Topics

In Australia, 24.4% of newborn Aboriginal or Torres Strait Islander infants were admitted to neonatal intensive care units (NICUs) or special care nurseries during 2022, compared with 16.3% of non‐Indigenous infants.1 For Aboriginal and Torres Strait Islander people, culture is a protective factor for strong health and wellbeing,2 but neonatal care can disrupt usual parent–infant care and cultural care practices. Understanding the characteristics of Aboriginal and Torres Strait Islander families receiving neonatal care is important for supporting their needs. Routinely collected national and state data do not typically provide detailed information about Aboriginal and Torres Strait Islander infants admitted to NICUs,1 leading to gaps in knowledge about how to optimise care, particularly at the local level.

1 The University of Newcastle, Newcastle, NSW
2 John Hunter Children's Hospital, Newcastle, NSW
3 Priority Research Centre for Health Behaviour, University of Newcastle, Newcastle, NSW

Correspondence: jessica.bennett@newcastle.edu.au

Data Sharing:

In line with Indigenous data sovereignty and Aboriginal and Torres Strait Islander ethical research principles, data sharing is available for this study.

Acknowledgements:

This study was funded by an Ikara–Flinders Ranges Challenge Grant. We respectfully acknowledge all Aboriginal and Torres Strait Islander people whose data were included in our analysis, and the governing services (Tamworth Aboriginal Medical Service, Tamworth Aboriginal Land Council, Walgett Aboriginal Medical Service, and the Aboriginal Advisory Group) for the leadership, knowledge, and wisdom shared with the investigators.

Competing interests:

No relevant disclosures.

1. Australian Institute of Health and Welfare. Australia's mothers and babies. Updated 24 Sept 2024. https://www.aihw.gov.au/reports/mothers‐babies/australias‐mothers‐babies/contents/about (viewed Oct 2024).
2. Lovett R, Brinckley MM, Phillips B, et al; Mayi Kuwayu Study investigators and partners. Marrathalpu mayingku ngiya kiyi. Minyawaa ngiyani yata punmalaka; wangaaypu kirrampili kara [Ngiyampaa title]; In the beginning it was our people's law. What makes us well; to never be sick. Cohort profile of Mayi Kuwayu: the national study of Aboriginal and Torres Strait Islander wellbeing [English title]. Australian Aboriginal Studies (Canberra) 2020; (2): 8‐30. https://mkstudy.com.au/wp‐content/uploads/2021/03/Lovett‐et‐al_Mayi‐Kuwayu_AAS‐2020_2.pdf (viewed Oct 2024).
3. Walter MA, Anderson, C. Indigenous statistics: a quantitative research methodology. London: Taylor & Francis, 2013.
4. Agency for Clinical Innovation. Neonatal intensive and special care units’ data registry. Undated. https://aci.health.nsw.gov.au/networks/maternity‐and‐neonatal/nicus (viewed Apr 2024).
5. Australian Department of Health and Aged Care. Modified Monash Model. Updated 12 Dec 2023. https://www.health.gov.au/topics/rural‐health‐workforce/classifications/mmm (viewed Apr 2024).
6. Huria T, Palmer SC, Pitama S, et al. Consolidated criteria for strengthening reporting of health research involving indigenous peoples: the CONSIDER statement. BMC Med Res Methodol 2019; 19: 173.
7. United Nations (General Assembly). Declaration on the rights of Indigenous People. 13 Sept 2007. https://www.un.org/development/desa/indigenouspeoples/wp‐content/uploads/sites/19/2018/11/UNDRIP_E_web.pdf (viewed Apr 2024).
8. Nolan‐Isles D, Macniven R, Hunter K, et al. Enablers and barriers to accessing healthcare services for Aboriginal people in New South Wales, Australia. Int J Environ Res Public Health 2021; 18: 3014.

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Disorders of gut–brain interaction, eating disorders and gastroparesis: a call for coordinated care and guidelines on nutrition support

Trina Kellar, Chamara Basnayake, Rebecca E Burgell, Michael Kamm, Hannah W Kim, Kate Lane, Kate Murphy and Nicholas J Talley

Med J Aust || doi: 10.5694/mja2.52537
Published online: 2 December 2024

ARTICLE
AUTHORS
REFERENCES

Topics

Digestive system diseases

Mental disorders

Untangling the complex interplay between eating disorders, gut–brain disorders and motility disorders is challenging. Nationally and internationally, there has been a concerning increase in patients receiving artificial nutrition that may be unnecessary.1 This places patients at risk of iatrogenic harm and results in considerable economic burden to health services. There is a clear need for high quality research to guide care, but in its absence, now more than ever, we require a national treatment consensus to support clinicians working in this field. This article aims to highlight the current status, knowledge, and service limitations in treating this difficult cohort of patients, and make recommendations on future strategies within Australia to move forward for better patient outcomes.

1 University of Queensland, Brisbane, QLD
2 St Vincent's Hospital Melbourne, Melbourne, VIC
3 Alfred Health, Melbourne, VIC
4 University of Melbourne, Melbourne, VIC
5 Orygen the National Centre of Excellence in Youth Mental Health, Melbourne, VIC
6 Queensland Eating Disorder Service, Brisbane, QLD
7 Hunter Medical Research Institute, University of Newcastle, Newcastle, NSW

Correspondence: rbwh-nmc-admin@health.qld.gov.au

Competing interests:

Nicholas Talley is the Emeritus Editor‐In‐Chief of the MJA. We confirm that he was not involved in any review, decision making, or editorial processes for this manuscript.

