Topics

Abstract

Objectives: To determine the incidence of self‐reported non‐coeliac wheat sensitivity (SR‐NCWS) and factors associated with its onset and resolution; to describe the prevalence of factors associated with gluten avoidance.

Design: Longitudinal cohort study; analysis of responses to self‐administered validated questionnaires (Digestive Health and Wellbeing surveys, 2015 and 2018).

Setting, participants: Subset of an adult population sample randomly selected in 2015 from the electoral rolls for the Newcastle and Gosford regions of New South Wales.

Main outcome measures: Prevalence of SR‐NCWS (2015, 2018) and incidence and resolution of SR‐NCWS, each by demographic and medical factors; prevalence of gluten avoidance and reasons for gluten avoidance (2018).

Results: 1322 of 2185 eligible participants completed the 2018 survey (response rate, 60.5%). The prevalence of SR‐NCWS was similar in 2015 (13.8%; 95% CI, 12.0–15.8%) and 2018 (13.9%; 95% CI, 12.1–15.9%); 69 of 1301 respondents (5.3%) reported developing new onset (incident) SR‐NCWS between 2015 and 2018 (incidence, 1.8% per year). Incident SR‐NCWS was significantly associated with a diagnosis of functional dyspepsia, and negatively associated with being male or older. Gluten avoidance was reported in 2018 by 24.2% of respondents (20.5% partial, 3.8% complete avoidance); general health was the most frequent reason for avoidance (168 of 316 avoiders, 53%). All 13 participants with coeliac disease, 56 of 138 with irritable bowel syndrome (41%), and 69 of 237 with functional dyspepsia (29%) avoided dietary gluten.

Conclusions: The prevalence of SR‐NCWS was similar in 2015 and 2018. Baseline (2015) and incident SR‐NCWS (2018) were each associated with functional gastrointestinal disorders. The number of people avoiding dietary gluten exceeds that of people with coeliac disease or SR‐NCWS, and general health considerations and abdominal symptoms are the most frequently reported reasons for avoidance.

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1 University of Newcastle, Newcastle, NSW
2 John Hunter Hospital, Newcastle, NSW
3 Macquarie University, Sydney, NSW
4 University of Queensland, Brisbane, QLD
5 Princess Alexandra Hospital, Brisbane, QLD

Correspondence: Michael.Potter@hnehealth.nsw.gov.au

Acknowledgements:

This project was partially supported by a grant from Prometheus Laboratories.

Competing interests:

No relevant disclosures.

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Research

The incidence of childhood cancer in Australia, 1983–2015, and projections to 2035

Danny R Youlden, Peter D Baade, Adèle C Green, Patricia C Valery, Andrew S Moore and Joanne F Aitken

Med J Aust 2020; 212 (3): . || doi: 10.5694/mja2.50456
Published online: 17 February 2020

ARTICLE
AUTHORS
REFERENCES

Topics

Pediatric medicine

Neoplasms

Statistics, epidemiology and research design

Abstract

Objectives: To describe changes in childhood cancer incidence in Australia, 1983–2015, and to estimate projected incidence to 2035.

Design, setting: Population‐based study; analysis of Australian Childhood Cancer Registry data for the 20 547 children under 15 years of age diagnosed with cancer in Australia between 1983 and 2015.

Main outcome measures: Incidence rate changes during 1983–2015 were assessed by joinpoint regression, with rates age‐standardised to the 2001 Australian standard population. Incidence projections to 2035 were estimated by age‐period‐cohort modelling.

