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    COVID‐19, children and schools: overlooked and at risk

    Zoë Hyde
    Med J Aust 2020; 213 (10): . || doi: 10.5694/mja2.50823
    Published online: 16 November 2020

    Children may be more susceptible than originally thought and could play a role in community transmission

    An early cause for hope in the coronavirus disease 2019 (COVID‐19) pandemic was the observation that children are much less likely to experience severe illness than adults.1 This remains true, but has created a perception that children are less susceptible to infection and do not play a substantial role in transmission. In Australia, this perception has been reinforced by assurances from the Prime Minister that schools are safe and that physical distancing is unnecessary in this setting.2 However, emerging research suggests greater caution is needed.

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      Mental health and COVID‐19: are we really all in this together?

      Patrick McGorry
      Med J Aust 2020; 213 (10): . || doi: 10.5694/mja2.50834
      Published online: 9 November 2020

      The pandemic is a vast, expanding disaster with no end in sight, producing chronic stress, disruption, and multiple losses

      The coronavirus disease 2019 (COVID‐19) pandemic has been a once‐in‐100‐years event. The scale of the disaster overshadows all others in living memory. Most disasters are focal and time‐limited. This one will span a considerable period of time and the economic impact will last years. This means the mental health effects will be deeper and more sustained than in other disasters. A survey during the first month of the pandemic in Australia assessed the nation's “temperature” early, as reported in this issue of the Journal.1 This survey and other information2,3 confirm that the initial mental health impact has been severe, and worse may be coming. Scientific models predicted that Australia would face a second curve of mental ill health and suicide,4,5 and this has now clearly arrived. We have been willing to turn our society and lives upside down to flatten the COVID‐19 curve. The same commitment is now required to flatten the mental health curve.

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      • 1 Orygen, Melbourne, VIC
      • 2 Centre for Youth Mental Health, the University of Melbourne, Melbourne, VIC


      Correspondence: pmcgorry@unimelb.edu.au
      Acknowledgements: 

      I am supported by a National Health and Medical Research Council Senior Principal Research Fellowship (1155508).

      Competing interests:

      No relevant disclosures.

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        Understanding the diagnosis of prostate cancer

        Xuan Rui S Ong, Dominic Bagguley, John W Yaxley, Arun A Azad, Declan G Murphy and Nathan Lawrentschuk
        Med J Aust 2020; 213 (9): . || doi: 10.5694/mja2.50820
        Published online: 2 November 2020

        Summary

        • Prostate cancer continues to be the most commonly diagnosed cancer, and the second leading cause of cancer death among Australian men.
        • Prostate‐specific antigen testing is personalised (not dichotomous in nature) and its interpretation should take into account the patient's age, symptoms, previous results and medication (eg, 5‐α reductase inhibitors such as dutasteride).
        • Multiparametric magnetic resonance imaging of the prostate has been proven to have a 93% sensitivity for detecting clinically significant prostate cancer. It has the potential to decrease unnecessary prostate biopsies by around 27%.
        • International Society of Urological Pathology (ISUP) grade 1 (Gleason score 6) has been shown to have very little, if any, risk of metastasis
        • ISUP grade 1 (Gleason score 3 +3 = 6) and low percentage ISUP grade 2 (Gleason score 3 + 4 [< 10%] = 7) can be offered active surveillance. The goal of active surveillance is to defer treatment but is still curative when required.
        • With better imaging (magnetic resonance imaging and emerging prostate‐specific membrane antigen positron emission tomography–computed tomography) and transperineal prostate biopsy, more men can be offered screening after discussion of risks and benefits, knowing that overdiagnosis has been minimised and radical treatment is reserved for only the most aggressive disease.

        • 1 EJ Whitten Prostate Cancer Research Centre at Epworth, Melbourne, VIC
        • 2 University of Melbourne, Melbourne, VIC
        • 3 University of Queensland, Brisbane, QLD
        • 4 Royal Brisbane and Women's Hospital, Brisbane, QLD
        • 5 Peter MacCallum Cancer Centre, Melbourne, VIC


        Correspondence: lawrentschuk@gmail.com
        Competing interests:

        No relevant disclosures.