1. Lal S, Paine P, Tack J, et al. Avoiding the use of long‐term parenteral support in patients without intestinal failure: a position paper from the European Society of Clinical Nutrition & Metabolism, the European Society of Neurogastroenterology and Motility and the Rome Foundation for Disorders of Gut‐Brain Interaction. Neurogastroenterol Motil 2024; 36: e14853.
2. Emmanuel AV, Stern J, Treasure J, et al. Anorexia nervosa in gastrointestinal practice. Eur J Gastroenterol Hepatol 2004; 16: 1135‐1142.
3. Hollis E, Murray HB, Parkman HP. Relationships among symptoms of gastroparesis to those of avoidant/restrictive food intake disorder in patients with gastroparesis. Neurogastroenterol Motil 2024; 36: e14725.
4. Schalla MA, Stengel A. Gastrointestinal alterations in anorexia nervosa ‐ a systematic review. Eur Eat Disord Rev 2019; 27: 447‐461.
5. Murray HB, Bailey AP, Keshishian AC, et al. Prevalence and characteristics of avoidant/restrictive food intake disorder in adult neurogastroenterology patients. Clin Gastroenterol Hepatol 2020; 18: 1995‐2002.
6. Peters JE, Basnayake C, Hebbard GS, et al. Prevalence of disordered eating in adults with gastrointestinal disorders: a systematic review. Neurogastroenterol Motil 2022; 34: e14278.
7. Gallo R, Armstrong E, Griffin H, et al. Impact of enteral tube feeding for individuals with disorders of the gut brain interaction. Clin Nutr ESPEN 2023; 58: 604.
8. Martin LD, Wang X, Day C, et al. Enteral tube feeding in functional gastrointestinal disorders: a game of chance? Clin Nutr ESPEN 2023; 57: 849.
9. Gillanders L, Angstmann K, Ball P, et al. AuSPEN clinical practice guideline for home parenteral nutrition patients in Australia and New Zealand. Nutrition 2008; 24: 998‐1012.
10. Camilleri M, Kuo B, Nguyen L, et al. ACG clinical guideline: gastroparesis. Am J Gastroenterol 2022; 117: 1197‐1220.
11. Cobbaert L, Hay P, Mitchell PB, et al. Sensory processing across eating disorders: a systematic review and meta‐analysis of self‐report inventories. Int J Eat Disord 2024; 57: 1465‐1488.
12. Chiarioni G, Bassotti G, Monsignori A, et al. Anorectal dysfunction in constipated women with anorexia nervosa. Mayo Clin Proc 2000; 75: 1015‐1019.
13. Joyeux MA, Pierre A, Barrois M, et al. Stomach size in anorexia nervosa: a new challenge? Eur Eat Disord Rev 2024; 32: 784‐794.
14. West M, McMaster CM, Staudacher HM, et al. Gastrointestinal symptoms following treatment for anorexia nervosa: a systematic literature review. Int J Eat Disord 2021; 54: 936‐951.
15. Riedlinger C, Schmidt G, Weiland A, et al. Which symptoms, complaints and complications of the gastrointestinal tract occur in patients with eating disorders? A systematic review and quantitative analysis. Front Psychiatry 2020; 11: 195.
16. Andreani NA, Sharma A, Dahmen B, et al. Longitudinal analysis of the gut microbiome in adolescent patients with anorexia nervosa: microbiome‐related factors associated with clinical outcome. Gut Microbes 2024; 16: 2304158.
17. Powell N, Walker MM, Talley NJ. The mucosal immune system: master regulator of bidirectional gut‐brain communications. Nat Rev Gastroenterol Hepatol 2017; 14: 143‐159.
18. Aguilera‐Lizarraga J, Hussein H, Boeckxstaens GE. Immune activation in irritable bowel syndrome: what is the evidence? Nat Rev Immunol 2022; 22: 674‐686.
19. Simons J, Shajee U, Palsson O, et al. Disorders of gut‐brain interaction: highly prevalent and burdensome yet under‐taught within medical education. United European Gastroenterol J 2022; 10: 736‐744.
20. Denman E, Parker EK, Ashley MA, et al. Understanding training needs in eating disorders of graduating and new graduate dietitians in Australia: an online survey. J Eat Disord 2021; 9: 27.
21. Knowles SR, Apputhurai P, Palsson OS, et al. The epidemiology and psychological comorbidity of disorders of gut–brain interaction in Australia: results from the Rome Foundation Global Epidemiology Study. Neurogastroenterol Motil 2023; 35: e14594.

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Perspective

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The equitable challenges to quality use of modulators for cystic fibrosis in Australia

Laura K Fawcett, Shafagh A Waters and Adam Jaffe

Med J Aust || doi: 10.5694/mja2.52527
Published online: 2 December 2024

ARTICLE
AUTHORS
REFERENCES

Topics

Respiratory tract diseases

Health services administration

Cystic fibrosis, an autosomal recessive disease, causes premature mortality with a current life expectancy of 56 years.1 Variations in a single gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR), an anion channel, cause this multisystemic disease.2 Bronchiectasis remains the most significant contributor to mortality, with other affected systems including the gastrointestinal, pancreatic, hepatobiliary, sweat glands and reproductive systems.3 Clinical manifestations of cystic fibrosis vary widely, leading to diverse phenotypic expressions.

1 Sydney Children's Hospital Randwick, Sydney, NSW
2 University of New South Wales, Sydney, NSW

Correspondence: laura.fawcett@health.nsw.gov.au

Acknowledgements:

LF is supported by the Rotary Club of Sydney Cove/Sydney Children's Hospital Foundation and UNSW postgraduate award scholarships. SW is supported by the UNSW Scientia program and the Australian National Health and Medical Research Council. There was no role of the funding sources in the planning, writing or publication of the work. Colman Taylor provided feedback on a draft manuscript regarding health technology assessment pathways.

Competing interests:

AJ is chair of the scientific and medical advisory committee of Rare Voices Australia and has received speaker payments from Vertex Pharmaceuticals. LF has been a sub‐investigator on Vertex clinical trials and received sponsorship of travel costs to attend educational meetings. SW has received competitive funding sponsored by Vertex Pharmaceuticals. Vertex Pharmaceuticals had no involvement in the planning, writing or publication of this article.