Results: The overall age‐standardised incidence rate of childhood cancer increased by 34% between 1983 and 2015, increasing by 1.2% (95% CI, +0.5% to +1.9%) per annum between 2005 and 2015. During 2011–2015, the mean annual number of children diagnosed with cancer in Australia was 770, an incidence rate of 174 cases (95% CI, 169–180 cases) per million children per year. The incidence of hepatoblastoma (annual percentage change [APC], +2.3%; 95% CI, +0.8% to +3.8%), Burkitt lymphoma (APC, +1.6%; 95% CI, +0.4% to +2.8%), osteosarcoma (APC, +1.1%; 95%, +0.0% to +2.3%), intracranial and intraspinal embryonal tumours (APC, +0.9%; 95% CI, +0.4% to +1.5%), and lymphoid leukaemia (APC, +0.5%; 95% CI, +0.2% to +0.8%) increased significantly across the period 1983–2015. The incidence rate of childhood melanoma fell sharply between 1996 and 2015 (APC, –7.7%; 95% CI, –10% to –4.8%). The overall annual cancer incidence rate is conservatively projected to rise to about 186 cases (95% CI, 175–197 cases) per million children by 2035 (1060 cases per year).

Conclusions: The incidence rates of several childhood cancer types steadily increased during 1983–2015. Although the reasons for these rises are largely unknown, our findings provide a foundation for health service planning for meeting the needs of children who will be diagnosed with cancer until 2035.

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1 Cancer Council Queensland, Brisbane, QLD
2 Menzies Health Institute Queensland, Griffith University, Gold Coast, QLD
3 Queensland University of Technology, Brisbane, QLD
4 QIMR Berghofer Medical Research Institute, Brisbane, QLD
5 Cancer Research UK Manchester Institute, Manchester University, Manchester, United Kingdom
6 Children's Health, Queensland Hospital and Health Service, Brisbane, QLD
7 Child Health Research Centre, University of Queensland, Brisbane, QLD
8 Institute for Resilient Regions, University of Southern Queensland, Brisbane, QLD
9 University of Queensland, Brisbane, QLD

Correspondence: dannyyoulden@cancerqld.org.au

Acknowledgements:

Patricia Valery was supported by an NHMRC Career Development Fellowship (1083090). We thank Leisa O'Neill for her work in the Australian Childhood Cancer Registry. We also acknowledge the assistance of all Australian state and territory cancer registries, the Australian Institute of Health and Welfare, and each of the major paediatric oncology treating hospitals throughout Australia.

Competing interests:

No relevant disclosures.

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Perspectives

Implementing value‐based health care at scale: the NSW experience

Elizabeth Koff and Nigel Lyons

Med J Aust 2020; 212 (3): . || doi: 10.5694/mja2.50470
Published online: 17 February 2020

ARTICLE
AUTHORS
REFERENCES

Topics

Global health

Health services administration

Statistics, epidemiology and research design

General medicine

What is value in health care and how can the system deliver it at scale?

The New South Wales health system exemplifies the worldwide challenge of health service sustainability. With 234 public hospitals and facilities employing over 130 000 staff, the system provides universal access to health care for a growing population of almost 8 million people across a diverse geography of over 800 000 km². The NSW Health budget in 2018–19 was $25 billion,1 representing over 25% of the annual state budget. As with all health systems, NSW Health is experiencing growing pressure from chronic disease, an ageing population and the use of new technology. In response, optimising health system access and efficiency has been central to health reform in NSW.2

NSW Health, Sydney, NSW

Correspondence: elizabeth.koff@health.nsw.gov.au

Competing interests:

No relevant disclosures.

1. NSW Government. Budget 2018–19. Budget Paper 1. Chapter 6 – Expenditure. https://www.budget.nsw.gov.au/sites/default/files/budget-2018-06/6._Expenditure-BP1-Budget_201819.pdf (viewed Apr 2019).
2. Garling P. First Report of the Special Commission of Inquiry into Acute Care Services in New South Wales Public Hospitals. Sydney: State of NSW, 2008. https://www.dpc.nsw.gov.au/publications/special-commissions-of-inquiry/special-commission-of-inquiry-into-acute-care-services-in-new-south-wales-public-hospitals/ (viewed Apr 2019).
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5. Gray M. Value based healthcare. BMJ 2017; 356: j437.
6. Li LC, Maetzel A, Pencharz JN, Maguire L, et al. Use of mainstream nonpharmacologic treatment by patients with arthritis. Arthritis Rheum 2004; 51: 203–209.
7. Cavalieri TA. Pain management at the end of life. Clin Geriatr 2005; 13: 44–52.
8. Deloitte Access Economics, for the NSW Agency for Clinical Innovation. Osteoarthritis Chronic Care Program evaluation. Deloitte Access Economics, 2014. https://www.aci.health.nsw.gov.au/__data/assets/pdf_file/0004/338242/OACCP_Evaluation.pdf (viewed Dec 2019).
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Narrative review

