Similitudes y diferencias entre Sind. Fatiga Crónica y Fibro

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Similitudes y diferencias entre Sind. Fatiga Crónica y Fibro

Mensaje por elipoarch » 09 Ago 2014, 18:02


Cort Johnson vuelve a hacer un análisis magnífico en su blog Health Rising, en este caso explicando las diferencias OBJETIVABLES entre la Fibromialgia y el Síndrome de Fatiga Crónica / Encefalomielitis Miálgica (SFC/EM). ¿Cuántas veces habéis oído (incluso a médicos) diciendo que ambas enfermedades son una sola? Pues no, existen estudios que constatan diferencias entre ambas, de tal modo que queda claro que no es una única enfermedad con diferentes expresiones, sino dos enfermedades que pueden ser comórbidas, pero diferentes. Uno de los últimos estudios que colgamos aquí mostraba más similitud entre el SFC/EM y la Esclerosis Múltiple que entre el SFC/EM y la Fibromialgia, si atendemos a los niveles de BDNF http://www.sfc-em-investigacion.com/vie ... 365#p21365" onclick="window.open(this.href);return false;, estudio al que se refiere este artículo en inicio, pero hay más.

Bueno, he pegado aquí el artículo para quien quiera leerlo entero, pero quiero destacar las diferencias y similitudes que señala, para un acceso más inmediato: (nota: algunos de los enlaces que pongo difieren del artículo original, porque no me casaban algunos... creo que se pueden haber liado un poco con tanto enlace... espero que a mí no me haya pasado lo mismo - además de que no me había dado cuenta de que ellos ya habían puesto los enlaces hasta la mitad de mi trabajo de búsqueda, en que he hecho clic en un enlace por casualidad :lol: )

En qué se parecen el Síndrome de Fatiga Crónica y la Fibromialgia
* Disminución de la variabilidad de frecuencia cardíaca – Activación Sistema Nervioso Simpático – FM y SFC/EM (http://www.ncbi.nlm.nih.gov/pubmed/24662556" onclick="window.open(this.href);return false;)
* Reducción de la capacidad aeróbica - FM (http://www.ncbi.nlm.nih.gov/pubmed/23527918" onclick="window.open(this.href);return false;) y SFC/EM (http://www.ncbi.nlm.nih.gov/pubmed/24755065" onclick="window.open(this.href);return false;)
* Aumento lactato en músculos – FM (http://www.ncbi.nlm.nih.gov/pubmed/20603699" onclick="window.open(this.href);return false;) / Problemas con el metabolismo del lactato – FM (http://www.ncbi.nlm.nih.gov/pubmed/16376018" onclick="window.open(this.href);return false;) / Aumento de lactato en el cerebro – SFC/EM (http://www.ncbi.nlm.nih.gov/pubmed/22281935" onclick="window.open(this.href);return false;)
* Aumento de la homicisteína en el líquido cefalorraquídeo - FM y SFC/EM (http://www.ncbi.nlm.nih.gov/pubmed/9310111" onclick="window.open(this.href);return false;)
* Reducción del flujo sanguíneo al cerebro - FM (http://www.ncbi.nlm.nih.gov/pubmed/17657679" onclick="window.open(this.href);return false;) y SFC/EM (http://www.ncbi.nlm.nih.gov/pubmed/16494597" onclick="window.open(this.href);return false;)
* Aumento Neuropeptido Y - FM (http://www.ncbi.nlm.nih.gov/pubmed/20074444" onclick="window.open(this.href);return false;) y SFC/EM (http://www.ncbi.nlm.nih.gov/pubmed/21190576" onclick="window.open(this.href);return false;)
* Implicación polimorfismo COMT - FM (http://www.ncbi.nlm.nih.gov/pubmed/24951880" onclick="window.open(this.href);return false;) y SFC/EM (http://www.ncbi.nlm.nih.gov/pubmed/21059181" onclick="window.open(this.href);return false;)
* Reducción matinal del cortisol en saliva - FM (http://www.ncbi.nlm.nih.gov/pubmed/21764519" onclick="window.open(this.href);return false;) y SFC/EM (http://www.ncbi.nlm.nih.gov/pubmed/23916911" onclick="window.open(this.href);return false;)
* Aumento IL-6 – FM (http://www.ncbi.nlm.nih.gov/pubmed/24462815" onclick="window.open(this.href);return false;) y SFC/EM (http://www.ncbi.nlm.nih.gov/pubmed/19909538" onclick="window.open(this.href);return false;)
* Disminución de la materia gris - tronco encefálico– FM (http://www.ncbi.nlm.nih.gov/pubmed/24179860" onclick="window.open(this.href);return false;) y SFC/EM (http://www.ncbi.nlm.nih.gov/pubmed/21560176" onclick="window.open(this.href);return false;)

