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[vivolenta]

Comparing the Fukuda et al. Criteria
and the Canadian Case Definition
for Chronic Fatigue Syndrome

Leonard A. Jason, PhD Susan R. Torres-Harding, PhD Amber Jurgens, BA Jena Helgerson, BA

link.. http://www.theonecli...t...n - CFS.pdf

Allega File(s)

•  jason2004CFSCCCFull.pdf   175,84K   95 Numero di downloads

Messaggio modificato da vivolenta, 13 gennaio 2009 - 09:54:27

[VITTORIA]

Tutti i documenti tradotti sinora, e quelli in corso o in attesa di essere tradotti, li trovate qui: http://www.cfsitalia...&st=0#entry8658 mentre questo link http://www.cfsitalia...hp?showforum=89 porta al subforum dedicato solo ai documenti tradotti.

[romy]

Mi capita che non riesco più a scaricare la maggioranza degli allegati,solo geroclifici non si legge una parola,come mai?.Romy

[admin]

Non so a cosa sia dovuto il problema, meglio quindi postare il link al pdf che si vuole segnalare.

[vivolenta]

Notes on Human Herpes Virus Type 6 Research in ME

There is continued interest in HHV6. It was discovered in 1986 by Dr Dharem Ablashi et al and has two sub-types: variants A and B. It is of the same herpes family as the Epstein-Barr virus (which is responsible for mononucelosis / glandular fever).
HHV6 is closely associated with cytomegalovirus (CMV) and with HHV7.
It has been found to interact with the human immunodeficiency virus (HIV) -- the GS strain is the one implicated in HIV infections; research has found HHV6 in 100% of AIDS patients tested. HHV6 is known to interact with other viruses, making those viruses more severe.
HHV6 has also been found in patients suffering from multiple sclerosis.
HHV6 has been linked to other known autoimmune conditions including systemic lupus erethyamtosus (SLE / lupus) and to Sjorgren’s syndrome.
HHV6 can attack the brain, lymph system, bone marrow and lungs. (ref: ACFS Conference will report high HHV6 results. ME Today / BRAME:September 1999:9:50-57)
Variant B (found in childhood roseola) affects most people quite early in life and then remains latent unless reactivated.
8 Variant A is less common. In 1986 Ablashi was contacted by three of the eading US experts in ME / CFIDS / CFS (Drs Cheney,Peterson and Komaroff) and asked to test for HHV6 in ME / CFIDS. He found that 70% of those patients had variant A instead of variant B.

9 Ablashi is now working with Professor Robert Suhadolnik (see pp.12 & 243 above), as HHV6 is directly related to the low molecular weight protein which Suhadolnik hopes will become a marker for ME / CFIDS / CFS.

Other research has also shown that HHV6A is active in ME / CFIDS. Evidence of this was presented at the Fourth International AACFS Research and Clinical Conference on CFIDS (Massachusets, October 1998) by Dr Konstance Knox of Herpesvirus Diagnostics Inc and the Institute for Viral Pathogenesis (Winsconsin) (ref: Abstract of Proceedings, page 38).
Tests for HHV6 detect only active infection, so the tests need to be re-run over several months, as patients are only intermittently positive for HHV6
A patients with ME or multiple sclerosis is most likely to show a positive HHV6 result if tested during a relapse / flare-up. (Even the concept of a relapse rarely features in papers by psychiatrists of the "Wessely School").
Some laboratories use pcr techniques (polymerase chain reaction) but this is not as reliable as using an early antigen assay.
A further herpes link with ME has been postulated by David Berg, Director of HEMEX Laboratories Inc, Phoenix, Arizona who at the Fourth International AACFS Research and Clinical Conference on CFIDS, Mass, October 1998 presented evidence that antibodies (caused by various antigens, including HHV6) attack capillary endothelial cells, thereby activating coagulation (with the formation of fibrin), resulting in increased blood viscosity.
This well-understood and serious blood disorder (known as disseminated intravascular coagulation or DIC) has been found in nearly 100% of tested ME / CFIFDS patients; it has also bee found in fibromyalgia patients; following silicone breast implants, and in Gulf War syndrome.
Berg’s data point to the immune system as activating this coagulation (by removing protective proteins and then by effectively agglutinating other proteins, resulting in fibrin deposition.
Whilst this process does not usually cause a thrombus in most ME patients, it does interfere with the body’s ability to transfer nutrients and oxygen via the capillary network.
Known as "Antibody Mediated Thrombosis", this work was also presented at the International Society of Thrombosis and Hemostasis Symposium, Washington DC, in August 1999. (ref: ME Today / BRAME: 1999:9:51-57).