1. Ruseckaite R, Salimi F, Earnest A, et al. Survival of people with cystic fibrosis in Australia. Sci Rep 2022; 12: 1‐9.
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3. Elborn JS. Cystic fibrosis. Lancet 2016; 388: 2519‐2531.
4. Clinical and Functional Translation of CFTR, CFTR2 Variant List History [website]. US Cystic Fibrosis Foundation, John Hopkins University, The Hospital for Sick Children. https://cftr2.org/mutations_history (viewed Feb 2024).
5. Australian Cystic Fibrosis Data Registry [website]. Cystic Fibrosis Australia. https://www.cysticfibrosis.org.au/cf‐data‐registry/ (viewed Feb 2024).
6. Middleton PG, Mall MA, Dřevínek P, et al. Elexacaftor–Tezacaftor–Ivacaftor for cystic fibrosis with a single Phe508del allele. N Engl J Med 2019; 381: 1809‐1819.
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10. McGarry ME, Gibb ER, Oates GR, Schechter MS. Left behind: the potential impact of CFTR modulators on racial and ethnic disparities in cystic fibrosis. Paediatr Respir Rev 2022; 42: 35‐42.
11. Kerem E, Reisman J, Corey M, et al. Prediction of mortality in patients with cystic fibrosis. N Engl J Med 1992; 326: 1187‐1191.
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13. Gee L, Abbott J, Conway SP, et al. Development of a disease specific health related quality of life measure for adults and adolescents with cystic fibrosis. Thorax 2000; 55: 946‐954.
14. Sontag MK. Sweat chloride: the critical biomarker for cystic fibrosis trials. Am J Respir Crit Care Med 2016; 194: 1311‐1313.
15. Boyle MP, Bell SC, Konstan MW, et al. A CFTR corrector (lumacaftor) and a CFTR potentiator (ivacaftor) for treatment of patients with cystic fibrosis who have a phe508del CFTR mutation: a phase 2 randomised controlled trial. Lancet Respir Med 2014; 2: 527‐538.
16. Sondo E, Cresta F, Pastorino C, et al. The L467F‐F508del complex allele hampers pharmacological rescue of mutant CFTR by elexacaftor/tezacaftor/ivacaftor in cystic fibrosis patients: the value of the ex vivo nasal epithelial model to address non‐responders to CFTR‐modulating drugs. Int J Mol Sci 2022; 23: 3175.
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20. Fawcett LK, Wakefield CE, Sivam S, et al. Avatar acceptability: views from the Australian cystic fibrosis community on the use of personalised organoid technology to guide treatment decisions. ERJ Open Res 2021; 7: 1‐10.
21. Berkers G, van Mourik P, Vonk AM, et al. Rectal organoids enable personalized treatment of cystic fibrosis. Cell Rep 2019; 26: 1701‐1708.
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30. Rosenfeld M, Wainwright CE, Higgins M, et al. Ivacaftor treatment of cystic fibrosis in children aged 12 to <24 months and with a CFTR gating mutation (ARRIVAL): a phase 3 single‐arm study. Lancet Respir Med 2018; 6: 545‐553.
31. Davies JC, Wainwright CE, Sawicki GS, et al. Ivacaftor in infants aged 4 to <12 months with cystic fibrosis and a gating mutation results of a two‐part phase 3 clinical trial. Am J Respir Crit Care Med 2021; 203: 585‐593.
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33. Milla CE, Ratjen F, Marigowda G, et al. Lumacaftor/Ivacaftor in patients aged 6‐11 years with cystic fibrosis and homozygous for F508del‐CFTR. Am J Respir Crit Care Med 2017; 195: 912‐920.
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37. Taylor‐Cousar JL, Munck A, McKone EF, et al. Tezacaftor–ivacaftor in patients with cystic fibrosis homozygous for Phe508del. N Engl J Med 2017; 377: 2013‐2023.
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40. Heijerman HGM, McKone EF, Downey DG, et al. Efficacy and safety of the elexacaftor/tezacaftor/ivacaftor combination regimen in people with cystic fibrosis homozygous for the F508del mutation: a double‐blind, randomised, phase 3 trial. Lancet 2019; 394: 1940.
41. Sutharsan S, McKone EF, Downey DG, et al. Efficacy and safety of elexacaftor plus tezacaftor plus ivacaftor versus tezacaftor plus ivacaftor in people with cystic fibrosis homozygous for F508del‐CFTR: a 24‐week, multicentre, randomised, double‐blind, active‐controlled, phase 3b trial. Lancet Respir Med 2022; 10: 267‐277.
42. Zemanick ET, Taylor‐Cousar JL, Davies J, et al. A phase 3 open‐label study of elexacaftor/tezacaftor/ivacaftor in children 6 through 11 years of age with cystic fibrosis and at least one F508del allele. Am J Respir Crit Care Med 2021; 203: 1522‐1532.
43. Mall MA, Brugha R, Gartner S, et al. Efficacy and safety of elexacaftor/tezacaftor/ivacaftor in children 6 through 11 years of age with cystic fibrosis heterozygous for F508del and a minimal function mutation A phase 3b, randomized, placebo‐controlled study. Am J Respir Crit Care Med 2022; 206: 1361‐1369.
44. Goralski JL, Hoppe JE, Mall MA, et al. Phase 3 open‐label clinical trial of elexacaftor/tezacaftor/ivacaftor in children aged 2–5 years with cystic fibrosis and at least one F508del allele. Am J Respir Crit Care Med 2023; 208: 59‐67.
45. Lorentzos MS, Metz D, Moore AS, et al. Providing Australian children and adolescents with equitable access to new and emerging therapies through clinical trials: a call to action. Med J Aust 2024; 220: 121‐125. https://www.mja.com.au/journal/2024/220/3/providing‐australian‐children‐and‐adolescents‐equitable‐access‐new‐and‐emerging
46. Burgel PR, Sermet‐Gaudelus I, Durieu I, et al. The French Compassionate Program of elexacaftor‐tezacaftor‐ivacaftor in people with cystic fibrosis with advanced lung disease and no F508del CFTR variant. Eur Respir J 2023; 61: 2202437.

