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    Translating health professional education research evidence into effective continuous professional development

    Ruth M Sladek, Sue McAllister and Kieran M Walsh
    Med J Aust 2019; 210 (3): . || doi: 10.5694/mja2.12111
    Published online: 18 February 2019

    Biases and assumptions often arise from past experiences and, when unquestioned, can negatively influence the development of effective educational strategies

    Knowledge is frequently considered as the panacea for all ills, and its acquisition is often proposed as the solution for ensuring we deliver the best quality health care. For example, training and continuing professional development (CPD) have been proposed as the first steps for medical colleges to address some troubling variations in health care practice in Australia.1 However, while proposing educational strategies to address health outcomes is logical, appropriate and defensible, it is well established that “knowing” something is quite different from “doing” something.2 Nevertheless, CPD curricula are frequently limited to “knowing”.3 While knowledge is a key prerequisite to transforming practice, how do we maximise CPD effectiveness as a strategy to improve care? And is changing individual practice through education all that is needed to change health practices and outcomes?4

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      Emerging diabetes and metabolic conditions among Aboriginal and Torres Strait Islander young people

      Angela Titmuss, Elizabeth A Davis, Alex Brown and Louise J Maple‐Brown
      Med J Aust 2019; 210 (3): . || doi: 10.5694/mja2.13002
      Published online: 18 February 2019

      Intersectoral collaboration is needed to engage communities and design effective culturally and age‐appropriate interventions

      The gap between the health of Aboriginal and Torres Strait Islander and non‐Indigenous Australians is well documented, with many policies and programs currently working towards improving outcomes. Despite these efforts, life expectancy is 10–11 years less than that of non‐Indigenous Australians,1 and 65% of deaths occur before 65 years of age, compared with 19% in the non‐Indigenous population.1

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      • 1 Royal Darwin Hospital, Darwin, NT
      • 2 Menzies School of Health Research, Darwin, NT
      • 3 Princess Margaret Hospital for Children, Perth, WA
      • 4 Aboriginal Health Research Accord, South Australian Health and Medical Research Institute, Adelaide, SA
      • 5 University of South Australia, Adelaide, SA


      Acknowledgements: 

      We acknowledge other members of the Hot North Diabetes in Youth collaboration (Northern Australia Tropical Disease Collaborative Research Program, NHMRC project grant 1131932): Peter Azzopardi, Elizabeth Barr, Paul Bauert, Gavin Cleland, Christine Connors, James Dowler, Sandra Eades, Keith Forrest, Aveni Haynes, Renae Kirkham, Elizabeth Moore, Vicki O'Donnell, Glenn Pearson, Lydia Scott, Jonathan Shaw, Sally Singleton, Ashim Sinha and Mark Wenitong. Angela Titmuss is supported by an NHMRC Postgraduate Scholarship and RACP Woolcock Scholarship. Alex Brown is supported by an NHMRC Research Fellowship (1137563). Louise Maple‐Brown is supported by an NHMRC Practitioner Fellowship (1078477).

      Competing interests:

      No relevant disclosures.

      • 1. Australian Institute of Health and Welfare. The health and welfare of Australia's Aboriginal and Torres Strait Islander peoples: 2015 (AIHW Cat. No. IHW 147). Canberra: AIHW, 2015. https://www.aihw.gov.au/reports/indigenous-health-welfare/indigenous-health-welfare-2015/contents/table-of-contents (viewed Nov 2018).
      • 2. Azzopardi PS, Sawyer SM, Carlin JB, et al. Health and wellbeing of Indigenous adolescents in Australia: a systematic synthesis of population data. Lancet 2018; 391: 766–782.
      • 3. Haynes A, Kalic R, Cooper M, et al. Increasing incidence of type 2 diabetes in Indigenous and non‐Indigenous children in Western Australia, 1990‐2012. Med J Aust 2016; 204: 303. https://www.mja.com.au/journal/2016/204/8/increasing-incidence-type-2-diabetes-indigenous-and-non-indigenous-children
      • 4. Craig ME, Femia G, Broyda V, et al. Type 2 diabetes in Indigenous and non‐Indigenous children and adolescents in New South Wales. Med J Aust 2007; 186: 497–499. https://www.mja.com.au/journal/2007/186/10/type-2-diabetes-indigenous-and-non-indigenous-children-and-adolescents-new
      • 5. Stone M, Baker A, Maple‐Brown L. Diabetes in young people in the Top End of the Northern Territory. J Paed Child Health 2013; 49: 976–979.
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      • 7. Valery PC, Moloney A, Cotterill A, et al. Prevalence of obesity and metabolic syndrome in Indigenous Australian youths. Obes Rev 2009; 10: 255–261.
      • 8. Australian Bureau of Statistics. Australian Aboriginal and Torres Strait Islander Health Survey: first results, Australia, 2012‐13 (ABS Cat. No. 4747.0.055.001). Canberra: ABS, 2013. http://www.abs.gov.au/ausstats/abs@.nsf/mf/4727.0.55.001 (viewed Nov 2018).
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      • 10. Viner R, White B, Christie D. Type 2 diabetes in adolescents: a severe phenotype posing major clinical challenges and public health burden. Lancet 2017; 389: 2252–2260.
      • 11. Mendelson M, Cloutier J, Spence L, et al. Obesity and type 2 diabetes mellitus in a birth cohort of First Nation children born to mothers with pediatric‐onset type 2 diabetes. Pediatr Diabetes 2011; 12: 219–228.
      • 12. Chow E, Chan JCN. Explaining the high prevalence of young‐onset diabetes among Asians and Indigenous Australians. Med J Aust 2017; 207: 331–332. https://www.mja.com.au/journal/2017/207/8/explaining-high-prevalence-young-onset-diabetes-among-asians-and-indigenous
      • 13. Dabelea D, Hanson RL, Lindsay RS, et al. Intrauterine exposure to diabetes conveys risks for type 2 diabetes and obesity: a study of discordant sibships. Diabetes 2000; 49: 2208–2211.
      • 14. Chen P, Piaggi P, Traurig M, et al. Differential methylation of genes in individuals exposed to maternal diabetes in utero. Diabetologia 2017; 60: 645–655.
      • 15. Wheelock KM, Sinha M, Knowler WC, et al. Metabolic risk factors and type 2 diabetes incidence in American Indian children. J Clin Endocrinol Metab 2016; 101: 1437–1244.
      • 16. Dabelea D, Mayer‐Davis EJ, Lamichhane AP, et al. Association of intrauterine exposure to maternal diabetes and obesity with type 2 diabetes in youth: the SEARCH case‐control study. Diab Care 2008; 31: 1422–1426.
      • 17. Lindberg SM, Adams AK, Prince RJ. Early Predictors of Obesity and Cardiovascular Risk Among American Indian Children. Mat Child Health J 2012; 16: 1879–1886.
      • 18. Van Buren DJ, Tibbs TL. Lifestyle interventions to reduce diabetes and cardiovascular risk among children. Curr Diab Rep 2014; 14: 557–567.
      • 19. Paul CL, Ishiguchi P, D'Este CA, et al. Testing for type 2 diabetes in Indigenous Australians: guideline recommendations and current practice. Med J Aust 2017; 207: 206–210. https://www.mja.com.au/journal/2017/207/5/testing-type-2-diabetes-indigenous-australians-guideline-recommendations-and
      Online responses are no longer available. Please refer to our instructions for authors page for more information.

