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Is ME due to Ehlers-Danlos Syndrome "stretchy veins"

Discussion in 'Connective Tissue Disorders/Ehlers-Danlos Syndrome' started by Allyson, Nov 12, 2012.

  1. Allyson

    Allyson *****

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    Hi SHell and thanks

    yes my sister had to be rushed to a city hosopital for a post partum haemorrage too and nearly died - I think she has EDS as well - has many other symptoms.

    Good luck in the reading on EDS , would love to hear further updates.
    Best,
    Ally
     
  2. VeganMonkey

    VeganMonkey Senior Member

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    I use compression stockings I still have from hospital, they cover the whole legs so not just the bottom half, I was told its important to compress complete legs, otherwise blood will pool in the upper legs. Also was told that if you compress the body only all the blood will be pushed to the legs.
    It would be nice indeed if they invent lightweight ones that are cool in summer. In winter I don't mind thos heavy things as they keep me warm.
     
    Allyson likes this.
  3. Allyson

    Allyson *****

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    not sure about that VM - i do find abdo ony helps pullme out of a rash - eg singlet dress clingy
    they say if you do legs it shoud be upt o the waist- yes calvesolny stocking useless - most of the blood is inthe abdominal vessels as they are larger,
    my doc said not to wear in bed tho - baro receptor thingo sends message your BP is higha nd drop BP further
    but sometimes if crashed that helps me in bed so better than feeling like Sh**.
     
  4. VeganMonkey

    VeganMonkey Senior Member

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    Bark receptor thingy? Hahaha sounds funny :D but makes sense. However the few times I slept with those on I woke up feeling better than normal. I haven't experimented with that enough, once it's cold enough to keep them on at night I will test it again.
     
    Allyson likes this.
  5. Allyson

    Allyson *****

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    yes i fell better when i sleep in stretchy stuff

    baro receptors - the indicators of your bp - in the neck or kidneys or both i forget

    they tell your body what your bp is so it can regulate it - so if you sleep with your feet elevated my doc says not a good idea - Baro receptors tell your brain your bp is high so it drops it eve further
     
  6. Allyson

    Allyson *****

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    CONNECTIVE TISSUE DOC IN SYDNEY AUSTRALIA INTERESTED IN EDS


    Merylg I got sent this by PM from a kind reliable source and thought it may be of interest to you and others in Sydney and Brisbane, Australia

    quote
    I found a connective tissue specialist in Brisbane and emailed him my history, he agrees my history is suggestive of connective tissue disease / Ehlers Danlos. He is on annual leave and returning to a new job running the connective tissue dysphasia clinic at Westmead Children's hospital in Sydney from Sept. He is happy to take us on ... if we don't mind travelling to Sydney. His name is Andreas Zankyl. Thanks so much for all your information, I'm so grateful.

    unquote

    (that may be meant ot read dyplasia not dysphasia)
     
    merylg likes this.
  7. VeganMonkey

    VeganMonkey Senior Member

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    I read somewhere that some people with POTS sleep half upright on some sort of wedge, but wouldn't that push all the blood to the legs?
     
  8. Sushi

    Sushi Moderator and Senior Member Albuquerque

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    shazinoz

    I am not sure what you are referring to, but I haven't read this whole thread. Does
    refer to a post in this thread?

    Thanks,
    Sushi
     
    Allyson likes this.
  9. becc

    becc

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    Thanks for posting all this information, Allyson and others. I have POTS and several doctors have commented on my hypermobility and skin over the years. I also have a lot of the other symptoms of EDS.

    I live in Melbourne so I'm going to ask my GP for a referral to the Genetics Department at the Royal Melbourne Hospital. I've no idea if it will end up being the answer to my ME but perhaps at least a component.

    Thanks!
     
    Allyson likes this.
  10. Allyson

    Allyson *****

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    Hi Bed, you are most welcome and
    You are most welcome Bec, glad to hear it has helped you as well as myself and so may other
    It is the best expalation of all our symptoms i have every heard.

    best of luck with the referral; this sentence was just posted on an EDS forum - MY capitalization.
    i have not read thee link yet
    best,
    Ally


    World-renowned EDS Expert Dr Rodney Grahame points out that, in America, almost 650,000 cases of EDS are missed ANNUALLY, based on studies that suggest almost 95% of cases presenting to clinics are missed, most often diagnosed with other things (fibro, chronic fatigue, somatization, etc.).