        • 1. Roberts MJ, Papa N, Perera M, et al. A contemporary, nationwide analysis of surgery and radiotherapy treatment for prostate cancer. BJU Int 2019; 124 (Suppl 1): 31–36.
        • 2. Australian Institute of Health and Welfare. Cancer in Australia 2019 (Cancer Series No. 119; Cat. No. CAN 123). Canberra: AIHW, 2019. https://www.aihw.gov.au/getmedia/8c9fcf52-0055-41a0-96d9-f81b0feb98cf/aihw-can-123.pdf.aspx?inline=true (viewed Aug 2020).
        • 3. Wang MC, Valenzuela LA, Murphy GP, Chu TM. Purification of a human prostate specific antigen. J Urol 2017; 197 (2 Suppl): S148–S152.
        • 4. Stamey TA, Yang N, Hay AR, et al. Prostate‐specific antigen as a serum marker for adenocarcinoma of the prostate. N Engl J Med 1987; 317: 909–916.
        • 5. Lilja H, Ulmert D, Vickers AJ. Prostate‐specific antigen and prostate cancer: prediction, detection and monitoring. Nat Rev Cancer 2008; 8: 268–278.
        • 6. Thompson IM, Pauler DK, Goodman PJ, et al. Prevalence of prostate cancer among men with a prostate‐specific antigen level < or =4.0 ng per milliliter. N Engl J Med 2004; 350: 2239–2246.
        • 7. Loeb S, Roehl KA, Antenor JA, et al. Baseline prostate‐specific antigen compared with median prostate‐specific antigen for age group as predictor of prostate cancer risk in men younger than 60 years old. Urology 2006; 67: 316–320.
        • 8. Litchfield MJ, Cumming RG, Smith DP, et al. Prostate‐specific antigen levels in men aged 70 years and over: findings from the CHAMP study. Med J Aust 2012; 196: 395–398. https://www.mja.com.au/journal/2012/196/6/prostate-specific-antigen-levels-men-aged-70-years-and-over-findings-champ-study.
        • 9. Oesterling JE, Jacobsen SJ, Chute CG, et al. Serum prostate‐specific antigen in a community‐based population of healthy men. Establishment of age‐specific reference ranges. JAMA 1993; 270: 860–864.
        • 10. Morgan TO, Jacobsen SJ, McCarthy WF, et al. Age‐specific reference ranges for serum prostate‐specific antigen in black men. N Engl J Med 1996; 335: 304–310.
        • 11. Partin AW, Criley SR, Subong EN, et al. Standard versus age‐specific prostate specific antigen reference ranges among men with clinically localized prostate cancer: a pathological analysis. J Urol 1996; 155: 1336–1339.
        • 12. DeAntoni EP, Crawford ED, Oesterling JE, et al. Age‐ and race‐specific reference ranges for prostate‐specific antigen from a large community‐based study. Urology 1996; 48: 234–239.
        • 13. Anderson JR, Strickland D, Corbin D, et al. Age‐specific reference ranges for serum prostate‐specific antigen. Urology 1995; 46: 54–57.
        • 14. Oesterling JE, Jacobsen SJ, Klee GG, et al. Free, complexed and total serum prostate specific antigen: the establishment of appropriate reference ranges for their concentrations and ratios. J Urol 1995; 154: 1090–1095.
        • 15. Borer JG, Sherman J, Solomon MC, et al. Age specific prostate specific antigen reference ranges: population specific. J Urol 1998; 159: 444–448.
        • 16. D'Amico AV, Roehrborn CG. Effect of 1 mg/day finasteride on concentrations of serum prostate‐specific antigen in men with androgenic alopecia: a randomised controlled trial. Lancet Oncol 2007; 8: 21–25.
        • 17. Marks LS, Andriole GL, Fitzpatrick JM, et al. The interpretation of serum prostate specific antigen in men receiving 5alpha‐reductase inhibitors: a review and clinical recommendations. J Urol 2006; 176: 868–74.
        • 18. Marks LS, Andriole GL, Fitzpatrick JM, et al. The interpretation of serum prostate specific antigen in men receiving 5α‐reductase inhibitors: a review and clinical recommendations. J Urol 2006; 176: 868–874.
        • 19. Thompson IM, Chi C, Ankerst DP, et al. Effect of finasteride on the sensitivity of PSA for detecting prostate cancer. J Natl Cancer Inst 2006; 98: 1128–1133.
        • 20. Helfand BT, Anderson CB, Fought A, et al. Postoperative PSA and PSA velocity identify presence of prostate cancer after various surgical interventions for benign prostatic hyperplasia. Urology 2009; 74: 177–183.
        • 21. Nadler RB, Humphrey PA, Smith DS, et al. Effect of inflammation and benign prostatic hyperplasia on elevated serum prostate specific antigen levels. J Urol 1995; 154 (2 Pt 1): 407–413.
        • 22. Neal DE, Jr., Clejan S, Sarma D, Moon TD. Prostate specific antigen and prostatitis. I. Effect of prostatitis on serum PSA in the human and nonhuman primate. Prostate 1992; 20: 105–111.
        • 23. Washino S, Okochi T, Saito K, et al. Combination of prostate imaging reporting and data system (PI‐RADS) score and prostate‐specific antigen (PSA) density predicts biopsy outcome in prostate biopsy naïve patients. BJU Int 2017; 119: 225–233.
        • 24. Vickers AJ, Brewster SF. PSA velocity and doubling time in diagnosis and prognosis of prostate cancer. Br J Med Surg Urol 2012; 5: 162–168.
        • 25. Pannek J, Rittenhouse HG, Chan DW, et al. The use of percent free prostate specific antigen for staging clinically localized prostate cancer. J Urol 1998; 159: 1238–1242.
        • 26. Catalona WJ, Partin AW, Slawin KM, et al. Use of the percentage of free prostate‐specific antigen to enhance differentiation of prostate cancer from benign prostatic disease: a prospective multicenter clinical trial. JAMA 1998; 279: 1542–1547.
        • 27. Catalona WJ, Partin AW, Sanda MG, et al. A multicenter study of [‐2] pro‐prostate specific antigen combined with prostate specific antigen and free prostate specific antigen for prostate cancer detection in the 2.0 to 10.0 ng/ml prostate specific antigen range. J Urol 2011; 185: 1650–1655.
        • 28. Vickers AJ, Cronin AM, Aus G, et al. A panel of kallikrein markers can reduce unnecessary biopsy for prostate cancer: data from the European Randomized Study of Prostate Cancer Screening in Göteborg, Sweden. BMC Med 2008; 6: 19.
        • 29. Russo GI, Regis F, Castelli T, et al. A systematic review and meta‐analysis of the diagnostic accuracy of Prostate Health Index and 4‐kallikrein panel score in predicting overall and high‐grade prostate cancer. Clin Genitourin Cancer 2017; 15: 429–439.e1.
        • 30. Mottet N, van den Bergh R, Briers E. EAU‐EANM-ESTRO‐ESUR-SIOG guidelines on prostate cancer. Eur Urol 2019; 75: 889–890.
        • 31. Grossman DC, Curry SJ, Owens DK, et al. Screening for prostate cancer: US Preventive Services Task Force recommendation statement. JAMA 2018; 319: 1901–1913.
        • 32. Prostate Cancer Foundation of Australia and Cancer Council Australia. Clinical practice guidelines for PSA testing and early management of test‐detected prostate cancer. 2015. https://wiki.cancer.org.au/australia/Guidelines:PSA_Testing (viewed Aug 2020).
        • 33. Catalona WJ, Richie JP, Ahmann FR, et al. Comparison of digital rectal examination and serum prostate specific antigen in the early detection of prostate cancer: results of a multicenter clinical trial of 6,630 men. J Urol 2017; 197 (2 Suppl): S200–S207.
        • 34. Patel MI, Kakala B, Beattie K. Teaching medical students digital rectal examination: a randomized study of simulated model vs rectal examination volunteers. BJU Int 2019; 124 (Suppl 1): 14–18.