        New guidelines from the Thrombosis and Haemostasis Society of Australia and New Zealand for the diagnosis and management of venous thromboembolism

        Huyen A Tran, Harry Gibbs, Eileen Merriman, Jennifer L Curnow, Laura Young, Ashwini Bennett, Chee Wee Tan, Sanjeev D Chunilal, Chris M Ward, Ross Baker and Harshal Nandurkar
        Med J Aust 2019; 210 (5): . || doi: 10.5694/mja2.50004
        Published online: 11 February 2019
        Correction(s) for this article: Erratum | Published online: 13 April 2025

        Abstract

        Introduction: Venous thromboembolism (VTE), including deep vein thrombosis (DVT) and pulmonary embolism (PE), is the third most common cardiovascular disease and, globally, more than an estimated 10 million people have it yearly. It is a chronic and recurrent disease. The symptoms of VTE are non‐specific and the diagnosis should actively be sought once considered. The mainstay of VTE treatment is anticoagulation, with few patients requiring additional intervention.

        A working group of experts in the area recently completed an evidence‐based guideline for the diagnosis and management of DVT and PE on behalf of the Thrombosis and Haemostasis Society of Australia and New Zealand (www.thanz.org.au/resources/thanz-guidelines).

        Main recommendations:

        • The diagnosis of VTE should be established with imaging; it may be excluded by the use of clinical prediction rules combined with D‐dimer testing.
        • Proximal DVT or PE caused by a major surgery or trauma that is no longer present should be treated with anticoagulant therapy for 3 months.
        • Proximal DVT or PE that is unprovoked or associated with a transient risk factor (non‐surgical) should be treated with anticoagulant therapy for 3–6 months.
        • Proximal DVT or PE that is recurrent (two or more) and provoked by active cancer or antiphospholipid syndrome should receive extended anticoagulation.
        • Distal DVT caused by a major provoking factor that is no longer present should be treated with anticoagulant therapy for 6 weeks.
        • For patients continuing with extended anticoagulant therapy, either therapeutic or low dose direct oral anticoagulants can be prescribed and is preferred over warfarin in the absence of contraindications.
        • Routine thrombophilia testing is not indicated.
        • Thrombolysis or a suitable alternative is indicated for massive (haemodynamically unstable) PE.

         

        Changes in management as a result of the guideline: Most patients with acute VTE should be treated with a factor Xa inhibitor and be assessed for extended anticoagulation.


        • 1 Alfred Health, Melbourne, VIC
        • 2 Monash University, Melbourne, VIC
        • 3 Waitemata District Health Board, Auckland, New Zealand
        • 4 Haemophilia Treatment Centre, Westmead Hospital, Sydney, NSW
        • 5 Auckland District Health Board, Auckland, New Zealand
        • 6 Monash Medical Centre, Melbourne, VIC
        • 7 Royal Adelaide Hospital, Adelaide, SA
        • 8 Monash Health, Melbourne, VIC
        • 9  Royal North Shore Hospital, Sydney, NSW
        • 10 Perth Blood Institute, Perth, WA
        • 11 Australian Centre of Blood Diseases, Melbourne, VIC


        Correspondence: huyen.tran@monash.edu
        Competing interests:

        No relevant disclosures.

