Treatment works best when autoimmune hepatitis is diagnosed early. With proper treatment, autoimmune hepatitis can usually be controlled. In fact, recent studies show that sustained response to treatment not only stops the disease from getting worse, but also may actually reverse some of the damage.
The primary treatment is medicine to suppress (slow down) an overactive immune system.
Both types of autoimmune hepatitis are treated with daily doses of a corticosteroid called prednisone. Your doctor may start you on a high dose (20 to 60 mg per day) and lower the dose to 5 to 15 mg/day as the disease is controlled. The goal is to find the lowest possible dose that will control your disease.
Another medicine, azathioprine (Imuran) is also used to treat autoimmune hepatitis. Like prednisone, azathioprine suppresses the immune system, but in a different way. It helps lower the dose of prednisone needed, thereby reducing its side effects. Your doctor may prescribe azathioprine, in addition to prednisone, once your disease is under control.
Most people will need to take prednisone, with or without azathioprine, for years. Some people take it for life. Corticosteroids may slow down the disease, but everyone is different. In about one out of every three people, treatment can eventually be stopped. After stopping, it is important to carefully monitor your condition and promptly report any new symptoms to your doctor because the disease may return and be even more severe, especially during the first few months after stopping treatment.
In about 7 out of 10 people, the disease goes into remission, with a lessening of severity of symptoms, within 2 years of starting treatment. A portion of persons with a remission will see the disease return within 3 years, so treatment may be necessary on and off for years, if not for life."
I occurs to me that your prednisone dose could be higher if your disease is not controlled at this dose. That is something you should address with your doctor.
It is hard for me to determine the extent of your liver injury on the basis of what you report. The Ishak score can be tricky to understand.
"The necroinflammatory components of the HAI include periportal inflammation and necrosis (0-10), lobular inflammation and necrosis (0-4), and portal inflammation (0-4). Instead of the HAI fibrosis score (0-4), the Ishak score was used, which stages fibrosis from 0-6 (1-2, portal fibrotic expansion; 3-4, bridging fibrosis; 5-6, cirrhosis). Steatosis was scored based on the proportion of hepatocytes with fat (1+, 25%; 2+, 26%-50%; 3+, 51%-75%; 4+, 76%). "
I am confused by your doctor saying the Ishak range is 1 to 10. Regardless, if we assume that you do have some cirrhosis, and I think that is a reasonable assumption, then maybe your goal should be to control the disease with medication and carefully watch your diet and work toward keeping your own liver. People can and do live long lives with cirrhosis and you might well be one of those people.
Older donors' livers have been successfully transplanted so it's conceivable that your grandmother's liver might be a possibility. I believe the oldest liver donor was 92 years of age. I know nothing about the protocol in India regarding organ allocation so I really can't add anything more to this subject.
This is a very complex subject and I apologize for my incompetence. I think you need to sit down with your doctor and thoroughly discuss the condition of your liver, the likelihood of controlling your disease with medication and his/her prognosis as far as your life expectancy and quality of life is concerned. And then get his/her opinion of the benefit and possibility of transplantation should it come to that.
I wish you good luck and good health.
I think Mike has covered everything very well. He has given you good advise and great information. I completely agree with him! Thanks Mike! I can only add that we are always here for you. We all understand what you are going through. Know that you have our full support. ~Kande
I apologise for not responding to your update as i was on a vacation for 2 weeks and wanted to spend some time with my kids away from my regular routine.
Thanks for your valuable advise. It has releived me to some extent.
I was shattered when i came to know i had cirrhosis. I was diognised in January 2008 and the Prednisone dose started off with 30 MG and and now reduced to 10 MG for last 2 months. I have an appointment on 15 MAY 2008.
My doctor did not give proper response to my querries. He just said that i had someting called ANA & AMA in my blood which has caused the Autoimmune hepatitis.
I was really worried bcos from my childhood i have been told that only excessive alchohol consumption will lead to Lever problem and i do not drink or smoke.
1. Just keen to know what is that i need to enquire when i go to the Doctor next?
2. Can a O+ve donor donate his lever to A+ve ( was keen because ..i want to make sure that i have some to donate when i need. My Wife is having o+ve .I .i dont have any brothers or sisters who can donate. so just thinking of possibiliteis proactively ..as it may help when the situation arises.)
You must have a blood type compatible with the recipient or you will not be able to donate. Here is who can donate to whom:
Type A can donate to types A and AB.
Type B can donate to types B and AB.
Type AB can donate to type AB.
Type O can donate to types A, B, AB, and O.
Blood Type Can receive liver from: Generally can donate a liver to:
O O O, A, B, AB
A A, O A, AB
B B, O B, AB
AB O, A, B, AB AB
I am feeling very strained nowadays.
Even after a sound sleep when i get up in the morning i am very tired and have no interest in anything. Is this due to side affects of the prednisone?
I do not have enough strength in my limbs either. Though i ve gained some weight and my complexion has changed i am not that very active as before.
