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CFS 2004 Conference Blurb


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By Dr. Bell

Literature Review

There were several lectures at the recent AACFS meetings that were so exciting they made my socks roll up and down. The CFS scientific community is maturing and beginning to put together the knowledge that has existed in a fragmentary way over the past twenty years.

The first outstanding lecture was by the Centers for Disease Control and Prevention and delivered by Dr. J. Jones, called the Dubbo Infection Outcomes Study. Dubbo is a region of Australia where several illnesses that seem to initiate CFS are seen. It is a prospective study with 101 patients with EBV mononucleosis, 88 patients with Ross River virus, and 65 patients with Q fever followed over time to see who develops the symptom pattern of CFS. At 12 months, 6% of subjects met criteria for CFS. The most important predictor of developing CFS was the severity of initiating infection, and emotions were not a predictive factor.

This outstanding study is formalizing the post-infective aspect of CFS. The study is not yet finished, and we will have to eagerly await full results: is there a difference between the CFS after EBV or the CFS after Ross River virus? What is the reason some people get CFS and others do not? What role does abnormal interferon or genetic markers play? Stay tuned.

The second lecture that was outstanding in my opinion was about Hepatitis C. Dr. Charles Raison presented a study he and co-workers have been working on concerning the treatment of hepatitis C with interferon (IFN). All patients had active hepatitis C, and prior to treatment, 22% had moderate fatigue with 3% bad enough to qualify for the diagnosis of CFS. During interferon treatment, the fatigue had risen to 70% with 30% having the severity and associated symptoms of CFS. Therefore, IFN clearly causes fatigue, worsening fatigue, and/or CFS-like symptoms in this group of patients with a known active infection with hepatitis C.

Well, we sort of knew that already, so it is not that big a deal. What is a big deal is what Dr. Raison said. The patients were monitored by measuring the viral load, and those patients with difficulty in clearing hepatitis C virus with interferon were the ones more likely to develop CFS type symptoms.

If proven true in subsequent and follow-up studies, this is remarkable. It implies that hepatitis C is a CFS-causing infection like the ones seen in the Dubbo study. Moreover, there seems to be a link between post-infectious fatigue, interferon, and difficulty clearing the virus (immune difficulties) even with interferon treatment. I would hope that this group of researchers is continuing to look into these relationships. This study is also a great reason why we cannot have blinders on ? we need to look at experiences from illnesses causing the symptom of fatigue such as cancer and specific infections like hepatitis C.

The third and fourth superb studies followed. The third was presented by Dr. Julian Stewart titled ?Regional blood volume and peripheral blood flow?. Dr. Stewart has been studying autonomic intolerance in young people with CFS. What he has shown with tilt-table testing is that there are regional changes in blood flow that are not normal. Among these is a marked reduction in thoracic blood volume related to inadequate cardiac venous return.

I love it. Perhaps even those patients who measure a normal circulating blood volume may, in effect, be hypovolemic in the heart and lungs. Kazuhiro Yoshiuchi presented a paper shortly after Dr. Stewart showing a reduction in cerebral blood flow in CFS patients.

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Interesting! Thanks for posting!


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