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          Current thinking in the health care management of children with cerebral palsy

          David Graham, Simon P Paget and Neil Wimalasundera
          Med J Aust 2019; 210 (3): . || doi: 10.5694/mja2.12106
          Published online: 11 February 2019

          Summary

           

          • Cerebral palsy is a developmental disorder of movement and posture which is often associated with comorbidities.
          • While there is currently a limited range of evidence‐based treatments that change the underlying pathology of cerebral palsy, there are many areas in which health care professionals can change the natural history of cerebral palsy and improve participation and quality of life for children with this condition.
          • Early identification has become of paramount importance in the management of cerebral palsy, and it is hoped that it will allow earlier access to cerebral palsy interventions that may improve the natural history of the condition.
          • Common challenges in the management of cerebral palsy include spasticity and dystonia, management of pain, hip surveillance, sleep and feeding, swallowing and nutrition.
          • The six Fs framework (function, family, fitness, fun, friends and future) provides a guide to developing shared goals with families in the management of cerebral palsy.

           


          • 1 Concord Centre for Mental Health, Sydney, NSW
          • 2 Kids Neuroscience Centre, Kids Research, Sydney, NSW
          • 3 Kids Rehab, Children's Hospital at Westmead, Sydney, NSW
          • 4 Royal Children's Hospital Melbourne, Melbourne, VIC


          Competing interests:

          No relevant disclosures.

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          • 37. Aquilina K, Graham D, Wimalasundera N. Selective dorsal rhizotomy: an old technique re‐emerging. Arch Dis Child 2015; 100: 798–802.
          • 38. Hasnat MJ, Rice JE. Intrathecal baclofen for treating spasticity in children with cerebral palsy. Cochrane Database Syst Rev 2015; (11): CD004552.
          • 39. Soo B, Howard JJ, Boyd RN, et al. Hip displacement in cerebral palsy. J Bone Joint Surg Am 2006; 88: 121–129.
          • 40. Wynter M, Gibson N, Kentish M, et al. Australian hip surveillance guidelines for children with cerebral palsy 2014 [website]. Australasian Academy of Cerebral Palsy and Developmental Medicine; 2014. https://www.ausacpdm.org.au/resources/australian-hip-surveillance-guidelines (viewed Nov 2017).
          • 41. Novak I, Hines M, Goldsmith S, Barclay R. Clinical prognostic messages from a systematic review on cerebral palsy. Pediatrics 2012; 130: e1285–e1312.
          • 42. Penner M, Xie W, Binepal N, et al. Characteristics of pain in children and youth with cerebral palsy. Pediatrics 2013; 132: e407–e413.
          • 43. Dang VM, Colver A, Dickinson HO, et al. Predictors of participation of adolescents with cerebral palsy: a European multi‐centre longitudinal study. Res Dev Disabil 2014; 36C: 551–564.
          • 44. Kingsnorth S, Orava T, Provvidenza C, et al. Chronic pain assessment tools for cerebral palsy: a systematic review. Pediatrics 2015; 136: e947–e960.
          • 45. Pin TW, Elmasry J, Lewis J. Efficacy of botulinum toxin A in children with cerebral palsy in Gross Motor Function Classification System levels IV and V: a systematic review. Dev Med Child Neurol 2013; 55: 304–313.
          • 46. Beecham E, Candy B, Howard R, et al. Pharmacological interventions for pain in children and adolescents with life‐limiting conditions. Cochrane Database Syst Rev 2015; (3): CD010750.
          • 47. Dahlseng MO, Andersen GL, da Graca Andrada M, et al; Surveillance of Cerebral Palsy in Europe Network. Gastrostomy tube feeding of children with cerebral palsy: variation across six European countries. Dev Med Child Neurol 2012; 54: 938–944.
          • 48. Reid SM, Johnson HM, Reddihough DS. The Drooling Impact Scale: a measure of the impact of drooling in children with developmental disabilities. Dev Med Child Neurol 2010; 52: e23–e28.
          • 49. Parr JR, Todhunter E, Pennington L, et al. The Drooling Reduction Intervention (DRI) trial: is hyoscine or glycopyrronium more effective and acceptable for the treatment of drooling in children with neurodisability? Arch Dis Child 2016; 101: A55–A56.
          • 50. Henderson RC, Lark RK, Gurka MJ, et al. Bone density and metabolism in children and adolescents with moderate to severe cerebral palsy. Pediatrics 2002; 110: e5.
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            Food protein‐induced enterocolitis syndrome: guidelines summary and practice recommendations

            Sam Mehr and Dianne E Campbell
            Med J Aust 2019; 210 (2): . || doi: 10.5694/mja2.12071
            Published online: 4 February 2019

            Summary

             

            • Food protein‐induced enterocolitis syndrome (FPIES) is a poorly understood non‐IgE gastrointestinal‐mediated food allergy that predominantly affects infants and young children.
            • Cells of the innate immune system appear to be activated during an FPIES reaction.
            • Acute FPIES typically presents between one and 4 hours after ingestion of the trigger food, with the principal symptom being profuse vomiting, and is often accompanied by pallor and lethargy. Additional features can include hypotension, hypothermia, diarrhoea, neutrophilia and thrombocytosis.
            • In Australia, the most commonly reported foods responsible for FPIES are (in descending order) rice, cow's milk, egg, oats and chicken.
            • Most children with FPIES react to only one food trigger, and thus, avoidance of multiple foods is often not indicated.
            • FPIES is often misdiagnosed as sepsis or gastroenteritis. However, a diagnosis of FPIES is favoured if there is rapid resolution of symptoms within hours of presentation, an absence of fever, and a lack of a significant rise in C‐reactive protein at presentation.
            • Diagnosis is often hampered by the lack of awareness of FPIES, absence of reliable biomarkers, the non‐specific nature of the presenting symptoms, and the delay between allergen exposure and symptoms.
            • Although some national peak allergy bodies have attempted to improve the diagnosis and management of FPIES, up until 2017 there were no internationally agreed guidelines for its diagnosis and management.