I never had that particular reaction to prednisone but that doesn't mean it cannot affect you differently from the way it affected me. I don't know why you're feeling that way. I hope you start feeling better as the day goes on. Mike
I was on Prednisone for a short while after my liver transplant. I had some rejection issues early on and Prednisone was the drug of choice, to help with the rejection. I had a lot of energy while I was on the medicine. I lost 6lbs. while on Prednisone, the reason was I just couldn't stop moving. I remember cleaning my home for 16 hours. It had the opposite effect with me. My doctors told me, my reaction to the medicine, was normal. Do you think you could be anemic? That can be a problem with pre & post transplant patients. I believe I would have some blood tests done. You should not feel that weak.
NOSE Bleed Common in Cirrhosis?
Had Nose Bleeds twice yesterday.
Yes, nose bleeds are common. The reason is the liver makes certain proteins that help the blood to clot. When the proteins are not made properly, the blood doesn't clot like it should. That is one more issue to deal with, with cirrhosis. I started having nose bleeds about 6 months before I had my transplant. At the same point in time I had esophagel vein bleeds also. Seven in all, that took around 13 bandings to stop the bleeding. You need to report the nose bleeds to your doctor, if you haven't already. Both are signs of advanced liver disease.
Impossible!!! LOL!!! But the vacation has been fun! :o)
I came to know about this form and I really found some useful informaion.
My father have lever psyriosis and also have heart patient. he is sufferring everyday from to much pain in heart and facing gestric problem even after control diet.
We talked with doctor and doctor advice that there is only way that we need to transplantent lever.
We have not taken further advice regarding this from other doctors but Before I consult with any doctor I need to know about transplantation Costing and can any live and young person dontate his lever part?
Father Blood group is 0+ , have diabetis,have heart problem son blood group is B+ and normal.
Father is 60+ and son is 30+
After donation can onr live his normal life or one should change his/her lifestyle?
I also need to know in india at what places this facilities available ?
and what is the best place.
If I get these information than I think further step will be easy for us and might be this advice will be useful to someoneelse.
You can reply on ***@****
Thanks for your advice in Advance.
An O blood type can receive a liver ONLY from another O blood type.
Here is a chart that explains it in detail:
Blood Type Can receive liver from: Can donate a liver to:
O O O, A, B, AB
A A, O A, AB
B B, O B, AB
AB O, A, B, AB AB
There are mainly 4 centers in India where lever transplants are done.
New Delhi - Gangaram Hospital
Hyderabad - Global Hospitals
Bangalore - Narayana Hrudayalaya
Delhi - Appollo
The cost is around 14 - 18 Laks INR. The success rates are as good as any center in US / UK at 85% +
Check the Link below for one of the center
There are few other centers as well Like Christiam Medical Mission Vellore , St Johns Medical Hospital Bangalore. But not inthe scale of the 4 mentioned above.
Please let me know if u further need any Information will try to get it.
I can't comment on what the staging means yet because I have yet to have a liver biopsy, but have been diagnosed with another autoimmune disease....I feel your dispair. I was told that more than lively I may develop autoimmune hepatitis. My LFT's are only going up and all of my serum inflammation markers are elevated and going up each time I'm tested. Prograf or prednisone is in my future.
You CANNOT live without a liver. 10mg prednisone is not a lot. We usually start our patients on a taper. You don't want an 84 year old liver. Plus, you don't know if she is the right match. She may have the same blood type as you, but her antibodies may be different...and an aged liver is not always the best...may have fibrotic chages as well as fatty deposits.
What did you mean when you said "....but her antibodies may be different"? This is the first I've heard that. I posted the blood type compatibility chart. Blood type compatibility and size of the donor pretty much sums it up as far as I know.
"The donor must be:
* Approximately the same weight and body size as the recipient
* Free from disease, infection, or injury that affects the liver
* Usually of the same or a compatible blood type" (see table in above post)
You're right that an older liver may not be the best but, when you're up against the wall and old liver is a whole lot better than a non functioning liver - notwithstanding the possibility of fibrosis and other architectural abnormalities. I wouldn't prefer an old liver but I wouldn't absolutely rule it out either.
I'm not Ashley, but my understanding is that there is more than just blood groups to consider. Rh is a factor as well. (i.e. O neg can only receive O neg, but O pos can receive both O pos and O neg.) In addition, some people carry antibodies (I believe referred to as Kel antibodies, usually designated by letter identity, for example, anti-c, anti-E, etc.) that will attack certain bloods if not "compatible". Too bad it's not just blood groups and size to determine the match...
I was talking about liver transplantation but I didn't make that clear. I apologize for that. Mike
I was wrong and I stand corrected. I really didn't know that HLA matching was relevant in cadaver liver transplants but I do now. I am still mot sure how significant it is with livers - as it is with other organs but, at least I know it is a factor.
Thanks for educating me. I do appreciate it.
From Janis siting a University of Pittsburgh article:
"Better Matching Tests, Better Outcomes?
