Dr. Charles W. Lapp har skrevet en omfattende oppsummering som utgjør hele 11 “word-sider” og som dekker de fleste emner og tema som ble diskutert og presentert på den store ME konferansen. I denne oppsummeringen har Lapp også tatt med en del egne kommentarer. Oppsummeringen bærer altså preg av subjektivitet.
Dette er hva Dr. Lapp sier innledningsvis:
“The biennial meeting of the IACFS was held in Ottawa, Ontario, this year. Those who expected Fall leaves and falling temperatures were greeted instead with temperatures in the high 70’s and sticky humidity. The theme of the conference could have been “Not What You Expected,” instead of “Translating Evidence Into Practice”!
While well attended, there was a notable absence of the “Old Guard” such as David Bell, Jacob Teitelbaum, Ritchie Shoemaker , Suzanne Vernon, Rich Podell, Pat Fennell, and many others. The large support groups (AFSA, NFA, CFIDS Association, CFS Knowledge) were not represented. We missed you all, but I have to say that this meeting attracted a large number of new and active participants. Overall about 200 patients and 200 providers attended, representing over 20 different countries.”
Noen utdrag fra oppsummeringen til Lapp:
Første dag av konferansen ble preget av annonseringen av resultatet fra BWG. Dersom XMRV hypotesen allerede var i store problemer kan det vel neppe sies at resultatene fra denne studien minsket tvilen. Dette er noe av hva Lapp skriver om XMRV-krigen:
“Everybody was braced for the Point-Counterpoint between Dr. Mikovitz and Dr. Coffin. However, the heat was extinguished by the introductory presentation of Dr. Graham Simmons who eloquently summarized the results of XMRV testing in 7 laboratories, all of whom were provided blinded specimens (negative controls, spiked (known) positives, and patient samples). Overall, XMRV/MLV was not confirmed in Persons with CFS (PWCs). Only Dr. Mikovits and her colleague Dr. Ruscetti found positive controls, and even these showed disagreement with replicate samples. Thus the work of Mikovits and Ruscetti seemed tainted right from the start.
Nevertheless, Dr. Mikovits (of the Whittemore-Peterson Institute, Reno NV) made a very nice presentation of her own work, explaining that she had double checked all specimens from the original article and found only 6 that were possibly contaminated, and sticking firmly to her hypothesis that XMRV is associated with ME/CFS.”
Det er diskusjon rundt de nye ME kriteriene også og tydeligvis en del av termologien i kriteriene.
Presentasjonene angående belastningstester og hva som foregår på biokjemisk og molekylær biologisk nivå har vi godt dekket via Jørgen Jelstads blogg. Signifikante endringer i ME pasienter under og etter fysisk aktivitet!
Etiologi og biomarkører – funn
Dette er noe av hva Lapp skriver:
The possibility of an enteroviral infection as a trigger for ME/CFS in some patients remains intriguing. Enteroviral infections mostly cause flu-like gastrointestinal symptoms (nausea, diarrhea) during the Summer months. John Chia MD (a pathologist and infectious disease specialist in Torrance, California) has long maintained that he and his son contracted ME/CFS from an enterovirus. Using paraffin-embedded biopsies from 132 PWCs, enteroviral protein VP1 was detected in 82% and and dsDNA in 64% of cases. He and his son both recovered by using an herbal antiviral (Equilibrant, see “Treatments” below).
Dr. Martin Lerner, an infectious disease specialist at Wayne State University (Michigan) presented an interesting poster concerning EB virus and ME/CFS. He treated 6 PWCs with valacyclovir (Valtrex, 14.3 mg/kg every 6 hours) for more than 12 months. Checking periodically for the continued presence of EBV, he found no evidence of EBV replication, but instead found “latent abortive reactive replication.” That is, the whole virus was not being manufactured in the body, but various parts of the virus were. These fragments were not infective.
Our old friend, Byron Hyde (Nightingale Foundation, Ottawa) was on hand to warn about a high incidence of thyroid cancer in Canadian patients. One hundred consecutive patients underwent “total body investigation” including thyroid ultrasound and/or scanning. The incidence of thyroid malignancy in this group exceeded 6000 per 100,000, whereas the natural incidence is only 30 per 100,000. Malignant nodules were usually solitary, hypervascular, and > 1cm in diameter.
Changing gears, Ekua Brenu, a young PhD candidate and very active researcher from Queensland AU, studied cytotoxic function and markers in PWCs at 6 month intervals to determine the stability of these observations over time. She confirmed that suppression of NK cells (CD56) was the most reliable finding, and could be a potential biomarker for ME/CFS. On the other hand, a number of other markers (TH1, TH2, TH17 cytokines, IL1α, IL1β, and TGF-β) varied over time.
Mary Ann Fletcher and Nancy Klimas (University of Miami) performed prospective cytokine studies in PWCs to determine which biomarkers were most abnormal compared to controls. They found that Lymphotoxin A (or LT, increased 257%), IL4 (240%), IL6 (100%), IL 12 (120%) IL5 (95%), and Neuropeptide Y were most increased above controls, while NK cell numbers were decreased. Lymphocyte Proliferation to mitogen stimulation was decreased, and lymphocyte activation markers (CD26, CD38) were increased. They found little difference in IL13, IL10, IL2, TNFα, IFN, IL15, and IL8. These findings may lead to markers for ME/CFS, and suggest that T cells are metabolically limited in performing their helper function.
