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DOCUMENTS 1
 REPORT BY ROSEMARY BIGGS
 QUOTES FROM DR. CHARLES RIZZA OXFORD HAEMOPHILIA CENTRE
 WORLD IN ACTION: BLOOD MONEY SCREENED 1975.
 WORLD HEALTH ORGANISATION GUIDELINES
 ARTICLE IN “ THE JOURNAL”
 GOVERNMENT REPORTS ON THE INADEQUACY OF ELSTREE
 LETTER FROM DAVID OWEN
 LANCET ARTICLE
British Journal of Haematology, 1977, 35, 487.
Haemophilia Treatment in the United Kingdom
From 1969 to 1974
Rosemary Biggs
From data collected by the Haemophilia Centre Directors of the United Kingdom and Northern Ireland
(see appendix) which was compiled and analysed by Rosemary Spooner.
(Received 8 September 1976; accepted 18 October 1976)
Summary. A study has been made by the Haemophilia Centre Directors of the United Kingdom and
Northern Ireland. From 1969 to 1974 2600 patients with haemophilia A and 388 with haemophilia B
attended Haemophilia Centres for treatment.
Of these patients, 71 are known to have died in the survey period. A record is presented of the
amounts and types of therapeutic materials used each year during this time. The incidence of jaundice
and anti-factor VIII and anti-factor IX antibodies was recorded.
Since 1967 increasing amounts of cryoprecipitate and of factor VIII and factor IX concentrate have
greatly improved the prospect for treatment of patients suffering from haemophilia A and haemophilia
B. Since 1969 the Directors of Haemophilia Centres have collected data about the amounts and types of
therapeutic material used to treat patients having haemophilia A (factor VIII deficiency) or B (factor IX
deficiency) and about the complications of treatment. It is hoped that this information will help in the
formulation of National Policy for the provision and use of therapeutic materials and help to define the
types of organisations required for the care of these patients. These two diseases have been considered
because between them they account for more than 95% of all patients having serious congenital
coagulation defects which require treatment by coagulation factor replacement.
In a report on the first 3 years of this survey in 1974 (Biggs, 1974), the amount of factor VIII used
to treat haemophilic patients was expressed as the number of blood donations (donor units) which were
needed to supply therapeutic material, this was helpful in assessing the amount of blood required to
supply factor VIII from the United Kingdom blood transfusion service. The concept of donor units was
also used to see if the occurrence of jaundice in patients could be related to the number of donors
contributing to the factor VIII that they had received. Analysis of the data did not suggest any
significant correlation.
Since the data was collected for the first report, improved methods for detecting hepatitis B surface
antigen have been developed and commercial human factor VIII has become available and used in
increasing amounts. It seems that commercial donors have had a higher incidence of hepatitis than
unpaid donors (Maycock, 1972; Alter et al, 1972; Prince, 1975), although commercial suppliers are
now making more efforts to reduce the potential infectivity of their product. Much of the commercial
human factor VIII is made by plasmapheresis from commercial donors. Thus the source of the blood
used to make factor VIII could have been more important than the number of donations contributing to
pools of plasma and in any case the number of donations contributing the commercial factor VIII is
seldom known. Also the amount of factor VIII activity derived from one donation will depend on the
amount of plasma removed from each donation and on the subsequent fractionation procedures.
There are other reasons other than cost which should encourage every effort to have the supply of
factor VIII made from United Kingdom blood. For one thing our haemophilic patients should not be
dependent on commercial blood donors recruited in other countries.
Also blood from these donors may be more likely to transmit infection than the blood of voluntary
donors. In addition it must be undesirable for a major source of supply of factor VIII to be from foreign
companies whose policy may be affected by political and other decisions outside the United Kingdom.
Dr Charles Rizza, Oxford Haemophilia Centre