First statewide meningococcal B vaccine program in infants, children and adolescents: evidence for implementation in South Australia

Helen S Marshall, Noel Lally, Louise Flood and Paddy Phillips

Med J Aust 2020; 212 (2): . || doi: 10.5694/mja2.50481
Published online: 3 February 2020

ARTICLE
AUTHORS
REFERENCES

Topics

Infectious diseases

Summary

Invasive meningococcal disease (IMD) is an uncommon but life‐threatening infection caused by Neisseria meningitidis. Serogroups B, C, W and Y cause most IMD cases in Australia. The highest incidence occurs in children under 5 years of age. A second peak occurs in adolescents and young adults, which is also the age of highest carriage prevalence of N. meningitidis.
Meningococcal serogroup B (MenB) disease predominated nationally before 2016 and has remained the predominant cause of IMD in South Australia with 82% of cases, compared with 35% in New South Wales, 35% in Queensland, 9% in Victoria, 29% in Western Australia and 36% nationally in 2016.
MenB vaccination is recommended by the Australian Technical Advisory Group on Immunisation for infants up to 2 years of age and adolescents aged 15–19 years (age 15–24 years for at‐risk groups, such as people living in close quarters or smokers), laboratory workers with exposure to N. meningitidis, and Aboriginal and Torres Strait Islander children from age 2 months to 19 years.
Due to the epidemiology and disease burden from MenB, a meningococcal B vaccine program has been implemented in South Australia for individuals with age‐specific incidence rates higher than the mean rate of 2.8/100 000 population in South Australia in the period 2000–2017, including infants, young children (< 4 years) and adolescents (15–20 years).
Program evaluation of vaccine effectiveness against IMD is important. As observational evidence also suggests 4CMenB may have an impact on Neisseria gonorrhoeae with genetic homology between bacterial species, the vaccine impact on gonorrhoea will also be assessed.

1 Women's and Children's Health Network, Adelaide, SA
2 Robinson Research Institute, University of Adelaide, Adelaide, SA
3 Communicable Disease Control Branch, Department for Health and Wellbeing, , Adelaide, SA

Correspondence: helen.marshall@adelaide.edu.au

Acknowledgements:

Helen Marshall is supported by the National Health and Medical Research Council: Career Development Fellowship (1084951). We thank Rodney Pearce and Celia Cooper, members of the South Australian Meningococcal B Expert Working Group, for reviewing the manuscript.

Competing interests:

The University of Adelaide, Helen Marshall's employer, has received funding from GlaxoSmithKline and Pfizer to undergo investigator‐led research. Helen Marshall is a member of ATAGI, but the views expressed in this article are her own views. She does not receive any personal payments from the pharmaceutical industry.

