Total Bilirrubine: *1.6 (0-1.2)
Direct Bilirrubine: *0.5 (0-0.4)
Indirect Bilirrubine: *1.10 (0-1)
Amonio in serum: *60 (11-35)
Total Cholesterol: 215 (<220)
Triglicéridos: 92 (35-200)
HDL: *36 (>45 normalidad <35 Riesgo)
TC/(HDL-TC): *6 (<4.5)
LDL: *161 (<155 normalidad >180 Riesgo)
(LDL-TC)/(HDL-TC) *4.5 (<3.55)
GOT 28 (<45)
GPT 31 (<45)
GGT 12 (8-61)
Fosfotasa Alkaline 54 (25-100)
AC. Antitransglutaminasa IgA 14.9 (>15 Positive) (It is negative, but very close to the limit)
Recent News
Tuesday, January 24, 2012
Friday, December 23, 2011
Cryptogenic Chronic Hepatitis ¿Cause or effect of CFS?
I've seen my results with the hepatologist, no trace of virus B, C or CMV in my liver. But if there is a chronic inflammation that should not be there, and I have been diagnosed with cryptogenic chronic hepatitis (unknown etiology). I was prescribed a non fat diet, ursobilane 300mg (2-2-2) and sports. I see him again in 2 or 3 months.
He tells me that the reference values of GPT and GOT are about to be changed next year to "30" by medical consensus in Spain, instead of 42 as they are now. I have a current value of 41.
He assures me that I have chronic hepatitis, because He has touched my liver and it is confirmed my biopsy and high transaminases, although within range in the current standard reference range. It is also supported by the rest of analisis done before showing apoptosis along these years, such as a high granzyme B, RNase-L, elastase, PKR, free DNA circulating in blood and the FAS ligands.
I keep on wondering if this is cause or consequence of CFS, because cryptogenic does not really solve the puzzle.
One theory that comes to my mind is the following:
- CFS patients with undiagnosed autoimmune hepatitis, might be responding to Rituximab for being an autoimmune disease.
- CFS patients with chronic mutant hepatitis B or hidden hepatitis C, could be responding to Tenofovir (retroviral) for being a chronic viral disease.
- CFS patients with cryptogenic chronic hepatitis might respond to GcMaf if they carry an unknown pathogen.
They are just my theories, but in any case keep them in mind, because these are difficult to diagnose hepatitis cases and often go unnoticed by doctors.
In fact if your GPT and GOT are over 30 you should at least suspect, my hepatologist told me that in 2012 they will lower reference ranges for transaminases at 30 instead of 43 as they are today.
He also mentioned that physical examination of the liver requires a lot of experience and is not easy to detect hepatitis with the hands.
Finally, the 3 hepatitis described will not necessarily yield positive serology or even on PCR. Only a biopsy can rule it out with certainty.
He tells me that the reference values of GPT and GOT are about to be changed next year to "30" by medical consensus in Spain, instead of 42 as they are now. I have a current value of 41.
He assures me that I have chronic hepatitis, because He has touched my liver and it is confirmed my biopsy and high transaminases, although within range in the current standard reference range. It is also supported by the rest of analisis done before showing apoptosis along these years, such as a high granzyme B, RNase-L, elastase, PKR, free DNA circulating in blood and the FAS ligands.
I keep on wondering if this is cause or consequence of CFS, because cryptogenic does not really solve the puzzle.
One theory that comes to my mind is the following:
- CFS patients with undiagnosed autoimmune hepatitis, might be responding to Rituximab for being an autoimmune disease.
- CFS patients with chronic mutant hepatitis B or hidden hepatitis C, could be responding to Tenofovir (retroviral) for being a chronic viral disease.
- CFS patients with cryptogenic chronic hepatitis might respond to GcMaf if they carry an unknown pathogen.
They are just my theories, but in any case keep them in mind, because these are difficult to diagnose hepatitis cases and often go unnoticed by doctors.
In fact if your GPT and GOT are over 30 you should at least suspect, my hepatologist told me that in 2012 they will lower reference ranges for transaminases at 30 instead of 43 as they are today.
He also mentioned that physical examination of the liver requires a lot of experience and is not easy to detect hepatitis with the hands.
Finally, the 3 hepatitis described will not necessarily yield positive serology or even on PCR. Only a biopsy can rule it out with certainty.
Thursday, December 08, 2011
Is CFS an Undiagnosed Liver disease?
Today, they have started to see my biopsy, they still need to do more tests for the B virus, but they told me that I should not worry about my liver. There is no fibrosis there and is quite "healthy". But there is injury to the hepatocytes, but they still need to know if they are infected with hepatitis B virus, which could cause the injury.