We recognised in the mid 70s and early 80s that all of the concentrates were infected with non-A nonB hepatitis. The only way we knew was that when we had someone who needed Factor VIII but who
did not have hepatitis, we would transfuse him and he would invariably get hepatitis but not hepatitis-A
or hepatitis-B. All we know is that there is that agent in the Factor VIII. The companies were going
through a variety of tests to make Factor VIII safe and they were halfway there when Aids came along
and presented a new problem. Factor VIII is still very impure, it could be called a crude protein
concentrate contaminated with Factor VIII.
In the US it is estimated that as many as 19,000 severe illnesses or deaths may be attributed to non –A
non- B hepatitis. It is less glamorous than Aids for which there were 9,784 deaths in 1986, the worst
year of the epidemic, but it is still deadly.
World Health Organisation Geneva 1981
The Collection, Fractionation, Quality Control, And Uses Of Blood And Blood Products: Guidelines 1975.
Donor populations showing a prevalence of acute or chronic hepatitis higher than that found in the
general population should be avoided for collection both of single donor products (whole blood and its
components) and of plasma for pooling for the manufacture of plasma fractions known to be capable of
transmitting hepatitis, such as clotting factor concentrates.
Countries with a low incidence of hepatitis should NOT use whole blood or blood products obtained
from source material collected from an area, which there is a high incidence of hepatitis.
In countries where Malaria is NOT endemic, donors should have a negative history of Malaria
exposure during the past six months and a negative history of clinical Malaria.
WORLD IN ACTION: BLOOD MONEY SCREENED 1975.
Paragraphs from letters shown
DR J GARROTT ALLEN (AMERICAN) WORLD –RENOWNED EXPERT ON HEPATITIS TO
WILLIAM MAYCOCK HEAD OF BRITISH BLOOD TRANSFUSION SERVICE.
“Commercial blood banking perpetuates the high-risk rates for hepatitis we encounter with their
products and it also tempts these same firms to sell residual products”.
“It does not take much commercial blood in a mixed combination to bring up an astounding attack rate
from one that is relatively unnoticed, this is the basis of my concern about Britain purchasing
commercial blood products from our country.”
Feb 19 2001
Louella Houldcraft,
The Journal
The world’s leading expert on haemophilia said last night he felt responsible for the deaths of 78 of his North-East
patients who were given blood infected with HIV and hepatitis C. Dr Peter Jones, medical director for the World
Federation of Haemophilia, claims he was forced to give his patients at Tyneside hospital blood products taken from
prisoners, drunks and drug addicts in America because of a lack of funding for the British transfusion service to
meet demand in this country. His patients were also given blood products - known as Factor VIII - taken from the
slums of South Africa, now the country with the highest rate of HIV and Aids in the world. Of his 105 haemophilia
patients, 95 became infected with HIV and hepatitis C and just 18 are still alive. Dr Jones, former director of the
regional haemophilia centre at Newcastle’s Royal Victoria Infirmary, said he and his patients had been betrayed by
the Government.
Speaking to The Journal hours before flying out to Dublin, where he will speak as an expert witness at the
Lindsay Tribunal on behalf of infected haemophiliacs in the Republic of Ireland, he called for an independent
inquiry into the blood scandal.
“We were all devastated when the true horror of what had happened started to unfold in the mid 1980s,” he said.
“At the haemophilia centre we were like one big family and myself and my colleagues had always tried to be
completely open and honest with our patients.” But the Government covered up and lied to us - just as it has
with BSE. “So many of my patients died, as they did at centres across the UK, and as their doctor I felt
responsible for their deaths.” The Government of the time promised us that Britain would be self-sufficient in
blood products by 1977 but in fact we have never been able to meet demand and we are still importing plasma
from the US. “I think my patients and their families deserve the same treatment as haemophiliacs in the
Republic of Ireland and I would fully support a public inquiry into the whole horrific episode.”