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Systematic review

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Interventions for Aboriginal and Torres Strait Islander people with type 2 diabetes that modify its management and cardiometabolic risk factors: a systematic review

Ciying Tan, Zoe Williams, Mohammad Ashraful Islam, Ray Kelly, Tuguy Esgin and Elif I Ekinci

Med J Aust || doi: 10.5694/mja2.52508
Published online: 25 November 2024

ARTICLE
AUTHORS
REFERENCES

Topics

Endocrine system diseases

Indigenous health

Statistics, epidemiology and research design

Abstract

Objectives: To review studies of interventions for reducing the impact of type 2 diabetes in Aboriginal and Torres Strait Islander people. The primary aim was to review and summarise the characteristics and findings of the interventions. The secondary aims were to assess their effects on diabetes and cardiometabolic risk factors, and the proportions of people with type 2 diabetes who achieved therapeutic targets with each intervention.

Study design: We searched eight electronic databases for publications of studies including Aboriginal or Torres Strait Islander people aged 15 years or older with diagnoses of type 2 diabetes, describing one or more diabetes interventions, and published in English during 1 January 2000 – 31 December 2020. Reference lists in the assessed articles were checked for further relevant publications.

Data sources: MEDLINE (Ovid), Web of Science (Clarivate), the Cochrane Library, Global Health (EBSCO), Indigenous Collection and Indigenous Australia (Informit), Cumulative Index to Nursing and Allied Health Literature (CINAHL), and the World Health Organization International Clinical Trials Registry Platform (WHO‐ICTRP).

Results: The database searches yielded 1424 unique records; after screening by title and abstract, the full text of 55 potentially relevant articles were screened, of which seventeen met our eligibility criteria: eleven cohort studies (seven retrospective audits and four prospective studies), three randomised controlled trials, and three observational, non‐randomised follow‐up studies. Twelve publications reported site‐based (Aboriginal or Torres Strait Islander health service or diabetes clinic) rather than individual‐based diabetes interventions. Interventions with statistically significant effects on mean glycated haemoglobin (HbA_1c) levels were laparoscopic adjustable gastric banding, a 5‐day diabetes self‐management camp, treatment of Strongyloides stercoralis infections, community‐based health worker‐led management, point‐of‐care testing, and self‐management approaches.

Conclusions: Few interventions for Aboriginal and Torres Strait Islander people with type 2 diabetes have been reported in peer‐reviewed publications. Improving diabetes care services resulted in larger proportions of people achieving therapeutic HbA_1c targets. Outcomes were better when Aboriginal and Torres Strait Islander communities were involved at all levels of an intervention. High quality studies of holistic, culturally safe and accessible interventions should be the focus of research.

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1 The Australian Centre for Accelerating Diabetes Innovations, Melbourne Medical School, the University of Melbourne, Melbourne, VIC
2 Austin Health, Melbourne, VIC
3 The University of Sydney, Sydney, NSW
4 Edith Cowan University, Perth, WA

Correspondence: elif.ekinci@unimelb.edu.au

Acknowledgements:

We thank Anita Horvath (Medical Education, University of Melbourne) for her support and advice in the standard structure and format of the review.

Competing interests:

Elif I Ekinci has received payment for sitting on an advisory panel for Eli Lilly Australia; and donated the money to her institution for diabetes research. She has received research support from Eli Lilly Australia, Novo Nordisk, Boehringer Ingelheim, the Eli Lilly Alliance, Versanis, Endogenex Insulet Corporation, and Medtronic.

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23. Chung F, Herceg A, Bookallil M. Diabetes clinic attendance improves diabetes management in an urban Aboriginal and Torres Strait Islander population. Aust Fam Physician 2014; 43: 797‐802.
24. Stoneman A, Atkinson D, Davey M, Marley JV. Quality improvement in practice: improving diabetes care and patient outcomes in Aboriginal Community Controlled Health Services. BMC Health Serv Res 2014; 14: 481.
25. McDermott RA, Schmidt B, Preece C, et al. Community health workers improve diabetes care in remote Australian Indigenous communities: results of a pragmatic cluster randomized controlled trial. BMC Health Serv Res 2015; 15: 68.
26. O'Brien PE, DeWitt DE, Laurie C, et al. The effect of weight loss on Indigenous Australians with diabetes: a study of feasibility, acceptability and effectiveness of laparoscopic adjustable gastric banding. Obes Surg 2016; 26: 45‐53.
27. Kapellas K, Mejia G, Bartold PM, et al. Periodontal therapy and glycaemic control among individuals with type 2 diabetes: reflections from the PerioCardio study. Int J Dent Hyg 2017; 15: e42‐e51.
28. Hays R, Giacomin P, Olma L, et al. The relationship between treatment for Strongyloides stercoralis infection and type 2 diabetes mellitus in an Australian Aboriginal population: a three‐year cohort study. Diabetes Res Clin Pract 2017; 134: 8‐16.
29. Lean ME, Leslie WS, Barnes AC, et al. Durability of a primary care‐led weight‐management intervention for remission of type 2 diabetes: 2‐year results of the DiRECT open‐label, cluster‐randomised trial. Lancet Diabetes Endocrinol 2019; 7: 344‐355.
30. Evans J, Canuto K, Kelly R, et al. Physical activity interventions to prevent and manage type 2 diabetes among Aboriginal and Torres Strait Islander peoples: a systematic review protocol. JBI Evid Synth 2021; 19: 177‐183.
31. Harfield S, Davy C, Kite E, et al. Characteristics of Indigenous primary health care models of service delivery: a scoping review protocol. JBI Database System Rev Implement Rep 2015; 13: 43‐51.
32. O'Dea K. Marked improvement in carbohydrate and lipid metabolism in diabetic Australian Aborigines after temporary reversion to traditional lifestyle. Diabetes 1984; 33: 596‐603.
33. Esgin T, Hersh D, Rowley KG, et al. Physical activity and self‐reported metabolic syndrome risk factors in the Aboriginal population in Perth, Australia, measured using an adaptation of the Global Physical Activity Questionnaire (GPAQ). Int J Environ Res Public Health 2021; 18: 5969.
34. Esgin T, Hersh D, Rowley K, et al. Indigenous research methodologies: decolonizing the Australian sports sciences. Health Promot Int 2019; 34: 1231‐1240.
35. Esgin T, Johnston N, Rowley K, et al. Effect of 12 weeks combined aerobic and resistance training on fitness, arterial stiffness and body composition in Indigenous Australian men and women [abstract: ASICS Sports Medicine Australia Conference, Langkawi, Malaysia, 25–28 Oct 2017]. J Sci Med Sport 2017; 20 (Suppl 3): 43.
36. Jack S. Closing the gap on diabetes: a social determinants of health perspective. Aborig Isl Health Work J 2012; 36: 27‐30.
37. Bate KL, Jerums G. Preventing complications of diabetes. Med J Aust 2003; 179: 498‐503. https://www.mja.com.au/journal/2003/179/9/3‐preventing‐complications‐diabetes
38. Riddle MC, Cefalu WT, Evans PH, et al. Consensus report: definition and interpretation of remission in type 2 diabetes. J Clin Endocrinol Metab 2022; 107: 1‐9.
39. Brown LM. A randomised trial of pioglitazone versus metformin monotherapy in Indigenous Australians with type 2 diabetes: effects on metabolic and cardiovascular parameters [Trial registered on ANZCTR: ACTRN12607000135415]. Updated 25 July 2008. https://anzctr.org.au/ACTRN12607000135415.aspx (viewed Mar 2021).
40. Ekinci EI, Pyrlis F, Hachem M, et al. Feasibility of once weekly exenatide–LAR and enhanced diabetes care in Indigenous Australians with type 2 diabetes (Long‐acting–once‐weekly‐exenatide laR–SUGAR, “Lower SUGAR” study). Intern Med J 2021; 51: 1463‐1472.