        • 35. Schröder FH, Kruger AB, Rietbergen J, et al. Evaluation of the digital rectal examination as a screening test for prostate cancer. J Natl Cancer Inst 1998; 90: 1817–1823.
        • 36. Carvalhal GF, Smith DS, Mager DE, et al. Digital rectal examination for detecting prostate cancer at prostate specific antigen levels of 4 ng/ml or less. J Urol 1999; 161: 835–839.
        • 37. Thompson J, Van Leeuwen P, Moses D, et al. The diagnostic performance of multiparametric magnetic resonance imaging to detect significant prostate cancer. J Urol 2016; 195: 1428–1435.
        • 38. Ahmed HU, El‐Shater Bosaily A, Brown LC, et al. Diagnostic accuracy of multi‐parametric MRI and TRUS biopsy in prostate cancer (PROMIS): a paired validating confirmatory study. Lancet 2017; 389: 815–822.
        • 39. Hu Y, Ahmed HU, Carter T, et al. A biopsy simulation study to assess the accuracy of several transrectal ultrasonography (TRUS)‐biopsy strategies compared with template prostate mapping biopsies in patients who have undergone radical prostatectomy. BJU Int 2012; 110: 812–820.
        • 40. Norberg M, Egevad L, Holmberg L, et al. The sextant protocol for ultrasound‐guided core biopsies of the prostate underestimates the presence of cancer. Urology 1997; 50: 562–566.
        • 41. Kasivisvanathan V, Rannikko AS, Borghi M, et al. MRI‐targeted or standard biopsy for prostate‐cancer diagnosis. N Engl J Med 2018; 378: 1767–1777.
        • 42. Weinreb JC, Barentsz JO, Choyke PL, et al. PI‐RADS prostate imaging ‐ reporting and data system: 2015, version 2. Eur Urol 2016; 69: 16–40.
        • 43. Park SY, Jung DC, Oh YT, et al. Prostate cancer: PI‐RADS version 2 helps preoperatively predict clinically significant cancers. Radiology 2016; 280: 108–116.
        • 44. Padhani AR, Weinreb J, Rosenkrantz AB, et al. Prostate Imaging‐Reporting and Data System Steering Committee: PI‐RADS v2 status update and future directions. Eur Urol 2019; 75: 385–396.
        • 45. Woo S, Kim SY, Lee J, et al. PI‐RADS version 2 for prediction of pathological downgrading after radical prostatectomy: a preliminary study in patients with biopsy‐proven Gleason Score 7 (3+4) prostate cancer. Eur Radiol 2016; 26: 3580–3587.
        • 46. Hansen NL, Barrett T, Kesch C, et al. Multicentre evaluation of magnetic resonance imaging supported transperineal prostate biopsy in biopsy‐naïve men with suspicion of prostate cancer. BJU Int 2018; 122: 40–49.
        • 47. Wei TC, Lin TP, Chang YH, et al. Transrectal ultrasound‐guided prostate biopsy in Taiwan: A nationwide database study. J Chin Med Assoc 2015; 78: 662–665.
        • 48. Grummet JP, Weerakoon M, Huang S, et al. Sepsis and ‘superbugs’: should we favour the transperineal over the transrectal approach for prostate biopsy? BJU Int 2014; 114: 384–388.
        • 49. Symons JL, Huo A, Yuen CL, et al. Outcomes of transperineal template‐guided prostate biopsy in 409 patients. BJU Int 2013; 112: 585–593.
        • 50. Yaxley AJ, Yaxley JW, Thangasamy IA, et al. Comparison between target magnetic resonance imaging (MRI) in‐gantry and cognitively directed transperineal or transrectal‐guided prostate biopsies for Prostate Imaging‐Reporting and Data System (PI‐RADS) 3‐5 MRI lesions. BJU Int 2017; 120 (Suppl 3): 43–50.
        • 51. Stefanova V, Buckley R, Flax S, et al. Transperineal prostate biopsies using local anesthesia: experience with 1,287 patients. prostate cancer detection rate, complications and patient tolerability. J Urol 2019; 201: 1121–1126.
        • 52. Grummet J, Gorin MA, Popert R, et al. “TREXIT 2020”: why the time to abandon transrectal prostate biopsy starts now. Prostate Cancer Prostatic Dis 2020; 23: 62–65.
        • 53. Gleason DF, Mellinger GT. Prediction of prognosis for prostatic adenocarcinoma by combined histological grading and clinical staging. J Urol 2017; 197 (2 Suppl): S134–S139.
        • 54. Humphrey PA, Moch H, Cubilla AL, et al. The 2016 WHO classification of tumours of the urinary system and male genital organs – Part B: prostate and bladder tumours. Eur Urol 2016; 70: 106–119.
        • 55. Epstein JI, Egevad L, Amin MB, et al. The 2014 International Society of Urological Pathology (ISUP) Consensus Conference on Gleason Grading of Prostatic Carcinoma: definition of grading patterns and proposal for a new grading system. Am J Surg Pathol 2016; 40: 244–252.
        • 56. Epstein JI, Zelefsky MJ, Sjoberg DD, et al. A contemporary prostate cancer grading system: a validated alternative to the Gleason score. Eur Urol 2016; 69: 428–435.
        • 57. Ross AE, Marchionni L, Vuica‐Ross M, et al. Gene expression pathways of high grade localized prostate cancer. Prostate 2011; 71: 1568–1577.
        • 58. Ross HM, Kryvenko ON, Cowan JE, et al. Do adenocarcinomas of the prostate with Gleason score (GS) ≤6 have the potential to metastasize to lymph nodes? Am J Surg Pathol 2012; 36: 1346–1352.
        • 59. Amin A, Scheltema MJ, Shnier R, et al. The Magnetic Resonance Imaging in Active Surveillance (MRIAS) trial: use of baseline multiparametric magnetic resonance imaging and saturation biopsy to reduce the frequency of surveillance prostate biopsies. J Urol 2020; 203: 910–917.
        • 60. Hofman MS, Lawrentschuk N, Francis RJ, et al. Prostate‐specific membrane antigen PET‐CT in patients with high‐risk prostate cancer before curative‐intent surgery or radiotherapy (proPSMA): a prospective, randomised, multicentre study. Lancet 2020; 395: 1208–1216.
        • 61. Kalapara AA, Nzenza T, Pan HYC, et al. Detection and localisation of primary prostate cancer using (68) gallium prostate‐specific membrane antigen positron emission tomography/computed tomography compared with multiparametric magnetic resonance imaging and radical prostatectomy specimen pathology. BJU Int 2020; 126: 83–90.
        • 62. Scheltema MJ, Chang JI, Stricker PD, et al. Diagnostic accuracy of 68Ga‐prostate‐specific membrane antigen (PSMA) positron‐emission tomography (PET) and multiparametric (mp) MRI to detect intermediate‐grade intra‐prostatic prostate cancer using whole‐mount pathology: impact of the addition of 68Ga‐PSMA PET to mp MRI. BJU Int 2019; 124: 42–49.
        • 63. Donato P, Morton A, Yaxley J, et al. (68)Ga‐PSMA PET/CT better characterises localised prostate cancer after MRI and transperineal prostate biopsy: is (68)Ga‐PSMA PET/CT guided biopsy the future? Eur J Nucl Med Mol Imaging 2020; 47: 1843–1851.
        • 64. Amin A, Blazevski A, Thompson J, et al. Protocol for the PRIMARY clinical trial, a prospective, multicentre, cross‐sectional study of the additive diagnostic value of gallium‐68 prostate‐specific membrane antigen positron‐emission tomography/computed tomography to multiparametric magnetic resonance imaging in the diagnostic setting for men being investigated for prostate cancer. BJU Int 2020; 125: 515–524.
        • 65. Rao K, Manya K, Azad A, et al. Uro‐oncology multidisciplinary meetings at an Australian tertiary referral centre–impact on clinical decision‐making and implications for patient inclusion. BJU Int 2014; 114: 50–54.
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          Opioid stewardship can reduce inappropriate prescribing of opioids at hospital discharge