But last night a spokeswoman for the Department of Health again repeated that the Government felt there was no
case to answer. “We do not believe anybody’s interests would be served by holding a public inquiry,” she said.
“Little was known about HIV and Aids at the time and a test did not
exist until 1985. “Factor VIII was in great demand from haemophiliacs and vastly improved their quality of life.”
We imported plasma to meet that demand.” We have great sympathy for the people affected but Government
policy remains that compensation, or other financial help to patients, is only paid when the NHS or individuals
working in it are at fault.
”The bad blood scandal was first exposed in The Journal in August when we revealed blood taken from US
prisons and so-called “skid row” had been used to make Factor VIII products given to a Newcastle haemophiliac
during the 1970s and 80s. During this time, over 4,500 haemophiliacs in Britain contracted hepatitis C while
1,200 also became infected with HIV. Although HIV sufferers received a one-off “sympathy” payment in 1991
for the “prejudice” they experienced because of the virus, no one has ever accepted responsibility for the scandal
or offered help to those with hepatitis C.
A spokeswoman for Haemophilia Action UK, formerly Haemophilia North, said last night it was a relief that
doctors were at last speaking out in support of their patients.” The latest scare over CJD has become a catalyst
for people’s anger,” she said.” It has been known for almost 50 years that viruses can be transmitted in blood and
if the Government had listened to the warnings in 1973 then I believe many of the deaths could have been
prevented.” The destruction of the haemophilia community continues to be portrayed as some huge accident.”
But the importation of blood products was based on an informed decision and someone has to answer for the
thousands of lives that have been lost and devastated as a result.”
HOUSE OF COMMONS
LONDON SW1A 0AA
The Rt. Hon John Moore MP,
Secretary of State for Health
And Social Security,
Elephant and Castle,
London SE1 6BY.
17 November 1987
Dear John.
I am glad to see that you have made an ex-gratia payment for haemophiliacs who, as a result of
transfusion, find themselves HIV Positive.
What concerns me however is how this situation has been allowed to occur. I note that in Hansard 393
on 22 January 1975, I said “I believe it is vitally important that the National Health Service should
become self-sufficient as soon as practicable in the production of Factor VIII, including AHG
concentrates”.
On 22 April in a written answer I was even more explicit “I hope that the National Health Service can
become self-sufficient in the production of all forms of Factor VIII within two or three years”. The
same answer was very much reiterated on 8 July (column 108).
I would be grateful if you could let me know what happened to the extra money that was allocated to
the regional transfusion centres, and why they did not become self –sufficient. I think I should in
fairness warn you that I have it in mind to refer the issue to the Ombudsman on grounds of
misadministration unless I receive a satisfactory explanation.
Yours sincerely
David
DAVID OWEN
1: Lancet 1985 Jun 29;1(8444):1495-8
Progressive liver disease in hemophilia: an understated problem?
Hay CR, Preston FE, Triger DR Underwood JC
In an 8-year study of 79 unselected patients with hemophilia who had received clotting factor
concentrates, there was evidence of chronic progressive liver disease in at least 17 (21%). 8 patients
had chronic active hepatitis and 9 had cirrhosis (5 with esophageal varies). Histological Evidence
suggested that non-A non-B hepatitis was mainly responsible, although the influence of other viruses
could not be excluded. Serial liver biopsies showed progression from chronic persistent hepatitis to
chronic active hepatitis and cirrhosis within 6 years, suggesting that chronic persistent hepatitis in
haemophiliacs is not as benign as hitherto supposed. Symptoms and abnormal physical signs were
uncommon in these patients. There was no relation between degree of abnormality of serum
aminotransferase levels and severity of the underlying liver disease. It is anticipated that liver disease
in hemophiliacs will become an increasing clinical problem in the future.
PMID:2861420
DOCUMENTS 2
 GOVERNMENT REPORTS ON THE INADEQUACY OF ELSTREE