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Towards a cure for long COVID: the strengthening case for persistently replicating SARS‐CoV‐2 as a driver of post‐acute sequelae of COVID‐19

Michelle JL Scoullar, Gabriela Khoury, Suman S Majumdar, Emma Tippett and Brendan S Crabb

Med J Aust || doi: 10.5694/mja2.52517
Published online: 25 November 2024

ARTICLE
AUTHORS
REFERENCES

Topics

Infectious diseases

New insights into post‐acute sequelae of coronavirus disease 2019 (PASC) or long COVID are emerging at great speed. Proposed mechanisms driving long COVID include the overlapping pathologies of immune and inflammatory dysregulation, microbiota dysbiosis, autoimmunity, endothelial dysfunction, abnormal neurological signalling, reactivation of endogenous herpesviruses, and persistence of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2).1,2 In this commentary, we describe some of these advances that indicate that long COVID may be driven by “long infection” and that persistent replicating SARS‐CoV‐2 may be the potentially mechanistically unifying driver for long COVID.

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1 Burnet Institute, Melbourne, VIC
2 Clinic Nineteen, Melbourne, VIC
3 Monash University, Melbourne, VIC
4 University of Melbourne, Melbourne, VIC

Correspondence: michelle.scoullar@burnet.edu.au

Acknowledgements:

The Burnet Institute is supported by an Operational Infrastructure Grant from the State Government of Victoria, Australia, and the Independent Research Institutes Infrastructure Support Scheme of the NHMRC of Australia.

Competing interests:

No relevant disclosures.

