SFC-Info: mayo 2009

En la actualidad me trata la Dra. Josepa Rigau desde hace 18 meses: Josepa Rigau Av Catalunya, 12, 3º, 1ª 43002 Tarragona Spain +34977220358 Anteriormente me trate con el Dr. Kenny de Meirleir (www.redlabs.be) y Ana Garcia Quintana.
Recordad que esto solo es parte de mi blog, el total lo podeis ver en www.sfc-tratamiento.blogspot.com o la version en ingles: www.pochoams.blogspot.com.

Me acaban de realizar el Perfil Mitocondrial, y los resultados muestran un fallo mitocondrial en mi caso muy importante que explica mis dias malos...De momento lo pongo en ingles, y mas adelante los comentare en espanol.

El ADN extracelular es una novedad biológica, de la cual se desconoce su significado clínico y fisiopatológico.Los primeros resultados espectrales, permiten la cuantificación de los niveles de ADN libre en suero y orina humanos de personas sanas
y enfermas, los cuales contribuirán a realizar las comparaciones para entender la biología del ADN libre en la salud y la enfermedad con miras a obtener ayudas diagnósticas pronósticas y terapéuticas en enfermedades tan complejas como el cáncer, infecciones crónicas, enfermedades autoinmunes etc.

Actualmente la detección de niveles de ADN circulante es utilizada para el diagnóstico de tumores, diferentes tipos de cáncer, y enfermedades virales como hepatitis, para lo cual se utilizan normalmente kits comerciales de un costo elevado, lo que limita el uso de la técnica a laboratorios de altos recursos en muy pocos paises del mundo. Lo curioso es que en los pacientes de SFC los titulos de ADL libre circulante en sangre son elevados tambien, asi como ocurre en los pacientes con cancer, enfermedades autoinmunes (lupus) o infecciones cronicas... No es de extranar por tanto que el grado de discapacidad pueda llegar a ser similar en los dias malos. En mi caso se da este hecho de un titulo elevado de ADN circulante en sangre, 22 frente a 9 que es el maximo del rango de referencia.

Note: DNA and ATP disability score do not match my present physical ability.The only thing I could suggest is that the mitochondria in my neutrophils, which are evaluated in the ATP profiles test, are in worse condition than those in my muscle cells. I don't know why this would occur.

ATP (adenosine triphosphate), studies on neutrophils
ATP is hydrolysed to ADP and phosphate as the major energy source in muscle and other tissues. It is regenerated by oxidative phosphorylation of ADP in the mitochondria. When aerobic metabolism provides insufficient energy, extra ATP is generated during the anaerobic breakdown of glucose to lactic acid. ATP reactions require magnesium. ADP to ATP conversion can be blocked by environmental contaminants as can the transiocator [TLj in the mitochondrial membrane. [TL] efficiency is also sensitive to pH and other metabolic-factor changes. [TL] defects may demand excessive ADP to AMP conversion (not re-converted to ADP or through to ATP). Defects in Mg-ATP, ADP - ATP conversion and enzyme or [TL] blocking can all result in chronic fatigue - a factor in any disease where biochemical energy availability is reduced.

ATP whole cells:
With excess Mg added 1.37 nmol/106 cells 1.6-2.9
(Standard method of measuring ATP)
Endogenous Mg only 0.74 nmol/106 cells 0.9 - 2.7
(Measured ATP result is lowered during intracellular magnesium deficiency)
Ratio ATP/ATPMg 0.53………………………………….. > 0.6
ADP to ATP conversion efficiency (whole cells):
ATPMg (from above) 1.37 nmol/106 cells (1*) 1.6-2.9
ATPMg (inhibitor present) 0.41 nmol/106 cells (2*) <0.3
AXpMg (inhjbitor removed) 0.78 nmol/106 cells (3*) > 1.4
ADP to ATP efficiency [(3*- 2*)/(l*- 2*)] x 100 = 38.5 % > 60
Blocking of active sites (2*/!*) x 100 = 29.9 % upto 14

ADP-ATP TRANSLOCATOR fTLj (mitochondria, not whole cells):

ATP Ref. range change % ref. range
(pmol/106 cells)
Start 244 290-700

[TL] 'ouf 309 410-950 26.6 over 35% (Increase)
(in-vitro test) reflects ATP supply for cytoplasm
[TL] W 191 140 - 330 21.7 55 to 75% (Decrease)
(in-vitro test) reflects normal use of ATP on energy demand

Comments
Very Low whole-cell ATP. Poor ATP-related Mg availability.
30% blocking of active sites leading to: Very Poor ADP-ATP re-conversion.
Low mt-ATP and poor provision of 'new' mt-ATP. Restricted access to rrit-ATP
secondary to the 3/10 blocking of transiocator function.

