Intra-cerebral haemorrhage but not neurodegenerative disease appears over-represented in deaths of Australian cadaveric pituitary hormone recipients.


Journal

Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
ISSN: 1532-2653
Titre abrégé: J Clin Neurosci
Pays: Scotland
ID NLM: 9433352

Informations de publication

Date de publication:
Nov 2020
Historique:
received: 28 04 2020
revised: 28 07 2020
accepted: 06 09 2020
entrez: 23 11 2020
pubmed: 24 11 2020
medline: 9 2 2021
Statut: ppublish

Résumé

Recent scientific reports and epidemiological studies have engendered mounting concerns regarding the potential human-to-human transmissibility of non-prion neurodegenerative and related diseases. This study investigated whether recipients of cadaveric pituitary hormone treatments are at increased risk of death from non-prion neurodegenerative and related diseases. A retrospective national cohort study based on death certificates of recipients of the cadaveric pituitary hormone treatments (n = 184) as part of the Australian Human Pituitary Hormone Program (AHPHP; n = 2940) 1967-1985. Standardised mortality ratios (SMR) from non-prion neurodegenerative and other diseases were estimated based on the Australian population. Allowing for potential diagnostic mis-attributions, there was no significant increase in the SMR from non-prion central nervous system (CNS) neurodegenerative disease, especially dementia and/or Alzheimer's disease (0.47; [95% CI: 0.19, 1.12] P = 0.081). The SMR for intra-cerebral haemorrhage, potentially related to cerebral amyloid angiopathy (CAA), was increased (2.77; [95% CI: 1.12-5.75] P = 0.009), although accommodation of possible mis-diagnosis through conflation of this category with other stroke causes of death emphasising likely intra-cranial haemorrhage showed no persisting significant increase in mortality in cadaveric pituitary hormone recipients, including all deaths recorded as due to intra-cranial haemorrhage (1.72; [95% CI: 0.80, 3.26] P = 0.123). In the setting of recent evidence strongly supporting the likelihood of brain-to-brain horizontal transmission and subsequent propagation and deposition of abnormally folded proteins associated with non-prion neurodegenerative and related disorders, this study offers further tentative support for deaths directly stemming from transmission of non-prion disease related to cadaveric pituitary hormone treatment. Acknowledging the limitations of the present study, however, ongoing detailed assessments of this potential risk are necessary.

Sections du résumé

BACKGROUND AND PURPOSE OBJECTIVE
Recent scientific reports and epidemiological studies have engendered mounting concerns regarding the potential human-to-human transmissibility of non-prion neurodegenerative and related diseases. This study investigated whether recipients of cadaveric pituitary hormone treatments are at increased risk of death from non-prion neurodegenerative and related diseases.
METHODS METHODS
A retrospective national cohort study based on death certificates of recipients of the cadaveric pituitary hormone treatments (n = 184) as part of the Australian Human Pituitary Hormone Program (AHPHP; n = 2940) 1967-1985. Standardised mortality ratios (SMR) from non-prion neurodegenerative and other diseases were estimated based on the Australian population.
RESULTS RESULTS
Allowing for potential diagnostic mis-attributions, there was no significant increase in the SMR from non-prion central nervous system (CNS) neurodegenerative disease, especially dementia and/or Alzheimer's disease (0.47; [95% CI: 0.19, 1.12] P = 0.081). The SMR for intra-cerebral haemorrhage, potentially related to cerebral amyloid angiopathy (CAA), was increased (2.77; [95% CI: 1.12-5.75] P = 0.009), although accommodation of possible mis-diagnosis through conflation of this category with other stroke causes of death emphasising likely intra-cranial haemorrhage showed no persisting significant increase in mortality in cadaveric pituitary hormone recipients, including all deaths recorded as due to intra-cranial haemorrhage (1.72; [95% CI: 0.80, 3.26] P = 0.123).
CONCLUSION CONCLUSIONS
In the setting of recent evidence strongly supporting the likelihood of brain-to-brain horizontal transmission and subsequent propagation and deposition of abnormally folded proteins associated with non-prion neurodegenerative and related disorders, this study offers further tentative support for deaths directly stemming from transmission of non-prion disease related to cadaveric pituitary hormone treatment. Acknowledging the limitations of the present study, however, ongoing detailed assessments of this potential risk are necessary.

Identifiants

pubmed: 33222975
pii: S0967-5868(20)31498-3
doi: 10.1016/j.jocn.2020.09.021
pii:
doi:

Substances chimiques

Human Growth Hormone 12629-01-5

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

78-82

Commentaires et corrections

Type : ErratumIn

Informations de copyright

Copyright © 2020 Elsevier Ltd. All rights reserved.

Auteurs

Sultan H Alnakhli (SH)

Australian National Creutzfeldt-Jakob Disease Registry (ANCJDR), The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville 3010, Australia.

Handan Wand (H)

The Kirby Institute (formerly National Centre in HIV Epidemiology and Clinical Research), University of New South Wales, Coogee 2034, Australia.

Matthew Law (M)

The Kirby Institute (formerly National Centre in HIV Epidemiology and Clinical Research), University of New South Wales, Coogee 2034, Australia.

Shannon Sarros (S)

Australian National Creutzfeldt-Jakob Disease Registry (ANCJDR), The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville 3010, Australia.

Christiane Stehmann (C)

Australian National Creutzfeldt-Jakob Disease Registry (ANCJDR), The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville 3010, Australia.

Matteo Senesi (M)

Australian National Creutzfeldt-Jakob Disease Registry (ANCJDR), The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville 3010, Australia; Department of Medicine, Royal Melbourne Hospital, The University of Melbourne, Parkville 3010, Australia.

Genevieve M Klug (GM)

Australian National Creutzfeldt-Jakob Disease Registry (ANCJDR), The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville 3010, Australia.

Marion Simpson (M)

Australian National Creutzfeldt-Jakob Disease Registry (ANCJDR), The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville 3010, Australia.

Victoria Lewis (V)

Australian National Creutzfeldt-Jakob Disease Registry (ANCJDR), The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville 3010, Australia; Department of Medicine, Royal Melbourne Hospital, The University of Melbourne, Parkville 3010, Australia.

Colin L Masters (CL)

Australian National Creutzfeldt-Jakob Disease Registry (ANCJDR), The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville 3010, Australia.

Steven J Collins (SJ)

Australian National Creutzfeldt-Jakob Disease Registry (ANCJDR), The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville 3010, Australia; Department of Medicine, Royal Melbourne Hospital, The University of Melbourne, Parkville 3010, Australia. Electronic address: stevenjc@unimelb.edu.au.

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Classifications MeSH