In Pathology, they normally look at 3 parameters, in the first two I have a zero rank, which means I am okay. In the third one, which is the "hepatocyte necrosis" I rank 1 (range 1-3). So there is injury, but the liver is not really damaged as for today, therefore I have no prognosis for cirrhosis at all.
Nevertheless it could potentially explain part of my symptoms, because the liver lesion is present, but that's better to wait for the final report and the interpretation of my liver specialist.
Hepatocyte necrosis is closely linked to apoptosis (programmed cell death), and that is what I have seen in the many analysis that I have done since I fell sick in 2006:
- 2006 RNase-L, elastase and high PKR = programmed cell death -> immunity to fight against something (Redlabs-Belgium)
- 2009 free circulating DNA Very high = programmed cell death -> immunity to fight against something (Acumen-UK)
- 2010, abnormal levels of the ligands FAS = programmed cell death -> immunity to fight against something (Irsi Caixa, Barcelona)
- 2011, elevated Granzyme B = programmed cell death -> immunity to fight against something (Gregorio Marañón, Madrid)
So, apparently it does seem that whatever I have in the liver is related to my CFS history.
It was not easy at all to detect the damage in my liver:
During all these years, no wrong liver function blood standard test (2005-2011):
-All the blood work on liver enzymes came normal
-All liver function came normal (GPT/GOT)
-All B & C serologies came negative
-Even a PCR DNA on B virus came NEGATIVE! But that is because PCR has limitations in the number of copies per ml that they can detect, normally starting from 120 copies.
However, what was present in a more subliminal and less conclusive way, were these traces of other liver malfunction in "not liver exclusive link test": (2005-2011)
-Presence of ammonia in blood
-High levels of nitric oxide in blood
-frequent high levels of bilirubin in blood
-Occasional severe abdominal pain in the right upper quadrant that could last more than 8 hours, 3 times a year that I need to go to the hospital to get a pain killer in vein.
-Occasional mild jaundice
-Frequently elevated fibrinogen
-Protein C active frequently high
-Sleep inverted (cortisol inverted)
-Occasional itching
-Occasional acolia
-Occasional coluria
-Essential amino acid deficiency
-High levels of cholesterol and triglycerides
-HBc antibody-positive on three occasions, intercalated with negative results in many more occasions in the last 3 years.
In November 2011, a very sophisticated PCR technique was used to detect even a single copy of the virus per milliliter, and they found 13 copies in my case, so I was recommended a liver biopsy, which is where they have seen the damage to liver cells.
It is now clear to me that "something" has infected my hepatocytes, and that causes liver inflammation and injury.
The big question is whether it is a mutant version of hepatitis B virus in the pre-core S region, or a hidden hepatitis B virus in the liver, and that will tell me next week.
If this is confirmed, I believe many people with Chronic Fatigue Syndrome may be infected with an undiagnosed B virus that could explain at least part of the clinical symptoms they present. If that was the case, it could also explain why tenofovir therapy works in some patients with CFS.
Another possibility in many patients with CFS is a chronic autoimmune hepatitis is not my case. In autoimmune hepatitis predominantly female (78%) in the absence of virus serological markers, elevated serum levels of IgG, high titers of antibodies (ANA, SMA, anti-LKMI), and 60% have other autoimmune thyroiditis , rheumatoid arthritis, ulcerative colitis. In these cases, immunosuppressive therapy would be effective, so perhaps the work Rituximab in patients with CFS.
Bear in mind that both "autoimmune chronic hepatitis" and "chronic hepatitis by a mutan B virus of the Pre-core region" are not present in common serologies. Autoimmune hepatitis is treated with immunosupression, and chronic Hepatitis B is treated with retrovirals. That could potentially explain why Tenofovir or Rituximab have been effective in different subsets of CFS patients.
In Pathology, they normally look at 3 parameters, in the first two I have a zero rank, which means I am okay. In the third one, which is the "hepatocyte necrosis" I rank 1 (range 1-3). So there is injury, but the liver is not really damaged as for today, therefore I have no prognosis for cirrhosis at all.
Nevertheless it could potentially explain part of my symptoms, because the liver lesion is present, but that's better to wait for the final report and the interpretation of my liver specialist.
Hepatocyte necrosis is closely linked to apoptosis (programmed cell death), and that is what I have seen in the many analysis that I have done since I fell sick in 2006:
- 2006 RNase-L, elastase and high PKR = programmed cell death -> immunity to fight against something (Redlabs-Belgium)
- 2009 free circulating DNA Very high = programmed cell death -> immunity to fight against something (Acumen-UK)
- 2010, abnormal levels of the ligands FAS = programmed cell death -> immunity to fight against something (Irsi Caixa, Barcelona)
- 2011, elevated Granzyme B = programmed cell death -> immunity to fight against something (Gregorio Marañón, Madrid)
So, apparently it does seem that whatever I have in the liver is related to my CFS history.