1. Davis HE, McCorkell L, Vogel JM, Topol EJ. Long COVID: major findings, mechanisms and recommendations. Nat Rev Microbiol 2023; 21: 133‐146.
2. Merad M, Blish CA, Sallusto F, Iwasaki A. The immunology and immunopathology of COVID‐19. Science 2022; 375: 1122‐1127.
3. Office for National Statistics. Self‐reported coronavirus (COVID‐19) infections and associated symptoms, England and Scotland: November 2023 to March 2024 [website]. ONS, 2024. https://www.ons.gov.uk/peoplepopulationandcommunity/healthandsocialcare/conditionsanddiseases/articles/selfreportedcoronaviruscovid19infectionsandassociatedsymptomsenglandandscotland/november2023tomarch2024 (viewed Apr 2024).
4. National Center for Health Statistics. US Census Bureau, Household Pulse Survey, 2022–2024. Long COVID. Generated interactively [website]. CDC, 2024. https://www.cdc.gov/nchs/covid19/pulse/long‐covid.htm (viewed May 2024).
5. Bowe B, Xie Y, Al‐Aly Z. Postacute sequelae of COVID‐19 at 2 years. Nat Med 2023; 29: 2347‐2357.
6. Woldegiorgis M, Cadby G, Ngeh S, et al. Long COVID in a highly vaccinated but largely unexposed Australian population following the 2022 SARS‐CoV‐2 Omicron wave: a cross‐sectional survey. Med J Aust 2024; 220: 323‐330. https://www.mja.com.au/journal/2024/220/6/long‐covid‐highly‐vaccinated‐largely‐unexposed‐australian‐population‐following
7. Ledford H. Long COVID is a double curse in low‐income nations — here's why [media release]. Nature, 2024. https://www.nature.com/articles/d41586‐023‐04088‐x (viewed May 2024).
8. Rao S, Gross RS, Mohandas S, et al. Postacute sequelae of SARS‐CoV‐2 in children. Pediatrics 2024; 153: e2023062570.
9. Appelman B, Charlton BT, Goulding RP, et al. Muscle abnormalities worsen after post‐exertional malaise in long COVID. Nat Commun 2024; 15: 17.
10. Fedorowski A, Fanciulli A, Raj SR, et al. Cardiovascular autonomic dysfunction in post‐COVID‐19 syndrome: a major health‐care burden. Nat Rev Cardiol 2024; 21: 379‐395.
11. Greene C, Connolly R, Brennan D, et al. Blood–brain barrier disruption and sustained systemic inflammation in individuals with long COVID‐associated cognitive impairment. Nat Neurosci 2024; 27: 421‐432.
12. Hampshire A, Azor A, Atchison C, et al. Cognition and memory after Covid‐19 in a large community sample. N Engl J Med 2024; 390: 806‐818.
13. Cervia‐Hasler C, Brüningk SC, Hoch T, et al. Persistent complement dysregulation with signs of thromboinflammation in active Long Covid. Science 2024; 383: eadg7942.
14. Davitt E, Davitt C, Mazer MB, et al. COVID‐19 disease and immune dysregulation. Best Pract Res Clin Haematol 2022; 35: 101401.
15. Yin K, Peluso MJ, Luo X, et al. Long COVID manifests with T cell dysregulation, inflammation and an uncoordinated adaptive immune response to SARS‐CoV‐2. Nat Immunol 2024; 25: 218‐225.
16. Phetsouphanh C, Darley DR, Wilson DB, et al. Immunological dysfunction persists for 8 months following initial mild‐to‐moderate SARS‐CoV‐2 infection. Nat Immunol 2022; 23: 210‐216.
17. Phetsouphanh C, Jacka B, Ballouz S, et al. Improvement of immune dysregulation in individuals with long COVID at 24‐months following SARS‐CoV‐2 infection. Nat Commun 2024; 15: 3315.
18. Chen B, Julg B, Mohandas S, Bradfute SB, RECOVER Mechanistic Pathways Task Force. Viral persistence, reactivation, and mechanisms of long COVID. eLife 2023; 12: e86015.
19. Proal AD, VanElzakker MB, Aleman S, et al. SARS‐CoV‐2 reservoir in post‐acute sequelae of COVID‐19 (PASC). Nat Immunol 2023; 24: 1616‐1627.
20. Ghafari M, Hall M, Golubchik T, et al. Prevalence of persistent SARS‐CoV‐2 in a large community surveillance study. Nature 2024; 626: 1094‐1101.
21. Menezes SM, Jamoulle M, Carletto MP, et al. Blood transcriptomic analyses reveal persistent SARS‐CoV‐2 RNA and candidate biomarkers in post‐COVID‐19 condition. Lancet Microbe 2024; 5: 100849.
22. Peluso MJ, Swank ZN, Goldberg SA, et al. Plasma‐based antigen persistence in the post‐acute phase of COVID‐19. Lancet Infect Dis 2024; 24: E345‐E347.
23. Zuo W, He D, Liang C, et al. The persistence of SARS‐CoV‐2 in tissues and its association with long COVID symptoms: a cross‐sectional cohort study in China. Lancet Infect Dis 2024; 24: 845‐855.
24. Zollner A, Koch R, Jukic A, et al. Postacute COVID‐19 is characterized by gut viral antigen persistence in inflammatory bowel diseases. Gastroenterology 2022; 163: 495‐506.
25. Platt A, Singh M, Stein S, et al. Replication‐competent virus detected in blood of a fatal COVID‐19 case. Ann Intern Med 2024; 177: 113‐135.
26. Xu E, Xie Y, Al‐Aly Z. Long‐term gastrointestinal outcomes of COVID‐19. Nat Commun 2023; 14: 983.
27. Zhu A, Real F, Capron C, et al. Infection of lung megakaryocytes and platelets by SARS‐CoV‐2 anticipate fatal COVID‐19. Cell Mol Life Sci 2022; 79: 365.
28. Català M, Mercadé‐Besora N, Kolde R, et al. The effectiveness of COVID‐19 vaccines to prevent long COVID symptoms: staggered cohort study of data from the UK, Spain, and Estonia. Lancet Respir Med 2024; 12: 225‐236.
29. Xie Y, Choi T, Al‐Aly Z. Postacute sequelae of SARS‐CoV‐2 infection in the pre‐Delta, Delta, and Omicron eras. N Engl J Med 2024; 391: 515‐525.
30. Bramante CT, Beckman KB, Mehta T, et al. Favorable antiviral effect of metformin on severe acute respiratory syndrome Coronavirus 2 viral load in a randomized, placebo‐controlled clinical trial of Coronavirus disease 2019. Clin Infect Dis 2024; 79: 354‐363.

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Research

Cerebral palsy in Australia: birth prevalence, 1995–2016, and differences by residential remoteness: a population-based register study

Hayley Smithers‐Sheedy, Emma Waight, Shona Goldsmith, Sue Reid, Catherine Gibson, Heather Scott, Linda Watson, Megan Auld, Fiona Kay, Clare Wiltshire, Gina Hinwood, Annabel Webb, Tanya Martin, Nadia Badawi and Sarah McIntyre, the ACPR Group

Med J Aust 2024; 221 (10): . || doi: 10.5694/mja2.52487
Published online: 18 November 2024

ARTICLE
AUTHORS
REFERENCES

Topics

Nervous system diseases

Statistics, epidemiology and research design

Pediatric medicine

General medicine

Environment and public health

Abstract

Objective: To examine recent changes in the birth prevalence of cerebral palsy in Australia; to examine the functional mobility of children with cerebral palsy by residential remoteness.

Study design: Population‐based register study; analysis of Australian Cerebral Palsy Register (ACPR) data.

Setting, participants: Children with cerebral palsy born in Australia, 1995–2016, and included in the ACPR at the time of the most recent state/territory data provision (31 July 2022).

Main outcome measures: Change in birth prevalence of cerebral palsy, of cerebral palsy acquired pre‐ or perinatally (in utero to day 28 after birth), both overall and by gestational age group (less than 28, 28–31, 32–36, 37 or more weeks), and of cerebral palsy acquired post‐neonatally (day 29 to two years of age); gross motor function classification by residential remoteness.