INACTIVATING VIRUSES IN BLOOD
FROM THE KREVER REPORT
Inactivating viruses in blood products
During the late 1970s, the German pharmaceutical manufacturer Behringwerke began to develop a
method of inactivating hepatitis viruses. The process involved heating concentrates in a solution at
60ºC for ten hours. By 1978, Behringwerke had begun clinical trials of this new heat-sterilized factor
concentrate, which it named “Factor VIII HS.” The results were published by N. Heimburger and
colleagues in the German journal Die gelben Heften in 1980.
The results were impressive. The clinical trials, conducted at several German hemophilia centres,
demonstrated that the process inactivated not only hepatitis B but also non-A, non-B hepatitis. As of
the date of publication, none of the forty-four patients treated with the new factor concentrate showed
signs of hepatitis. In 1981, Behringwerke published the results of other studies performed using its new
heat-treated factor concentrate. The studies proved that he structure of the protein was unchanged by
heat inactivation and that the viral inactivation process yielded factor concentrates of higher purity. On
5 February 1981, heat-treated factor VIII concentrate manufactured by Behringwerke was licensed by
the Federal Health Office, with the condition that a clinical report be submitted after two years.
Although Behringwerke had succeeded in producing a demonstrably safer factor VIII concentrate
product, Factor VIII HS was not used extensively by hemophiliacs in Germany. The inactivation was
achieved at the expense of a 40 per cent loss in clotting activity. This loss meant that twice the amount
of plasma was needed to produce the factor concentrate, and the cost doubled. As a consequence, only
German hemophilia patients who tested negative for hepatitis B were eligible to receive the factor
concentrate free of charge under their health insurance plans.
During the early 1980s, several other blood product manufacturers also began to incorporate a viral
inactivation measure into their manufacturing processes. They sought and obtained regulatory approval
for the distribution of their heat-treated factor concentrates on the German market. On 22 October
1982, the Federal Health Office licensed Armour Pharma to distribute H.T. Factorate, and on 13
December 1982 it licensed the dry heat-treated factor VIII concentrate produced by Travenol
Laboratories Inc. The next year several other manufacturers, including Immuno, were licensed to
manufacture and distribute heat-treated factor VIII concentrate in Germany.
DOCUMENTS 3
 NICE GUIDELINES
 INFORMATION ON HEPATITIS C AND TREATMENT
N
NICE Issues Guidance on Interferon Alpha and Ribavirin for Hepatitis C
Information on Hepatitis C and Interferon Alpha and Ribavirin