             


            • 1 Royal Children's Hospital, Melbourne, VIC
            • 2 Children's Hospital at Westmead, Sydney, NSW
            • 3 University of Sydney, Sydney, NSW


            Competing interests:

            No relevant disclosures.

            • 1. Nowak‐Węgrzyn A, Chehade M, Groetch ME, et al. International consensus guidelines for the diagnosis and management of food protein‐induced enterocolitis syndrome: executive summary — workgroup report of the Adverse Reactions to Foods Committee, American Academy of Allergy, Asthma and Immunology. J Allergy Clin Immunol 2017; 139: 1111–1126.
            • 2. Katz Y, Goldberg MR, Rajuan N, et al. The prevalence and natural course of food protein‐induced enterocolitis syndrome to cow's milk: a large‐scale, prospective population‐based study. J Allergy Clin Immunol 2011; 127: 647–653.
            • 3. Mehr S, Frith K, Barnes EH, et al. Food protein‐induced enterocolitis syndrome in Australia: a population‐based study, 2012–2014. J Allergy Clin Immunol 2017; 140: 1323–1330.
            • 4. Mehr S, Frith K, Campbell DE. Epidemiology of food protein‐induced enterocolitis syndrome. Curr Opin Allergy Clin Immunol 2014; 14: 208–216.
            • 5. Caubet JC, Ford LS, Sickles L, et al. Clinical features and resolution of food protein‐induced enterocolitis syndrome: 10‐year experience. J Allergy Clin Immunol 2014; 134: 382–389.
            • 6. Powell GK. Enterocolitis in low‐birth‐weight infants associated with milk and soy protein intolerance. J Pediatr 1976; 88: 840–844.
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            • 8. Mehr S, Kakakios A, Frith K, Kemp AS. Food protein‐induced enterocolitis syndrome: 16‐year experience. Pediatrics 2009; 123: e459–e464.
            • 9. Mehr SS, Kakakios AM, Kemp AS. Rice: a common and severe cause of food protein‐induced enterocolitis syndrome. Arch Dis Child 2009; 94: 220–223.
            • 10. Australasian Society of Clinical Immunology and Allergy. Action plan for FPIES. ASCIA; 2015. https://www.allergy.org.au/patients/food-other-adverse-reactions/fpies-action-plan (viewed Feb 2018).
            • 11. Sampson HA, Aceves S, Bock SA, et al. Food allergy: a practice parameter update‐2014. J Allergy Clin Immunol 2014; 134: 1016–1025.
            • 12. Cruz JE, Fahim G, Moore K. Practice guideline development, grading and assessment. PT 2015; 40: 854–857.
            • 13. Ruffner MA, Ruymann K, Barni S, et al. Food protein‐induced enterocolitis syndrome: insights from review of a large referral population. J Allergy Clin Immunol Pract 2013; 1: 343–349.
            • 14. Sicherer SH, Eigenmann PA, Sampson HA. Clinical features of food protein‐induced enterocolitis syndrome. J Pediatr 1998; 133: 214–219.
            • 15. Sopo SM, Giorgio V, Dello Iacono I, et al. A multicentre retrospective study of 66 Italian children with food protein‐induced enterocolitis syndrome: different management for different phenotypes. Clin Exp Allergy 2012; 42: 1257–1265.
            • 16. Levy Y, Danon YL. Food protein‐induced enterocolitis syndrome — not only due to cow's milk and soy. Pediatr Allergy Immunol 2003; 14: 325–329.
            • 17. Burks AW, Casteel HB, Fiedorek SC, et al. Prospective oral food challenge study of two soybean protein isolates in patients with possible milk or soy protein enterocolitis. Pediatr Allergy Immunol 1994; 5: 40–45.
            • 18. Mullins RJ, Turner PJ, Barnes EH, Campbell DE. Allergic gastroenteritis hospital admission time trends in Australia and New Zealand. J Paed Child Health 2018; 54: 398–400.
            • 19. Fernandes BN, Boyle RJ, Gore C, et al. Food protein‐induced enterocolitis syndrome can occur in adults. J Allergy Clin Immunol 2012; 130: 1199–1200.