          Stephan A Schug
          Med J Aust 2020; 213 (9): . || doi: 10.5694/mja2.50818
          Published online: 2 November 2020

          The associated risks, particularly that of long term use, are underestimated, and appropriate measures are needed

          Before 1990, opioids were primarily used to treat severe acute and cancer pain. In the subsequent 30 years, opioids have been increasingly used for treating chronic non‐malignant pain; prescribing has increased exponentially in the developed world, particularly in the United States, but also in Canada and Australia.1 Regrettably, this has not only resulted in poor outcomes for patients living with chronic pain; the analgesic efficacy of opioids for this indication are limited, and they do not improve, and often reduce, function and quality of life.2 Further, diversion of prescribed opioids and their misuse have risen in parallel with increased prescribing, leading to higher numbers of overdoses deaths. In Australia, about 1100 people died following opioid overdoses during 2018, and 75% of cases involved prescription opioids (similar to the number of deaths from car accidents in that year).3


          • University of Western Australia, Perth, WA


          Correspondence: stephan.schug@uwa.edu.au
          Competing interests:

          The Anaesthesiology Unit of the University of Western Australia and Stephan Schug personally (since his retirement in October 2019) have received research and travel funding and speaking and consulting honoraria from Grünenthal, Indivior, Mundipharma, Pfizer, iX Biopharma, Seqirus, Xgene, Biogen, Luye Pharma and Foundry during the past 36 months.

          • 1. Häuser W, Schug S, Furlan AD. The opioid epidemic and national guidelines for opioid therapy for chronic noncancer pain: a perspective from different continents. Pain Rep 2017; 2: e599.
          • 2. Busse JW, Wang L, Kamaleldin M, et al. Opioids for chronic noncancer pain: a systematic review and meta‐analysis. JAMA 2018; 320: 2448–2460.
          • 3. Man N, Chrzanowska A, Dobbins T, et al. Trends in drug‐induced deaths in Australia, 1997–2018 (Drug Trends Bulletin Series). Sydney: National Drug and Alcohol Research Centre, UNSW Sydney, 2019. https://ndarc.med.unsw.edu.au/resource/trends-drug-induced-deaths-australia-1997-2018 (viewed Sept 2020).
          • 4. Roughead EE, Lim R, Ramsay E, et al. Persistence with opioids post discharge from hospitalisation for surgery in Australian adults: a retrospective cohort study. BMJ Open 2019; 9: e023990.
          • 5. Schug SA, Palmer GM, Scott DA, et al, editors. Acute pain management: scientific evidence. 4th edition. Melbourne: Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine, 2015; here: pp. 365–368.
          • 6. Macintyre PE, Huxtable CA, Flint SL, Dobbin MD. Costs and consequences: a review of discharge opioid prescribing for ongoing management of acute pain. Anaesth Intensive Care 2014; 42: 558–574.
          • 7. Stewart JE, Tuffin PH, Kay J, et al. The effect of guideline implementation on discharge analgesia prescribing (two years on). Anaesth Intensive Care 2019; 47: 40–44.
          • 8. McAnally H. Rationale for and approach to preoperative opioid weaning: a preoperative optimization protocol. Perioper Med (Lond) 2017; 6: 19.
          • 9. Stark N, Kerr S, Stevens J. Prevalence and predictors of persistent post‐surgical opioid use: a prospective observational cohort study. Anaesth Intensive Care 2017; 45: 700–706.
          • 10. Shah A, Hayes CJ, Martin BC. Characteristics of initial prescription episodes and likelihood of long‐term opioid use: United States, 2006–2015. MMWR Morb Mortal Wkly Rep 2017; 66: 265–269.
          • 11. Australian and New Zealand College of Anaesthetists, Faculty of Pain Medicine. Position statement on the use of slow‐release opioid preparations in the treatment of acute pain. Mar 2018. https://www.anzca.edu.au/getattachment/d9e2a7c5-0f17-42d3-bda7-c6dae7e55ced/Position-statement-on-the-use-of-slow-release-opioid-preparations-in-the-treatmentofacute-pain (viewed Oct 2020).
          • 12. Brat GA, Agniel D, Beam A, et al. Postsurgical prescriptions for opioid naive patients and association with overdose and misuse: retrospective cohort study. BMJ 2018; 360: j5790.
          • 13. Therapeutic Goods Administration. Return your unused opioids: resource kit. July 2019. https://www.tga.gov.au/publication/return-your-unused-opioids-resource-kit (viewed Sept 2020).
          • 14. Hopkins R, Bui T, Konstantatos AH, et al. Educating junior doctors and pharmacists to reduce discharge prescribing of opioids for surgical patients: a cluster randomised controlled trial. Med J Aust 2020; 213: 417–423.
          • 15. Stevens J, Trimboli A, Samios P, et al. A sustainable method to reduce postoperative oxycodone discharge prescribing in a metropolitan tertiary referral hospital. Anaesthesia 2019; 74: 292–299.
          • 16. Allen ML, Leslie K, Parker AV, et al. Post‐surgical opioid stewardship programs across Australia and New Zealand: current situation and future directions. Anaesth Intensive Care 2019; 47: 548–552.
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            Yellow nails syndrome: complete triad

            Adrián López Alba and Agustín Blanco Echevarría
            Med J Aust 2020; 213 (9): . || doi: 10.5694/mja2.50807
            Published online: 2 November 2020

            An 83‐year‐old male non‐smoker presented with chronic purulent cough. On physical examination, xanthonychia (yellow discoloration), onychauxis (thickened nails), onycholisis (separation of the nail from the nail bed), enhanced transverse curvature, and scleronychia (hardening and thickening of the nails) were observed (Figure, A). He had a 5 year history of decreased longitudinal nail growth and progressive adult onset bilateral lower limb lymphoedema. Findings on computed tomography scan demonstrated severe bilateral cystic bronchiectasis (Figure, B and C). Yellow nails syndrome is a disorder characterised by the triad of yellow thickened nails, lymphoedema and respiratory manifestations, typically chronic cough, bronchiectasis or pleural effusion. All three features appear in only 27–60% of patients.1 Treatment is symptomatic and includes antibiotic prescription for bronchiectasis and oral vitamin E alone or combined with triazole antifungals for yellow nails, achieving partial to complete responses.1


            • Hospital Universitario 12 de Octubre, Madrid, Spain


            Correspondence: alalba@salud.madrid.org
            Acknowledgements: 

            We thank the patient who made the article possible.