Chronic hepatitis C is a disease of the liver caused by the hepatitis C virus. Six major types of the
hepatitis C virus have been found, these are genetic types (genotypes) and at least 4 out of 10 people
who suffer from hepatitis C are infected with genotype 1.

The virus is generally transmitted parenterally (by any means except digestion). Patients often get the
virus through intravenous drug use and the sharing of needles. The virus was also spread through blood
transfusion prior to the introduction of screening in 1991, as well as through blood products before the
viral inactivation programme in the mid-1980s. There is a small risk of infection from tattooing,
electrolysis, ear piercing and acupuncture. Infection through sexual intercourse can also occur and if a
mother has the virus then there is a 6 in 100 chance she will pass it to her child. HIV infection is thought
to increase the risk of transmission.

People exposed to the virus, often do not have symptoms, however about 2 in 10 will quickly develop
acute hepatitis, and may feel weak and uncomfortable and loose their appetite, symptoms that have
been described as flu-like with jaundice. 85 out of 100 people exposed to the virus go on to develop
chronic hepatitis C.

Development of the disease is slow and variable and can happen over 20-50 years. Of those infected 2
to 3 out of 10 people develop advanced liver disease (cirrhosis) within 20 years and a small number of
these get cancer of the liver (hepatocellular carcinoma). People with end stage liver disease or cancer of
the liver develops severe symptoms and may require a liver transplant. A third of all people infected may
never progress to cirrhosis or will not progress for at least 50 years

Interferon alpha can be used alone to treat people with the Hepatitis C virus. This is called monotherapy
and the precise way it works is not known. Around 47 out of 100 people with the virus respond to this
treatment, but in more than half of those who respond the infection returns within six months of stopping
treatment. This treatment is given by an injection under the skin three times per week. Injections may be
given by clinical staff or by the patient after training. Patients who respond to this treatment usually do so
within three to four months, but some have had to continue with treatment for 12 months.

