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Royal Society of Medicine Conference
28th April 08
This article is taken from the Edmesh Newsletter Issue 64
There was more than a little disquiet amongst the ME community about the London based Royal Society
of Medicine (RSM) Conference, “Chronic Fatigue Syndrome”, which was held on 28 April 2008.
The Royal Society’s publicity for the event indicated that the aim of the meeting was to take a broad look
at CFS, examining its nature and definition. However, the concerns related to the lack of balance in the
agenda for the conference, which was biased towards the mental health perspective of ME as an illness of
psychiatric origin.
The lack of general publicity for the conference was also a concern. This was considered likely to deny
the majority of people with ME the opportunity to express their opinion.
The ME Association has said: “It is hard to understand why the RSM has failed to grasp the opportunity
to put on a meeting that really does takes a broad look at an illness that is classified as neurological by the
World Health Organisation.”
There was a peaceful protest at the venue by people with ME and their supporters on the day of the
conference.
Also see article in media section “Letter to Daily Telegraph by Derek Enlander, New York.
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BRIEF REPORT ON THE 3rd INTERNATIONAL INVEST IN ME CONFERENCE,
LONDON, 23.5.2008
This 4th UK conference on CFS/ME held between February and May 2008 was attended by approx. 165
people, including GPs, healthcare professionals, patients, carers and patient group representatives. MRC
and CMO representatives received a special welcome. The event was dedicated to Dr John Richardson
and chaired by Professor Malcolm Hooper. Presenter profiles and presentation abstracts are included in
the Journal of Invest in ME, Vol.2, Issue 1, available on www.investinme.org . A DVD is being prepared
- £15.
Dr Leonard Jason PhD, De Paul University, Chicago, spoke about ‘Case Definitions of ME/CFS,
including a Paediatric Case Definition’. These are very important in defining ME/CFS, because
sources of diagnostic unreliability in assessment can lead to disagreements amongst medics and scientists.
Operationally explicit criteria do not exist for ME/CFS – criterion variances account for the largest source
(of unreliability). Information from patients by structured interview schedules is needed for greater
reliability. ME/CFS fatigue can be described in different ways. He then spoke about various existing
case definitions, e.g. Fukuda 1994, Canadian 2003, Paediatric 2006 and the new Empirical CDC
definition. The latter is used for disability assessment, together with form MOS SF-36. New empirical
case definitions are important and have huge implications for prevalence rates and for patients, he
concluded.
Dr Jonathan Kerr, ST George’s University, London, presenting ‘Gene Expression in ME/CFS: A
Means of Subtyping’ was one example of revealing the complexities and seriousness of ME/CFS.
Essential epidemiological aspects: prevalence 0.5%, M:F ratio 6:1, sudden onset, preceding virus
infection, toxin exposure, pre-existing emotional stress. His team looked at a microarray of 47,000 genes
from 25 CFS patients and 50 normal blood donors. Genes showing differential expression were further
analysed using real-time PCR in 55 CFS patients and normal blood donors. CFS diagnosis was made a)
using the 1994 CDC Fukuda criteria and b) based on assessment and associated symptoms using 7
different measures. Findings: 13 transcription factors were over-represented and differential expression
confirmed in 88 genes, associated with haematological and immunological diseases and function, cancer,
cell death, immune response and infections. Graphs showed hugely different results in CFS groups
compared to controls. Clustering of data had revealed 7 subtypes with distinct differences in SF-36
scores, clinical phenotypes and severity. He suggested there was an immune system / brain interaction.