Behandlingstiltak av ME. Her er ett utdrag:
John Chia MD ( Torrance, California) has long maintained that he and his son contracted ME/CFS from an enterovirus infection. Enteroviruses (which include the coxsackie and polio viruses) usually cause flu-like symptoms in the Summer months (atypical for influenza, which occurs in the late Fall and Winter). At the last conference in 2009 Chia reported success treating himself, his son, as well as numerous patients who had stomach biopsies positive for enteroviral protein VP1. Treated subjects were given up to 600mg per day of oxymatrine for 3 to 6 months. 52% of the treated subjects improved on a 7-point scale (much better to unchanged to much worse), while only 6% of controls improved. In this year’s account, Chia reports an enhanced response when the antibiotic rifampin (300mg twice daily for 7 days) is given concurrently with oxymatrine. Of 48 subjects treated, 32 (67%) responded to such therapy. Two-thirds had a febrile response and transient worsening of symptoms, however, when rifampin was added. Oxymatrine (with or without rifampin) appears to be an effective therapy in a subset of PWCs with evidence of enteroviral infection in the gut.
An Ampligen update was provided by Dr. David Strayer (Hemispherx Biopharma Inc, Philadelphia), who reminded us that in previous studies 40 weeks of Ampligen therapy improved exercise tolerance by 16.6% (compared to 4.8% on placebo) and reduced concurrent medication use by 72% (56% on placebo). In the current study, 208 Ampligen subjects were analyzed for antibody against XMRV. 33.7% of subjects were positive for XMRV. These subjects were sicker (as measured by activities of daily living and actigraphy). On treatment with Ampligen these same subjects demonstrated a 14% greater exercise response and 24% more reduction in medication use, compared to XMRV-negative subjects. The generic name for Ampligen has now been designated as “rintatolimod” by the World Health Organization.
Richard Van Konynenburg (Rick vank) og melyleringshypotese (mangel på glutation). Video fra Sverige kan du se her.
(mhj kom: Metyleringshypotesen overlapper med hypotesene for nitros- og oksidativt stress. I videoen fra Sverige går Rick grundig igjennom den biokjemiske delen. Han skiller tydelig på hva som er hans hypotese og hva som er funnet i studier)
Norman Booth once again presented Dr. Sarah Myhill’s hypothesis that mitochondrial function is blocked or failed in ME/CFS. Nettsted for info her
Lapp om GcMAF:
GcMAF (pronounced “gee-see- MAFF”) is the newest fad in ME/CFS treatment. This compound is thought to activate macrophages that are not responding properly, whereby it is also known as Macrophage Activating Factor (MAF) derived from Vitamin D Binding Protein. GcMAF starts as an amino acid attached to three different sugars. B-lymphocytes cleave one sugar, and T-lymphocytes cleave the other, leaving just an amino acid – sugar complex. This complex (GcMAF) binds to dormant macrophages and activates them.
Macrophages are the “police” or “first responders” in our immune systems. When they contact “foreigners” such as viruses or bacteria, macrophages signal lymphocytes of the invasion, then gobble up the invader. Drs. Kenny DeMeirleir (Vrije University, Brussels BE) and Paul Cheney (Asheville NC) presented treatment papers featuring this compound, which has also been tried as an immune modulator in HIV and cancer.
DeMeirleir injected 0.25 to 1 ml weekly (subcu or intravenously) into adult subjects for up to 40 weeks. All were XMRV/MLV positive. He reported that 68/108 (63%) reported “noticeable improvement” in fatigue, sleep quality, pain, neurocognitive function, recovery time, orthostatic intolerance and digestive problems. Side effects occurred in 18%, mostly headache or sleep disturbance, and 7% dropped out due to these symptoms.
Cheney treated 21 patients for at least 2 months with sublingual GcMAF. 10/21 showed improvement in symptoms, and 5/21 failed to respond or got worse. Most subjects experienced exacerbation of their CFS symptoms, and two developed Vitamin D toxicity.
[Ed. note: We are all seeking new treatments for ME/CFS but I don’t think this is it. These posters only described very modest improvement, numbers were small, and side effects were legion. I have now seen several patients who were involved in these studies and they report utter failure. At one time there was a voluntary website where subjects could report their results. When I checked the site, none reported any significant response, but the website has since been shut down.]
I have included one study in the treatment section that might fit as well into epidemiology. Irma Pinxterhuis (Oslo University Hospital, NO) entitled her poster, “What Can Be Done To Prevent Deterioration and Promote Occupational Performance.” Studying 15 severely affected women over time, Pinxterhuis aptly defined what helped and did not help. Improvement was affected negatively by lack of support and understanding, expectations or demands from themselves and others, and financial insecurity. What helped is worth emphasizing:
Support of health care providers and others
Lowered expectations for themselves and from others
Balanced nutrition and healthy or whole foods
Pinxterhuis wrote, “they needed above all peace of mind and a feeling that they and their family were taken care of, so that they could use all their energy on getting better.”
En kommentar fra Lapp angående sykdomsforløp og varighet av ME tilstand:
[Ed. note: To my recollection, Dr. David Bell reported an 80% recovery rate over 15 years in his Lyndonville population of children. This is in keeping with Rowe’s findings, which suggests that the prognosis for children is far better than for adults. Bell and Rowe have both pointed out, however, that “recovery” is relative, and many children must continue to pace, set limits, and monitoring activity well into adult life. Note that continuing engagement in education was the best predictor of outcome.]