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Interesting article https://www.frontiersin.org/article...TltN1Y3VK9XkSYQH6j9TVR-PbH1HxCQ37K3hdv9NC8#B2
Any possible pragmatic approach ?
Any possible pragmatic approach ?
The Role of Cell Adhesion and Cytoskeleton Dynamics in the Pathogenesis of the Ehlers-Danlos Syndromes and Hypermobility Spectrum Disorders
- Thread starter CristianSerious
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The paper is summarized with this section:
"These findings suggest that what unites and defines the EDS/HSD subtypes may not be defects in the structure and/or organization of collagen itself, but in cell adhesion to collagen. If such a notion is correct, this may provide an ideal basis for the development of a universal or non-specific diagnostic test that truly captures all EDS/HSD subtypes, irrespective of the principal underlying defect. "
One of the most interesting sentences, to me, was this:
"Speculatively, any autoimmune or inflammatory condition that promotes a general disassembly of collagen in the ECM could initiate the same pathomechanism and promote connective tissue abnormalities, which then manifest through features of joint hypermobility, skin hyperextensibility, and tissue fragility. "
It's basically saying that hEDS like symptoms could be nonspecific manifestation of an unknown autoimmune or inflammatory condition, likely including CFS.
"These findings suggest that what unites and defines the EDS/HSD subtypes may not be defects in the structure and/or organization of collagen itself, but in cell adhesion to collagen. If such a notion is correct, this may provide an ideal basis for the development of a universal or non-specific diagnostic test that truly captures all EDS/HSD subtypes, irrespective of the principal underlying defect. "
One of the most interesting sentences, to me, was this:
"Speculatively, any autoimmune or inflammatory condition that promotes a general disassembly of collagen in the ECM could initiate the same pathomechanism and promote connective tissue abnormalities, which then manifest through features of joint hypermobility, skin hyperextensibility, and tissue fragility. "
It's basically saying that hEDS like symptoms could be nonspecific manifestation of an unknown autoimmune or inflammatory condition, likely including CFS.
- Messages
- 67
- Location
- Bucharest, Romania
Hi,
This is understandable what can you do about it ?
This is understandable what can you do about it ?
- Messages
- 67
- Location
- Bucharest, Romania
From a old CFS groupe from Captain Dave:
"
Matrix metallopeptidase 9 (MMP-9), also known as 92 kDa type IV collagenase, 92 kDa gelatinase or gelatinase B (GELB), is a class of enzymes that belong to the zinc-metalloproteinases family involved in the degradation of the extracellular matrix. In humans the MMP9 gene encodes for a signal peptide, a propeptide, a catalytic domain with inserted three repeats of fibronectin type II domain followed by a C-terminal.
There has always been a suspicion of a defect in the ability of bone marrow ability to turn out healthy red cells. Studies done on mice show that excess MMP9 induces a form of anemia. Many doctors has suspected a mycoplasma infection but I see raise MMP9 as being the culprit. At any rate, the treatment for mycoplasma was long term Doxycycline. Many CFS patients recovered and many did not.
I think the doctors blew it by not looking closely at MMP9. Doxycycline and minocycline also lower MMP9 and may well account for the recovery of those that took 100mg-day of either of these antibiotics for 3 months.
There is a lot of work to do in this area so be sure to consult a doctor.
"
"
Matrix metallopeptidase 9 (MMP-9), also known as 92 kDa type IV collagenase, 92 kDa gelatinase or gelatinase B (GELB), is a class of enzymes that belong to the zinc-metalloproteinases family involved in the degradation of the extracellular matrix. In humans the MMP9 gene encodes for a signal peptide, a propeptide, a catalytic domain with inserted three repeats of fibronectin type II domain followed by a C-terminal.
There has always been a suspicion of a defect in the ability of bone marrow ability to turn out healthy red cells. Studies done on mice show that excess MMP9 induces a form of anemia. Many doctors has suspected a mycoplasma infection but I see raise MMP9 as being the culprit. At any rate, the treatment for mycoplasma was long term Doxycycline. Many CFS patients recovered and many did not.
I think the doctors blew it by not looking closely at MMP9. Doxycycline and minocycline also lower MMP9 and may well account for the recovery of those that took 100mg-day of either of these antibiotics for 3 months.
There is a lot of work to do in this area so be sure to consult a doctor.
"
- Messages
- 67
- Location
- Bucharest, Romania
There are also people at https://www.roadback.org/ who achieved remission using pulse dose antibiotics.
- Messages
- 67
- Location
- Bucharest, Romania
Someone got remission using Doxy https://hellsbellsandmastcells.com/2021/06/16/remission/
@mitoMAN this might be of interest for you
@mitoMAN this might be of interest for you
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- 72
@Nasaud I achieved almost full remission temporarily while on doxy + cefdinir for 1.5 months from connective tissue symptoms (weakened muscles, weak joints, fat loss, throwing out back, joint paint, brain fog, pallor, fluid dysregulation). I've been trying to find a cause for my symptoms, but maybe it's time to get back on them since the symptoms have returned in full force.
Pyrrhus
Senior Member
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Related discussion:
Signs of Intracranial Hypertension, Hypermobility, and Craniocervical Obstructions in Patients With ME/CFS (Bragee et al., 2020)
https://forums.phoenixrising.me/thr...l-obstructions-in-patients-with-me-cfs.81446/
Signs of Intracranial Hypertension, Hypermobility, and Craniocervical Obstructions in Patients With ME/CFS (Bragee et al., 2020)
https://forums.phoenixrising.me/thr...l-obstructions-in-patients-with-me-cfs.81446/
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