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25. South Australian Meningococcal B Expert Working Group. A Meningococcal B Program for South Australia. Adelaide: SA Health, 2018. https://www.sahealth.sa.gov.au/wps/wcm/connect/public+content/sa+health+internet/about+us/reviews+and+consultation/meningococcal+b+program+for+south+australia (viewed Sept 2018).
26. Australian Government Department of Health. Invasive Meningococcal Disease National Surveillance report, with a focus on MenW — 9 January 2017. Canberra: Commonwealth of Australia, 2017. http://www.health.gov.au/internet/main/publishing.nsf/Content/5FEABC4B495BDEC1CA25807D001327FA/$File/1Jan-31-Dec2017-Consol-Invasive-Men-W.pdf (viewed Dec 2019).
27. Plikaytis BD, Stella M, Boccadifuoco G, et al. Interlaboratory standardization of the sandwich enzyme‐linked immunosorbent assay designed for MATS, a rapid, reproducible method for estimating the strain coverage of investigational vaccines. Clin Vaccine Immunol 2012; 19: 1609–1617.
28. Tozer S, Whiley D, Smith H, et al. Use of the meningococcal antigen typing system to assess the Australian meningococcal strain coverage with a multicomponent serogroup B vaccine. 20th International Pathogenic Neisseria Conference (IPNC); Manchester (UK); 4–9 September, 2016; p 257. http://ipnc2016.org/IPNC2016AbstractBook.pdf (viewed Nov 2019).
29. Koutangni T, Boubacar Mainassara H, Mueller JE. Incidence, carriage and case‐carrier ratios for meningococcal meningitis in the African meningitis belt: a systematic review and meta‐analysis. PLoS One 2015; 10: e0116725.
30. Australian Bureau of Statistics. Net interstate migration [Cat. No. 3412.0]. Canberra: ABS, 2018. https://www.abs.gov.au/ausstats/abs@.nsf/Latestproducts/3412.0Main%20Features52017-18?opendocument&tabname=Summary&prodno=3412.0&issue=2017-18&num=&view= (viewed Jan 2019).
31. Australian Bureau of Statistics. Net overseas migration. Canberra: ABS, 2018. https://www.abs.gov.au/ausstats/abs@.nsf/Latestproducts/3412.0Main%20Features42017-18?opendocument&tabname=Summary&prodno=3412.0&issue=2017-18&num=&view= (viewed Dec 2019).
32. Bryan P, Seabroke S, Wong J, et al. Safety of multicomponent meningococcal group B vaccine (4CMenB) in routine infant immunisation in the UK: a prospective surveillance study. Lancet Child Adolesc Health 2018; 2: 395–403.
33. Marshall H, Koehler A, Pratt N, et al. Enhanced passive surveillance of adverse events following implementation of a meningococcal B vaccine program in senior school students. 16th National Immunisation Conference; Adelaide (Australia); 4–6 June, 2018; p 63.
34. Nainani V, Galal U, Buttery J, et al. An increase in accident and emergency presentations for adverse events following immunisation after introduction of the group B meningococcal vaccine: an observational study. Arch Dis Child 2017; 102: 958–962.
35. Fiorito TM, Baird GL, Alexander‐Scott N, et al. Adverse events following vaccination with bivalent rLP2086 (Trumenba): an observational, longitudinal study during a college outbreak and a systematic review. J Pediatr Infect Dis 2018; 37: e13–e19.
36. Marshall HS, McMillan M, Koehler A, et al. B Part of It protocol: a cluster randomised controlled trial to assess the impact of 4CMenB vaccine on pharyngeal carriage of Neisseria meningitidis in adolescents. BMJ Open 2018; 8: e020988.
37. Marshall HS, McMillan M, Koehler AP, et al. Meningococcal B vaccine and meningococcal carriage in adolescents, Australia. N Engl J Med 2019. In press.
38. Petousis‐Harris H, Paynter J, Morgan J, et al. Effectiveness of a group B outer membrane vesicle meningococcal vaccine against gonorrhoea in New Zealand: a retrospective case‐control study. Lancet 2017; 390: 1603–1610.
39. Longtin J, Dion R, Simard M, et al. Possible impact of wide‐scale vaccination against serogroup B Neisseria meningitidis on gonorrhea incidence rates in one region of Quebec, Canada. Open Forum Infect Dis 2017; 4 (Suppl): S734–S735.
40. Graham S, Guy RJ, Donovan B, et al. Epidemiology of chlamydia and gonorrhoea among Indigenous and non‐Indigenous Australians, 2000–2009. Med J Aust 2012; 197: 642–646. https://www.mja.com.au/journal/2012/197/11/epidemiology-chlamydia-and-gonorrhoea-among-indigenous-and-non-indigenous

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Editorials

Caesarean section births for twins: rational choice, or a non‐evidence‐based intervention that may cause harm?

