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

A

Allyson

Senior Member
Messages
1,684
Location
Australia, Melbourne
no it was not in your pst sorry Meryl - i put it up separately but you are right it was not appropriate so remived it
basically it was interesting as she had medical info tattood on her arm - POTS OI low BP etc etc all down her arm

sorry for the mix up and inconveneince
 
WillowJ

WillowJ

คภภเє ɠรค๓թєl
Messages
4,940
Location
WA, USA
Allyson said:
Great thanks Willow - yes my specialist also says you do NOT nd joint HM. I suos that got picked u as it was recogniable - then all the invisible sympotms tended to be overlooked by doc as they are in ME/cfs.
DO you have any Julia Newton reference please? I don not know her; si will sentd this to my docs - the arterial stiffness is new to me too but sounds logical. And yoeu the 2011 International concensus doc on ME says that joint HM is common in those with ME.

thanks again - is it OK if i it elswhere? ( I have made a condensed thread on this topic on NC as this one had got too long for people to read.)

cheers
Ally
Click to expand...

yes, that's fine to post on NC or elsewhere.

It was Gwen Kennedy, not Julia Newton, the arterial finding seems limited to adults. I will fix my other post accordingly. Here are the refs.

http://www.ncbi.nlm.nih.gov/pubmed/20819963
RESULTS:

Children with CFS/ME had increased oxidative stress compared with control individuals (isoprostanes: 252.30 vs 215.60 pg/mL, P = .007; vitamin C, mean [SD]: 0.84 [0.26] vs 1.15 [0.28] mg/dL, P < .001; vitamin E, 8.72 [2.39] vs 10.94 [3.46] microg/mL, P = .01)

and increased white blood cell apoptosis (neutrophils: 53.7% vs 35.7%, P = .005; lymphocytes: 40.1% vs 24.6%, P = .009).

Arterial stiffness variables did not differ significantly between groups (mean augmentation index, -0.57% vs -0.47%, P = .09);

however, the derived variables significantly correlated with total (r = 0.543, P = .02) and low-density lipoprotein (r = 0.631, P = .004) cholesterol in patients with CFS/ME but not in controls.
CONCLUSIONS:

Biomedical anomalies seen in adults with CFS/ME-increased oxidative stress and increased white blood cell apoptosis-can also be observed in children with clinically diagnosed CFS/ME compared with matched controls.

Unlike in their adult counterparts, however, arterial stiffness remained within the reference range in these pediatric patients.
Click to expand...

http://www.ncbi.nlm.nih.gov/pubmed/18031285
In the present study, we investigated the relationship between inflammation and oxidative stress and augmentation index, a measure of arterial stiffness,
...
The combination of increased arterial wave reflection, inflammation and oxidative stress may result in an increased risk of future cardiovascular events. Assessment of arterial wave reflection might be useful for determining cardiovascular risk in this patient group.
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full text is free

other than that one paper, I can't find any indication that arterial stiffness is related to CTD in a quick search

here are a couple of recent papers from Julia Newton, btw
http://www.ncbi.nlm.nih.gov/pubmed/22273713
http://www.ncbi.nlm.nih.gov/pubmed/21749371
 
A

Allyson

Senior Member
Messages
1,684
Location
Australia, Melbourne
or anyone who is interested in POTS (Postural Orthostatic Tachycardia Syndrome) and learning about what it is in very simple and layperson terms, I can't say enough about this book, written by Jodi Epstein Rhum, and with the medical portion edited by Svetlana Blitshteyn, MD (an exceptional neurologist and POTS specialist in New York). It's called:
"POTS: Together We Stand, Riding the Waves of Dysautonomia"

You can get it on amazon.com. For anyone who has POTS, or has a loved one with POTS; also for medical professionals who wish to know what it is, and what life is like for the patients who have to deal with it.

This book is very important to us, because there's not a lot of information out there about POTS, and we are desperately trying to spread awareness of this debilitating syndrome. Although it is invisible to those looking on, it is very real to those experiencing it. Research has shown that patients with POTS have a quality of life similar to those with congestive heart failure or chronic lung disease.


A
 
Sushi

Sushi

Moderation Resource Albuquerque
Messages
19,935
Location
Albuquerque
Allyson

I think the POTS patients would find the information you posted more easily if it were posted in the
Problems Standing: Orthostatic Intolerance; POTS

section of the forum.