            Competing interests:

            No relevant disclosures.

            • 1. Vignes S, Baran R. Yellow nail syndrome: a review. Orphanet J Rare Dis 2017; 12: 42.
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              Gut microbiota‐derived trimethylamine N‐oxide is associated with poor prognosis in patients with heart failure

              Wensheng Li, Anqing Huang, Hailan Zhu, Xinyue Liu, Xiaohui Huang, Yan Huang, Xiaoyan Cai, Jianhua Lu and Yuli Huang
              Med J Aust 2020; 213 (8): . || doi: 10.5694/mja2.50781
              Published online: 19 October 2020

              Abstract

              Objective: Gut microbiota‐produced trimethylamine N‐oxide (TMAO) is a risk factor for cardiovascular events. However, conflicting findings regarding the link between plasma TMAO level and prognosis for patients with heart failure have been reported. We examined the association of plasma TMAO concentration with risk of major adverse cardiac events (MACEs) and all‐cause mortality in patients with heart failure.

              Study design: Meta‐analysis of prospective clinical studies.

              Data sources: We searched electronic databases (PubMed, EMBASE) for published prospective studies examining associations between plasma TMAO level and MACEs and all‐cause mortality in adults with heart failure.

              Data synthesis: Hazard ratios (HRs) with 95% confidence intervals for associations between TMAO level and outcomes were estimated in random effects models. In seven eligible studies including a total of 6879 patients (median follow‐up, 5.0 years) and adjusted for multiple risk factors, higher plasma TMAO level was associated with greater risks of MACEs (TMAO tertile 3 v tertile 1: HR, 1.68; 95% CI, 1.44–1.96; per SD increment: HR, 1.26; 95% CI, 1.18–1.36) and of all‐cause mortality (TMAO tertile 3 v tertile 1: HR, 1.67; 95% CI, 1.17–2.38; per SD increment: HR, 1.26; 95% CI, 1.07–1.48). Higher TMAO level was also associated with greater risk of MACEs after adjusting for estimated glomerular filtration rate (eGFR; six studies included); however, the heterogeneity of studies in which risk was adjusted for eGFR was significant (I2 = 76%).

              Conclusions: Elevated plasma TMAO level in patients with heart failure is associated with poorer prognoses. This association is only partially mediated by renal dysfunction.

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              • 1 Shunde Hospital of Southern Medical University, Foshan (Guangdong), China
              • 2 George Institute for Global Health, Sydney, NSW


              Acknowledgements: 

              Our investigation was supported by the Science and Technology Innovation Project in Foshan, Guangdong (FS0AA‐KJ218‐1301‐0006), the Clinical Research Startup Program of Shunde Hospital, Southern Medical University (CRSP2019001, CRSP2019008), the self‐financing Science and Technology Plan Project of Foshan, Guangdong (Medical Science and Technology Research Key Project; 2018AB00208), and the Medical Science and Technology Research Foundation of Guangdong Province (A2018209).We thank Julia Jenkins (Liwen Bianji, Edanz Editing China; www.liwenbianji.cn/ac), for editing the English text of our manuscript.

              Competing interests:

              No relevant disclosures.

