New precautionary measures against the possible risk of transmission of variant Creutzfeldt Jakob Disease

The UK Department of Health (DOH) has said today that recipients of blood transfusions are to be excluded from donating blood in the future as a further precautionary measure against the possible risk of transmission of variant Creutzfeldt Jakob Disease (vCJD), Health Secretary John Reid announced today.

Variant Creutzfeldt-Jakob disease (vCJD) is a rare and fatal human neurodegenerative condition. As with Creutzfeldt-Jakob disease, vCJD is classified as a Transmissible Spongiform Encephalopathy (TSE) because of characteristic spongy degeneration of the brain and its ability to be transmitted. vCJD is a new disease that was first described in March 1996.

New precautionary measures to change the eligibility for blood donation will be implemented from April 5th. It will exclude people who confirm they have received a transfusion after 1 January 1980 because it is generally accepted that there will have been no exposure to BSE in the UK before than date.

The Health Secretary, John Reid said, "We are following a highly precautionary approach. Although people may have concerns about the implications of this announcement, I would emphasise again that this action is being taken because of an uncertain but slight risk. People should, indeed, continue to have a blood transfusion when it is really necessary. Any slight risk associated with receiving blood must be balanced against the significant risk of not receiving that blood when it is most needed.

"People who can should continue to give blood. Blood donation is a safe procedure and people should continue to donate blood regularly. We place great value on those who already donate and would welcome new donors."

The prion that is believed to cause Creutzfeldt-Jakob exhibits an amino acid sequence and configuration which makes it insoluble in water, while the normal protein is highly soluble. So, as the numbers of defective prion proteins propagate and increase exponentially, the process leads to a huge load of insoluble prions in affected cells. This load of proteins disrupts cell function and causes cell death. Once the prion is transmitted, the defective proteins invade the brain like a forest fire and the patient dies within a few months (a few patients live for about 1-2 years). The defective protein can be transmitted by human growth hormone products, corneal grafts or dural grafts (acquired form) or it can be inherited (hereditary form) or appear for the first time in the patient (sporadic form). In the latter two forms the defective protein is not transmitted from an external source but already exists in the genes of the individual.

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