Dr Martin Lerner, a US Infectious Diseases Specialist – his presentation ‘A Twenty Year Journey to
Understanding and Treatment of the CFS, including a Longitudinal Study of Groups A and B CFS
Patients, 2000-2006’ reinforced the message that the study and treatment of subsets of CFS/ME patients
is highly complex. One achievement was the establishment of the Martin Lerner Foundation, with a
mission to advance research, treatment and dissemination of understanding CFS. He developed an
Energy Index Score (EI) – a simple reliable metric to evaluate the functional capacity of CFS patients at
physician visits and in measuring recovery after treatment with anti-viral drugs. He had identified
subgroups of patients whose illness was associated with herpesvirus infections (e.g. EBV, CMV + HHV6) and treated these with Valacyclovir and/or Valgancyclovir with significant success rates, notably in
those with persistent single (EBV) infection. A longitudinal study had identified 2 distinct groups: Group
A whose illness was due to herpesvirus infections only; Group B where herpesvirus infections occurred
with major co-infections (e.g. Lyme Disease, Babesiosis and Adult Rheumatic Fever). Anti-viral
treatment of Group A patients resulted in significant EI effect size changes. There was evidence of
abnormal T-waves (tachycardia) and abnormal cardiac wall motion at rest and during stress, and cardiac
biopsies showed evidence of pathogenic cardiomyopathy. Concluding he said a study of 187 CFS
patients treated from 2001-2007 at a single CFS treatment centre in Beverly Hills, Michigan, indicates
that CFS in Group A was caused by persistent, often abortive herpesvirus infections.
Dr Julia Newton, Newcastle University – her lecture was entitled ‘Standing up for Fatigue –
Autonomic Nervous System Response to Standing in CFS/ME’. She discussed blood pressure (BP) –
there was a constant drive to reduce BP in the UK, but low BP had major implications. The Autonomic
Nervous System (ANS) has 2 arms: the Sympathetic Nervous System, which raises BP, and the
Parasympathetic Nervous System, which sends signals to the brain to slow down. The Newcastle ‘Falls
and Syncope Service’ cares for patients who faint and fall. She spoke about Autonomic Dysfunction in
the pathogenesis of fatigue – there is a strong association between fatigue and the ANS (e.g. in MS and
heart failure). In CFS/ME symptoms of ANS dysfunction can be ascertained by an Orthostatic Grading
Scale (OGS); problems manifest when standing up and are evident in 89% of patients. CFS/ME patients
suffer from Dysautonomia; response to orthostasis is hypotension (low BP), which can result in syncope
(fainting due to low BP), Presyncope and fatigue. Changes from a 40 min. tilt-table test can be measured:
heart rate + BP (haemodynamic), autonomic changes, Impedence Cardiography, cardiac output and stroke
volume. A study of 63 patients tested on orthostasis showed that 48% had symptoms during the head-up
tilt and 52% suffered from orthostatic hypotension. There also was the Positional Orthostatic
Tachycardia Syndrome (POTS) – the maximum heart rate in CFS patients was 120, compared to 70 in
controls. Muscle magnetic resonance studies on 16 CFS patients and 8 controls showed CFS patients
generated a lot of acid in muscles after exercise. These symptoms can be treated; she said dried fruit and
a pinch of salt daily may help. – Many questions followed.
Dr John Chia, Infectious Disease Specialist, California, spoke about ‘The Role of Enterovirus
Infection in CFS/ME’ The enteroviral link with CFS/ME originated in the UK, but had not been
followed in the US, he said. He related his observations in a 19 year old student, from an initial severe
respiratory infection to finding extensive viral antibodies in a stomach biopsy. He spoke about
Picornaviruses – enteroviruses are one group (> 70 types), which are small, non-enveloped icoshedral
viruses. Very many cases of acute enteroviral infections occur every year in the US manifesting as
rhinitis, sinusitis, pharyngitis, bronchitis, pleuritis and pneumonia; they affect the gastrointestinal tract,
the central nervous system, the cardiovascular system, the musculoskeletal system and the skin. He spoke
about Th1/Th2 polarisation, which determines the outcome of intracellular infections. Atopic diseases,
steroids, vigorous exercise and prior infections are factors which determine eradication or persistence of
infections. Polioviral RNAs play different roles in infected cells; acute infections produce higher levels
of RNÁ; in chronic persistent infections there are double-stranded RNA formations. Similar findings had
been documented by Nairn, Gow et al, Galbraith et al. In their own study they found that 135/165 (82%)
of biopsies from CFS patients stained positive for VP1 within parietal cells, compared to 7/34 (20%) in
controls. Administering alpha interferon or ribavirin, or a combination of these to CFS/ME patients with
persistent EV infection resulted in significant improvement of clinical symptoms and suppression of EV
RNA. He proposed a model of pathogenesis of CFS – there is a genetic predisposition for the
development of these problems.