            • 20. Tan JA, Smith WB. Non‐IgE‐mediated gastrointestinal food hypersensitivity syndrome in adults. J Allergy Clin Immunol Pract 2014; 2: 355–357.
            • 21. Nowak‐Węgrzyn A, Katz Y, Mehr SS, Koletzko S. Non‐IgE‐mediated gastrointestinal food allergy. J Allergy Clin Immunol 2015; 135: 1114–1124.
            • 22. Berin MC. Immunopathophysiology of food protein‐induced enterocolitis syndrome. J Allergy Clin Immunol 2015; 135: 1108–1113.
            • 23. Goswami R, Blazquez AB, Kosoy R, et al. Systemic innate immune activation in food protein‐induced enterocolitis syndrome. J Allergy Clin Immunol 2017; 139: 1885–1896.
            • 24. Mehr S, Lee E, Hsu P, et al. Innate immune activation in food reactions in infants with food protein induced enterocolitis syndrome (abstract). Fifth Pediatric Allergy and Asthma Meeting (PAAM); London (UK), 26–28 Oct 2017. Clin Transl Allergy 2018; 8 (Suppl): 26. https://ctajournal.biomedcentral.com/track/pdf/10.1186/s13601-018-0204-0 (viewed Nov 2018).
            • 25. Nowak‐Węgrzyn A, Sampson HA, Wood RA, Sicherer SH. Food protein‐induced enterocolitis syndrome caused by solid food proteins. Pediatrics 2003; 111: 829–835.
            • 26. Miceli Sopo S, Bersani G, Monaco S, et al. Ondansetron in acute food protein‐induced enterocolitis syndrome, a retrospective case‐control study. Allergy 2017; 72: 545–551.
            • 27. Murray KF, Christie DL. Dietary protein intolerance in infants with transient methemoglobinemia and diarrhea. J Pediatr 1993; 122: 90–92.
            • 28. Nomura I, Morita H, Ohya Y, et al. Non‐IgE‐mediated gastrointestinal food allergies: distinct differences in clinical phenotype between Western countries and Japan. Curr Allergy Asthma Rep 2012; 12: 297–303.
            • 29. Nomura I, Morita H, Hosokawa S, et al. Four distinct subtypes of non‐IgE‐mediated gastrointestinal food allergies in neonates and infants, distinguished by their initial symptoms. J Allergy Clin Immunol 2011; 127: 685–688.
            • 30. Delahaye C, Chauveau A, Kiefer S, Dumond P. Food protein‐induced enterocolitis syndrome (FPIES) in 14 children [French]. Arch Pediatr 2017; 24: 310–316.
            • 31. Lee E, Campbell DE, Barnes EH, Mehr SS. Resolution of acute food protein‐induced enterocolitis syndrome in children. J Allergy Clin Immunol Pract 2017; 5: 486–488.
            • 32. Lee E, Mehr S. What is new in the diagnosis and management of food protein‐induced enterocolitis syndrome. Current Pediatrics Reports 2016; 4: 138–146.
            • 33. Järvinen KM, Nowak‐Węgrzyn A. Food protein‐induced enterocolitis syndrome (FPIES): current management strategies and review of the literature. J Allergy Clin Immunol Pract 2013; 1: 317–322.
            • 34. Nowak‐Węgrzyn A, Assa'ad AH, Bahna SL, et al. Work group report: oral food challenge testing. J Allergy Clin Immunol 2009; 123: S365–S383.
            • 35. Sicherer SH. Food protein‐induced enterocolitis syndrome: case presentations and management lessons. J Allergy Clin Immunol 2005; 115: 149–156.
            • 36. Holbrook T, Keet CA, Frischmeyer‐Guerrerio PA, Wood RA. Use of ondansetron for food protein‐induced enterocolitis syndrome. J Allergy Clin Immunol 2013; 132: 1219–1220.
            • 37. Tan J, Campbell D, Mehr S. Food protein‐induced enterocolitis syndrome in an exclusively breastfed infant‐an uncommon entity. J Allergy Clin Immunol 2012; 129: 873.
            • 38. Kemp AS, Hill DJ, Allen KJ, et al. Guidelines for the use of infant formulas to treat cow's milk protein allergy: an Australian consensus panel opinion. Med J Aust 2008; 188: 109–112. https://www.mja.com.au/journal/2008/188/2/guidelines-use-infant-formulas-treat-cows-milk-protein-allergy-australian
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              Silent but deadly: patients with enterococcal bacteraemia should be assessed for colorectal neoplasia