    See: http://tinyurl.com/cc5qk57
     
  11. WillowJ

    WillowJ Senior Member

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    sorry if this was answered already... I jumped randomly into the middle of the thread. :b

    it used to disqualify people because the standard-issue boots would not fit. Now, however, the US military contracts with Klingbeil (they also make ice skates) to make custom boots (for those who need it?), so flat feet is no longer a disqualification. Or so I'm told.
     
    Allyson likes this.
  12. WillowJ

    WillowJ Senior Member

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    I agree that if there's an EDS connection, it would most likely be a subset.

    I've heard some relevant things from CTD geneticists. One is that EDS-type disorders can have a sudden exacerbation, like from a motor vehicle accident.

    Another is that having a hereditray connective tissue disease (which could be mild) would make having an acquired connective tissue disease more likely (and it's plausible to me that ME is a connective tissue disease in its own right).
     
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  13. VeganMonkey

    VeganMonkey Senior Member

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    I'm wondering if hypermobility could affect a person if they didn't have EDS.

    Btw I am thinking of taking pictures of my hypermobility I can keep in an album here so it's easier for people to look up examples straight here on the forum since it takes a bit of googling to find pictures.
     
    Allyson likes this.
  14. Allyson

    Allyson *****

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    post from on anohter page but copy her too; for xmrv and oothers who have commented on cold baths helping

    yes i think aching feet is from the fluid pooling in the feet - my face is puffy when i wake up and it settles if is stay up a few hours but my feet ache from being up few hours as the fluid settles there - so that i think is the typical EDS picture as blood is not circulating but sitting in the viens of legs and abdomen; so lymphatic massage helps as does deep water - cool - as it forces fluid back from lymph to venous circulation

    I would like to make a short version of this thread - condensing the input - for others to read as it is so long now but do not know how - i cannot even copy and paste- all the formatting shows up.
     
  15. Allyson

    Allyson *****

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    good idea about the pics VM

    I have read that you can be hypermobilea nd not have EDS 3 but not sure i believe it - i thing symptosm often not appaarent til you are in your 20 s so young gymnasts and dancers are unawared until later of oher EDS symptoms - tht is just a guess though.


    But I know you can have EDS 3 and NOT be hypermobile - the apttern seems to be form thsi site and PM feedbacks that you are either hypermobile or very very stiff in the muscles.
     
  16. Allyson

    Allyson *****

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    this article just in too is useful

    Ehlers-Danlos Syndrome, Hypermobility Type

    Synonyms: EDS Hypermobility Type, EDS Type III, Ehlers-Danlos Syndrome Type III

    Howard P Levy, MD, PhD
    Department of Medicine, Division of General Internal Medicine
    McKusick-Nathans Institute of Genetic Medicine
    Johns Hopkins University School of Medicine
    Baltimore, Maryland

    Initial Posting: October 22, 2004; Last Update: September 13, 2012.

    Go to:

    Summary .

    Disease characteristics. Ehlers-Danlos syndrome (EDS), hypermobility type is generally considered the least severe type of EDS, although significant complications, primarily musculoskeletal, can and do occur. The skin is often soft or velvety and may be mildly hyperextensible. Subluxations and dislocations are common; they may occur spontaneously or with minimal trauma and can be acutely painful. Degenerative joint disease is common. Chronic pain, distinct from that associated with acute dislocations, is a serious complication of the condition and can be both physically and psychologically disabling. Easy bruising is common. Functional bowel disorders are likely underrecognized. Autonomic dysfunction, such as orthostatic intolerance, may also be seen. Aortic root dilation is typically of a mild degree with no increased risk of dissection in the absence of significant dilation. Psychological dysfunction, psychosocial impairment, and emotional problems are common.

    Diagnosis/testing. The diagnosis of EDS, hypermobility type is based entirely on clinical evaluation and family history. In most individuals with EDS, hypermobility type, the gene in which mutation is causative is unknown and unmapped. Haploinsufficiency of tenascin-X (encoded by TNXB) has been associated with EDS, hypermobility type in a small subset of affected individuals. Testing for TNXB mutations is available on a limited clinical basis.

    Management. Treatment of manifestations: Physical therapy tailored to the individual; assistive devices (braces to improve joint stability; wheelchair or scooter to offload stress on lower-extremity joints; suitable mattress to improve sleep quality); pain medication tailored to symptoms; appropriate therapy for gastritis/reflux /delayed gastric emptying/irritable bowel syndrome; possible beta-blockade for progressive aortic enlargement; psychological and/or pain-oriented counseling.