Dr Irving Spurr, a GP with over 20 years experience in ME/CFS, gave ‘A GPs experience of Diagnosis
and Treatment of ME/CFS’. He worked with Dr John Richardson on enteroviruses and their role in
ME/CFS for most of that time. He outlined the illness spectrum of enteroviruses: they affect the
oropharynx, the gut, skin, muscle, CNS/PNS, cardiovascular and glandular systems, result in
autoimmunity and can cause foetal abnormalities and tumours, causing an array of symptoms, including
anergy, myalgia, memory defect, dysequilibrium, parasthesia etc. He explained how various signs can be
investigated, e.g. mobility by a Romberg test. Further investigations to include standard blood tests,
antibody screen, thyroid function, viral serology. ECG Trop T, Buspirone / Prolactin / Cortisol; brain
scans. He listed the various enteroviruses: polioviruses, Coxsackie viruses A+B, Echoviruses and new
enteroviruses, some of which have more than one serotypes. Host range and transmission occurs amongst
humans, from animals + birds, by faecal and oral spread. Incubation period is 2-5 days. If the immune
system is OK – infection is fought off; if it’s too weak, it can’t be fought; if it’s too strong, severe
reactions can occur. He described cases and statistics from his own practice. Aims of management are
prevention and minimizing the turbulent phase.
Prevention involves vaccinations (which is
controversial), efficient early warning and notification, isolation, use of anti-virals. He outlined a number
of methods aimed at reducing the impact of these infections, including early diagnosis, immune regulation
with immunoglobulin, stress reduction, home tuition, benefit payments, toxin-free food/drink,
choline/Vit.C. He concluded saying the role of enteroviruses in ME was very important. Dr Jean
Monro, Medical Director of the Breakspear Hospital, described ‘Subgrouping of and Treatments for
ME/CFS’. She explained that she works with a team at the small hospital; they get health insurance and
insurance companies to pay for patients. Their clinical case definition and guidelines for medical
practitioners include the following: Consider factors in fatigue states (each with detailed descriptions):
Food, gastrointestinal function, oxygen, cellular integrity (all these interact), then investigations into
factors relating to fatigue - again considering each aspect in detail; e.g. gastrointestinal aspects include
aerobic and anaerobic bacterial antibodies, lactulose breath tests, comprehensive stool analysis and
parasitology, … gut permeability tests. The aim then is to detoxify the body. She spoke about capillary
circulation, which is affected by infectious agents. They carry out autonomic assessments, brainstem
autonomic functions, resting cardiac function. She spoke about ‘the irritable brainstem’, which she said
was almost like epilepsy, and the ‘fatiguable heart’, which could be measured. She mentioned
transcutaneous blood gases, discussed the function of sleep – the purpose of which was conservation of
energy in reducing the metabolic rate, and the various stages of sleep. She mentioned supersensitivity,
food sensitivities, Lyme Disease, Coeliac Disease, delayed hypersensitivity and much more. Finally she
outlined briefly 4 different case histories.
Dr Judy Mikovits, Research Director of the Whittemore Peterson Nevada CFS Centre for NeuroImmune Disorders, elaborated on ‘How Sub Grouping will affect Research Strategies: Towards a
Molecular Definition of ME/CFS’. She asked if this conference would mark a turning point. ME/CFS,
Atypical MS, Fibromyalgia, Autism and GWI were very complex. Their mission was to facilitate and
advance patient care and train medical students. Their clinical priorities include: Patient treatment
stratification based on genetic signature of disease subsets; microbial co-infections; HHV6A and novel
viruses; identification and validation of biomarkers through immunological profiling. She spoke of a
Sample Repository – the world’s largest CFS sample repository containing over 5,000 samples,
categorized in a searchable database of patient and sample data. Their current hypothesis is that a chronic
inflammatory stimulation occurs from acute and reactivated systemic infections of multiple viruses on a
susceptible host, where a genetic background leads to the pathogenesis characterized as ME/CFS. She
outlined various viral and co-infections which had been observed – a total of 1608 viral transcripts, micro
RNA or endogenous viral elements were observed and how many were tested for. Viral evasive
mechanisms of viruses associated with CFS were identified, etc etc.
Comment: This was another exciting and well-organised conference. – Grateful thanks to the 25% ME Group for paying the fee to
attend. 12.6.2008 Doris Jones