It was not easy at all to detect the damage in my liver:
During all these years, no wrong liver function blood standard test (2005-2011):
-All the blood work on liver enzymes came normal
-All liver function came normal (GPT/GOT)
-All B & C serologies came negative
-Even a PCR DNA on B virus came NEGATIVE! But that is because PCR has limitations in the number of copies per ml that they can detect, normally starting from 120 copies.
However, what was present in a more subliminal and less conclusive way, were these traces of other liver malfunction in "not liver exclusive link test": (2005-2011)
-Presence of ammonia in blood
-High levels of nitric oxide in blood
-frequent high levels of bilirubin in blood
-Occasional severe abdominal pain in the right upper quadrant that could last more than 8 hours, 3 times a year that I need to go to the hospital to get a pain killer in vein.
-Occasional mild jaundice
-Frequently elevated fibrinogen
-Protein C active frequently high
-Sleep inverted (cortisol inverted)
-Occasional itching
-Occasional acolia
-Occasional coluria
-Essential amino acid deficiency
-High levels of cholesterol and triglycerides
-HBc antibody-positive on three occasions, intercalated with negative results in many more occasions in the last 3 years.
In November 2011, a very sophisticated PCR technique was used to detect even a single copy of the virus per milliliter, and they found 13 copies in my case, so I was recommended a liver biopsy, which is where they have seen the damage to liver cells.
It is now clear to me that "something" has infected my hepatocytes, and that causes liver inflammation and injury.
The big question is whether it is a mutant version of hepatitis B virus in the pre-core S region, or a hidden hepatitis B virus in the liver, and that will tell me next week.
If this is confirmed, I believe many people with Chronic Fatigue Syndrome may be infected with an undiagnosed B virus that could explain at least part of the clinical symptoms they present. If that was the case, it could also explain why tenofovir therapy works in some patients with CFS.
Another possibility in many patients with CFS is a chronic autoimmune hepatitis is not my case. In autoimmune hepatitis predominantly female (78%) in the absence of virus serological markers, elevated serum levels of IgG, high titers of antibodies (ANA, SMA, anti-LKMI), and 60% have other autoimmune thyroiditis , rheumatoid arthritis, ulcerative colitis. In these cases, immunosuppressive therapy would be effective, so perhaps the work Rituximab in patients with CFS.
Bear in mind that both "autoimmune chronic hepatitis" and "chronic hepatitis by a mutan B virus of the Pre-core region" are not present in common serologies. Autoimmune hepatitis is treated with immunosupression, and chronic Hepatitis B is treated with retrovirals. That could potentially explain why Tenofovir or Rituximab have been effective in different subsets of CFS patients.
Tuesday, November 29, 2011
Mutant Chronic Hepatitis-B or Hidden Hepatitis-C
Today I am going to talk about something I think is very important for all that you have a diagnosis of CFS.
As you know I have CFS diagnosed for 6 years now, and despite the fact that my serologies for hepatitis A, B and C were negative during these years, this year Gregorio Marañón Hospital and last year Carlos III detected B viruses in my blood test. This came as a surprise because I was vaccinated against Hepatitis B and I already passed Hepatitis A.
As you can see the evolution of these blood tests, surface antigen HBs came out negative ALWAYS, however HBc core antibody was positive on 2 occasions since 2009. Moreover HBe antigen was detected in blood also on two occasions, and there is as well signs of an infectious component when we observe 2 (IL-2R) in December 2010.
The interpretation of this evolution is NOT easy. Firstly because normally is not standardized to test for HBc nor HBe, and secondly because these results may be interpreted in isolation as a "false positive" because they do not fit together well with a negative HBs Ag.
However Gregorio Marañón Hospital advised me to go for a good Liver specialist to undertake a thorough study, because the B virus that they saw was not from the vaccine. For this reason I went to Vicente Carreño, which is the number 1 in Spain.
Dr. Carreño checked my liver with his hands and it was 2 cm rhomboid (sorry for this translation), which signals inflammation, and because of the abnormalities observed in the blood work, He stated that I could be infected with the Hepatitis B virus, despite of the vaccine. Apparently this is a possibility, although not everybody is aware of it.
