A Fellow Patient's Treatment History

[cajim]

1975 born in August;
1991 HBsAg+, HBeAg+ found;
2003 liver pain, liver function normal, DNA 8th power, tried Chinese herbal medicine for one year, ineffective;
2004 liver pain, liver function normal, DNA 8th power, started Lamivudine;
2005 Lamivudine, liver function normal, DNA is only down to 4th power, decreased liver pain;
2006 Lamivudine, ALT slightly abnormal, liver function slightly abnormal, DNA up to 6th power, YMDD mutation detected;
2006 Lamivudine plus Adefovir, liver function normal, DNA down to 4th power;
2006 Lamivudine plus a different branch of Adefovir, liver function normal, DNA-;
2007 Adefovir alone, unable to control the virus, DNA up to 6th power, added Lamivudine, DNA became negative again;
2008 mutation despite combined Lamivudine and Adefovir, changed to Adefovir plus Entecavir;
2009 Adefovir plus Entecavir, liver function normal, DNA negative;
2009 Adefovir plus Entecavir till now (October 2009), liver function slightly abnormal, DNA increased to 7th power, virus detection showed mutation.

[cajim]

Case 7  Male
1962:  Born;
1987:  Got married, diagnosed HBeAg- HBV
1995:  HBeAg+ HBV, ALT 112;
02/06: Cirrhosis, ascites;
03/06: Massive bleeding, hospitalization, hardener treatment
04/08: Cirrhosis, no ascites, enlarged spleen, DNAHBV-, normal ALT/AST;
05/08: Cirrhosis, no ascites, enlarged spleen, DNAHBV 10^6, ALT/AST about 200;
08/08: Hospitalization, started ADV, discharged from hospital in 45 days;
12/08: ALT/AST/HBVDNA no much change;
04/09: Hospitalization again;
05/09: Started Entecavir, in 15 days HBVDNA to 10^3, ALT 70, AST 50, discharged from hospital:
07/09: HBVDNA-, ALT 170, AST 70;
08/09: 3 months of Entecavir, ALT 109, AST 102, HBVDNA 1.25x10^3
09/09: 4 months of Entecavir, ALT 59, AST 56, HBVDNA <100;
10/09: 5 months of Entecavir, ALT 55, AST 50, HBVDNA <100;
11/09: 6 months of Entecavir, ALT 36, AST 44;
01/10: ALT 46, AST 35;
02/10: AST 42;

[cajim]

Case 6  Male
1987:  diagnosed HbeAg+ HBV, tried Chinese herbs and Western pills, no effect, stopped treatment.
2005:  B-US showed slight thickening of spleen, nothing done.
2007:  balted belly, B-US showed cirrhosis and ascites, started LAM and diuresis, one month later, liver function, HBVDNA, etc. became normal, ascites subsided.
2008:  Till 03/06/08 patient reported stable status, then he tested varices of esophagus, ALT 66.5, AST 38.9, AFP 11.29, HBVDNA <1000, HBeAg-, HBVDNA-, to avoid resisteance and mutation, patient added ADV himself (03/25/08).
05/04/08:  ALT 45, AST 37, HBVDNA-
06/14/08:  ALT 30, AST 28, HBVDNA-
09/02/08:  HBsAg+, HBsAB-, HBeAg- HBeAB-, HBcAB+, HBVprs+, AFP 2.43, HBVDNA <1000,
12/06/08:  ALT 39, AST 28, HBVDNA <1000;
03/22/09:  Varices of esophagus CBRC+ F1LEME-, normal liver and kidney functions, HBVDNA <1000.