              • 1. Ziaeian B, Fonarow GC. Epidemiology and aetiology of heart failure. Nat Rev Cardiol 2016; 13: 368–378.
              • 2. Benjamin EJ, Muntner P, Alonso A, et al. American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics: 2019 update. A report from the American Heart Association. Circulation 2019; 139: e56–e528.
              • 3. Tang W, Bäckhed F, Landmesser U, Hazen SL. Intestinal microbiota in cardiovascular health and disease. J Am Coll Cardiol 2019; 73: 2089–2105.
              • 4. Brown JM, Hazen SL. Microbial modulation of cardiovascular disease. Nat Rev Microbiol 2018; 16: 171–181.
              • 5. Antza C, Stabouli S, Kotsis V. Gut microbiota in kidney disease and hypertension. Pharmacol Res 2018; 130: 198–203.
              • 6. Kanbay M, Onal EM, Afsar B, et al. The crosstalk of gut microbiota and chronic kidney disease: role of inflammation, proteinuria, hypertension, and diabetes mellitus. Int Urol Nephrol 2018; 50: 1453–1466.
              • 7. Qi J, You T, Li J, et al. Circulating trimethylamine N‐oxide and the risk of cardiovascular diseases: a systematic review and meta‐analysis of 11 prospective cohort studies. J Cell Mol Med 2018; 22: 185–194.
              • 8. Schiattarella GG, Sannino A, Toscano E, et al. Gut microbe‐generated metabolite trimethylamine‐N-oxide as cardiovascular risk biomarker: a systematic review and dose‐response meta‐analysis. Eur Heart J 2017; 38: 2948–2956.
              • 9. Heianza Y, Ma W, Manson JE, et al. Gut microbiota metabolites and risk of major adverse cardiovascular disease events and death: a systematic review and meta‐analysis of prospective studies. J Am Heart Assoc 2017; 6: e004947.
              • 10. Tang WH, Hazen SL. Microbiome, trimethylamine N‐oxide, and cardiometabolic disease. Transl Res 2017; 179: 108–115.
              • 11. Tang WHW, Wang Z, Fan Y, et al. Prognostic value of elevated levels of intestinal microbe‐generated metabolite trimethylamine‐N‐oxide in patients with heart failure: refining the gut hypothesis. J Am Coll Cardiol 2014; 64: 1908–1914.
              • 12. Tang WHW, Wang Z, Shrestha K, et al. Intestinal microbiota‐dependent phosphatidylcholine metabolites, diastolic dysfunction, and adverse clinical outcomes in chronic systolic heart failure. J Card Fail 2015; 21: 91–96.
              • 13. Trøseid M, Ueland T, Hov JR, et al. Microbiota‐dependent metabolite trimethylamine‐N-oxide is associated with disease severity and survival of patients with chronic heart failure. J Intern Med 2015; 277: 717–726.
              • 14. Suzuki T, Heaney LM, Bhandari SS, et al. Trimethylamine N‐oxide and prognosis in acute heart failure. Heart 2016; 102: 841–848.
              • 15. Schuett K, Kleber ME, Scharnagl H, et al. Trimethylamine‐N-oxide and heart failure with reduced versus preserved ejection fraction. J Am Coll Cardiol 2017; 70: 3202–3204.
              • 16. Suzuki T, Yazaki Y, Voors AA, et al. Association with outcomes and response to treatment of trimethylamine N‐oxide in heart failure: results from BIOSTAT‐CHF. Eur J Heart Fail 2019; 21: 877–886.
              • 17. Salzano A, Israr MZ, Yazaki Y, et al. Combined use of trimethylamine N‐oxide with BNP for risk stratification in heart failure with preserved ejection fraction: findings from the DIAMONDHFpEF study. Eur J Prev Cardiol 2019; https://doi.org/10.1177/2047487319870355. [online ahead of print].
              • 18. Stroup DF, Berlin JA, Morton SC, et al. Meta‐analysis of observational studies in epidemiology: a proposal for reporting. Meta‐analysis Of Observational Studies in Epidemiology (MOOSE) group. JAMA 2000; 283: 2008–2012.
              • 19. Wells GA, Shea B, O'Connell D, et al. The Newcastle–Ottawa Scale (NOS) for assessing the quality of nonrandomised studies in meta‐analyses. http://www.ohri.ca/programs/clinical_epidemiology/oxford.asp (viewed Oct 2019).
              • 20. Chowdhury R, Stevens S, Gorman D, et al. Association between fish consumption, long chain omega 3 fatty acids, and risk of cerebrovascular disease: systematic review and meta‐analysis. BMJ 2012; 345: e6698.
              • 21. Huang Y, Cai X, Mai W, et al. Association between prediabetes and risk of cardiovascular disease and all cause mortality: systematic review and meta‐analysis. BMJ 2016; 355: i5953.
              • 22. Pasini E, Aquilani R, Testa C, et al. Pathogenic gut flora in patients with chronic heart failure. JACC Heart Fail 2016; 4: 220–227.
              • 23. Cui X, Ye L, Li J, et al. Metagenomic and metabolomic analyses unveil dysbiosis of gut microbiota in chronic heart failure patients. Sci Rep 2018; 8: 635.
              • 24. An D, Zhan Q, Bai Y, et al. The clinical significance of serum trimethylamine N‐oxide (TMAO) level in patients with chronic heart failure [abstract]. J Am Coll Cardiol 2017; 70: C145.
              • 25. Tomlinson J, Wheeler DC. The role of trimethylamine N‐oxide as a mediator of cardiovascular complications in chronic kidney disease. Kidney Int 2017; 92: 809–815.
              • 26. Organ CL, Otsuka H, Bhushan S, et al. Choline diet and its gut microbe‐derived metabolite, trimethylamine N‐oxide, exacerbate pressure overload‐induced heart failure. Circ Heart Fail 2016; 9: e002314.
              • 27. Koeth RA, Levison BS, Culley MK, et al. γ‐Butyrobetaine is a proatherogenic intermediate in gut microbial metabolism of L‐carnitine to TMAO. Cell Metab 2014; 20: 799–812.
              • 28. Wang Z, Klipfell E, Bennett BJ, et al. Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Nature 2011; 472: 57–63.
              • 29. Livshits G, Kalinkovich A. Inflammaging as a common ground for the development and maintenance of sarcopenia, obesity, cardiomyopathy and dysbiosis. Ageing Res Rev 2019; 56: 100980.
              • 30. Kitai T, Kirsop J, Tang WH. Exploring the microbiome in heart failure. Curr Heart Fail Rep 2016; 13: 103–109.
              • 31. Kumemoto R, Yusa K, Shibayama T, Hatori K. Trimethylamine N‐oxide suppresses the activity of the actomyosin motor. Biochim Biophys Acta 2012; 1820: 1597–1604.
              • 32. Makrecka‐Kuka M, Volska K, Antone U, et al. Trimethylamine N‐oxide impairs pyruvate and fatty acid oxidation in cardiac mitochondria. Toxicol Lett 2017; 267: 32–38.
              • 33. Tang WH, Kitai T, Hazen SL. Gut microbiota in cardiovascular health and disease. Circ Res 2017; 120: 1183–1196.
              • 34. Chioncel O, Ambrosy AP. Trimethylamine N‐oxide and risk of heart failure progression: marker or mediator of disease. Eur J Heart Fail 2019; 21: 887–890.
              • 35. Cho CE, Taesuwan S, Malysheva OV, et al. Trimethylamine‐N‐oxide (TMAO) response to animal source foods varies among healthy young men and is influenced by their gut microbiota composition: a randomized controlled trial. Mol Nutr Food Res 2017; 61: 1600324.
              • 36. Mayerhofer C, Awoyemi AO, Moscavitch SD, et al. Design of the GutHeart — targeting gut microbiota to treat heart failure — trial: a Phase II, randomized clinical trial. ESC Heart Fail 2018; 5: 977–984.
              • 37. Abbasi J. TMAO and heart disease: the new red meat risk? JAMA 2019; 321: 2149–2151.
              • 38. Cui X, Ye L, Li J, et al. Metagenomic and metabolomic analyses unveil dysbiosis of gut microbiota in chronic heart failure patients. Sci Rep 2018; 8: 635.
              • 39. Ponikowski P, Voors AA, Anker SD, et al. ESC Scientific Document Group. 2016 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure. The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Eur Heart J 2016; 37: 2129–2200.
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                “No jab, no pay” pays off

                Terence M Nolan
                Med J Aust 2020; 213 (8): . || doi: 10.5694/mja2.50796
                Published online: 19 October 2020

                The policy has been effective, albeit with modest closure of coverage gaps, and without substantial backlash

                In April 1998, the Australian government linked the payment of childcare subsidies (Childcare Assistance and Childcare Cash Rebate) and the Maternity Immunisation Allowance to childhood vaccination status.1 To receive these benefits, families needed to show that their child was fully vaccinated according to the National Immunisation Program Schedule.2 Further, the Victorian government passed legislation in 2015 that required childcare proprietors to record and regularly update the vaccination status of each child in their care, and to restrict admission to children who were up to date (“No jab, no play”).3 Other states have since followed suit.


                • 1 Peter Doherty Institute for Infection and Immunity, University of Melbourne, Melbourne, VIC
                • 2 Murdoch Children's Research Institute, Melbourne, VIC


                Correspondence: t.nolan@unimelb.edu.au
                Competing interests:

                No relevant disclosures.