There are several types of the B virus, and to some of them the vaccine is not effective. Also it can go unnoticed in a normal hepatitis blood work. So He prescribed some special molecular blood work at NUCLEOTEX laboratory in Spain that performs molecular tests to detect two possible cases:
-Hidden Hepatitis C
-Mutant Hepatitis B in Pre-S region
My Results:
Hepatitis B virus:
PCR DNA (ultracentrifugation): 13 copies / ml
HBV-DNA-PCR PBMC NEGATIVE
Proliferation of CD4 + T lymphocytes specific B virus
S (HBs) NEGATIVE
Core (HBc) NEGATIVE
E (HBe) NEGATIVE
Hepatitis C virus:
HCV RNA-(PCR) in PBMC NEGATIVE
PCR-RNA (ultracentrifugation) NEGATIVE
Proliferation of CD4 + T lymphocytes specific to hepatitis C virus
Core NEGATIVE
NS3 (Helicase) NEGATIVE
NS4 NEGATIVE
Although at first glance it seems all negative, it is not. These tests show there is B virus in my blood (13 copies per ml).
Bear in mind that the standard DNA testing for B & C virus are not as sensible as the one I did here in Spain, normally they have a limitation: (116 to 989,400,000 copies/mL). In my case, I only had 13 copies/ml, therefore I would have come negative in standard DNA testing. This is a very low titer, but still shows is positive. At this point is not contagious, but if it peaks, it could be. Another important factor is that the titer might be very low in blood but not necessarily in the liver. It could also be a "false positive" therefore it needs to be confirmed with a biopsy.
For this reason He recommends a biopsy to confirm the infection and liver status, which not only going to look Hepatitis B and C, but also inflammation, tissue conditions, etc. The sample will frozen just in case more things need to be tested at a later stage (i.e. HGRV) .
In view of these results, the observed abnormalities in previous blood test and my clinical history, it is in the opinion of Dr. Carreño a must to perform a biopsy to confirm the findings.
When confirmed, chronic mutant hepatitis B, is treated with retrovirals (Tenofovir), normally for 6 months, given that this kind of hepatitis is more easily cured than regular chronic Hepatitis B.
I've asked him if it is possible that during these 6 years that I have thought to have CFS, perhaps I simply have had chronic mutant Hepatitis B undiagnosed, and his answer was YES.
It is too early to draw conclusions, however I think it's important enough share this writing, when I know the final results of the biopsy I will let you know. If it turns to be the case, I think everyone with a diagnosis of CFS should go through a good hepatologist who can rule out this possibility.
The standard treatment for this kind of mutant hepatitis is Tenofovir, and it comes to mind to think that people with XMRV treated with Tenofovir, might actually be responding because they might carry an undiagnosed B mutant B virus in the pre core S region.
As I said, it has taken me 6 years of running from one doctor to another to find out, is not an easy diagnosis. And I am not suspect of a wrong CFS diagnosis, De Meirleir, among 6 other specialist diagnosed me in 2006 with my RNASe-L, PKR, Elastase etc. Shara Mhyll also did with my mitochondrial failure. I also met the criteria of Cheney of diastolic disfunction of the left ventricle, Irsi Caixa also observed the same pattern than the CFS group studied with NK & CD8 abnormalities.
I could go on and on...but what I mean with this is that this B virus may be behind many many CFS diagnosed patients, and Tenofovir may be doing the trick for that reason. I also read that GcMAF is a more efficient treatment for Hepatitis B than retrovirals, and that would explain why some patients are responding to this therapy.
Having normal levels of GPT/GPO, and negative serology for hepatitis is not enough to rule it out as you could see. Not that you can do biopsy directly, first make the liver specialist need to run the molecular blood work, and if the virus is found, it is recommended to run the biopsy to confirm it. To be completely honest, in the opinion of my doctor, even if the blood work came negative He would have recommended a biopsy to make sure, given the many years of symptoms of hepatitis like that I had. Bear in mind that you need a very good specialist that is aware of these advances. They are published by the way.
To be continued ...
As you know I have CFS diagnosed for 6 years now, and despite the fact that my serologies for hepatitis A, B and C were negative during these years, this year Gregorio Marañón Hospital and last year Carlos III detected B viruses in my blood test. This came as a surprise because I was vaccinated against Hepatitis B and I already passed Hepatitis A.
As you can see the evolution of these blood tests, surface antigen HBs came out negative ALWAYS, however HBc core antibody was positive on 2 occasions since 2009. Moreover HBe antigen was detected in blood also on two occasions, and there is as well signs of an infectious component when we observe 2 (IL-2R) in December 2010.
The interpretation of this evolution is NOT easy. Firstly because normally is not standardized to test for HBc nor HBe, and secondly because these results may be interpreted in isolation as a "false positive" because they do not fit together well with a negative HBs Ag.