    Prevention of primary manifestations: Low-resistance exercise to increase both core and extremity muscle tone for improved joint stability; appropriate writing utensils to reduce finger and hand strain.

    Prevention of secondary complications: Calcium, vitamin D, low-impact weight-bearing exercise to maximize bone density.

    Surveillance: DEXA every other year if bone loss is confirmed.

    Pregnancy management: Labor and delivery may progress very rapidly, even in primigravid women. There is no clear advantage to vaginal vs cesarean delivery. Pregnant women with known aortic root dilation should have an echocardiogram in each trimester.

    Agents/circumstances to avoid: Joint hyperextension; resistance/isometric exercise can exacerbate joint instability and pain; high-impact activity increases the risk of acute subluxation/dislocation, chronic pain, and osteoarthritis; crutches, canes, and walkers, which put increased stress on the upper extremities, should be used with caution.

    Genetic counseling. EDS, hypermobility type is inherited in an autosomal dominant manner. Most individuals diagnosed with the syndrome have an affected parent. The proportion of cases caused by de novo mutations is unknown. Each child of an individual with EDS, hypermobility type has a 50% chance of inheriting the disorder. Prenatal testing is available on a limited basis if the disease-causing mutation has been identified in the family.

    Go to:

    Diagnosis .

    Clinical Diagnosis

    Clinical diagnostic criteria and a revised nomenclature for all forms of Ehlers-Danlos syndrome (EDS) were proposed by Beighton et al [1998] (click for full text). EDS, hypermobility type is characterized chiefly by joint laxity with soft skin and easy bruising, but other organ systems (especially gastrointestinal and cardiovascular) are frequently involved. EDS, classic type has more significant skin and soft tissue manifestations, but in mild cases may be difficult to clearly distinguish from EDS, hypermobility type.

    The diagnosis of EDS, hypermobility type is based entirely on clinical evaluation and family history. The criteria listed below reflect those proposed by Beighton et al [1998] as modified by the author's experience.

    Major diagnostic criteria should all be met to establish a diagnosis of EDS, hypermobility type:

    Joint hypermobility, which is often confirmed by a score of five or more on the nine-point Beighton scale [Beighton et al 1973], although some individuals with objective joint laxity score fewer than five points (see below for the sensitivity and specificity of examination for joint hypermobility). One point is scored for each of the following:

    Passive dorsiflexion of each fifth finger greater than 90°


    Passive apposition of each thumb to the flexor surface of the forearm


    Hyperextension of each elbow greater than 10°


    Hyperextension of each knee greater than 10°


    Ability to place the palms on the floor with the knees fully extended


    Soft skin with normal or only slightly increased extensibility

    Soft skin is subjectively assessed, preferably in an area in which moisturizer has not been applied.


    Skin hyperextensibility is assessed at a site lacking excess or loose skin and without evidence of prior trauma by gently pulling until resistance is met. An ideal location is the volar surface of the distal forearm or wrist, where the upper limit of normal extensibility is 1-1.5 cm. Extensor surfaces of joints have excess skin and should not be used.


    Absence of fragility or other significant skin or soft tissue abnormalities, which are suggestive of other types of EDS. Such findings could include:

    Spontaneous or easily induced skin cuts or tears


    Spontaneous or easily induced tears or ruptures of tendons, ligaments, arteries, or other internal organs


    Surgical complications, such as arterial rupture or sutures tearing through tissues and failing to hold


    Spontaneous wound dehiscence


    Recurrent or incisional hernias


    Significant skin hyperextensibility (>1.5 cm on the volar wrist)


    Thin, translucent skin


    Atrophic ("cigarette paper") scars (although mildly atrophic scars are sometimes seen in EDS, hypermobility type, especially in areas subject to physical stress, such as extensor surfaces and the abdominal wall)


    Molluscoid pseudotumors

    Minor diagnostic criteria are supportive of but not sufficient to establish a diagnosis of EDS, hypermobility type:

    Positive family history of EDS, hypermobility type (or family history of joint laxity), without significant skin or soft tissue fragility, in a pattern consistent with autosomal dominant inheritance


    Recurrent joint dislocations or subluxations


    Chronic joint, limb, and/or back pain


    Easy bruising


    Functional bowel disorders (functional gastritis, irritable bowel syndrome)


    Neurally mediated hypotension or postural orthostatic tachycardia


    High, narrow palate


    Dental crowding

    The sensitivity and specificity of examination for joint hypermobility is dependent in part on the individual's age, gender, and medical history.