David A Ellwood

Med J Aust 2020; 212 (2): . || doi: 10.5694/mja2.50454
Published online: 3 February 2020

ARTICLE
AUTHORS
REFERENCES

Topics

Women's health

The change from vaginal births to operative births may entail unforeseen longer term consequences

The benefits and risks of birth by caesarean section are debated, with passionate proponents on each side of the discussion.1 The most recent national data (for 2017) indicate that in Australia more than one‐third of babies (35%) were born after caesarean section.2 While its safety has undoubtedly improved, it is still reported that greater maternal and perinatal morbidity and mortality are associated with caesarean section than with vaginal births.3 The longer term health outcomes for mother and child are also important.4 In this issue of the MJA, Liu and her colleagues5 report that the caesarean rate for twin pregnancies in Victoria has almost tripled over the past three decades, and that the most frequent reason for operative intervention was the twin pregnancy itself. It is pertinent to examine the reasons for this trend and to ask whether it is justified.

1 Griffith University, Gold Coast, QLD
2 Gold Coast University Hospital, Gold Coast, QLD

Correspondence: d.ellwood@griffith.edu.au

Competing interests:

No relevant disclosures.

1. Ellwood DA, Oats J. Every caesarean section must count. Aust N Z J Obstets Gynaecol 2016; 56: 450–452.
2. Australian Institute of Health and Welfare. Australia's mothers and babies 2017: in brief (Cat. No. PER 100; Perinatal statistics series no. 35). Canberra: AIHW, 2019.
3. Keag OE, Norman JE. Stock SJ. Long‐term risks and benefits associated with cesarean delivery for mother, baby, and subsequent pregnancies: systematic review and meta‐analysis. PLoS Med 2018; 15: e1002494.
4. Bentley JP, Roberts CL, Bowen JR, et al. Planned birth before 39 weeks and child development: a population‐based study. Pediatrics 2016; 138: e20162002.
5. Liu Y, Davey MA, Lee R, et al. Changes in the modes of twin birth in Victoria, 1983–2015. Med J Aust 2020; 212: 82–88.
6. Barrett JFR, Hannah ME, Hutton EK, et al. A randomized trial of planned cesarean or vaginal delivery for twin pregnancy. New Engl J Med 2013; 369: 1295–1305.
7. Hannah ME, Hannah WJ, Hewson SA, et al. Planned caesarean section versus planned vaginal birth for breech presentation at term: a randomised multicentre trial. Term Breech Trial Collaborative Group. Lancet 2000; 356: 1375–1383.
8. Australian Department of Health. Pregnancy care guidelines: 61.3. Breech presentation. Updated 17 May 2019. https://www.health.gov.au/resources/pregnancy-care-guidelines/part-j-clinical-assessments-in-late-pregnancy/fetal-presentation#613-breech-presentation (viewed Nov 2019).
9. Coates D, Thirukumar P, Spear V, et al. What are women's mode of birth preferences and why? A systematic scoping review. Women Birth; https://doi.org/10.1016/j.wombi.2019.09.005. [Epub ahead of print]

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Editorials

The cheques and balances of national universal screening of patients with new colorectal cancer for Lynch syndrome

Megan Hitchins

Med J Aust 2020; 212 (2): . || doi: 10.5694/mja2.50453
Published online: 3 February 2020

ARTICLE
AUTHORS
REFERENCES

Topics

Neoplasms

Health services administration

Tiered universal screening systems that save lives are cost‐effective

About 15–20% of colorectal cancers exhibit microsatellite instability (MSI) caused by deficient DNA mismatch repair (MMR).1 Most of these cancers (80%) are sporadic, associated with hypermethylation of the MLH1 gene promoter. Lynch syndrome is caused by germline mutations affecting one of the MMR genes (MLH1, MSH2, MSH6, PMS2), and accounts for 15–20% of MMR‐deficient (dMMR) colorectal cancers, or 2–5% of all colorectal cancers, making it the most common hereditary colorectal cancer predisposition syndrome.2 People with Lynch syndrome are at increased risk of several cancer types, especially colorectal cancer: the risk by age 70 years is 10–82%, depending on the mutant gene, considerably higher than that of the general population (4.5%).3

Cedars‐Sinai Center for Bioinformatics and Functional Genomics, Los Angeles, CA, United States of America

Correspondence: megan.hitchins@cshs.org

Competing interests:

No relevant disclosures.