Results: Data for 10 855 children with cerebral palsy born during 1995–2016 were available, 6258 of whom were boys (57.7%). The birth prevalence of cerebral palsy in the three states with complete case ascertainment (South Australia, Victoria, Western Australia) declined from 2.1 (95% confidence interval [CI], 1.9–2.4) cases per 1000 live births in 1995–1996 to 1.5 (95% CI, 1.3–1.7) cases per 1000 live births in 2015–2016. The birth prevalence of pre‐ or perinatally acquired cerebral palsy declined from 2.0 (95% CI, 1.7–2.3) to 1.4 (95% CI, 1.2–1.6) cases per 1000 live births; statistically significant declines were noted for all gestational ages except 32–36 weeks. The decline in birth prevalence of post‐neonatally acquired cerebral palsy, from 0.15 (95% CI, 0.11–0.21) to 0.08 (95% CI, 0.05–0.12) cases per 1000 live births, was not statistically significant. Overall, 3.4% of children with cerebral palsy (307 children) lived in remote or very remote areas, a larger proportion than for all Australians (2.0%); the proportion of children in these areas who required wheelchairs for mobility was larger (31.3%) than that of children with cerebral palsy in major cities or regional areas (each 26.1%).

Conclusions: The birth prevalence of cerebral palsy declined markedly in Australia during 1995–2016, reflecting the effects of advances in maternal and perinatal care. Our findings highlight the need to provide equitable, culturally safe access to antenatal services for women, and to health and disability services for people with cerebral palsy, across Australia.

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1 Cerebral Palsy Alliance Research Institute, the University of Sydney, Sydney, NSW
2 Murdoch Children's Research Institute, the Royal Children's Hospital, Melbourne, VIC
3 SA Birth Defects and Cerebral Palsy Registers, Women's and Children's Health Network, Adelaide, SA
4 WA Register of Developmental Anomalies, Western Australian Department of Health, Perth, WA
5 Queensland Cerebral Palsy Register: Choice, Passion, Life, Brisbane, QLD
6 Northern Territory Top End Health Service, Darwin, NT
7 Royal Hobart Hospital, Hobart, TAS
8 Children's Hospital at Westmead, Sydney, NSW

Correspondence: hsmitherssheedy@cerebralpalsy.org.au

Data Sharing:

The authors had access to all raw data, statistical reports, and tables. The de‐identified data are not publicly available, but requests to the corresponding author will be considered on a case‐by‐case basis.

Acknowledgements:

The Australian Capital Territory, New South Wales, and Australian cerebral palsy registers are funded by the Cerebral Palsy Alliance Research Foundation, the Northern Territory register by Women, Children and Youth, Royal Darwin Hospital, the Queensland register by Choice, Passion, Life, the South Australian register by the Women's and Children's Health Network (with additional support from Novita), and the Tasmanian register by St Giles and the Tasmanian Department of Health. The Victorian register received funding from the Victorian Department of Health and Human Services and the Cerebral Palsy Alliance Research Foundation, and infrastructure support from the Victorian Government Operational Infrastructure Support Program. The Western Australian Register of Developmental Anomalies: Cerebral Palsy is funded by the Western Australian Department of Health. The funding sources support the work of the cerebral palsy registers, which included the preparation of this report.

The ACPR Group acknowledge all the children with cerebral palsy and their families, and the clinicians who support them. We thank the Consultative Council on Obstetric and Paediatric Mortality and Morbidity (CCOPMM) for providing access to Victorian denominator data for this analysis and for the assistance of Safer Care Victoria staff. The conclusions, findings, opinions, and views or recommendations expressed in this article are those of the authors, and do not necessarily reflect those of CCOPMM.

Competing interests:

No relevant disclosures.

1. Rosenbaum P, Paneth N, Leviton A, et al. A report: the definition and classification of cerebral palsy April 2006. Dev Med Child Neurol Suppl 2007; 49: 8‐14.
2. Australian Cerebral Palsy Register. Australian Cerebral Palsy Register report 2023: birth years 1995–2016. Jan 2023. https://cpregister.wpengine.com/wp‐content/uploads/2023/01/2023‐ACPR‐Report.pdf (viewed Jan 2024).
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19. Crowther CA, Ashwood P, Middleton P, et al; MAGENTA Study Group. Prenatal intravenous magnesium at 30–34 weeks’ gestation and neurodevelopmental outcomes in offspring: the MAGENTA randomized clinical trial. JAMA 2023; 330: 603‐614.
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21. Shepherd E, Salam RA, Middleton P, et al. Antenatal and intrapartum interventions for preventing cerebral palsy: an overview of Cochrane systematic reviews. Cochrane Database Syst Rev 2017; 8: CD012077.
22. Chow S, Creighton, P, Holberton, JR, et al. 2021 Report of the Australian and New Zealand Neonatal Network. 2023. https://anznn.net/Portals/0/AnnualReports/Report%20of%20the%20Australian%20and%20New%20Zealand%20Neonatal%20Network%202021%20amended2.pdf (viewed Jan 2024).
23. McIntyre S, Blair E, Badawi N, et al. Antecedents of cerebral palsy and perinatal death in term and late preterm singletons. Obstet Gynecol 2013; 122: 869‐877.
24. Palmer K, Mockler J, Davies‐Tuck M, et al. Protect‐me: a parallel‐group, triple blinded, placebo‐controlled randomised clinical trial protocol assessing antenatal maternal melatonin supplementation for fetal neuroprotection in early‐onset fetal growth restriction. BMJ Open 2019; 9: e028243
25. Waight E, McIntyre S, Woolfenden S, et al; Australian Cerebral Palsy Register Group. Temporal trends, clinical characteristics, and sociodemographic profile of post‐neonatally acquired cerebral palsy in Australia, 1973–2012: a population‐based observational study. Dev Med Child Neurol. 2023; 65: 107‐116
26. Martin T, McIntyre S, Waight E, et al; ACPR Birds‐Eye View Group. Prevalence and trends for Aboriginal and Torres Strait Islander children living with cerebral palsy: a birds‐eye view. Dev Med Child Neurol 2023; 65: 1475‐1485
27. Bizuayehu HM, Harris ML, Chojenta C, et al. Maternal residential area effects on preterm birth, low birth weight and caesarean section in Australia: a systematic review. Midwifery 2023; 123: 103704.
28. Woolfenden S, Galea C, Smithers‐Sheedy H, et al; Australian Cerebral Palsy Register Group; CP Quest. Impact of social disadvantage on cerebral palsy severity. Dev Med Child Neurol 2019; 61: 586‐592.