    Young children (especially age ≤5 years) tend to be very flexible and are therefore difficult to assess.


    Women are, on average, more flexible than men.


    Older individuals tend to lose flexibility, and post-surgical or arthritic joints often have reduced range of motion. A history of former joint laxity or clinical demonstration of substantial laxity in multiple joints is sometimes accepted in lieu of a positive Beighton score in such cases, if the family history and other minor criteria are strongly suggestive.
     
  17. lastgasp

    lastgasp

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    Sorry but you've been misinformed, there have been around *60* recorded outbreaks of M.E, from the 1930s to 1990s, ranging from Los Angeles to Durban to New Zealand and so on..

    The first ones were called atypical polio, Icelandic disease or something else, then later deemed to be the same disease, as the signs were quite clear. Muscle testing and post-mortems elucidated some of the common features and pathologies, and epidemiology showed it to be linked to the spread of polio, to whom ME survivors developed immunity.

    ME was classified as a neurological disease by the World Health Org in 1969. There was even a test for it in the 1980/90s and you could get experimental immune therapy but the psychiatrists soon put paid to that (they removed the few signs originally in Holmes' CFS too for Fukuda 1994 and made the cardinal exercise problem very *optional*).
     
  18. lastgasp

    lastgasp

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    All those things have plenty other explanations other than stretchy veins. You're picking features that fit in with your hypothethis and choosing to ignore alternative explanations which certainly exist because CFS is not simply another name for EDS or ME.

    Cold as well as heat exacerbtes ME - perhaps even more so because it's pernicious to mitochondria. Posture is NOT the only thing that explains fluctuations, clearly mitochondrial defects do that, as well as infection and autoimmunity.
    .
    Standing uses muscle activity and is a huge strain on a weak heart - for whatever reason (including possibly mitos again)

    Alcohol requires a liver enzyme to detoxify which pwME are deficient in (cytochrome? Can't remember). It also dehydrates.

    Poor oxygen delivery to muscle could be due to cellular muscle defect or RBC deformity, or too much muscle injury.

    Photophobia and hyperaccusis (rare to have one without the other in ME) could be due to gating dysfunction in the brain as well as other things. Pupil dilation may be neurologically impaired in ME. We also have poor muscle control for fine eye movements (saccading) which is one of the things that can make reading difficult. ME sufferers may have allodynia as well, and even olfactory hypersensitivity (often confused with MCS). We're also hypersensitive to visual movement signals, such as a bustling supermarket.

    I don't know how much adrenalin we can output - we have some insufficiency there, and often an all-round loss of hormonal responsiveness.

    Stomach pain has been found to be caused by inflammation on examination, it can also be due to reduced gastric emptying or low stomach acid. PwME have been found to have chronic enteroviral infection in the stomach.

    I prefer not to use the term PEM or "malaise", it's meaninglessly subjective, vague and trivial. A person coming down with a headcold has "malaise". With ME it's more the exacerbation of any and all symptoms, what in heart disease they call decompensation, and the muscle recovery time is extraordinary.


    Abnormally delayed recovery of muscle strength - you wouldn't wake up feeling okay the next day.
    I'd like to know if the mitochondrial and muscle tissue injury seen in ME occurs in EDS. What about EMG muscle jitter? Cogwheel leg movements? Fasciculations or spasms? Irregular respiration, slowed or paradoxical breathing?

    Temporary paralysis - willing a limb to move (while lying down) but the signal just not "getting through" is common particularly in early stages or bad relapses. there's some evidence of reduced nerve transmission.

    Sleep dysfunction - pwME often have a sleep disorder that's not simply be explained by symptom interference alone. Usually sleep very poorly at night, may have extreme torpor during the day and may sleep better then. Forced "sleep hygeine" leads to spiralling deterioration and more infections.

    Cognitive exertion - too much intellectual effort while lying down leads to a flare. How is that explained by posture?

    Causes of death - in ME includes pancreatic failure and certain cancers as well as cardio-vascular.

    Autoantibodies and immune disease (T cell insufficiency etc), I can't see any mention of these in an EDS search but maybe I missed something?

    Food intolerance - clearly if someone eats wheat and goes out for an unaccustomed walk before or after they're a bit daft. More likely over weeks, months and years people try to pace and only notice an association when it's clear. It's reality that certain foods cause some people problems and your telling them they're being daft is not helpful. Severe cases very easily get oral candida from carbs or fruit.