However Gregorio Marañón Hospital advised me to go for a good Liver specialist to undertake a thorough study, because the B virus that they saw was not from the vaccine. For this reason I went to Vicente Carreño, which is the number 1 in Spain.
Dr. Carreño checked my liver with his hands and it was 2 cm rhomboid (sorry for this translation), which signals inflammation, and because of the abnormalities observed in the blood work, He stated that I could be infected with the Hepatitis B virus, despite of the vaccine. Apparently this is a possibility, although not everybody is aware of it.
There are several types of the B virus, and to some of them the vaccine is not effective. Also it can go unnoticed in a normal hepatitis blood work. So He prescribed some special molecular blood work at NUCLEOTEX laboratory in Spain that performs molecular tests to detect two possible cases:
-Hidden Hepatitis C
-Mutant Hepatitis B in Pre-S region
My Results:
Hepatitis B virus:
PCR DNA (ultracentrifugation): 13 copies / ml
HBV-DNA-PCR PBMC NEGATIVE
Proliferation of CD4 + T lymphocytes specific B virus
S (HBs) NEGATIVE
Core (HBc) NEGATIVE
E (HBe) NEGATIVE
Hepatitis C virus:
HCV RNA-(PCR) in PBMC NEGATIVE
PCR-RNA (ultracentrifugation) NEGATIVE
Proliferation of CD4 + T lymphocytes specific to hepatitis C virus
Core NEGATIVE
NS3 (Helicase) NEGATIVE
NS4 NEGATIVE
Although at first glance it seems all negative, it is not. These tests show there is B virus in my blood (13 copies per ml).
Bear in mind that the standard DNA testing for B & C virus are not as sensible as the one I did here in Spain, normally they have a limitation: (116 to 989,400,000 copies/mL). In my case, I only had 13 copies/ml, therefore I would have come negative in standard DNA testing. This is a very low titer, but still shows is positive. At this point is not contagious, but if it peaks, it could be. Another important factor is that the titer might be very low in blood but not necessarily in the liver. It could also be a "false positive" therefore it needs to be confirmed with a biopsy.
For this reason He recommends a biopsy to confirm the infection and liver status, which not only going to look Hepatitis B and C, but also inflammation, tissue conditions, etc. The sample will frozen just in case more things need to be tested at a later stage (i.e. HGRV) .
In view of these results, the observed abnormalities in previous blood test and my clinical history, it is in the opinion of Dr. Carreño a must to perform a biopsy to confirm the findings.
When confirmed, chronic mutant hepatitis B, is treated with retrovirals (Tenofovir), normally for 6 months, given that this kind of hepatitis is more easily cured than regular chronic Hepatitis B.
I've asked him if it is possible that during these 6 years that I have thought to have CFS, perhaps I simply have had chronic mutant Hepatitis B undiagnosed, and his answer was YES.
It is too early to draw conclusions, however I think it's important enough share this writing, when I know the final results of the biopsy I will let you know. If it turns to be the case, I think everyone with a diagnosis of CFS should go through a good hepatologist who can rule out this possibility.
The standard treatment for this kind of mutant hepatitis is Tenofovir, and it comes to mind to think that people with XMRV treated with Tenofovir, might actually be responding because they might carry an undiagnosed B mutant B virus in the pre core S region.
As I said, it has taken me 6 years of running from one doctor to another to find out, is not an easy diagnosis. And I am not suspect of a wrong CFS diagnosis, De Meirleir, among 6 other specialist diagnosed me in 2006 with my RNASe-L, PKR, Elastase etc. Shara Mhyll also did with my mitochondrial failure. I also met the criteria of Cheney of diastolic disfunction of the left ventricle, Irsi Caixa also observed the same pattern than the CFS group studied with NK & CD8 abnormalities.
I could go on and on...but what I mean with this is that this B virus may be behind many many CFS diagnosed patients, and Tenofovir may be doing the trick for that reason. I also read that GcMAF is a more efficient treatment for Hepatitis B than retrovirals, and that would explain why some patients are responding to this therapy.
Having normal levels of GPT/GPO, and negative serology for hepatitis is not enough to rule it out as you could see. Not that you can do biopsy directly, first make the liver specialist need to run the molecular blood work, and if the virus is found, it is recommended to run the biopsy to confirm it. To be completely honest, in the opinion of my doctor, even if the blood work came negative He would have recommended a biopsy to make sure, given the many years of symptoms of hepatitis like that I had. Bear in mind that you need a very good specialist that is aware of these advances. They are published by the way.
To be continued ...