Sushi
 
A

Allyson

Senior Member
Messages
1,684
Location
Australia, Melbourne
I see the news showing they use DNA from 3 people in an embryo to eliminate genetic diosrders - another very good reason to seek an EDS diagnosis if you or yours are thinking of haveing children. Now it will be possible to have children without passing on the faulty EDS genes.


A
 
A

Allyson

Senior Member
Messages
1,684
Location
Australia, Melbourne
I found this list of the 17 types of EDS ( 2013) interesting


Classi!cation of EDSs.

Subtype Inheritance Gene(s)

Major forms

Classic AD
COL5A1, COL5A2

Hypermobility/JHS AD? Mostly unknown

Vascular AD
COL3A1

Kyphoscoliotic AR
PLOD1

Arthrochalasia AD
COL1A1, COL1A2

Dermatosparaxis AR
ADAMTS2

Rare/emerging forms



Tenascin X-de!cient AR, AD?
TNXB

Classic with vascular rupture AD
COL1A1

Cardiac-valvular AR
COL1A2

EDS/OI overlap AD
COL1A1, COL1A2

With periventricular heterotopia XLD
FMNA

Musculocontractural AR
CHST14

Spondylocheirodysplastic AR
SLC39A13

Progeroid AR
B4GALT7

Kyphoscoliotic with deafness AR
FKBP14

Parodontitis AD Unknown

Fibronectin-de!cient AR Unknown

AD: autosomal dominant; AR: autosomal
 
A

Allyson

Senior Member
Messages
1,684
Location
Australia, Melbourne
Someone else with ME has just had his blood volume measured and it was also low and he required urgent trransfusions

Docs could not understand how he was functioning.....

Have not heard how low it was yet - awaiting news and will post updates.

Still waiting on follow up for why I got no treatment or explanation for my low blood volume


A
 
ukxmrv

ukxmrv

Senior Member
Messages
4,413
Location
London
Did they write a letter to your GP Allyson? I'm wondering if your local hospital would be able to do a saline infusion and if so, who was supposed to be doing it. In the UK I've heard of the A&E Department being asked to do it.
 
A

Allyson

Senior Member
Messages
1,684
Location
Australia, Melbourne
merylg said:
ISRN Dermatol. 2012; 2012: 751768.
Published online 2012 November 22. doi: 10.5402/2012/751768
PMCID: PMC3512326
Ehlers-Danlos Syndrome, Hypermobility Type: An Underdiagnosed Hereditary Connective Tissue Disorder with Mucocutaneous, Articular, and Systemic Manifestations

Marco Castori*

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3512326/?report=classic
Click to expand...

thanks for postig that Meryl!

this is for @ Mya Symmons - I cannot fnd your post on this topic so hope you see it here"
http://www.ncbi.nlm.nih.gov/books/NBK1462/

Bookshelf ID: NBK1462PMID: 20301635




Ehlers-Danlos Syndrome, Kyphoscoliotic Form



Synonyms: EDS, Kyphoscoliotic Form; EDS Type VI; EDS VI; Ehlers-Danlos Syndrome Type VI; Lysyl-Hydroxylase Deficiency. Includes: Ehlers-Danlos Syndrome Type VIA, Nevo Syndrome

Heather N Yeowell, PhD and Beat Steinmann, MD.




　

Initial Posting: February 2, 2000; Last Update: January 24, 2013.

Go to:




Summary



Disease characteristics. Ehlers-Danlos syndrome (EDS), kyphoscoliotic form (previously known as EDS VI) is a generalized connective tissue disorder characterized by friable, hyperextensible skin, thin scars, and easy bruising; generalized joint laxity; severe muscular hypotonia at birth; progressive scoliosis, present at birth or within the first year of life; and scleral fragility with increased risk of rupture of the globe. Intelligence is normal; life span may be normal, but affected individuals are at risk for rupture of medium-sized arteries and respiratory compromise if kyphoscoliosis is severe.

Diagnosis/testing. EDS, kyphoscoliotic form is caused by deficient activity of the enzyme procollagen-lysine, 2-oxoglutarate 5-dioxygenase 1 (PLOD1, or lysyl hydroxylase 1). The diagnosis of EDS, kyphoscoliotic form relies on the demonstration of a markedly increased ratio of deoxypyridinoline to pyridinoline crosslinks in urine measured by high-performance liquid chromatography (HPLC) (a highly sensitive, specific, and inexpensive test) and/or assay of lysyl hydroxylase enzyme activity in skin fibroblasts. Molecular genetic testing of PLOD1, the only gene in which mutations are known to cause EDS, kyphoscoliotic form, is available.

Ally
 
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