[cajim]

Case 5  Female
12/52:  Born
About 1990:  poor appetite, tired, diagnosed HBsAg+, took herbs, symptoms basically disappeared;
About 2 years later:  HBV, symptoms included fatigue, balted behind ribs, took meds on and off;
About 1999-2000:  diagnosed cirrhosis, took herbs, 03/01:  B-US showed slight ascites;
04/00:  ALT 60, AST 53;
08/00:  ALT 46, AST 50;
02/01:  ALT 55, AST 64;
07/01:  ALT 50, AST 35;
08/01:  ALT 52, AST 55, PCR HBV 0;
08/02:  ALT 70, AST 70, B-US showed splenomegaly, took herbs on and off for 2 years;
09/02:  ALT 36, AST 57;
01/03:  ALT 30, AST 53;
04/03:  ALT 14.7, AST 40.1;
06/03:  ALT 28, AST 39;
11/03:  ALT 37, AST 66;
06/04:  ALT 38, AST 37;
02/05:  ALT 31, AST 52;
05/05:  ALT 29, AST 69, PCR HBV 0;
06/05:  ALT 15, AST 36;
10/05:  ALT 20, AST 72;
11/05:  ALT 24, AST 84;
01/06:  ALT 25, AST 64;
03/06:  AFP 3.2, hepatic encephalopathy, HBVDNA10 to 4th power, ALT 21.3, AST 39.6, HBsAg+, HBsAB-, HBeAg+, HBeAB-, HBcAB-;
04/06:  ALT 38.0, AST 54.0;
05/06:  ALT 33.0, AST 41.0, started Entecavir;
07/06:  ALT 32.0, AST 42.0;
07/06-2:  ALT 31.0, AST 85.0;
10/06:  ALT 27.0, AST 62.0, HBVDNA <500copies/ml;
12/06:  ALT 24.0, AST 61.0;
03/07:  ALT 41.0, AST 67.0;
04/07:  ALT 32.0, AST 58.0;
05/07:  ALT 21.0, AST 53.0;
07/07:  ALT 31.0, AST 55.0, HBVDNA 112.9->85.6, HBsAg 7430 (25.9, AST 60.5->44.3, AFP 63.4, HBVDNA ,5x10^2;
07/09:  ALT 24.4, AST 43.3;
08/09:  ALT 33.6->113.0->75.1, AST 79.0->271.6->81.3;
09/09:  ALT 41.7, AST 49.3;
10/09:  ALT 29.0, AST 56.0;
11/09:  ALT 31.4->30.7->39.2, AST 67.2->70.2->74.9, AFP 40.3, metastasis to bones.

As patient went from HBV to cirrhosis to ascites to splenomegaly to hepatic encephalopathy to primary ca of liver to metastasis to bones, did the ALT/AST/HBVDNA correspond to the disease course?  Yet how many patients were persuaded into life-long dependence on antiviral drugs?

[cajim]

1970 born
1989 diagnosed with HBV
1997 wife gave birth to son, wife is immune, son vaccinated and has antibody against HBV;
1989 HBeAg-;
1999 cirrhosis as shown by B-US;
2001 splenic embolism, started LAM;
2005 developed LAM resistance, switched to Adefovirdipivoxil;
2009 in May developed Adefovirdipivoxil resistance, AFP 200, GGT 220, HBVDNA to 6th power, switched to Entecavir 2 pills daily, AFP 200, GGT 200, HBVDNA to 4th power, liver slightly reduced in size, surface uneven, edges indented, many nodes, two of them about 2cms, AFP 200, GGT200, with Entecavir AFP and GGT come down slightly;
12/02/09  diagnosed severe varicosity on esophagus and fundus of stomach, loop ligature twice, now liver function and HBVDNA roughly normal.
09/20/09  diagnosed in decompensation status
09/23/09  HBDNA <1000
10/21/09  did 6 loop ligature on esophagus,
11/22/09  ALT 43.3, AST 54.9, GGT 171.4, AFP 43.5, HBVDNA <1000

[cajim]

Sun Tzu, a Chinese militarist 2500 years ago, said: “是故百战百胜，非善之善者也；不战而屈人之兵，善之善者也。”

Translation:  Thus to fight a hundred battles and win a hundred battles, is not a reflection of the most supreme strategy.  The ability to subdue the enemy without battle is a reflection of the ultimate supreme strategy.

A Chinese doctor says: “to cure without treatment is the highest level; to cure with treatment is only the second level; of course, to fail to cure with treatment is the lowest level.”

Isn’t it the situation today that modern medicine aims at the second level and most often ends at the lowest level?

