chronic fatigue syndrome'
A Martin Lerner1, Safedin Beqaj2, James T Fitzgerald3, Ken Gill4,
Carol Gill4, James Edington4
Published Date May 2010 , Volume 2010:2
1Department of Medicine, William Beaumont Hospital, Royal Oak; 2Wayne
State University School of Medicine, Detroit; 3Department of Medical
Education, University of Michigan Medical School, Ann Arbor, Michigan;
4The Dr A Martin Lerner Chronic Fatigue Syndrome Foundation, Beverly
Hills, Michigan, USA
Purpose: We hypothesized that chronic fatigue syndrome (CFS) may be
caused by single or multiple Epstein–Barr virus (EBV), cytomegalovirus
(HCMV), or human herpesvirus 6 (HHV6) infection. To determine if CFS
life-altering fatigue and associated findings including muscle aches,
tachycardia at rest, chest aches, left ventricular dysfunction,
syncope, and elevated herpesvirus serum antibody titers are reversed
by long-term subset-directed valacyclovir and/or valganciclovir.
Patients and methods: Data were collected at physician visits every
4–6 weeks from 142 CFS patients at one clinic from 2001 to 2007. To be
included in this study, patients had to be followed for at least six
months. The data captured included over 7000 patient visits and over
35,000 fields of information. Severity of fatigue was monitored by a
validated Energy Index Point Score® (EIPS®). Baseline and follow-up
serum antibody titers to EBV, HCMV, and HHV6, as well as coinfections
with Borrelia burgdorferi, Anaplasma phagocytophila, Babesia microti,
and antistreptolysin O, 24-hour ECG Holter monitors, 2D
echocardiograms, cardiac dynamic studies, symptoms, and toxicity were
captured and monitored. International criteria for CFS plus a
specifically designed CFS diagnostic panel were used.
Results and conclusions: The Group A herpesvirus CFS patients (no
coinfections) returned to a near-normal to normal life (P = 0.0001).
The long-term EIPS value increased (primary endpoint, P < 0.0001) with
subset-directed long-term valacyclovir and/or valganciclovir therapy.
Secondary endpoints (cardiac, immunologic, and neurocognitive
abnormalities) improved or disappeared. Group B CFS patients
(herpesvirus plus coinfections) continued to have CFS.