    I personally have virtually none of the characteristics of EDS usually given for all the types, I wouldn't discount it's remotely possible, and definitely so for some - but it's a differential diagnosis.
    your list is too vague and commonplace, I wouldn't use it to diagnose ME. For instance, multiple sclerosis also has heat intolerance, IBS is very common, no mention of the cardinal muscle slow recovery or fluctuations from hour to hour even without doing anything or immune symptoms.


    "also it is the only theory tat expalins why we have normal days and bad days - for me they correlate with posture."

    I don't doubt that EDS is being widely misdiagnosed but just because you've reached Damascus doesn't mean everyone with "ME" has EDS or that EDS is suddenly the only explanation. Why would EDS occur in 60 sudden onset epidemics and why would patients develop immunity to polio. I often see people getting their diagnosis corrected then trying to convince others they've all got what they have.
     
  19. Allyson

    Allyson *****

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    Dear Last gasp,

    thanks for the thoughtful reply.

    Firstly it is not my theory - it comes from a professor of medicine at one of Australia's top universities and was news to me too.

    Seondly no-where do I state that this is the answer to everyone's problem - as many have already said in this thread, no one needs a diagnosis to be on this forum. Many people are now being diagnosed with Lyme disease after many years thinking they had ME , for just one example.

    I have written several times this is just one theory than many could consider and have had hundreds of contacts from others here and elswhere saying they though it applied to them too and thanking me for pointing out the link.

    I have learned about my illness from the effort and contributions of many people here and on other forums like this who have educated me over the years and I am extremely grateful for that, and started this link as a way of giving back to others who re seeking answers too.

    I myself have multiiple food intolerances and allergies- that is part of the picture of both EDS and ME and no-where do i state or, I hope even imply, that people with these "are daft".

    My point about the gluten is that being upright can also cause a lot of the symptoms that people have attributed just to food ntolerance - I wish I had realised that before. Thi is something that is potenetially estable but no- one is testing for that that I am aware of.

    EDS research is still in flux too - the more people diagnosed or even seen by specialists the better for finding answers.

    PWME have many varied symptoms and not evey one has all the symptoms you mention here. I do not get a flare from cognitive exertion while recumbant that I am aware of for example (But could you define what you mean by flare though please?)

    I don t have time atm to address all your points - and I am no expert in ME or EDS either but the immune system rests largely in the gut .....and gut is connective tissue.

    you say _" Alcohol requires a liver enzyme to detoxify which pwME are deficient in (cytochrome? Can't remember). It also dehydrates."

    That may well be but alcohol is also a potent vasodilator; dehydration from alcohol does not take place within the firs 20 minutes of a drink - but that is when i feel the effects,a decrease in blood supply to the brain can happen within afew minutes of standing ( postural drop - that we then correct for with and adrenalin surge) . But yes that is a good connection you make becaue for me a crash form ME is like a very very bad hangover, so dehydration is likely to be a factor in ME crashes - and thus hangover research could feed back to our illness.

    No-one has answers for all the many seemingly strange symptoms that occur in Me and many other diseases

    This s one thread in the search for those answers - the EDS pages feature the same search for answers ( they do not seem to have a forum of this qulaity alas yet).

    I do think that there are many easily testable hypotheses in this theory and I would like to see them explored, however, if only as a step in the elimination process of scientific discovery.

    Thanks again for the interesting input.

    Cheers,
    Ally

    PS I note you are new to the forum - welcome - and that all your few posts so far have been solely in response to my threads on this topic and seem to be somewhat vitriolic in nature.

    Not sure why that should be so.

    I do know there is a lot of money to be made from selling anti-viral and other medications to severly ill and deperate people. There is no money to be made from this theory. I have no vested or financial interest in it apart from the strong desire to find the cause - and hopefully a cure..

    And also as this thread has had over 15,000 hits I think there are many others who find it a worthwhile path to explore too.
     
  20. Allyson

    Allyson *****

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    Post in on this topic from Crux on another thread re-poted here for thaos following here - many thanks indeed Crux:

    Thanks Allyson;

    There's alot to be learned about EDS.

    Luckily, I have also had great results from the B12. (Many of the symptoms of B12 deficiency and EDS overlap.)

    It looks like getting enough of the collagen strenthening amino acids would also help. ( I make alot of bone broth, high in glycine, proline, with some lysine.)

    I've read a little about some minerals that may help with collagen, skin, joints. Copper and Zinc are brought up. ( I take zinc, and get copper from foods.)
    .....
    I have no doubt that genetics have been the biggest part of my health problems.
     

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