Current HBV picture:  we try to control HBV and end up with fighting resistance and mutations, taking drugs for life, etc.

Proof from Israel:  March, 2000, Israeli physicians in public hospitals implemented a program of sanctions in response to a labor dispute over a contract proposal by the government and canceled hundreds of thousands of visits to outpatient clinics and postponed tens of thousands of elective operations.   The result: the Jerusalem Post interviewed non-profit making Jewish burial societies, which perform funerals for the vast majority of Israelis and found out the number of funerals performed had fallen drastically.  Meir Adler, manager of the Shamgar Funeral Parlour, which buries most other residents of Jerusalem, declared with much more certainty: "There definitely is a connection between the doctors sanctions and fewer deaths. We saw the same thing in 1983 when the Israel Medical Association applied sanctions for four and a half months."

What does this mean to the patient?  Try to find a way to cure without treatment and be willing to do what it takes.

[cajim]

In China there are villages of HIV patients who were infected with virus through selling blood.  Compared with their US counterparts, they are much poorer and cannot afford most of the treatments here.  Yet they live longer and their quality of life is better in that they can still work in the fields.  I am not saying they are cured and maybe slowly they become weak too.  According to the reporting doctor, the difference between the Chinese and western treatments is the former aims at helping the body while the latter aims at killing/controlling the virus.

Coming back to HBV, the concern with the western style of dealing with HBV is that the HBV may never be killed, only the carrier.  The effect of LAM for 2 to 3 years is beautiful:  undetectable HBVDNA, normal liver function, and the patients think their disease is controlled.  But when the virus comes back it comes back with vengeance.  There are even patients who after years of entecavir their HBsAg even becomes negative but their conditions are poorer than most of those with positive HBsAg.

Which is more successful?  Living a life taking care of the body to let it deal with HBV or living a life dealing with HBV with treatments that are known to be harmful to the body?  The answer takes time.

[stevenNYer]

cajim: To respond to Steven's comment above:  Yes, with hindsight we can say it is "poor management of using" what were available then.  But what I fear is: 10 years from now, how do we know combo Entecavir and Tenofovir is not the same as LAM?


You're right, no one has a crystal ball but we go by what we know now.  There are no guarantees in life.  But what we know now is alot more than before.  Remeber we don't say everyone should treat, we say in certain cases because the alternative in these cases is active hepatitis.  Also, alot of the treatment for HepB is acutally from the HIV model.  HIV combination treatment is the norm for the same reason, to prevent resistance.  And it has been successful for many many years.  For HIV, the alternative is a rather quick death.


jhakas:  "liver pain" is commonly reported for those sith chronic HepB.  The liver itself feels no pain, but inflammation could pressure surrounding organs, tissues, veins, etc, so the pain is from that.

[BeachTiePurist]

Yes, a pain in the lower right ribcage is due to a swollen liver.  Hepatitis is a word meaning inflammation of the liver.  The pain is due to the swelling.

[cajim]

Male, born 11/03.
09/03, diagnosed  with HBeAg-, HBeAB, normal liver function.
06/06, ALT 210, AST 120, took herbs, 1 week to ALT 970, AST 360, liver biopsy G2, hospitalized, used some Chinese medicines, 1 week later ALT 220, AST 120, started LAM
LAM for 1 year, liver function normal, HBVDNA-, 2 more years of LAM.
08/09, stopped LAM, 3 months later ALT 740, AST 340, HBVDNA 2.96 x 10 to 7th power.
10/09, ALT 365, AST 110, TBA 24.9, CBE 400, GGT 511, tried some other western drugs, ALT 430, AST 200, tried herbs again, 1 week later, ALT 740, AST 374.
12/09, ALT 1800, AST 800, HBVDNA 5.1 x 10 to 7th power, tried western medicines again, 1 month later ALT 555, AST 330, HBVDNA 5.1 x 10 to 7th power.

To respond to Steven's comment above:  Yes, with hindsight we can say it is "poor management of using" what were available then.  But what I fear is: 10 years from now, how do we know combo Entecavir and Tenofovir is not the same as LAM?