1. Boland CR, Thibodeau SN, Hamilton SR, et al. A National Cancer Institute Workshop on Microsatellite Instability for cancer detection and familial predisposition: development of international criteria for the determination of microsatellite instability in colorectal cancer. Cancer Res 1998; 58: 5248–5257.
2. Lynch HT, Snyder CL, Shaw TG, et al. Milestones of Lynch syndrome: 1895–2015. Nat Rev Cancer 2015; 15: 181–194.
3. Møller P, Seppälä T, Bernstein I, et al. Cancer incidence and survival in Lynch syndrome patients receiving colonoscopic and gynaecological surveillance: first report from the prospective Lynch syndrome database. Gut 2017; 66: 464–472.
4. Hampel H, Frankel WL, Martin E, et al. Screening for the Lynch syndrome (hereditary nonpolyposis colorectal cancer). N Engl J Med 2005; 352: 1851–1860.
5. Hampel H, Frankel W, Panescu J, et al. Screening for Lynch syndrome (hereditary nonpolyposis colorectal cancer) among endometrial cancer patients. Cancer Res 2006; 66: 7810–7817.
6. Evaluation of Genomic Applications in Practice and Prevention (EGAPP) Working Group. Recommendations from the EGAPP Working Group: genetic testing strategies in newly diagnosed individuals with colorectal cancer aimed at reducing morbidity and mortality from Lynch syndrome in relatives. Genet Med 2009; 11: 35–41.
7. Giardiello FM, Allen JI, Axilbund JE, et al; US Multi‐Society Task Force on Colorectal Cancer. Guidelines on genetic evaluation and management of Lynch syndrome: a consensus statement by the US Multi‐Society Task Force on colorectal cancer. Gastroenterology 2014; 147: 502–526.
8. Stoffel EM, Mangu PB, Gruber SB, et al; American Society of Clinical Oncology; European Society of Clinical Oncology. Hereditary colorectal cancer syndromes: American Society of Clinical Oncology Clinical Practice Guideline endorsement of the familial risk‐colorectal cancer: European Society for Medical Oncology Clinical Practice Guidelines. J Clin Oncol 2015; 33: 209–217.
9. Gallego CJ, Shirts BH, Bennette CS, et al. Next‐generation sequencing panels for the diagnosis of colorectal cancer and polyposis syndromes: a cost‐effectiveness analysis. J Clin Oncol 2015; 33: 2084–2091.
10. Kang YJ, Killen J, Caruana M, et al. The predicted impact and cost‐effectiveness of systematic testing of people with incident colorectal cancer for Lynch syndrome. Med J Aust 2020; 212: 72–81.
11. Ladabaum U, Wang G, Terdiman J, et al. Strategies to identify the Lynch syndrome among patients with colorectal cancer: a cost‐effectiveness analysis. Ann Intern Med 2011; 155: 69–79.
12. Webber EM, Kauffman TL, O'Connor E, Goddard KA. Systematic review of the predictive effect of MSI status in colorectal cancer patients undergoing 5FU‐based chemotherapy. BMC Cancer 2015; 15: 156.
13. Le DT, Uram JN, Wang H, et al. PD‐1 blockade in tumors with mismatch‐repair deficiency. N Engl J Med 2015; 372: 2509–2520.

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Medical education
Lessons from practice

Use of botulinum toxin to heal atypical pressure ulcers in the palm

Anupam Datta Gupta and David H Wilson

Med J Aust 2020; 212 (2): . || doi: 10.5694/mja2.50452
Published online: 3 February 2020

ARTICLE
AUTHORS
REFERENCES

Topics

Anatomy and physiology

Nervous system diseases

Rehabilitation

A 59‐year‐old woman attended our spasticity clinic with treatment‐resistant atypical pressure ulcer in the right hand caused by focal spasticity secondary to upper motor neuron lesion. She had suffered subarachnoid haemorrhage from a ruptured arteriovenous malformation and underwent craniotomy. She was deemed not suitable for structured rehabilitation due to her significant disability and was placed in a residential accommodation. The patient was using an electrical wheelchair and was requiring full assistance with her personal care. She had typical, dense post‐stroke right‐sided spastic hemiplegia. In the upper limb, she had shoulder adduction and internal rotation, elbow flexion, wrist palmar flexion with flexed fingers at the metacarpophalangeal and proximal interphalangeal joints. She had a baclofen pump that controlled her lower limb spasticity.