Ribavirin is a tablet that is currently licensed for use in combination with interferon alpha for the
treatment of certain people with the hepatitis C virus.

. Results from clinical trials (involving 1744 individual patients) show that 67 out of 100 patients infected
with hepatitis C virus (not genotype 1) respond to combination treatment within 24 weeks, this response
is sustained and there is no gain from a further 24 weeks of treatment.

Adverse effects related to combination therapy include influenza-like symptoms (fatigue, headache,
fever), anaemia, , gastrointestinal complaints (loss of appetite, nausea), dermatological symptoms
(alopecia), psychiatric disturbances (depression, anxiety) and hypo- or hyperthyroidism.

The total budget impact for the NHS of combination therapy depends on a number of factors:
prevalence, proportion of patients diagnosed, proportion of these who attend for assessment, and
proportion considered suitable for treatment. It is estimated that there will be about 7,000 patients in
England and Wales treated in the first instance. Assuming that treatment of these patients is spread out
over three years, that all receive 6 months' treatment and two-thirds receive 12 months' treatment, the
drug cost would amount to about £55 million, or about £18 million per year.

As knowledge of the disease and its treatment becomes more widespread, it is also likely that more
people than otherwise will be diagnosed and will seek treatment. It is estimated that the annual
continuing drug cost would be about £5 million. However, it is most likely that rates of diagnosis, referral
to specialists, biopsy and acceptance of the therapy will all increase, so this estimate of annual costs
after three years is likely to be an underestimate.