Friday, November 05, 2010
XMRV Workshop in Barcelona (November 2010)
A new XMRV Workshop has taken place today in Vall Hebron Hospital in Barcelona. We have had five lectures, all of them full of the history of all the papers that have been published since Dr. Judy Mikovits’s paper came out in September 2009. But each speaker has also given a summary of what are they working on.
Dr. José Alegre opened the session and was the first to speak. He is one of the most well known specialists in CFS, and as soon as the Science paper was published, he immediately tried to involve a group of Biologists from his Hospital in this research. One of the things mentioned by Dr. Alegre was the fact that pregnant women seem to have a remission of their symptoms during their pregnancy and a relapse right after they give birth, which points out a hormonal component in this illness. He also mentioned that it would be interesting to research the genome of post polio patients given that they have similar fatigue symptoms as CFS patients, and in that way it could be understood for both conditions.
Dr. Cecilia Cabrera from IrsiCaixa talked for an hour. Dr. Cabrera discussed that the structure of XMRV was simpler that HIV, and so far, only 3 genes had been identified: gag, pal and M. She mentioned the great importance of Dr. Ila Singh’s study with animals, and all they have learned about XMRV. Then she said that they have tested 11 patients and done 4 controls, that they have identified sequences of XMRV (not polytrophic virus) in B cells of CFS patients and controls, and that they are developing models of infection in human tissues in vitro, and in this way was able to study the viral pathogenicity. In their studies they had observed that XMRV was being restricted by the APO-B system, and also that the lymphoid tissue could act as a reservoir.
Dr. Cabrera also motioned that there is a common effort overseas to find a common assay to allow everybody to detect XMRV in the same way, and this is being developed by the SRWG (Scientific Research Working Group) which is conformed by the Blood Working Group, Retrovirologist teams, CFS researchers and Federal Agencies.
Dr. José Montoya of Stanford University was next. He started explaining that six years ago he met his first CFS patient, and since then he has visited more than 450. He is sure that you can develop CFS after a viral infection, and he believes that 11 % of patients that suffer EBV, Q fever, Ross River virus, etc, can end up with a CFS. About Dr. Judy Mikovit’s paper he remarked that since it was published everybody is turning to CFS with the intention to find out all they can because they have completely changed their opinion.
In a random, double-blind, placebo-controlled study they have found that there was a clinical improvement in patients who were taking valganciclovir for a period of more than six months, compared with placebo. CFS patients met Fukuda’s international criteria and had high antibody data against HHV-6 and EBV. Several immunological markers changed significantly in the treated patients that were not seen in patients taking placebo. This study will be submitted for publication this month, and provides evidence that CFS is a real illness that can be caused by an infectious agent that can be treated with prolonged antiviral intervention. They are also working on the hypothesis that besides the antiviral mechanism there could also be an immune modulator component in the good results.
The dramatic improvement of these patients was both cognitive and physical. Also worth to mention that the medication did not work in every case, and they are working on markers that could help ascertain the suitability of the medication each individual patient. Among the markers monocytes are a good candidate given that in the study they came down significantly and then normalized in the patients where the drug did work. The cytokine profile of the patients also played a role in following the good effects of this medication, specifically:IL5, IL17F, ENA78, EOTAXIN, IP10… Additionally, Dr. Montoya mentioned that HHV6 plays a unique role because it integrated in the chromosome of CFS patients, which is simply not normal in a virus.
Dr. Montoya remarked that the Early Antigen was used to prevent the relapses in naso-pharyngeal cancer, and in CFS patients is very elevated even after 20 years of the acute infection, which is simply not normal. Therefore this is a marker He uses for patients selection in the study.
Dra. Carmen Mendoza from Hospital Carlos III of Madrid did not talked much on XMRV, but instead on HIV. Off the record She mentioned that they have found 0% of XMRV in their lab, and in my view She was a bit lost on the latest advances on XMRV research, as She was still talking about geographical distribution and contamination as potential reasons not to find XMRV in Europe, We had to remind her that XMRV has been found in Spain, Italy, Holland, Norway, UK…It was a bit discouraging to find out that the “extra effort” that Carlos III plans to do is to send to Abbot Labs in the US, the blood of the patients that already they declared “negative” to perform a serological test, that on the other hand has already been criticized of not being accurate out of the animal model, this means in humans. Therefore we do not expect Carlos III to advance on the XMRV research, and postulates to be the Spanish publicly financed entity that slows down the research process with meaningless negative studies.
Dr. Jordi Petriz, of the Vall Hebron Hospital. He told us that the aim of his research with Dr. Alegre was the development of a diagnosis tool for the disease based on the functional response of the cells of CFS patients. It was also mentioned that the interferon response was key to allow XMRV to do damage in the health of CFS patients.