1 Queen Elizabeth Hospital, Adelaide, SA
2 University of Adelaide, Adelaide, SA

Correspondence: anupam.dattagupta@adelaide.edu.au

Acknowledgements:

We thank Barbara Brougham for her help with the editing of the manuscript.

Competing interests:

No relevant disclosures.

1. Gupta AD, Wilson W. Botulinum toxin for spasticity: a case for change to the Pharmaceutical Benefits Scheme. Med J Aust 2018; 208: 379–381. https://www.mja.com.au/journal/2018/208/9/botulinum-toxin-spasticity-case-change-pharmaceutical-benefits-scheme
2. Meijer R, Wolswijk A, Eijsden HV. Prevalence, impact and treatment of spasticity in nursing home patients with central nervous system disorders: a cross‐sectional study. Disabil Rehabil 2017; 39: 363–371.
3. Jaul E. Cohort study of atypical pressure ulcers development. Int Wound J 2014; 11: 696–700.
4. Atiyeh BS, Hayek SN. Pressure sores with associated spasticity: a clinical challenge. Int Wound J 2005; 2: 77–80.
5. Nair KP, Marsden J. The management of spasticity in adults. BMJ 2014; 349: g4737.
6. Ward AB. A summary of spasticity management — a treatment algorithm. Eur J Neurol 2002; 9 (Suppl): 48–52.
7. Tarsy D, Simon DK. Dystonia. N Engl J Med 2006; 355: 818–828.
8. Graham LA. Management of spasticity revisited. Age Ageing 2013; 42: 435–441.

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Perspectives

Understanding the proportion of cervical cancers attributable to HPV

Julia ML Brotherton, Alison C Budd and Marion Saville

Med J Aust 2020; 212 (2): . || doi: 10.5694/mja2.50477
Published online: 3 February 2020

ARTICLE
AUTHORS
REFERENCES

Topics

Sexual health

Neoplasms

Women's health

Environment and public health

Most cervical cancers can be prevented with HPV vaccination and screening

Since Walboomers and colleagues1 published their findings in 1999, citing that 99.7% of cervical cancers are related to the human papillomavirus (HPV), this has become the standard understanding of the proportion of cervical cancers attributable to HPV.

1 VCS Foundation, Melbourne, VIC
2 Australian Institute of Health and Welfare, Canberra, ACT

Correspondence: jbrother@vcs.org.au

Competing interests:

Julia Brotherton and Marion Saville are investigators on the Compass Trial, conducted and funded by VCS Foundation. VCS Foundation have received equipment and a funding contribution for the Compass Trial from Roche Molecular Systems and Roche Tissue Diagnostics.