              Eugene Athan, Ivana Cabiltes, Sarah Coghill and Steven J Bowe
              Med J Aust 2019; 210 (2): . || doi: 10.5694/mja2.12027
              Published online: 4 February 2019

              The epidemiology of bloodstream infections has changed during the early 21st century, and our understanding of complex host–pathogen relationships continues to evolve. Enterococci have emerged as major community and health care pathogens; the association of colorectal neoplasia with enterococcal infections has recently been reported, particularly with community‐acquired Enterococcus faecalis bacteraemia of unknown source.1,2

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              • 1 Barwon Health, Geelong, VIC
              • 2 Deakin University, Melbourne
              • 3 University Hospital Geelong, Geelong, VIC
              • 4 Swinburne University of Technology, Melbourne, VIC


              Correspondence: eugene@barwonhealth.org.au
              Competing interests:

              No relevant disclosures.

              • 1. Correidoira J, García‐País MJ, Coira A, et al. Differences between endocarditis caused by Streptococcus bovis and Enterococcus spp. and their association with colorectal cancer. Eur J Clin Microbiol Infect Dis 2015; 34: 1657–1665.
              • 2. Pericàs JM, Corredoira J, Moreno A, et al. Relationship between Enterococcus faecalis infective endocarditis and colorectal neoplasm: preliminary results from a cohort of 154 patients. Rev Esp Cardiol (Engl Ed) 2017; 70: 451–458.
              • 3. Murray HW, Roberts RB: Streptococcus bovis bacteremia and underlying gastrointestinal disease. Arch Intern Med 1978; 138: 1097–1099.
              • 4. Reynolds JG, Silva E, McCormack WM. Association of Streptococcus bovis bacteremia with bowel disease. J Clin Microbiol 1983; 17: 696–697.
              • 5. Leport C, Bure A, Leport J, Vilde JL. Incidence of colonic lesions in Streptococcus bovis and enterococcal endocarditis. Lancet 1987; 1: 748.
              • 6. Corredoira J, Alonso MP, Coira A, et al. Characteristics of Streptococcus bovis endocarditis and its differences with Streptococcus viridans endocarditis. Eur J Clin Microbiol Infect Dis 2008; 27: 285–291.
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                High intensity lipid‐lowering therapy after acute coronary syndromes: room for improvement

                Karam Kostner
                Med J Aust 2019; 210 (2): . || doi: 10.5694/mja2.12055
                Published online: 4 February 2019

                Effective therapies are available, but too few patients are receiving them

                There is a significant amount of evidence that intensive statin therapy reduces the likelihood of cardiovascular events in people who have had an acute coronary syndrome (ACS), and such therapy is given the highest grade of recommendation in Australian clinical practice guidelines.1 Post hoc analyses of randomised trials of treatment with statins, statins and ezetimibe, or, more recently, proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors indicate that patients who achieve very low low‐density lipoprotein cholesterol (LDL‐C) levels are at very low risk of cardiovascular events after an ACS, and that the rates of adverse events related to attaining such levels are not increased.2,3 In the Improved Reduction of Outcomes: Vytorin Efficacy International Trial (IMPROVE‐IT), the combination of simvastatin and a non‐statin LDL‐lowering treatment (ezetimibe) reduced LDL‐C levels to a median 1.4 mmol/L, and this was associated with reduced numbers of clinical events.4 In the Odyssey Outcomes trial, a combination of statins and alirocumab (a PCSK9 inhibitor) reduced LDL‐C levels to below 1.0 mmol/L and this was associated with reduced numbers of major adverse cardiovascular events.3 These trials provide further support for the LDL‐C hypothesis of cardiovascular risk, which suggests that the risk of a cardiovascular event is reduced by about 22% for each 1.0 mmol/L reduction in LDL‐C levels.2


                • Mater Hospital, Brisbane, QLD


                Correspondence: k.kostner@uq.edu.au
                Competing interests:

                No relevant disclosures.

                • 1. Chew DP, Scott IA, Cullen L, et al. National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand: Australian clinical guidelines for the management of acute coronary syndromes 2016. Heart Lung Circ 2016; 25: 895–951.
                • 2. Shepherd J, Barter P, Carmena R, et al. Effect of lowering LDL cholesterol substantially below currently recommended levels in patients with coronary heart disease and diabetes: the Treating to New Targets (TNT) study. Diabetes Care 2006; 29: 1220–1226.
                • 3. Schwartz GG, Steg PG, Szarek M, et al. Alirocumab and cardiovascular outcomes after acute coronary syndrome. N Engl J Med 2018; 379: 2097–2107
                • 4. Cannon CP, Blazing MA, Giugliano RP, et al. Ezetimibe added to statin therapy after acute coronary syndromes. N Engl J Med 2015; 372: 2387–2397.
                • 5. De Vera MA, Bhole V, Burns LC, Lacaille D. Impact of statin adherence on cardiovascular disease and mortality outcomes: a systematic review. Br J Clin Pharmacol 2014; 78: 684–698.
                • 6. Brieger D, D'Souza M, Huyn K, et al. Intensive lipid‐lowering therapy in the 12 months after an acute coronary syndrome in Australia: an observational analysis. Med J Aust 2019; 210: 000–000.
                • 7. Jackevicius CA, Mamdani M, Tu JV. Adherence with statin therapy in elderly patients with and without acute coronary syndromes. JAMA 2002; 288: 462–467.
                • 8. Wouters H, Van Dijk L, Geers HC, et al. Understanding statin non‐adherence: knowing which perceptions and experiences matter to different patients. PLoS One 2016; 11: e0146272.73.
                • 9. Wu JY, Leung WY, Chang S, et al. Effectiveness of telephone counselling by a pharmacist in reducing mortality in patients receiving polypharmacy: randomised controlled trial. BMJ 2006; 333: 522.
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                  Pregabalin misuse: the next wave of prescription medication problems

                  Bridin Murnion and Katherine M Conigrave
                  Med J Aust 2019; 210 (2): . || doi: 10.5694/mja2.12056
                  Published online: 4 February 2019

                  Overseas experience need not portend the future of prescription drug misuse in Australia

                  Dispensing data indicate that pregabalin prescribing in Australia is rising rapidly, and the numbers of self‐poisonings and deaths are also increasing.1 This mirrors the European and North American experience of escalating misuse and harms.2,3 Although Australian guidelines recommend it only as second line treatment for neuropathic pain,4 pregabalin is now the seventh most expensive drug in terms of Pharmaceutical Benefits Scheme (PBS) expenditure.5


                  • 1 Drug and Alcohol Services, Wyong Hospital, Wyong, NSW
                  • 2 University of Sydney, Sydney, NSW
                  • 3 Drug Health Services, Royal Prince Alfred Hospital, Sydney, NSW


                  Competing interests:

                  No relevant disclosures.