Coenzyme 010

ref. range
Serum coenzyme Q10 0.64 jamol/L 0.55 - 2.00

Coenzme Q10 is synthesised naturally in humans and is also found in foods, such as vegetables and fish, it acts as a cofactor in the electron transfer pathway which produces energy (in the form of adenosine triphosphate - ATP) within the mitochondria of human cells. The energy is used for muscie contraction and other vital functions. It is also an antioxidant which may have a sparing effect on vitamins C and E in situations of oxidative stress

SUPEROXIDE DISMUTASE and GLUTATHIONE PEROXIDASE
A functional test looks at the in-vitro efficiency of the patient's red cell superoxide dismutase (SOD) when their neutrophil superoxide production is maximally stimulated. The activity of the individual forms of SOD are explored. General cell protection from damage by superoxide is provided by intracellular zmc:copper-SOD (Zn/Cu-SOD). Mitochondria are protected by manganese-dependent SOD (Mn-SOD). Extracellular SOD (EC-SOD - another Zn/Cu SODase) protects the nitric oxide pathways that relax vascular smooth muscle.
For each form of SODase, genetic variations are known, mutations can occur during excessive oxidative stress on DNA and polymorphisms may be present. DNA adducts can chemically block these genes. Glutathione peroxidase (GSH-PX) activity is measured in red blood cells. It is a selenium-dependent enzyme and selenium deficiency is the commonest cause of poor enzyme activity. As poor glutathione (GSH) availability is easily overlooked as an additional reason for poor GSH-PX activity, we also measure total GSH in red cells.

Blood test results:

Test Result Units Reference range
Functional test 42 % Over 40 (mostly 41 -47)
Zn/Cu-SOD 269 Enzyme activity (u) 240-410
Mn-SOD 158 Enzyme activity (u) 125-208
EC-SOD 31 Enzyme activity (u) 28-70

Gene studies:

Sod form Gene(s) Comments
Zn/Cu-SOD chromosome 21 Normal Normal enzyme activity
Mn-SOD chromosome 6 Normal Normal enzyme activity
EC-SOD chromosome 4 Normal Normal enzyme activity

Result Reference range
Glutathione peroxidase (GSH-PX)
Red cell Glutathione peroxidase (GSH-PX) 48 U/gHb 67-90
Red cell Glutathione (GSH) 1.31mmol/1 1.7-2.6

NIACIN STATUS (vitamin B3)
Red cell nicotinamide adenine dinucleotide (NAD) is a good indicator of B3 status.

Red cell nicotinamide adenine dinucleotide = 12,7 ug/ml 14.0 - 30.0

Interpretation of result:
Reference range (14.0 - 30.0)
Mild B3 deficiency (12.5 - 13.9)
Moderate B3 deficiency (11.0 - 12.4)
Fairly marked B3 deficiency (10.0 - 10.9)
Marked B3 deficiency (8.5 - 9.9)
Severe B3 deficiency (less than 8.5)

References:
1) Fu CS, Swendseid ME, Jacob RA, McKee RW. Biochemical markers for assessment of niacin status in young men: levels of erythrocyte coen2ymes and plasma tryptophan. JNutr 1989: 1949 - 1955.
2) Critical review. Assessment of niacin status in humans. Nutrition Reviews 1990; 48: 318-320

Note:
The amino acid tryptophan is a precursor of niacin. However, protein synthesis has a higher metabolic priority than the conversion of tryptophan to niacin coenzyme and adequate niacin levels cannot always be obtained from tryptophan.

Cell-free DNA in blood plasma

Background. Most of the cell-free DNA present in blood plasma is associated with cell degradation. Very low levels are present in healthy people and increases are associated with serious illnesses such as malignancy, stroke, auto¬immune diseases, severe infections and Chronic Fatigue Syndrome.

Patient's result: Reference range
Cell-free DNA 22.7 ug DNA per litre plasma up to 9.5

Comments:
Mild increase = 9.6 to 12.4
Some increase = 12.5 to 14.9
Definite increase = 15.0 to 20.0
Highiy significant = over 20.0

Method summary* Plasma is incubated with EDTA, a detergent and a proteinase prior to precipitation of the proteins. DNA is then precipitated with alcohol and re-dissolved in a Tris-acetate-EDTA Buffer. The DNA is measured in a Pharmacia GeneQuant™ or Jenway Genova analyser using a micro-cuvette.
*Schmidt B, Weickmann S, Witt C, Fleischhacker M. Improved Method for Isolating Cell-Free DNA. Clin Chem 2005:51(8); 1561-2

Cell-free DNA in chronic fatigue syndrome (CFS) In initial studies on 87 CFS patients, positive results were found in 93% of those with a disease duration of four months to five years (n = 75). In those with a disease duration of five to 14 years (n = 12), 75% had positive results.

SFC-Info

jueves, 21 de mayo de 2009

Perfil Mitocondrial de la Doctora Mhyll (ingles)

viernes, 15 de mayo de 2009

en el curso de iridiologia...

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