1. Walboomers JM, Jacobs MV, Manos MM, et al. Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. J Pathol 1999; 189: 12–19.
2. Brotherton JML, Tabrizi SN, Phillips S, et al. Looking beyond human papillomavirus (HPV) genotype 16 and 18: defining HPV genotype distribution in cervical cancers in Australia before vaccination. Int J Cancer 2017; 141: 1576–1584.
3. Australian Institute of Health and Welfare. Cervical screening in Australia 2018 [Cat. No. CAN 111]. Canberra: AIHW, 2018. https://www.aihw.gov.au/reports/cancer-screening/cervical-screening-in-australia-2018/contents/table-of-contents (viewed Dec 2019).
4. Li N, Franceschi S, Howell‐Jones R, et al. Human papillomavirus type distribution in 30,848 invasive cervical cancers worldwide: Variation by geographical region, histological type and year of publication. Int J Cancer 2011; 128: 927–35.
5. Saraiya M, Unger ER, Thompson TD, et al. HPV Typing of Cancers Workgroup. US assessment of HPV types in cancers: implications for current and 9‐valent HPV vaccines. J Natl Cancer Inst 2015; 107: djv086.
6. Lagheden C, Eklund C, Lamin H, et al. Nationwide comprehensive human papillomavirus (HPV) genotyping of invasive cervical cancer. Br J Cancer 2018; 118: 1377–1381.
7. Petry KU, Liebrich C, Luyten A, et al. Surgical staging identified false HPV‐negative cases in a large series of invasive cervical cancers. Papillomavirus Res 2017; 4: 85–89.
8. McCluggage WG. Recent developments in non‐HPV‐related adenocarcinomas of the lower female genital tract and their precursors. Adv Anat Pathol 2016; 23: 58–69.
9. Hodgson A, Park KJ. Cervical adenocarcinomas: a heterogeneous group of tumors with variable etiologies and clinical outcomes. Arch Pathol Lab Med 2019; 143: 34–46.
10. Stolnicu S, Barsan I, Hoang L, et al. International Endocervical Adenocarcinoma Criteria and Classification (IECC): a new pathogenetic classification for invasive adenocarcinomas of the endocervix. Am J Surg Pathol 2018; 42: 214–226.
11. Castle PE, Pierz A, Stoler MH. A systematic review and meta‐analysis on the attribution of human papillomavirus (HPV) in neuroendocrine cancers of the cervix. Gynecol Oncol 2018; 148: 422–429.
12. Casey S, Harley I, Jamison J, et al. A rare case of HPV‐negative cervical squamous cell carcinoma. Int J Gynecol Pathol 2015; 34: 208–212.
13. Higgins GD, Uzelin DM, Phillips GE, et al. Increased age and mortality associated with cervical carcinomas negative for human papillomavirus RNA. Lancet 1991; 338: 910–913.
14. Lei J, Ploner A, Lagheden C, et al. High‐risk human papillomavirus status and prognosis in invasive cervical cancer: a nationwide cohort study. PLoS Med 2018; 15: e1002666.
15. Hallowell BD, Saraiya M, Thompson TD, et al. Population‐based assessment of HPV genotype‐specific cervical cancer survival: CDC Cancer Registry Sentinel Surveillance System. JNCI Cancer Spectr 2018; 2: pky036.
16. World Health Organization. Cervical cancer elimination strategy. WHO, 2019. https://www.who.int/cancer/cervical-cancer/cervical-cancer-elimination-strategy (viewed Dec 2019).

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Incidence and prevalence of self‐reported non‐coeliac wheat sensitivity and gluten avoidance in Australia

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The incidence of childhood cancer in Australia, 1983–2015, and projections to 2035

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Implementing value‐based health care at scale: the NSW experience

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First statewide meningococcal B vaccine program in infants, children and adolescents: evidence for implementation in South Australia

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Caesarean section births for twins: rational choice, or a non‐evidence‐based intervention that may cause harm?

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The cheques and balances of national universal screening of patients with new colorectal cancer for Lynch syndrome

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Use of botulinum toxin to heal atypical pressure ulcers in the palm

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Understanding the proportion of cervical cancers attributable to HPV

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Victoria's Voluntary Assisted Dying Act: navigating the section 8 gag clause

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Gastro‐oesophageal reflux disease in infancy: a review based on international guidelines

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Incidence and prevalence of self‐reported non‐coeliac wheat sensitivity and gluten avoidance in Australia

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The incidence of childhood cancer in Australia, 1983–2015, and projections to 2035

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Implementing value‐based health care at scale: the NSW experience

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First statewide meningococcal B vaccine program in infants, children and adolescents: evidence for implementation in South Australia

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Caesarean section births for twins: rational choice, or a non‐evidence‐based intervention that may cause harm?

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The cheques and balances of national universal screening of patients with new colorectal cancer for Lynch syndrome

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Use of botulinum toxin to heal atypical pressure ulcers in the palm

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Understanding the proportion of cervical cancers attributable to HPV

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Victoria's Voluntary Assisted Dying Act: navigating the section 8 gag clause

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Gastro‐oesophageal reflux disease in infancy: a review based on international guidelines

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Pagination