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Lp-PLA2 Blood Test, a marker for vascular inflammation

Emootje

Senior Member
Messages
356
Location
The Netherlands
The Lp-PLA2 (PLAC) test is cleared by the FDA to help assess risk for vascular events. This Test is a blood test that measures the level of Lp-PLA2 (Lipoprotein-associated Phospholipase A2), an enzyme associated with the inflammation of arteries. http://www.plactest.com
Maybe this generally accepted test could detect our massive inflammation...

 

Emootje

Senior Member
Messages
356
Location
The Netherlands
Lp-PLA2: inflammatory biomarker of vascular risk in multiple sclerosis

A member of the A2 phospholipase superfamily, the enzyme lipoprotein-associated phospholipase A2 (Lp-PLA2), is involved in atherogenic processes. Lp-PLA2 mass and activity were measured by the enzyme-linked immunosorbent assay and by a colorimetric method, respectively, and compared among 63 multiple sclerosis (MS) patients and 47 age-matched healthy controls (HCs). Lp-PLA2 plasma levels were significantly higher in MS patients (236.7 ± 10 ng/ml) compared to HCs (197.0 ± 7 ng/ml) (p = 0.003), but LP-PLA2 activity did not differ between the two groups. Both Lp-PLA2 plasma mass and activity were higher in secondary progressive (mass 247.0 ±15.5 ng/ml, p = 0.05; activity 156.1 ±6 nmol/min/ml, p = 0.003) compared to relapsing-remitting MS patients (mass 227.0 ± 16 ng/ml; activity 128.8 ± 5 nmol/min/ml) and compared to HCs. Lp-PLA2 plasma activity was associated with measures of MS clinical disability. However, this association was attenuated after adjustment for the components of lipid profile
 

Emootje

Senior Member
Messages
356
Location
The Netherlands
Lp-PLA2 is also associated with endothelial dysfunction:

"Lp-PLA2 is a member of the phospholipase A2 family of enzymes and is a 45.4-kDa protein produced by macrophages, T lymphocytes, and mast cells"
"The production and release of Lp-PLA2 by lymphocytes and macrophages may become increased under inflammatory conditions. The metabolism of oxidized phospholipids by Lp-PLA2 increases the circulating levels of oxidized free fatty acid and lysophosphatidylcholine. Lysophosphatidylcholine can then have adverse effects on endothelial function via increased oxidative stress, modulation of leukocyte chemotaxis, and inhibition of endothelial cell migration to sites of endothelial damage"
http://atvb.ahajournals.org/content/26/1/106.full.pdf
 

Emootje

Senior Member
Messages
356
Location
The Netherlands
FYI, In the US, Life Extension Foundation offers this test for members for 125 bucks. Given the info provided by Emootje, I am going to have this tested. Interestingly enough, Lp-PLA2 is also released by mast cells.
Nice!
In Germany, Ganzimmune offers the Lp-PLA2 test for 54,56 euro. [order-form]
By the way, increased phospholipase activity could explain the high choline metabolites finding from this study and this study (phospholipase induced breakdown of cell membranes shows up as choline on a 1H MRS brain scan). http://www.imaios.com/en/e-Courses/...nce-Spectroscopy-MRS/metabolites-spectroscopy
 

Emootje

Senior Member
Messages
356
Location
The Netherlands
A phospholipase A (PLA2) article by Cort:
Putting It All Together – CFS is a Disease of Increased Phospholipase (PLA) Activity - Chaudhuri and Behan suggest increased choline levels contribute to cognitive dysfunction (effortful task processing) and reduced ATP levels impair aerobic metabolism and contribute to the exercise intolerance seen in CFS. What might increased brain choline and decreased ATP production have in common? Chaudhuri and Behan believe both are due to increased phospholipase (PLA) activity. This appears to suggest they believe increased PLA activity occurs not just in the brain but is system wide. Since PLA is ubiquitous in the body increased PLA activity could affect a wide variety of tissues.

Phospholipases (PLA’s) – are a superfamily of esterases that release phospholipids ‘moieties’ (fractions) including choline when they hydrolyze (break) the ester bonds in lipid membranes. Aside from actual trauma or lipid peroxidation (free radical damage) phospholipid release from cell membranes is usually caused by phospholipase activity. Phospholipids in the CNS cell membranes are high in polyunsaturated fatty acids (PUFA’s) and PUFA metabolism is ‘stringently controlled’ by PLA2 (and acetyltransferase). Normally when fatty acids are released by PLA2 they are rapidly taken up by membrane phospholipids by an energy dependent mechanism using CoA and ATP.

Phospholipase activity releases factors that exert widely varying effects in the cell. Phospholipids play a key role in regulating the release of arachidonic acid, the precursor of eicocanisoid synthesis. The eicocansoids (prostaglandins, thromboxanes, leukotrienes) mediate (trigger) the inflammatory process. A marker of cellular injury, the inflammatory process begins with the release of AA. AA is broken up to produce pro-inflammatory mediators such as prostaglandins (COX 1, 2) and leukotrienes. Prostaglandins then combine with cellular receptors to initiate signaling cascades which utilize G-proteins and cyclic CMP (cAMP) to produce pro-inflammatory substances.

PLA2 activity has been implicated in the pathology of a number of neurodegenerative diseases including Alzheimer’s and is thought to play a role in neuronal plasticity (Sun et. al. 2004). The activation of the P2Y nucleotide receptor on astrocytes triggers ‘reactive gliosis’, a process implicated in these neurodegenerative diseases and which Chaudhuri and Behan believe may be occurring in CFS.

TRIGGERING PHOSPHOLIPASE ACTIVITY - Why phospholipase activity would be increased in CFS patients is unclear. CFS patients appear to be subject, however, to several factors (infection, increased neurotransmitter/ cytokine levels, oxidative stress, neurotoxins) that could trigger phospholipase activity. Chaudhuri et. al. note that infection and/or neurotoxins can produce prolonged changes in membrane functioning (Chaudhuri et. al. 2003). The authors suggest the adaptation of the host cell to either a pathogen or its exotoxin (neurotoxin) could result in a long term derangement of the membranes