They will use, functional flow cytometry, a very sophisticated technology on the whole blood of people with CFS infected with XMRV, and compare the results with appropriate controls, in the hope of finding a pattern and goal differential characteristic of CFS. These techniques will also allow the analysis of the lymphocytes in the study of CFS patient’s immune system. He has also widely described the study that is focused on neutrophil oxidative metabolism and how this may affect their function. As they plan to study the membrane structure of CFS patients, it was suggested to him in the Q&A to have a look on the paper published on Mitochondrial dysfunction a bacterial translocation by Sarah Mhyll and Kenny De Meirleir.
Our conclusion is that all of them have mentioned the importance of an animal model to study the pathogenesis of XMRV. It’s also very important to have accepted tools to work with, and this means the urgent need of a universal kit. They are all working in the same direction, they are sharing lots of data, samples, etc, and they all agreed with the great complicity between the different groups, which they had not observed so far, for the other diseases they have worked on. Good long term perspectives.
Wednesday, October 27, 2010
Sunday, October 17, 2010
Friends of the Institute
Friends of the Institute
For a donation of as little as $60.00 per year, you can become a "Friend of the Institute." You will receive a beautiful WPI Butterfly logo pin, invitations to WPI events, our newsletter and special email updates.
Click here to find out how you can make a donation.
En Español:
Amigos del Instituto
Por una donación de tan sólo $ 60.00 por año, puedes convertirte en un "amigo del Instituto." Recibirás un hermoso pin del WPI con el logotipo de la mariposa, invitaciones a eventos del WPI, el boletín de noticias y actualizaciones especiales por correo electrónico.
Haz clic aquí para saber cómo se puede hacer una donación.
For a donation of as little as $60.00 per year, you can become a "Friend of the Institute." You will receive a beautiful WPI Butterfly logo pin, invitations to WPI events, our newsletter and special email updates.
Click here to find out how you can make a donation.
En Español:
Amigos del Instituto
Por una donación de tan sólo $ 60.00 por año, puedes convertirte en un "amigo del Instituto." Recibirás un hermoso pin del WPI con el logotipo de la mariposa, invitaciones a eventos del WPI, el boletín de noticias y actualizaciones especiales por correo electrónico.
Haz clic aquí para saber cómo se puede hacer una donación.
Tuesday, October 05, 2010
Natural treatments for lowering cholesterol
Treatments
1. Begin with an exercise program and, if overweight, bring your weight down.
2. In men, especially if you are overweight, have high blood pressure, and have diabetes (or are prediabetic), this may ALL be coming from too low of a testosterone level. If your total testosterone is under 450 on the blood test, I would consider using prescription natural testosterone (Androgel or Testim or compounded) to bring your level up over 700.
3. In women, consider a trial of prescription natural Armour Thyroid—even if the labs are normal. High cholesterol is often caused by low thyroid and the tests are horribly unreliable (they miss the majority of those who need thyroid hormone). Consider an exercise stress test before beginning exercise or thyroid. Both are very healthy for the heart, but could unmask heart disease in those with severe heart blockages.
4. Enjoy eating your eggs and cholesterol. Study after study shows that eating 6 eggs a day for 6 weeks has no effect on cholesterol blood levels. Yet this myth persists. Avoid saturated fats (hard fats) and margarine (butter is much healthier and tastier than margarine).
5. Eat 1-3 cloves of garlic a day. Crushed into olive oil, it makes a yummy treat that may drop your cholesterol. In addition, have a cereal with oats (e.g., Life, Cheerios, Quaker Oats Squares) for breakfast. Simply adding garlic and oats to your diet can lower your cholesterol almost as much as many medications. Artichokes also lower cholesterol.
6. Herbals can be quite effective as well at maintaining a healthy cholesterol level. If you can find one I recommend a product that contains inositol hexaniacinate (flush free niacin), berberine, chromium, artichoke, policosanol and deodorized garlic.
7. If triglycerides are also elevated, especially be sure to avoid sweets and add Acetyl-L-Carnitine 1,000 mg a day to the above for 3 months to see if it lowers the triglycerides.
8. If on cholesterol lowering medications (statins), be sure to take Coenzyme Q10 (200 mg a day).
Source: http://www.healthiertalk.com/8-tips-lower-your-cholesterol-naturally-2532
1. Begin with an exercise program and, if overweight, bring your weight down.
2. In men, especially if you are overweight, have high blood pressure, and have diabetes (or are prediabetic), this may ALL be coming from too low of a testosterone level. If your total testosterone is under 450 on the blood test, I would consider using prescription natural testosterone (Androgel or Testim or compounded) to bring your level up over 700.