[stevenNYer]

That August 1975 born chronic HepB patient is a classic example of poor treatment.

It's not the antivirals, it's poor management of using them.  

I would question why LAM for over 1 year, then why go mono Adefovir?, then why is Entecavir resistance NOT expected since there is already resistance to LAM.  And would it surprise anyone if even combo Entecavir and Tenofovir fail at this point?

[cajim]

Of course, doctors may cause mutations if they prescribe antivirals at the wrong time or in the wrong combination.

How about patients themselves?  How many of us don't feel we are being treated unless we get a bottle of drugs from our doctors?

[stef2011]

you have been very very unlucky to have met the wrong doctors, it was well known to researchers and advanced doctors about lam and adefovir worsening illness and not curing, now entecavir and tenofovir are another story but you have to be naive,i have been very lucky that the team of researchers in my city knew this and i also knew this reading trials

in your condition i would start alinia even if off label, it is active against all resistant strains hbv and change immediately adefovir with tenofovir (adefovir is very very weak and toxic) + entecavir and eventually Emtricitabine, unfortunately after all these mutations combo entecavir+adefovir is very weak and wil lead to another mutation

i also hope you are not under the same doctor who lead you to all these mutations because he is absolutely not a good doctor

you have to keep the virus und otherwise there is not a lot of meaning in treating with antivirals because they immediately lead to resistance, you have to get und for a couple of years and then when replicor drug will be available you will be free from resistance and hbv

[jhakas]

Hi
Just one question .. does the LIVER ever pain ... I had some pain in my rib case right side and when I asekd the doc he said the liver NEVER pains ...

[cajim]

Female, age 59, with HBV, HBeAg+, mother and brother died of HCC.

March to June, 2005, repeatedly abnormal liver function, max ALT 348, AST 230, globulin 38.5, normal when taking Tiopronin, high again when not on Tiopronin,  HBVDNA-.

July 2005, DNA-, globulin 38.4, albumin 33.3, others normal, AFP 219.5, as the AFP value is too high, did enhanced CT, CT results normal, the doctor suggested taking Lamivudine.

January 2008, DNA is 7 * 10 x 6th power, liver function normal, mutation, YMDD detection: YVDD+, started Lamivudine + Adefovir.

June 2008, taking Lamivudine + Adefovir for six months, DNA at 10 x 6th power. Lamivudine + a different brand of Adefovir for six months, HBVDNA low to 10 x 4th power, and later rose to 10 x 6th power, liver function normal.

January 2009, YMDD mutation detection: YVDD+, changed to Adefovir + Baraclude.

January to August 2009, used Adefovir + Baraclude, DNA sometimes 10 x 3rd power, sometimes 10 x 3rd power, normal liver function, B-US: 1, liver parenchyma damage, cirrhosis; 2, multiple small liver nodules, nodular sclerosis.

Mutation test:
Adefovir (181) Wild
Adefovir (236) Wild
Entecavir (184) Wild
Entecavir (202) Wild
Entecavir (250) Wild
YMDD mutation detection:  M-, v+, i-.

January 2010, DNA at 10 to 3rd power or 4th power, liver function normal.

[cajim]

antiviral treatments = all the oral treatments, e.g. Lamivudine, Adefovir, Entecavir, excluding interferon.

[heyjude1]

Sorry to ask you so many questions but you seem to have alot of  knowlege regarding HBV.  Can you give me an example of antiviral treatments?  Would that inclde the seasonal flu shot?  Would you be referring to interferon?  I understand some people undergo interferon treatments for HepB.  This is news to me bc I thought interferon wad used for HepC only. Is there a high risk of liver cancer from HepB also?

[cajim]

This case shows the pain and difficulty at dealing with HBV once it gets smart and learns to deal with the drugs.  So, be very cautious with starting antiviral treatments.

[heyjude1]

In layman's terms, what does this mean?  I think it means you still have active virus in your blood??  
I don't have all the stats on my blood tests over the years but I know my blood test still comes back positve for Hep. B and adnormal liver function does show up from time to time...something about protiens...any idea what this means without the stats? encome