                  • 1. Cairns R, Schaffer AL, Ryan N, et al. Rising pregabalin use and misuse in Australia: trends in utilization and intentional poisonings. Addiction 2018; https://doi.org/10.1111/add.14412.
                  • 2. Lyndon A, Audrey S, Wells C, et al. Risk to heroin users of polydrug use of pregabalin or gabapentin. Addiction 2017; 112: 1580–1589.
                  • 3. Gomes T, Greaves S, van den Brink W, et al. Pregabalin and the risk for opioid‐related death: a nested case‐control study. Ann Int Med 2018; 169: 732–734.
                  • 4. Siddall P, Hall A. Neuropathic pain: diagnosis and treatment today. Medicinewise News [online]. Mar 2018. https://cdn0.scrvt.com/08ab3606b0b7a8ea53fd0b40b1c44f86/07f7c27169bb23c8/1d249d6217dd/NPS1992_MW_News_NP_v2.pdf (viewed Oct 2018).
                  • 5. Australian Government Department of Health. PBS Expenditure and prescriptions, twelve months to 30 June 2017. http://www.pbs.gov.au/statistics/expenditure-prescriptions/2016-2017/expenditure-and-prescriptions-twelve-months-to-30-june-2017.pdf (viewed Oct 2018).
                  • 6. Crossin R, Scott D, Arunogiri S, et al. Pregabalin misuse‐related ambulance attendances in Victoria, 2012–2017: characteristics of patients and attendances. Med J Aust 2019; 210: 000–000.
                  • 7. Morrison EE, Sandilands EA, Webb DJ. Gabapentin and pregabalin: do the benefits outweigh the harms? J R Coll Physicians Edinb 2017; 47: 310–313.
                  • 8. Australian Institute of Health and Welfare. Impacts of chronic back problems (AIHW Bulletin 137). Aug 2016. https://www.aihw.gov.au/getmedia/9018da61-cdf0-4e3a-bd98-2508f515290d/19839.pdf.aspx?inline=true (viewed Oct 2018).
                  • 9. Shanthanna H, Gilron I, Rajarathinam M, et al. Benefits and safety of gabapentinoids in chronic low back pain: a systematic review and meta‐analysis of randomized controlled trials. PLoS Med 2017; 14: e1002369.
                  • 10. Mathieson S, Maher CG, McLachlan AJ, et al. Trial of pregabalin for acute and chronic sciatica. N Engl J Med 2017; 376: 1111–1120.
                  • 11. Hayes C, West C, Egger G. Rethinking chronic pain in a lifestyle medicine context. In: Egger G, Binns A, Rössner S, Sagner M, editors. Lifestyle medicine. Lifestyle, the environment and preventive medicine in health and disease. Third edition. London: Academic Press, 2017; pp. 339–353.
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                    International vascularised composite allotransplantation activity: implications for Australia

                    Karen M Dwyer, James D Burt and Tim Bennett
                    Med J Aust 2019; 210 (2): . || doi: 10.5694/mja2.12068
                    Published online: 4 February 2019

                    Although hand transplantation has the potential to transform lives, the procedure is not without risk

                    March 2018 heralded 7 years since the only Australian to date received a hand transplant. The recipient has physically and psychologically integrated the transplanted hand and reports significantly improved quality of life;1 motor and sensory functions continue to improve incrementally with ongoing hand therapy. The Transplantation Society of Australia and New Zealand (TSANZ) Vascular Composite Allograft (VCA) Advisory Committee met during the TSANZ annual scientific meeting held in Melbourne in April 2018. Transplant physicians and surgeons and reconstructive microsurgeons comprise the advisory committee, with scope to co‐opt expert members (eg, in bioethics) as required. Despite the success of the seminal hand transplant in Australia, no further patients have progressed to the transplant waiting list. In light of this, the Advisory Committee reflects in this article on the status of hand transplantation internationally and considers its relevance for Australia.


                    • 1 Deakin University, Geelong, VIC
                    • 2 St Vincent's Hospital Melbourne, Melbourne, VIC


                    Correspondence: karen.dwyer@deakin.edu.au
                    Acknowledgements: 

                    The views expressed in this manuscript reflect those of the TSANZ VCA Advisory Committee — Karen Dwyer (Chair), Jamie Burt, Tim Bennett, Frank Ierino, Sharon Ford, Kate Wyburn and Richard Allen — and have been ratified by the TSANZ Council — Stephen Alexander (President) and Toby Coates (President elect).

                    Competing interests:

                    No relevant disclosures.