3. In women, consider a trial of prescription natural Armour Thyroid—even if the labs are normal. High cholesterol is often caused by low thyroid and the tests are horribly unreliable (they miss the majority of those who need thyroid hormone). Consider an exercise stress test before beginning exercise or thyroid. Both are very healthy for the heart, but could unmask heart disease in those with severe heart blockages.
4. Enjoy eating your eggs and cholesterol. Study after study shows that eating 6 eggs a day for 6 weeks has no effect on cholesterol blood levels. Yet this myth persists. Avoid saturated fats (hard fats) and margarine (butter is much healthier and tastier than margarine).
5. Eat 1-3 cloves of garlic a day. Crushed into olive oil, it makes a yummy treat that may drop your cholesterol. In addition, have a cereal with oats (e.g., Life, Cheerios, Quaker Oats Squares) for breakfast. Simply adding garlic and oats to your diet can lower your cholesterol almost as much as many medications. Artichokes also lower cholesterol.
6. Herbals can be quite effective as well at maintaining a healthy cholesterol level. If you can find one I recommend a product that contains inositol hexaniacinate (flush free niacin), berberine, chromium, artichoke, policosanol and deodorized garlic.
7. If triglycerides are also elevated, especially be sure to avoid sweets and add Acetyl-L-Carnitine 1,000 mg a day to the above for 3 months to see if it lowers the triglycerides.
8. If on cholesterol lowering medications (statins), be sure to take Coenzyme Q10 (200 mg a day).
Source: http://www.healthiertalk.com/8-tips-lower-your-cholesterol-naturally-2532
Wednesday, September 15, 2010
Published positive XMRV studies
Published study by FDA in PNAS 2 weeks ago:
http://www.pnas.org/content/early/2010/08/16/1006901107.full.pdf+html
2009 Lombardi study in Science:
http://www.sciencemag.org/cgi/content/abstract/1179052?ijkey=m3wzKT4yJqEyk&keytype=ref&siteid=sci
Press releases of Iris Caixa about their XMRV study in Spain:
http://www.elperiodico.com/es/noticias/sociedad/20100907/detectado-virus-comun-dos-cada-tres-enfermos-fatiga-cronica/469776.shtml
http://www.irsicaixa.org/es/premsa
http://www.pnas.org/content/early/2010/08/16/1006901107.full.pdf+html
2009 Lombardi study in Science:
http://www.sciencemag.org/cgi/content/abstract/1179052?ijkey=m3wzKT4yJqEyk&keytype=ref&siteid=sci
Press releases of Iris Caixa about their XMRV study in Spain:
http://www.elperiodico.com/es/noticias/sociedad/20100907/detectado-virus-comun-dos-cada-tres-enfermos-fatiga-cronica/469776.shtml
http://www.irsicaixa.org/es/premsa
Saturday, July 24, 2010
Regarding the FDA/NIH paper, and its impact of retrovirologist in the world
I saw Dr. Soriano from Carlos III, 2 weeks ago, because He tested me for XMRV, and He told me that I was NEGATIVE, the same as the rest of CFS patients He tested. He was convinced that the was no link between CFS and XMRV because:
1) He was unable to find it in NONE of the CFS patients He tested, there was no control group, as there was no official study.
2) He was able to detect it in Prostate Cancer patients, and "other" patients, He said... I assume HIV patients, although He did not say. But He is number 1 in HIV in Spain.
3) For CFS patients He used the same primers than in the Science study, He did PCR and serological test from Abbott Labs.
I tried to explain him about the unpublished study by NIH and FDA, but He would not listen, He only talked about the CDC negative study, and He thinks the Lombardi study is a "bluff"
Both the CDC and the NIH/FDA groups submitted research articles to separate journals for publication, and those journals have completed their respective peer-reviews. However, in the "interest of scientific inquiry and collaboration across HHS", both groups of scientists agreed to conduct further assessments to investigate the discrepancies between their studies prior to publication.
CDC completed their assessment and their paper was published in Retrovirology on July 1, 2010. The NIH/FDA study was further reviewed by the journal editor and currently awaits publication. Its release is controlled by the journal.
The "second look" at both the CDC and the FDA/NIH papers, is kind of dogi, when only one paper is published after "revision".
Now the journal makes the final call, but if they are not satisfied, they can still reject the FDA/NIH paper. This is worrysome.
Scientist do not look at blogs, or articles in newspapers, they only look at published data, and NO positive study is published on CFS patients for XMRV besides the one in Science. If that preveils, they will stop paying attention to XMRV / ME.
I think is dangerous that by September the NIH has not released their study, but I would not know how to force that, other than the media.
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