People with
chronic fatigue syndrome suffer from a defect in an enzyme
the body uses to
inactivate viruses, a Philadelphia-based research
group reported this
week.
The discovery, if
it holds up to scrutiny, lends support to the idea
that the syndrome
can start with a common viral infection that leads
to a chronic, abnormal
immune response.
The enzyme abnormality
has shown up in all of more than 100 chronic
fatigue syndrome
patients tested so far, said Robert J. Suhadolnik of
Temple University,
who led the research effort. It appears in about 10
percent of healthy
individuals with no sign of chronic fatigue.
Suhadolnik and his
colleagues hope their discovery, which reportedly
has been confirmed
by Belgian researchers, will lead to a diagnostic
test for the elusive
disorder. Chronic fatigue syndrome disables
uncounted thousands
of people and frustrates physicians looking for
cause or effective
treatment.
The new finding could
also provide clues to the physiological
mechanism of the
syndrome, which has been attributed to dozens of
different immunologic,
neurologic, muscular, cellular, viral,
environmental, and
nutritional causes.
'Overactive and defective
antiviral enzymes may be involved in the
production of fatigue,
and also the cognitive symptoms,' Suhadolnik
said yesterday in
an interview.
Dr. Anthony Komaroff
of Brigham and Women's Hospital in Boston, a
leading authority
on chronic fatigue syndrome, praised the quality of
Suhadolnik's research
and said he was impressed with earlier findings
from his laboratory
indicating the antiviral enzyme system is
overactive in a
high percentage of fatigue patients.
However, Komaroff
said many more randomly selected chronic fatigue
sufferers would
have to be tested for the enzyme defect, along with
healthy subjects
and individuals with other kinds of diseases, to
determine its usefulness
as a diagnostic test.
'The world has been
waiting for a diagnostic test, and Suhadolnik
thinks he may have
it,' Komaroff said. 'But I don't see how that
claim can be made
because the numbers are too small.'
In the new report,
published in the current issue of the Journal of
Interferon and Cytokine
Research, the enzyme defect appeared in seven
patients with confirmed
chronic fatigue syndrome. It did not appear
among seven healthy
individuals of the same age in one test that
measures active,
functional enzymes; it sometimes appeared among
healthy subjects
using a different test, but Suhadolnik believes that
is because the second
test 'denatures,' or breaks down proteins.
In subsequent, unpublished
tests of more than 100 chronic fatigue
patients and equal
numbers of controls, or people without the
disorder, the same
results appeared, the Temple University biochemist
said.
The defect is an
unusually small form of an enzyme called RNase-L,
which breaks down
RNA, a molecule that is the principal genetic
substance of many
viruses.
Chronic fatigue syndrome
involves at least six months of severe
fatigue plus four
or more of the following symptoms: impairment in
short-term memory
or concentration; sore throat; tender lymph nodes in
the neck or armpit;
muscle pain; pain in multiple joints without
inflammation; headaches
of a new type, pattern, or severity;
unrefreshing sleep;
and long-lasting malaise following exertion.
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1997 Globe Newspaper Company
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