                • 1. Bond L, Nolan T, Lester R. Immunisation uptake, services required and government incentives for users of formal day care. Aust N Z J Public Health 1999; 23: 368–376.
                • 2. Bond L, Davie G, Carlin JB, et al. Increases in vaccination coverage for children in child care, 1997 to 2000: an evaluation of the impact of government incentives and initiatives. Aust N Z J Public Health 2002; 26: 58–64.
                • 3. Department of Health and Human Services (Victoria). No jab no play [website]. 2017. https://www2.health.vic.gov.au/public-health/immunisation/vaccination-children/no-jab-no-play (viewed Sept 2020).
                • 4. Lawrence GL, MacIntyre CR, Hull BP, McIntyre PB. Effectiveness of the linkage of child care and maternity payments to childhood immunisation. Vaccine 2004; 22: 2345–2350.
                • 5. Hull BP, Beard FH, Hendry AJ, et al. “No jab, no pay”: catch‐up vaccination activity during its first two years. Med J Aust 2020; 213: 364–369.
                • 6. Leask J, Danchin M. Imposing penalties for vaccine rejection requires strong scrutiny. J Paediatr Child Health 2017; 53: 439–444.
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                  Time for a new approach to funding residential aged care

                  Edward Strivens
                  Med J Aust 2020; 213 (8): . || doi: 10.5694/mja2.50799
                  Published online: 19 October 2020

                  Support should be tied to the health care needs of residents, not to how eligibility for subsidies is assessed

                  Government support for residential aged care facilities (RACFs) in Australia has undergone major periodic shifts in the attempt to match residents’ needs and the costs of care. The money involved is considerable: during 2018–19, the Australian government provided $13.3 billion in subsidies, with more than 200 000 people living in RACFs.1


                  • 1 James Cook University, Cairns, QLD
                  • 2 Cairns and Hinterland Hospital and Health Service, Cairns, QLD


                  Competing interests:

                  No relevant disclosures.

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                    Considerations for cancer immunotherapy during the COVID‐19 pandemic

                    Yada Kanjanapan and Desmond Yip
                    Med J Aust 2020; 213 (9): . || doi: 10.5694/mja2.50805
                    Published online: 14 October 2020
                    Correction(s) for this article: Erratum | Published online: 2 May 2025

                    Cancer immunotherapy during the COVID‐19 pandemic presents management challenges from immune‐related toxicities, requiring careful patient selection

                    The coronavirus disease 2019 (COVID‐19) pandemic has led to fundamental re‐evaluation of the benefits versus risks of treatment in oncology. Immunotherapy has had an expanding presence in oncology, becoming a primary systemic treatment option in diseases such as melanoma, lung, urothelial, renal, and head and neck cancers. Immune checkpoint inhibitor (ICI) therapy, namely anti‐programmed cell death protein 1 (anti‐PD‐1), anti‐programmed cell death ligand 1 (anti‐PD‐L1) and anti‐cytotoxic T‐lymphocyte‐associated protein 4 (anti‐CTLA‐4) antibodies, halt the negative regulatory checks of T lymphocytes, thus activating the immune response against tumours. Patients with cancer receiving these treatments are faced with a unique set of treatment‐related toxicities driven by an autoimmune mechanism.

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                    • 1 Canberra Hospital, Canberra, ACT
                    • 2 Australian National University, Canberra, ACT


                    Correspondence: yada.kanjanapan@act.gov.au
                    Competing interests:

                    No relevant disclosures.

                    • 1. Bersanelli M. Controversies about COVID‐19 and anticancer treatment with immune checkpoint inhibitors. Immunotherapy 2020; 12: 269–273.
                    • 2. Dai M, Liu D, Liu M, et al. Patients with cancer appear more vulnerable to SARS‐COV-2: a multicenter study during the COVID‐19 outbreak. Cancer Discov 2020; 10: 783–791.
                    • 3. Qin C, Zhou L, Hu Z, et al. Dysregulation of immune response in patients with COVID‐19 in Wuhan, China. Clin Infect Dis 2020; 71: 762–768.
                    • 4. Lim SY, Lee JH, Gide TN, et al. Circulating cytokines predict immune‐related toxicity in melanoma patients receiving anti‐PD‐1-based immunotherapy. Clin Cancer Res 2019; 25: 1557–1563.
                    • 5. Robilotti EV, Babady NE, Mead PA, et al. Determinants of COVID‐19 disease severity in patients with cancer. Nat Med 2020; 26: 1218–1223.
                    • 6. Garassino MC, Whisenant JG, Huang LC, et al. COVID‐19 in patients with thoracic malignancies (TERAVOLT): first results of an international, registry‐based, cohort study. Lancet Oncol 2020; 21: 914–922.
                    • 7. Wolchok JD, Rollin L, Larkin J. Nivolumab and ipilimumab in advanced melanoma. N Engl J Med 2017; 377: 2503–2504.
                    • 8. Motzer RJ, Tannir NM, McDermott DF, et al. Nivolumab plus ipilimumab versus sunitinib in advanced renal‐cell carcinoma. N Engl J Med 2018; 378: 1277–1290.
                    • 9. RECOVERY Collaborative Group. Dexamethasone in hospitalized patients with COVID‐19 — preliminary report. N Engl J Med 2020; https://doi.org/10.1056/nejmoa2021436 [Epub ahead of print].
                    • 10. Del Castillo M, Romero FA, Argüello E, et al. The spectrum of serious infections among patients receiving immune checkpoint blockade for the treatment of melanoma. Clin Infect Dis 2016; 63: 1490–1493.
                    • 11. Schwarz M, Kocher F, Niedersuess‐Beke D, et al. Immunosuppression for immune checkpoint‐related toxicity can cause Pneumocystis jirovecii pneumonia (PJP) in Non‐small‐cell lung cancer (NSCLC): a report of 2 cases. Clin Lung Cancer 2019; 20: e247–e250.
                    • 12. Fujita K, Kim YH, Kanai O, et al. Emerging concerns of infectious diseases in lung cancer patients receiving immune checkpoint inhibitor therapy. Respir Med 2019; 146: 66–70.
                    • 13. Picchi H, Mateus C, Chouaid C, et al. Infectious complications associated with the use of immune checkpoint inhibitors in oncology: reactivation of tuberculosis after anti PD‐1 treatment. Clin Microbiol Infect 2018; 24: 216–218.
                    • 14. Läubli H, Balmelli C, Kaufmann L, et al. Influenza vaccination of cancer patients during PD‐1 blockade induces serological protection but may raise the risk for immune‐related adverse events. J Immunother Cancer 2018; 6: 40.
                    • 15. Failing JJ, Ho TP, Yadav S, et al. Safety of influenza vaccine in patients with cancer receiving pembrolizumab. JCO Oncol Pract 2020; 16: e573–e580.
                    • 16. Segelov E, Underhill C, Prenen H, et al. Practical considerations for treating patients with cancer in the COVID‐19 pandemic. JCO Oncol Pract 2020; 16: 467–482.
                    • 17. Weinkove R, McQuilten ZK, Adler J, et al. Managing haematology and oncology patients during the COVID‐19 pandemic: interim consensus guidance. Med J Aust 2020; 212: 481–489. https://www.mja.com.au/journal/2020/212/10/managing-haematology-and-oncology-patients-during-covid-19-pandemic-interim-0
                    • 18. Friedlaender A, Kim C, Addeo A. Rethinking the optimal duration of immune checkpoint inhibitors in non‐small cell lung cancer throughout the COVID‐19 pandemic. Front Oncol 2020; 10: 862.
                    • 19. Robert C, Ribas A, Hamid O, et al. Durable Complete Response After Discontinuation of Pembrolizumab in Patients With Metastatic Melanoma. J Clin Oncol 2018; 36: 1668–1674.
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                      Demographics and performance of candidates in the examinations of the Australian Medical Council, 1978–2019