                    • 1. Dwyer KM, Webb AR, Furniss HS, et al. First hand transplant procedure in Australia: outcome at 2 years. Med J Aust 2013; 199: 285–287. https://www.mja.com.au/journal/2013/199/4/first-hand-transplant-procedure-australia-outcome-2-years
                    • 2. Shores JT, Brandacher G, Lee WP. Hand and upper extremity transplantation: an update of outcomes in the worldwide experience. Plast Reconstr Surg 2015; 135: 351e–360e.
                    • 3. Burloux G. Hand transplant and body image. In: Lanzetta M, Dubernard JM, Petruzzo P, editors. Hand transplantation. Milan, Italy: Springer Milano, 2007; pp. 375–379.
                    • 4. Kanitakis J, Jullien D, Petruzzo P, et al. Clinicopathologic features of graft rejection of the first human hand allograft. Transplantation 2003; 76: 688–693.
                    • 5. Bhaskaranand K, Bhat AK, Acharya KN. Prosthetic rehabilitation in traumatic upper limb amputees (an Indian perspective). Arch Orthop Trauma Surg 2003; 123: 363–366.
                    • 6. Salminger S, Sturma A, Roche AD, et al. Functional and psychosocial outcomes of hand transplantation compared with prosthetic fitting in below‐elbow amputees: a multicenter cohort study. PLoS One 2016; 11: e0162507.
                    • 7. Petruzzo P, Lanzetta M, Dubernard J. International Registry on Hand and Composite Tissue Transplantation. Transplantation 2014; 98: 44.
                    • 8. Weissenbacher A, Hautz T, Zelger B, et al. Antibody‐mediated rejection in hand transplantation. Transpl Int 2014; 27: e13–e17.
                    • 9. Dwyer KM, Carroll R, Hill P, et al. Refractory vascular rejection in a hand allograft in the presence of antibodies against angiotensin II (type 1) receptor. Transplantation 2017; 101: e344–e345.
                    • 10. Kanitakis J, Petruzzo P, Badet L, et al. Chronic rejection in human vascularized composite allotransplantation (hand and face recipients): an update. Transplantation 2016; 100: 2053–2061.
                    • 11. Krezdorn N, Tasigiorgos S, Wo L, et al. Kidney dysfunction after vascularized composite allotransplantation. Transplant Direct 2018; 4: e362.
                    • 12. Pei G, Xiang D, Gu L, et al. A report of 15 hand allotransplantations in 12 patients and their outcomes in China. Transplantation 2012; 94: 1052–1059.
                    • 13. Dillon MP, Fortington LV, Akram M, et al. Geographic variation of the incidence rate of lower limb amputation in Australia from 2007–12. PLoS One 2017; 12: e0170705.
                    • 14. Lantieri L, Grimbert P, Ortonne N, et al. Face transplant: long‐term follow‐up and results of a prospective open study. Lancet 2016; 388: 1398–1407.
                    • 15. Aycart MA, Kiwanuka H, Krezdorn N, et al. Quality of life after face transplantation: outcomes, assessment tools, and future directions. Plast Reconstr Surg 2017; 139: 194–203.
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                      Recruiting general practice patients for large clinical trials: lessons from the Aspirin in Reducing Events in the Elderly (ASPREE) study

                      Jessica E Lockery, Taya A Collyer, Walter P Abhayaratna, Sharyn M Fitzgerald, John J McNeil, Mark R Nelson, Suzanne G Orchard, Christopher Reid, Nigel P Stocks, Ruth E Trevaks and Robyn Woods
                      Med J Aust 2019; 210 (4): . || doi: 10.5694/mja2.12060
                      Published online: 28 January 2019

                      Abstract

                      Objective: To assess the factors that contributed to the successful completion of recruitment for the largest clinical trial ever conducted in Australia, the Aspirin in Reducing Events in the Elderly (ASPREE) study.

                      Design: Enrolment of GPs; identification of potential participants in general practice databases; screening of participants.

                      Setting, participants: Selected general practices across southeast Australia (Tasmania, Victoria, Australian Capital Territory, New South Wales, South Australia).

                      Major outcomes: Numbers of patients per GP screened and randomised to participation; geographic and demographic factors that influenced screening and randomising of patients.

                      Results: 2717 of 5833 GPs approached (47%) enrolled to recruit patients for the study; 2053 (76%) recruited at least one randomised participant. The highest randomised participant rate per GP was for Tasmania (median, 5; IQR, 1–11), driven by the high rate of participant inclusion at phone screening. GPs in inner regional (adjusted odds ratio [aOR], 1.45; 95% CI, 1.14–1.84) and outer regional areas (aOR, 1.86; 95% CI, 1.19–2.88) were more likely than GPs in major cities to recruit at least one randomised participant. GPs in areas with a high proportion of people aged 70 years or more were more likely to randomise at least one participant (per percentage point increase: aOR, 1.10; 95% CI, 1.05–1.15). The number of randomised patients declined with time from GP enrolment to first randomisation.

                      Conclusion: General practice can be a rich environment for research when barriers to recruitment are overcome. Including regional GPs and focusing efforts in areas with the highest proportions of potentially eligible participants improves recruitment. The success of ASPREE attests to the clinical importance of its research question for Australian GPs.

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                      • 1 Monash University, Melbourne, VIC
                      • 2 College of Health and Medicine, Australian National University School of Clinical Medicine, Canberra, ACT
                      • 3 Canberra Hospital, Canberra, ACT
                      • 4 University of Tasmania, Hobart, TAS
                      • 5 Curtin University, Perth, WA
                      • 6 University of Adelaide, Adelaide, SA


                      Correspondence: jessica.lockery@monash.edu
                      Acknowledgements: 

                      The ASPREE study, including the design and implementation of the recruitment strategy, was supported by the National Institute on Aging and the National Cancer Institute at the National Institutes of Health in the United States (U01AG029824), the National Health and Medical Research Council (334047 and 1127060), Monash University, and the Victorian Cancer Agency. Bayer provided aspirin and the matching placebo. We acknowledge the dedicated and skilled staff in Australia and the Unites States who undertook the ASPREE trial. We are also most grateful to the ASPREE participants who so willingly volunteered for this study, and the general practitioners and medical clinics who supported the participants in the ASPREE study., (ASPREE): International Standard Randomized Controlled Trial Number Register (ISRCTN83772183) and clinicaltrials.gov (NCT01038583).

                      Competing interests:

                      No relevant disclosures.

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