This guidance will be reviewed in October 2003.
Chronic Hepatitis C
The National Institute of Diabetes and Digestive and Kidney Diseases
Introduction
The hepatitis C virus (HCV) is one of the most important causes of chronic liver disease in the United
States. It accounts for about 20 percent of acute viral hepatitis, 60 to 70 percent of chronic hepatitis,
and 30 percent of cirrhosis, end-stage liver disease, and liver cancer. Almost 4 million Americans, or
1.8 percent of the U.S. population, have antibody to HCV (anti-HCV), indicating ongoing or previous
infection with the virus. Hepatitis C causes an estimated 8,000 to 10,000 deaths annually in the United
States.
A distinct and major characteristic of hepatitis C is its tendency to cause chronic liver disease. At least
75 percent of patients with acute hepatitis C ultimately develop chronic
Presently, there is no vaccine or other means of preventing hepatitis C infection. HCV exists in many
different forms, called genotypes, confounding researchers in their quest to develop a vaccine effective
for all variations. Also, HCV mutates frequently within infected patients, so even if an effective
vaccine is developed, it could be rendered useless by a new strain of mutant virus.
Currently, chronic hepatitis C patients who do not respond to therapy have few options. In many,
cirrhosis or other damage will eventually cause the liver to stop functioning. In these cases, a liver
transplant is the only recourse. However, even new livers often become infected with the virus
Genotyping and Serotyping of HCV
There are 6 known genotypes and more than 50 subtypes of hepatitis C. The genotype of infection is
helpful in defining the epidemiology of hepatitis C. Knowing the genotype or serotype (genotypespecific antibodies) of HCV is helpful in making recommendations and counselling regarding therapy.
Patients with genotypes 2 and 3 are almost three times more likely to respond to therapy with alpha
interferon or the combination of alpha interferon and Ribavirin. Furthermore, when using combination
therapy, the recommended duration of treatment depends on the genotype. For patients with genotypes
2 and 3, a 24-week course of combination treatment is adequate, whereas for patients with genotype 1,
a 48-week course is recommended. For these reasons, testing for HCV genotype is often clinically
helpful. Once the genotype is identified, it need not be tested again; genotypes do not change during the
course of infection.
Alpha interferon has multiple neuropsychiatric effects. Prolonged therapy can cause marked irritability,
anxiety, personality changes, depression, and even suicide or acute psychosis. Patients particularly
susceptible to these side effects are those with pre-existing serious psychiatric conditions and patients
with neurological disease. Interferon therapy is also associated with relapse in people with a previous
history of drug or alcohol abuse. Alpha interferon should not be given to a patient who has only
recently stopped alcohol or substance abuse. Typically a 2-year abstinence is recommended before
starting therapy. Strict abstinence from alcohol is recommended during therapy with interferon.
Alpha interferon therapy can induce autoantibodies, and a 6- to 12-month course triggers an
autoimmune condition in about 2 percent of patients, particularly if they have an underlying
susceptibility to autoimmunity (high titers of antinuclear or antithyroid antibodies, for instance).
Exacerbation of a known autoimmune disease (such as rheumatoid arthritis or psoriasis) occurs
commonly during interferon therapy.
Alpha interferon has bone marrow suppressive effects. Therefore, patients with bone marrow
compromise or cytopenias, such as low platelet count (75,000 cells/mm3) or neutropenia (1,000
cells/mm3) should be treated cautiously and with frequent monitoring of cell counts.
Ribavirin causes red cell haemolysis to a variable degree in almost all patients. Therefore, patients with
a pre-existing haemolysis or anaemia (haemoglobin 11 gm or hematocrit 33 percent) should not receive
Ribavirin. Similarly, patients who have significant coronary or cerebral vascular disease should not
receive Ribavirin, as the anaemia caused by treatment can trigger significant ischemia. Fatal
myocardial infarctions and strokes have been reported during combination therapy with alpha
interferon and Ribavirin.
Finally, Ribavirin causes birth defects in animal studies and should not be used in women who are not
practicing adequate means of birth control. Alpha interferon also should not be used in pregnant
women as it has direct antigrowth and antiproliferative effects. Combination therapy should therefore
be used with caution. Patients should be fully informed of the potential side effects before starting
therapy.
Side Effects of Treatment
Common side effects of alpha interferon (occurring in more than 10 percent of patients) include:

Fatigue

Muscle aches

Headaches

Nausea and vomiting

Skin irritation at the injection site

Low-grade fever

Weight loss

Irritability

Depression

Mild bone marrow suppression

Hair loss (reversible)
Most of these side effects are mild to moderate in severity and can be managed. They are worse during
the first few weeks of treatment, especially with the first injection. Thereafter, side effects diminish.
Acetaminophen may be helpful for the muscle aches and low-grade fever, and side effects may be less
troublesome if interferon is taken in the evening. Fatigue and depression are occasionally so
troublesome that the dose of interferon should be decreased or therapy stopped early. Depression and
personality changes can occur on interferon therapy and be quite subtle and not readily admitted by the
patient. These side effects need careful monitoring.
Ribavirin also causes side effects, and the combination is generally less well tolerated than interferon
monotherapy. The most common side effects of Ribavirin are:

Anaemia

Fatigue and irritability

Itching

Skin rash

Nasal stuffiness, sinusitis, and cough
Ribavirin causes a dose-related haemolysis of red cells; with combination therapy, haemoglobin
usually decreases by 2 to 3 gm/dL and the hematocrit by 5 to 10 percent. The amount of decrease in
haemoglobin is highly variable. The decrease starts between weeks 1 and 4 of therapy and can be
precipitous. Some patients develop symptoms of anaemia, including fatigue, shortness of breath,
palpitations, and headache. The sudden drop in haemoglobin can precipitate angina pectoris in
susceptible people, and fatalities from acute myocardial infarction and stroke have been reported in
patients receiving combination therapy for hepatitis C. For these important reasons, Ribavirin should
not be used in patients with pre-existing anaemia or with significant coronary or cerebral vascular
disease. If such patients require therapy for hepatitis C, they should receive alpha interferon
monotherapy.
Ribavirin has also been found to cause itching and nasal stuffiness. These are histamine-like side
effects; they occur in 10 to 20 percent of patients and are usually mild to moderate in severity. In some
patients, however, sinusitis, recurrent bronchitis, or asthma-like symptoms become prominent. It is
important that these symptoms be recognized as attributable to Ribavirin, because dose modification
(by 200 mg per day) or early discontinuation of treatment may be necessary.
Uncommon side effects of alpha interferon and combination therapy (occurring in less than 2 percent
of patients) include:

Autoimmune disease (especially thyroid disease)

Severe bacterial infections

Marked thrombocytopenia

Marked neutropenia

Seizures

Depression and suicidal ideation or attempts

Retinopathy (microhemorrhages)

Hearing loss and tinnitus
Rare side effects include acute congestive heart failure, renal failure, vision loss, pulmonary fibrosis or
pneumonitis, and sepsis. Deaths have been reported from acute myocardial infarction, stroke, suicide,
and sepsis.
A unique but rare side effect is paradoxical worsening of the disease. This is assumed to be caused by
induction of autoimmune hepatitis, but its cause is really unknown. Because of this possibility,
aminotransferases should be monitored. If ALT levels rise to greater than twice the baseline values,
therapy should be stopped and the patient monitored. Some patients with this complication have
required corticosteroid therapy to control the hepatitis.
DOCUMENTS 4
 TAKEN FROM THE KREVER REPORT
 TAKEN FROM HIV LITIGATION
 REPORT BY THE NORTHERN ECHO
TAKEN FROM THE KREVER REPORT
On 20 July 1990, counsel for the government gave opposing counsel a list of 600 documents relating to policy
decisions about the safety of the blood supply during the period 1972 to 1986, in respect of which public interest
immunity was claimed. The plaintiffs then made an application seeking disclosure of these documents. The High
Court ruled that not all the documents were protected by public interest immunity, and ordered that the
Haemophilia Society be given production of specific classes of documents. The production did not extend to
documents pertaining to self-sufficiency, allocation of resources, expansion of the Blood Products Laboratory,
reorganization of the National Blood Transfusion Service, and heat treatment of blood products. The order was
appealed. In the Court of Appeal, the government argued that the documents should not be disclosed for two
reasons. First, the case had no merit; and, second, confidentiality was required to safeguard the kind of full, free,
and uninhibited discussions that were integral to the policy process. On 20 September 1990, the Court of Appeal
rejected the government’s arguments and ordered the Department of Health to make production of a broader
class of documents. For the court, Lord Justice Gibson held that the hemophiliacs’ right to proper presentation of
their case overrode the right to public interest immunity, and that the plaintiffs had “a good arguable claim in
law based upon common law negligence.” He said that it was very likely that the documents in question would
contain material that would lend substantial weight to their claim:
The plaintiffs need the documents for the proper presentation of their case in order for them to obtain the
necessary expert evidence directed to the explanations for that failure which the documents will reveal. It seems
to me to be necessary for the fair and proper disposal of the case that there should be known to both sides the
actual grounds for the various decisions which led to the continued use of imported and other blood products
capable of infecting a patient with HIV.
Lord Justice Gibson accordingly held that all documents relating to self-sufficiency, allocation of resources, the
Blood Products Laboratory, the National Blood Transfusion Service, donor screening, testing, heat treatment,
and steps to minimize hepatitis infection must be produced. After the Court of Appeal’s decision, with the trial
scheduled to begin in March 1991, Mr. Justice Ognall urged the parties to settle, stating that the government had
a “moral duty” to the hemophiliacs. Regional health authorities then met with the Secretary of State for Health to
present their arguments in favour of settlement, going so far as to threaten that they would settle on their own,
independently of the Department of Health. They argued that legal costs were escalating and that physicians
were spending too much time preparing their case instead of caring for patients. The chief medical officer also
urged the Department of Health to settle the matter out of court. Finally, in December 1990, the government
acquiesced, on the condition that the action be discontinued. In addition to a settlement of £42 million (Can$94
million), the government agreed to pay for the plaintiffs’ reasonable legal costs, and specified that the settlement
applied to non-litigants. Prime Minister John Major announced on 11 December 1990 that the government
would pay the settlement moneys into a new special fund created within the Macfarlane Trust which, inclusive
of legal costs, exceeded £50 million (Can$112 million). The fund was formally established in May 1991 as the
Macfarlane (Special Payments) (No. 2) Trust, with the £42 million (Can$83 mil-lion) capital grant from the
government. Payments from the fund were made only on the express authorization of the Department of Health.
They were all made anonymously, using a code so that the recipient’s name could not be disclosed. As of 31
March 1991, 1,226 persons were registered with the fund and, on average, each had received a lump-sum
payment of £35,000 (Can$74,000). Payments were allocated on the basis of the family status of the applicant on
the day before the announcement of the settlement.
TAKEN FROM HIV LITIGATION
“Testing. First, the Department are likely to contend that successive generations of hepatitis B tests
virtually eliminated the risk of hepatitis B. Although there was also a danger in the 1970s from
hepatitis NANB, that risk was not considered to be very serious until the early 1980s.”
“In the case of hepatitis B testing, no tests were ever completely effective, although it must be
conceded that from the late 1970s the threat from hepatitis B was small. As for hepatitis NANB, the
acute phase of the disease is not serious. In the long term the effects are frequently devastating and can
lead to cirrhosis of the liver and death. Although this was not established until the 1980’s, in the late
1970’s there was concern that hepatitis NANB might lead to serious long -term consequences. Indeed,
the threat of hepatitis NANB was the cause of research into heat-treatment in the early 1980s.”
The Northern Echo
Saturday, March 10, 2001
Hepatitis sufferers ‘were kept in dark’
By Nick Morrison
A HAEMOPHILIAC was told he had a deadly virus five years before the test was made available to
other sufferers, The Northern Echo can reveal.
Campaigners claim the news supports their case that they were deliberately kept in the dark when
they agreed not to take legal action over the virus, before they knew they may have been infected.
Public inquiry call: Ollie Caruthers (Pictured) is believed to be the first in the North-east to be told
he had contracted hepatitis C, when he became ill following an operation to remove a tooth in 1989.
Mr Carruthers, 52, who lives in Washington UK, was given a blood transfusion during the
operation, at Newcastle’s Royal Victoria Infirmary.
When he later became feverish and weak, he arranged to see consultant Dr Peter Jones, who told
him in December 1989 that he had contracted hepatitis C.
Mr Carruthers said he was told that if he did not drink alcohol for six months he would be all right,
but when the symptoms persisted for several years, he eventually used the internet to find out that the
virus was potentially fatal.
He said: When I found out what was wrong with me I was really angry. There were nights when I
just cried.”
He said he was now backing calls for a public inquiry into contaminated blood and compensation
for haemophiliacs who had contracted hepatitis C.
Two years after Mr Caruthers was tested, haemophiliacs who had been infected with HIV through
contaminated blood accepted a compensation package from the Government.
Part of the deal included an undertaking not to take action over potential infection with hepatitis
viruses but it was only later in 1991 that a hepatitis C test was widely available and only in 1994 that
North-East haemophiliacs were told whether they had contracted the disease.
A spokeswoman for Haemophilia Action UK, whose partner has contracted hepatitis C and HIV,
said: “If the hepatitis test was available for one person it should have been available for others.”
“If people had been tested for hepatitis C they would have fought for more compensation in the HIV
settlement in 1991, for being infected with two viruses.”
A Department of Health spokesperson said pending legal action meant it could not comment on
events leading up to the introduction of a hepatitis C test.