                      Neville D Yeomans, Jillian R Sewell, Philip Pigou and Stuart Macintyre
                      Med J Aust 2021; 214 (2): . || doi: 10.5694/mja2.50800
                      Published online: 5 October 2020

                      Australia has relied, for most of its history, on international medical graduates (IMGs) to supplement its workforce. Since 1978, IMGs applying for general registration to practise in Australia have usually needed to pass the examinations of the Australian Medical Examining Council, or since 1986, its successor, the Australian Medical Council (AMC). The AMC provides several pathways to registration by the Australian Health Practitioner Regulation Agency (AHPRA). The route now termed “the standard pathway” consists of a two‐part assessment including a multiple choice question (MCQ) examination followed by a clinical examination. While most IMGs are required to pass both examinations, since 2007, IMGs who qualified in the so‐called competent authority countries (the United Kingdom, Ireland, the United States and Canada) have usually not been required to sit these examinations.1


                      • 1 University of Melbourne, Melbourne, VIC
                      • 2 Centre for Community Child Health, Melbourne, VIC
                      • 3 Australian Medical Council, Canberra, ACT


                      Correspondence: nyeomans@unimelb.edu.au
                      Acknowledgements: 

                      We acknowledge the assistance of Kevin Ng and Prathyusha Sama, Senior Computer Programmer and Software Developer at the AMC, for programming to extract the de‐identified data analysed in this article.

                      Competing interests:

                      No relevant disclosures.

                      • 1. Medical Board of Australia. Competent authority pathway [website]. AHPRA, 2019. https://www.medicalboard.gov.au/Registration/International-Medical-Graduates/Competent-Authority-Pathway.aspx (viewed July 2020).
                      • 2. Australian Government Publishing Service. Human Rights and Equal Opportunity Commission — annual report 1990–91. Canberra: Commonwealth of Australia; 1991. https://humanrights.gov.au/sites/default/files/Annual_Report_90-91.pdf (viewed July 2020).
                      • 3. Australian Competition and Consumer Commission and Australian Health Workforce Officials’ Committee. Review of Australian specialist medical colleges: report to Australian Health Ministers. Canberra: Commonwealth of Australia, 2005.
                      • 4. House of Representatives Standing Committee on Health and Ageing. Lost in the labyrinth: report on the inquiry into registration processes and support for overseas trained doctors. Canberra: Commonwealth of Australia, 2012. https://www.aph.gov.au/Parliamentary_Business/Committees/House_of_Representatives_Committees?url=haa/overseasdoctors/report.htm (viewed July 2020).
                      • 5. Geffen L. Assuring medical standards: the Australian Medical Council 1985–2010. Canberra, ACT: Australian Medical Council, 2010.
                      • 6. Australian Medical Council Limited. IMG guides. https://www.amc.org.au/publications/img-guides/ (viewed July 2020).
                      • 7. United Nations Statistics Division. Geographical regions 1999. https://unstats.un.org/unsd/methodology/m49 (viewed July 2020).
                      • 8. Australian Bureau of Statistics. Migration, Australia, 1993–2018 [Cat. No. 3412.0]. Canberra, ACT: ABS, 2018. https://www.abs.gov.au/AUSSTATS/abs@.nsf/DetailsPage/3412.02017-18?OpenDocument (viewed July 2020).
                      • 9. Breen K, Frank I, Walters T. Australian Medical Council: a view from the inside. Intern Med J 2001; 31: 243–248.
                      • 10. McCoubrie P. Improving the fairness of multiple‐choice questions: a literature review. Med Teach 2004; 26: 709–712.
                      • 11. Yeomans ND. They came to heal: Australia's medical immigrants, 1960 to the present [dissertation]. Melbourne: University of Melbourne, 2018: 120.
                      • 12. Dewhurst NG, McManus C, Mollon J, et al. Performance in the MRCP (UK) examination 2003–4: analysis of pass rates of UK graduates in relation to self‐declared ethnicity and gender. BMC Med 2007; 5: 8.
                      • 13. Shellito JL, Osland JS, Helmer SD, Chang FC. American Board of Surgery examinations: can we identify surgery residency applicants and residents who will pass the examinations on the first attempt? Am J Surg 2010; 199: 216–222.
                      • 14. Rubright JD, Jodoin M, Barone MA. Examining demographics, prior academic performance, and United States Medical Licensing Examination scores. Acad Med 2019; 94: 364–370.
                      • 15. Unwin E, Potts HWW, Dacre J, et al. Passing MRCP (UK) PACES: a cross‐sectional study examining the performance of doctors by sex and country. BMC Med Educ 2018; 18: 1–9.
                      • 16. Sandhu H, Adams A, Singleton L, et al. The impact of gender dyads on doctor–patient communication: A systematic review. Patient Educ Couns 2009; 76: 348–355.
                      • 17. Menzies L, Minson S, Brightwell A, et al. An evaluation of demographic factors affecting performance in a paediatric membership multiple‐choice examination. Postgrad Med J 2015; 91: 72–76.
                      • 18. Lipner R, Song H, Biester T, et al. Factors that influence general internists’ and surgeons’ performance on maintenance of certification exams. Acad Med 2011; 86: 53–58.
                      • 19. McGrail MR, Russell DJ. Australia's rural medical workforce: supply from its medical schools against career stage, gender and rural‐origin. Aust J Rural Health 2016; 25: 298–305.
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