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Five decades of debate on burnout

Renzo Bianchi and James F Sowden

Med J Aust || doi: 10.5694/mja2.52512
Published online: 11 November 2024

ARTICLE
AUTHORS
REFERENCES

Topics

Mental disorders

Diagnostic techniques and procedures

Environment and public health

Occupational diseases

First described in the mid‐1970s, “burnout” has elicited continued interest among occupational health specialists.1,2 The World Health Organization3 defines burnout as a triadic syndrome that comprises: (i) feelings of energy depletion or exhaustion; (ii) increased mental distance from one's job, or feelings of negativism or cynicism towards one's job; and (iii) a sense of ineffectiveness and lack of accomplishment. This definition closely aligns with the conceptualisation of burnout in the Maslach Burnout Inventory, the most prominent measure of the entity.2,4 Although burnout has become a popular indicator of job‐related distress, persistent controversies surround the construct. As burnout reaches its half‐century of existence, this article offers an overview of key research developments that have prompted investigators to revamp their views of the syndrome.

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1 Norwegian University of Science and Technology, Trondheim, TR, Norway
2 Flinders University, Adelaide, SA

Correspondence: renzo.bianchi@ntnu.no

Competing interests:

No relevant disclosures.

1. Freudenberger HJ. Staff burn‐out. J Soc Issues 1974; 30: 159‐165.
2. Maslach C, Schaufeli WB, Leiter MP. Job burnout (here: p. 404). Annu Rev Psychol 2001; 52: 397‐422.
3. World Health Organization. International Classification of Diseases. 11th ed. Geneva: WHO, 2022.
4. Maslach C, Jackson SE, Leiter MP. Maslach Burnout Inventory manual. 4th ed. Menlo Park: Mind Garden, 2016.
5. Maslach C, Leiter MP. The burnout challenge: managing people's relationships with their jobs (here: p. 3). Cambridge: Harvard University Press, 2022.
6. Lesener T, Gusy B, Wolter C. The job demands‐resources model: a meta‐analytic review of longitudinal studies. Work Stress 2019; 33: 76‐103.
7. Guthier C, Dormann C, Voelkle MC. Reciprocal effects between job stressors and burnout: a continuous time meta‐analysis of longitudinal studies. Psychol Bull 2020; 146: 1146‐1173.
8. Bianchi R, Verkuilen J, Schonfeld IS, et al. Is burnout a depressive condition? A 14‐sample meta‐analytic and bifactor analytic study. Clin Psychol Sci 2021; 9: 579‐597.
9. Rotenstein LS, Torre M, Ramos MA, et al. Prevalence of burnout among physicians: a systematic review. JAMA 2018; 320: 1131‐1150.
10. Haslam N. Concept creep: psychology's expanding concepts of harm and pathology. Psychol Inq 2016; 27: 1‐17.
11. Sowden JF, Schonfeld IS, Bianchi R. Are Australian teachers burned‐out or depressed? A confirmatory factor analytic study involving the Occupational Depression Inventory. J Psychosom Res 2022; 157: 110783.
12. Willner P, Scheel‐Krüger J, Belzung C. The neurobiology of depression and antidepressant action. Neurosci Biobehav Rev 2013; 37: 2331‐2371.
13. Sen S. Is it burnout or depression? Expanding efforts to improve physician well‐being. N Engl J Med 2022; 387: 1629‐1630.
14. Bianchi R, Schonfeld IS, Laurent E. Biological research on burnout‐depression overlap: long‐standing limitations and on‐going reflections. Neurosci Biobehav Rev 2017; 83: 238‐239.
15. Schaufeli WB, Leiter MP, Maslach C. Burnout: 35 years of research and practice. Career Dev Int 2009; 14: 204‐220.
16. Sterkens P, Baert S, Rooman C, Derous E. Why making promotion after a burnout is like boiling the ocean. Eur Sociol Rev 2023; 39: 516‐531.
17. Smith J, Cvejic E, Lal TJ, et al. Impact of alternative terminology for depression on help‐seeking intention: a randomized online trial (here: p. 80‐81). J Clin Psychol 2023; 79: 68‐85.
18. Bianchi R, Schonfeld IS. Examining the evidence base for burnout. Bull World Health Organ 2023; 101: 743‐745.
19. Friberg T. Burnout: from popular culture to psychiatric diagnosis in Sweden. Cult Med Psychiatry 2009; 33: 538‐558.
20. Schaufeli WB, Enzmann D. The burnout companion to study and practice: a critical analysis. London: Taylor & Francis, 1998.
21. Shirom A. Reflections on the study of burnout. Work Stress 2005; 19: 263‐270.
22. Bianchi R, Swingler G, Schonfeld IS. The Maslach Burnout Inventory is not a measure of burnout. Work 2024; https://doi.org/10.3233/WOR‐240095 [online ahead of print].
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Social media: the root cause of rising youth self‐harm or a convenient scapegoat?

Helen Christensen, Aimy Slade and Alexis E Whitton

Med J Aust || doi: 10.5694/mja2.52503
Published online: 4 November 2024

ARTICLE
AUTHORS
REFERENCES

Topics

Mental disorders

Information science

Recent events have reignited debate over whether social media is the root cause of increasing youth self‐harm and suicide. Social media is a fertile ground for disseminating harmful content, including graphic imagery and messages depicting gendered violence and religious intolerance. This proliferation of harmful content makes social media an unwelcoming space, especially for women, minority groups, and young people, who are more likely to be targeted by such content, strengthening the narrative that social media is at the crux of a youth mental health crisis.

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Black Dog Institute, Sydney, NSW

Correspondence: a.whitton@unsw.edu.au

Acknowledgements:

This work is supported by a Medical Research Future Fund Million Minds Suicide Prevention Grant (APP1200195). Alexis Whitton is supported by a National Health and Medical Research Council (NHMRC) Investigator Grant (grant # 2017521). Helen Christensen is a recipient of a NHMRC Investigator Grant (#1155614). The funding body did not play a role in the decision to write or publish this manuscript.

Competing interests:

No relevant disclosures.

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