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.

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.