasian College of Physicians. Evolve: evaluating evidence, enhancing efficiencies. Sydney: RACP. http://www.evolve.edu.au (accessed May 2017).
30. Turvill J. High negative predictive value of a normal faecal calprotectin in patients with symptomatic intestinal disease. Frontline Gastroenterol 2011; 3: 21-28.
31. National Institute for Health and Care Excellence. Faecal calprotectin diagnostic tests for inflammatory diseases of the bowel. Diagnostics guidance [DG11]. London: NICE; 2013. https://www.nice.org.uk/guidance/dg11 (accessed Sept 2016).
32. Zayyat R, Appleby RN, Logan RPH. Can we improve the negative predictive value of faecal calprotectin for the diagnosis of IBS in primary care? Gut 2011; 60(Suppl 1): A49-A50.
33. Williamson KD, Steveling K, Holtmann G, et al. Clinical triage for colonoscopy is useful in young women. Intern Med J 2015; 45: 492-496.
34. Lau MSY, Ford AC. Do lay people accept a positive diagnosis of irritable bowel syndrome? Gastroenterology 2015; 149: 252-253.
35. Collins J, Farrall E, Turnbull DA, et al. Do we know what patients want? The doctor-patient communication gap in functional gastrointestinal disorders. Clin Gastroenterol Hepatol 2009; 7: 1252-1254, 4.e1-e2.
36. Linedale EC, Chur-Hansen A, Mikocka-Walus A, et al. Uncertain diagnostic language affects further studies, endoscopies, and repeat consultations for patients with functional gastrointestinal disorders Clin Gastroenterol Hepatol 2016; 14: 1735-1741.
37. Linedale EC, Shahzad M, Mikocka-Walus A, et al. Referrals to a tertiary hospital: a clinical snapshot of patients with functional gastrointestinal disorders and effectiveness of primary care management. United European Gastroenterol J 2016; 3(5 Suppl 1): 484.
38. Harkness EF, Grant L, O’Brien SJ, et al. Using read codes to identify patients with irritable bowel syndrome in general practice: a database study. BMC Fam Pract 2013; 14: 183.
39. Stone L. Blame, shame and hopelessness: medically unexplained symptoms and the ‘heartsink’ experience. Aust Fam Physician 2014; 43: 191-195.
40. Dalrymple J, Bullock I. Diagnosis and management of irritable bowel syndrome in adults in primary care: summary of NICE guidance. BMJ 2008; 336: 556-558.
41. Hu LY, Ku FC, Lu T, et al. Risk of cancer in patients with irritable bowel syndrome: a nationwide population-based study. Ann Epidemiol 2015; 25: 924-928.
42. Hsiao CW, Huang WY, Ke TW, et al. Association between irritable bowel syndrome and colorectal cancer: a nationwide population-based study. Eur J Intern Med 2014; 25: 82-86.
43. Adeniji OA, Barnett CB, Di Palma JA. Durability of the diagnosis of irritable bowel syndrome based on clinical criteria. Dig Dis Sci 2004; 49: 572-574.
44. Owens DM, Nelson DK, Talley NJ. The irritable bowel syndrome: long-term prognosis and the physician-patient interaction. Ann Intern Med 1995; 122: 107.
45. Youn YH, Kim HC, Lim HC, et al. Long-term clinical course of post-infectious irritable bowel syndrome after shigellosis: a 10-year follow-up study. Neurogastroenterol Motil 2016; 22: 490.
46. Nørgaard M, Farkas DK, Pedersen L, et al. Irritable bowel syndrome and risk of colorectal cancer: a Danish nationwide cohort study. Br J Cancer 2011; 104: 1202.
47. Olafsdottir LB, Gudjonsson H, Jonsdottir HH, et al. Stability of the irritable bowel syndrome and subgroups as measured by three diagnostic criteria – a 10-year follow-up study. Aliment Pharmacol Ther 2010; 32: 670-680.
48. Madisch A, Holtmann G, Plein K, et al. Treatment of irritable bowel syndrome with herbal preparations: results of a double-blind, randomized, placebo-controlled, multi-centre trial. Aliment Pharmacol Ther 2004; 19: 271-279.
49. Ford AC, Quigley EM, Lacy BE, et al. Effect of antidepressants and psychological therapies, including hypnotherapy, in irritable bowel syndrome: systematic review and meta-analysis. Am J Gastroenterol 2014; 109: 1350-1365; quiz 66.
50. Liu JP, Yang M, Liu YX, et al. Herbal medicines for treatment of irritable bowel syndrome. Cochrane Database Syst Rev 2006; (1): CD004116.
51. Moayyedi P, Quigley EM, Lacy BE, et al. The effect of fiber supplementation on irritable bowel syndrome: a systematic review and meta-analysis. Am J Gastroenterol 2014; 109: 1367-1374.
52. Marsh A, Eslick EM, Eslick GD. Does a diet low in FODMAPs reduce symptoms associated with functional gastrointestinal disorders? A comprehensive systematic review and meta-analysis. Eur J Nutr 2016; 55: 897-906.
53. Enck P, Junne F, Klosterhalfen S, et al. Therapy options in irritable bowel syndrome. Eur J Gastroenterol Hepatol 2010; 22: 1402-1411.
54. Lackner JM, Mesmer C, Morley S, et al. Psychological treatments for irritable bowel syndrome: a systematic review and meta-analysis. J Consult Clin Psychol 2004; 72: 1100-1113.
55. Ford AC, Talley NJ, Schoenfeld PS, et al. Efficacy of antidepressants and psychological therapies in irritable bowel syndrome: systematic review and meta-analysis. Gut 2009; 58: 367-378.
56. Prior A, Colgan SM, Whorwell PJ. Changes in rectal sensitivity after hypnotherapy in patients with irritable bowel syndrome. Gut 1990; 31: 896-898.
57. Whorwell PJ, Houghton LA, Taylor EE, et al. Physiological effects of emotion: assessment via hypnosis. Lancet 1992; 340: 69-72.
58. Gonsalkorale WM, Houghton LA, Whorwell PJ. Hypnotherapy in irritable bowel syndrome: a large-scale audit of a clinical service with examination of factors influencing responsiveness. Am J Gastroenterol 2002; 97: 954-961.
59. Whorwell PJ, Prior A, Faragher EB. Controlled trial of hypnotherapy in the treatment of severe refractory irritable-bowel syndrome. Lancet 1984; 2: 1232-1234.
60. Vidakovic-Vukic M. Hypnotherapy in the treatment of irritable bowel syndrome: methods and results in Amsterdam. Scand J Gastroenterol Suppl 1999; 230: 49-51.
61. Calvert EL, Houghton LA, Cooper P, et al. Long-term improvement in functional dyspepsia using hypnotherapy. Gastroenterology 2002; 123: 1778-1785.
62. Gibson PR, Shepherd SJ. Evidence-based dietary management of functional gastrointestinal symptoms: The FODMAP approach. J Gastroenterol Hepatol 2010; 25: 252-258.
63. Halmos EP, Power VA, Shepherd SJ, et al. A diet low in FODMAPs reduces symptoms of irritable bowel syndrome. Gastroenterology 2014; 146: 67-75.
64. Shepherd SJ, Lomer MCE, Gibson PR. Short-chain carbohydrates and functional gastrointestinal disorders. Am J Gastroenterol 2013; 108: 707-717.
65. Barrett JS, Gearry RB, Muir JG, et al. Dietary poorly absorbed, short-chain carbohydrates increase delivery of water and fermentable substrates to the proximal colon. Aliment Pharmacol Ther 2010; 31: 874-882.
66. O’ Keeffe M, Lomer MC. Who should deliver the low FODMAP diet and what educational methods are optimal: a review. J Gastroenterol Hepatol 2017; 32 Suppl 1: 23-26.
67. Barrett JS. How to institute the low-FODMAP diet. J Gastroenterol Hepatol 2017; 32 Suppl 1: 8-10.
68. Tuck C, Barrett J. Re-challenging FODMAPs: the low FODMAP diet phase two. J Gastroenterol Hepatol 2017; 32 Suppl 1: 11-15.
69. Ford AC, Lacy BE, Talley NJ. Irritable bowel syndrome. N Engl J Med 2017; 376: 2566-2578.