Diferencias entre Fibromialgia y Síndrome de Fatiga Crónica / Encefalomielitis Miálgica
Aumento Substancia P en FM / Reducida en SFC/EM - enlace a estudio: Chronic fatigue syndrome differs from fibromyalgia. No evidence for elevated substance P levels in cerebrospinal fluid of patients with chronic fatigue syndrome
Aumento BDNF en FM - enlace a estudio: Increased BDNF serum concentration in fibromyalgia with or without depression or antidepressants / Reducida en SFC/EM - Brain Derived Neurotrophic Factor is Decreased in Chronic Fatigue Syndrome
Aumento IL-8 en FM enlace a estudio: Cytokines play an aetiopathogenetic role in fibromyalgia: a hypothesis and pilot study. / IL-8 Reducida en SFC/EM enlace a estudio: Plasma cytokines in women with chronic fatigue syndrome
Leptina reducida en FM - enlace al estudio: Serum leptin in Egyptian patients with fibromyalgia syndrome: relation to disease severity. / Leptina incrementada en SFC/EM enlace a estudio - Daily cytokine fluctuations, driven by leptin, are associated with fatigue severity in chronic fatigue syndrome: evidence of inflammatory pathology.



[t]Where Fibromyalgia and Chronic Fatigue Syndrome Part Ways (and Where They Don’t)[/t]

Lately we’ve seen what appears to be a great deal of similarity in muscle issues in Chronic Fatigue Syndrome and Fibromyalgia. We know that Dr. Bateman and others believe ME/CFS and Fibromyalgia occur on a fatigue-pain continuum – that they are similar disorders that differ in the amount of fatigue and pain present. They both predominantly affect women, and similar medications are used in both.

Both Dr. Natelson and the Lights, however, have found differences in ME/CFS + FM vs ME/CFS patients alone, and Natelson argues that they’re quite different disorders.

Now a recent study demonstrates an important way that this is so.

Reduced levels of BDNF – described as a nerve repair agent – were recently found in Chronic Fatigue Syndrome and multiple sclerosis. The levels found – less 25% of normal – were stunningly low, and this suggested that neuron functioning was taking a real hit in both these disorders. Given the nerve damage found in MS, that result was expected for MS – but not in ME/CFS.

A recent Fibromyalgia BDNF study seems to portray a very different disorder. It examined BDNF and a marker of central sensitization (S100B) in the blood of fifty-six FM patients and then determined if this correlated with pain pressure thresholds (the threshold at which pressure starts producing pain). The lower the pain threshold, the more pain a person is in. The study did not involve healthy controls and thus did not, strictly speaking, determine if BDNF levels were higher or lower than normal in FM.

Microglia Activation and Central Sensitization

Before we get to the findings, let’s look at S100B. S100B is such an intriguing factor that it’s surprising it hasn’t been studied before in FM or in any other pain disorders. S100B upregulates two key cytokines, IL-1b and TNF-a, both of which may be involved in FM and ME/CFS. It also activates the nuclear transcription factor which Maes proposes underlies the inflammatory milieu in ME/CFS and depression. It is also considered a surrogate for microglial activation.

Study Findings

This study found that increased BDNF and S100B levels were associated with increased pain sensitivity in FM. Other studies have found increased BDNF levels in FM as well. These FM findings contrast sharply with the decreased BDNF levels found in ME/CFS.

With regards to BDNF, ME/CFS looks more like multiple sclerosis than it does Fibromyalgia.

High Levels of Excitation vs Low Levels of Nerve Repair?