[vivolenta]

http://www.ijcem.com...IJCEM812001.pdf

Chronic fatigue syndrome and mitochondrial dysfunction
Sarah Myhill1, Norman E. Booth2, John McLaren-Howard3
1Sarah Myhill Limited, Llangunllo, Knighton, Powys, Wales LD7 1SL, UK; 2Department of Physics and Mansfield College, University of Oxford, Oxford OX1 3RH, UK; 3Acumen, PO Box 129, Tiverton, Devon EX16 0AJ, UK

Received December 2, 2008; accepted January 12, 2009; available online January 15, 2009
Abstract: This study aims to improve the health of patients suffering from chronic fatigue syndrome (CFS) by interventions based on the biochemistry of the illness, specifically the function of mitochondria in producing ATP (adenosine triphosphate), the energy currency for all body functions, and recycling ADP (adenosine diphosphate) to replenish the ATP supply as needed. Patients attending a private medical practice specializing in CFS were diagnosed using the Centers for Disease Control criteria. In consultation with each patient, an integer on the Bell Ability Scale was assigned, and a blood sample was taken for the “ATP profile” test, designed for CFS and other fatigue conditions. Each test produced 5 numerical factors which describe the availability of ATP in neutrophils, the fraction complexed with magnesium, the efficiency of oxidative phosphorylation, and the transfer efficiencies of ADP into the mitochondria and ATP into the cytosol where the energy is used. With the consent of each of 71 patients and 53 normal, healthy controls the 5 factors have been collated and compared with the Bell Ability Scale. The individual numerical factors show that patients have different combinations of biochemical lesions. When the factors are combined, a remarkable correlation is observed between the degree of mitochondrial dysfunction and the severity of illness (P<0.001). Only 1 of the 71 patients overlaps the normal region. The “ATP profile” test is a powerful diagnostic tool and can differentiate patients who have fatigue and other symptoms as a result of energy wastage by stress and psychological factors from those who have insufficient energy due to cellular respiration dysfunction. The individual factors indicate which remedial actions, in the form of dietary supplements, drugs and detoxification, are most likely to be of benefit, and what further tests should be carried out.
Key Words: Chronic fatigue syndrome; myalgic encephalomyelitis; mitochondria; neutrophils, oxidative phosphorylation.

[vivolenta]

http://www.prohealth...cfm?libid=14431
Decreased corneal sensitivity and tear production in Fibromyalgia - Source: Investigative Ophthalmaology & Visual Science, Mar 25, 2009
by J Gallar, et al.
March 28, 2009

……..
Conclusions: The reduced corneal sensitivity of patients with fibromyalgia is attributable to a moderate decrease of corneal polymodal and cold nociceptor [sensory receptors] sensitivity, that may be the consequence or the cause of the chronic reduction in tear secretion also observed in these patients.

Source: Investigative Ophthalmaology & Visual Science, Mar 25, 2009. PMID: 19324850, by Gallar J, Morales C, Freire V, Acosta MC, Belmonte C, Duran JA. Instituto de Neurociencias, Universidad Miguel Hernandez-CSIC, San Juan de Alicante, Spain.

AUTOMATICHEN STRACIO:
Risultati: La maggior parte (18 su 20) dei pazienti FM riferito occhio secco sintomi, essendo il cliente secchezza oculare significativamente superiore nei soggetti sani (2,3 + / -0,1 vs 0,05 + / -0,02; p <0,001). Schirmer's valori di prova sono stati significativamente ridotti in pazienti FM rispetto a quelle del gruppo di controllo (10,5 + / -. 2 mm e 30,6 + / -1,6 mm, rispettivamente, p <0,001).