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The kids are OK: it is discrimination not same-sex parents that harms children

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Reducing antibiotic prescribing in Australian general practice: time for a national strategy

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Cardiac Society of Australia and New Zealand position statement executive summary: coronary artery calcium scoring

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The incidence and multiplicity rates of keratinocyte cancers in Australia

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Whither melanoma in Australia?

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The rationale for action to end new cases of rheumatic heart disease in Australia

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Clinical practice guidelines for the diagnosis and management of melanoma: melanomas that lack classical clinical features

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Diagnosis and management of irritable bowel syndrome: a guide for the generalist

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The kids are OK: it is discrimination not same-sex parents that harms children

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Reducing antibiotic prescribing in Australian general practice: time for a national strategy

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Cardiac Society of Australia and New Zealand position statement executive summary: coronary artery calcium scoring

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Summary

Atopic dermatitis: the new frontier

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The prevalence of monogenic diabetes in Australia: the Fremantle Diabetes Study Phase II

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The incidence and multiplicity rates of keratinocyte cancers in Australia

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Whither melanoma in Australia?

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The rationale for action to end new cases of rheumatic heart disease in Australia

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Clinical practice guidelines for the diagnosis and management of melanoma: melanomas that lack classical clinical features

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Diagnosis and management of irritable bowel syndrome: a guide for the generalist

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