While high levels of BDNF in FM look like they’re enhancing the activity of excitatory pain pathways in FM, low levels of BDNF in ME/CFS look like they may be impeding neuron repair and slowing down nerve transmission. Could FM be a disorder of brain excitation while ME/CFS is a disorder of brain loss and slowed functioning? Could it be that simple?

A quick look at the research findings in ME/CFS and Fibromyalgia indicate more overlaps than dissimilarities. Both are characterized by sympathetic nervous system activation, reduced aerobic capacity, increased lactate levels (in one place or another), reduced brain blood flow, decreased cortisol, and decreased grey matter in the brainstem.

Similarities between the ME/CFS and Fibromyalgia
Reduced heart rate variability – sympathetic nervous system activation – FM and ME/CFS
Reduced aerobic capacity – FM / Reduced aerobic capacity – ME/CFS
Increased lactate – muscles – FM / Problems with lactate metabolism – FM / Increased lactate brain – ME/CFS
Homocysteine increased in spinal fluid - both disorders
Reduced brain blood flow - FM / Reduced brain blood flow - ME/CFS
Neuropeptide Y increased - FM / Neuropeptide Y increased - ME/CFS
COMT Polymorphism Implicated– FM /COMT Polymorphism – ME/CFS
Reduced salivary awakening response cortisol – ME/CFS / FM
IL-6 increased – FM / IL-6 increased ME/CFS
Decreased grey matter – brainstem – FM / Decreased brain matter – brainstem – ME/CFS

Differences between the ME/CFS and Fibromyalgia
Substance P increased in FM / Reduced in ME/CFS
BDNF increased in FM / Reduced in ME/CFS
IL-8 increased FM / IL-8 decreased ME/CFS
Leptin reduced – FM / Leptin increased – ME/CFS

Central Sensitization – the Key?

It’s intriguing that the two major differences between the two disorders, increased substance P and BDNF in FM, are associated with central nervous system activation.

Given the high amount of pain and problems with stimulus overload, we’ve assumed ME/CFS is also a central sensitization disorder. Yet two markers associated with central sensitization that are elevated in FM, BDNF and substance P, are not elevated–or are actually lowered–in ME/CFS.

The excitatory neurotransmitter glutamate is also clearly increased in some parts of FM patients’ brains, but a CDC gene expression study suggested decreased glutamate uptake may be present in ME/CFS. At the Stanford Symposium Dr. Zinn described an ME/CFS brain characterized by substantial ‘slowing’. It was a brain that seemed to be more asleep than awake.

On the other hand, Jason has proposed that limbic kindling produces a kind of ‘seizure activity’ in parts of the brain in ME/CFS, and high levels of neuropeptide Y and reduced heart rate variability indicate the sympathetic nervous system is activated in both disorders. Klonopin (clonazepam), a nervous system inhibitor, is used in treating both disorders.

In the end it may be that, like the immune system in ME/CFS, parts of the brain are over- and under-activated in both disorders.

Conclusion

Increased levels of BDNF and S100B levels are associated with increased pain sensitivity in Fibromyalgia. They join a variety of other markers of central sensitization markers found in FM.

Differing levels of BDNF and substance P in Chronic Fatigue Syndrome and Fibromyalgia suggest that the two disorders differ in important ways. However, the two disorders share many more commonalities than differences. The central nervous system could be, however, where the two disorders diverge.

Pain is common in ME/CFS, but it appears that the pain is, at least in part, being produced in different ways than it is in Fibromyalgia.

Pongo el enlace al artículo, para que podáis ver todos los enlaces y comentarios : http://www.cortjohnson.org/blog/2014/08 ... part-ways/" onclick="window.open(this.href);return false;
VINCIT QUI SE VINCIT (Vence quien se vence a sí mismo)
EX NOTITIA VICTORIA (En el conocimiento reside el triunfo) 12
(tomado prestado de un amiguete... gràcies, Fran)
___________

DONA al Estudio de Biomarcadores para EM/SFC en el Centro de Investigación Médica Aplicada de la Clínica de Navarra:
El EM/SFC como Posible Inmunodeficiencia Adquirida https://helpify.es/comunidades/todo-por ... a-cronica/
ENTRE TODOS PODEMOS!!! :V: :V: :V: :V:

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