Mal Washer (Moore, Liberal Party) Share this | Hansard source

I thank the member for McEwen for drawing the House’s attention to the male recipients of growth hormone between 1960 and the mid-1980s. In the mid-1950s scientists learnt how to extract human growth hormone from the pituitary glands of cadavers. This hormone was injected into children of short stature, increasing their height. Professor Allars’s inquiry demonstrated, unfortunately, a failure to adequately protect public safety in relation to the Australian Human Pituitary Hormone Program, AHPHP. There was evidence of failures in the production of product, including the collection of pituitary glands; failures in supervision of the product and programs by government agencies, including the health department, the National Biological Standards Laboratory and the Human Pituitary Advisory Committee, or HPAC; and failures of appropriate action undertaken by the department following suspension of the program in 1985. There were inadequacies in tracing the recipients, the information provided, the epidemiological studies, and blood and organ donation.

Around 2,100 Australians were treated with human pituitary hormone under AHPHP, which ran in Australia from 1967 until 1985. This program treated approximately 1,570 women and about 60 men for infertility with human pituitary gonadotrophin and approximately 660 children for short stature with human growth hormone. Five Australians have developed and died from Creutzfeldt-Jakob disease, or CJD, as a result of receiving human pituitary hormones. The program was suspended in 1985. Twenty-two years ago, genetically modified growth hormone became available and side effects with this hormone are rare. There is certainly no risk of CJD.

CJD is one of the transmissible spongiform encephalopathies. CJD was first described as a disease in 1920 and knowledge of CJD grew from the late 1960s as research was conducted into other spongiform encephalopathies including kuru, an encephalopathy associated with ritual endocannibolism of the Fore tribe in the remote highlands of New Guinea.

In 1968, transmissibility of CJD by inoculation of chimpanzee brains was reported. The first iatrogenic person-to-person transmission by corneal transplant was reported in 1974. In the same year, warnings appeared in the literature regarding the need for special precautions beyond routine sterilisation procedures. In 1976, UK scientist Dr A Dickinson expressed concerns about the possibility of CJD contamination of growth hormone produced in the UK.

Human-to-human transmission of CJD and other spongiform encephalopathies is now limited to cases of accidental transplantation of an organ from a diseased person or in parenteral exposure to CJD tissues through contaminated instruments, and in variant CJD transmission may be possible by blood transfusion. Bovine spongiform encephalopathy, BSE, or mad cow disease, was probably caused by dietary supplementation of cattle with processed organs from sheep with scrapie. People eating infected cattle can become infected themselves. In all spongiform encephalopathies there is the presence of a protease-resistant pathogenic form as an endogenous protein or prion in the brains of all infected species. Deformed prions corrupt other brain proteins that aggregate and expand, recruiting more proteins forming insoluble deposits that injure neurons and neuroglia. Neuroglia is the glue or supporting tissue for the neurons and when lost causes the holes of spongiform encephalopathy.

The disease has a long incubation period of typically many months to years. When it manifests itself, the dementia however progresses rapidly, unlike Alzheimer’s, which is slower. No single test other than brain biopsy can confirm CJD and this is not easy, so examination of the cerebral spinal fluid along with electroencephalography and MRI help confirm the diagnosis. We have no proven anti-prion drug or vaccine so our males deserve the same compensation as our females.

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