Doctors at the University of Pittsburgh conducted a retrospective study of more than 3,200 patients who underwent liver transplant surgery, and found that donors and recipients who are more compatible in terms of their immune systems and liver tissue type will likely lower the risk of organ rejection following surgery, but will face an increased risk of disease recurrence once the transplant procedure is over.
"This is particularly significant for hepatitis C, the most common indication for liver transplantation and where the absolute majority of the patients suffer recurrence after transplantation," said John Fung, M.D., Ph.D., a professor of transplantation surgery at the University of Pittsburgh, and a study investigator. "Perhaps by paying attention to histocompatibility, we may be able to reduce the numbers."
Immune system compatibility, also known as histocompatibility, is determined by the degree of similarity between a recipients and donors profiles of so-called "human leukocyte antigens", or HLA. These are molecules found on cells that serve as signals to antibodies and other cells of the immune system. Doctors who perform HLA testing can usually determine whether a liver that is about to be transplanted is compatible with the recipients own liver.
"We had performed an analysis in the late 1980s regarding the role of HLA matching in liver transplantation," said Fung, in an interview with Priority Healthcare. "With much greater numbers than we had before, we confirmed that in some cases, HLA matching could be a negative factor, while in others, a positive factor."
Donor/recipient matching is key prior to kidney transplantation, and is a routine pre-operative assessment.(3) However, the practicality and merits of its use have been questioned in liver transplant procedures. Time restraints make the test impractical most of the time. Most surgeons also believe matching is irrelevant for transplanting the liver, an organ that is better equipped to modulate any postoperative immune reactions. Instead, surgeons may pay more attention to the donor and recipients blood type compatibility and the size of the liver relative to the recipient.
Nonetheless, University of Pittsburgh researchers have been collecting information for a database on liver compatibility related to approximately 7,000 liver transplants performed there in the past 20 years."
This may interest you.
Human leukocyte antigen and adult living-donor liver transplantation outcomes: an analysis of the organ procurement and transplantation network database.
Jakab SS, Navarro VJ, Colombe BW, Daskalakis C, Herrine SK, Rossi S.
Department of Medicine, Division of Gastroenterology and Hepatology, Jefferson Medical College, Thomas Jefferson University, and Department of Tissue Typing, This
Thomas Jefferson University Hospital, Philadelphia, PA 19107, USA.
Human leukocyte antigen (HLA) compatibility has no clinically significant impact in cadaveric liver transplantation. Less is known regarding living-donor liver transplantation (LDLT). Our prior analysis of the Organ Procurement and Transplantation Network (OPTN) database suggested a higher graft failure rate in patients who underwent LDLT from donors with close HLA match. We further investigated the effect of HLA-A, -B, and -DR matching on 5-yr graft survival in adult LDLT by analyzing OPTN data regarding adult LDLT performed between 1998 and 2005. We evaluated associations between 5-yr graft survival and total, locus-specific, and haplotype match levels. Separate analyses were conducted for recipients with autoimmune (fulminant autoimmune hepatitis, cirrhosis secondary to autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis) or nonautoimmune liver disease. Multivariable Cox proportional hazard models were used to evaluate interactions and adjust for potential confounders. Among 631 patients with available donor/recipient HLA data, the degree of HLA match had no significant effect on 5-yr graft survival, even when analyzed separately in recipients with autoimmune vs. nonautoimmune liver disease. To be able to include all 1,838 adult LDLTs, we considered a first-degree related donor as substitute for a close HLA match. We found no difference in graft survival in related vs. unrelated pairs. In conclusion, our results show no detrimental impact of close HLA matching on graft survival in adult LDLT, including in recipients with underlying autoimmune liver disease. Copyright (c) 2007 AASLD.
Influence of donor/recipient HLA-matching on outcome and recurrence of hepatitis C after liver transplantation.
Langrehr JM, Puhl G, Bahra M, Schmeding M, Spinelli A, Berg T, Schönemann C, Krenn V, Neuhaus P, Neumann UP.
Department of Surgery, Charité, Campus Virchow-Clinic, Humboldt University, Berlin, Germany. jan.***@****
The aim of this study was to analyze the effect of human leukocyte antigen (HLA) matching on outcome, severity of recurrent hepatitis C and risk of rejection in hepatitis C positive patients after liver transplantation (LT). In a retrospective analysis, 165 liver transplants in patients positive for hepatitis C virus (HCV) with complete donor/recipient HLA typing were reviewed for recurrence of HCV and outcome. Follow-up ranged from 1 to 158 months (median, 74.5 months). Immunosuppression consisted of either cyclosporine-A- or tacrolimus-based quadruple induction therapy including or an interleukin 2-receptor antagonist. Protocol liver biopsies were performed after 1, 3, 5, 7, and 10 years and staged according to the Scheuer scoring system. The overall 1-, 5-, and 10-year graft survival figures were 81.8%, 69.11 and 62%, respectively. There was no correlation in the study population between number of HLA mismatches and graft survival. The number of rejection episodes increased significantly in patients with more HLA mismatches (P < 0.05). In contrast to this, the fibrosis progression was significantly faster in patients with 0-5 HLA mismatches compared to patients with a complete HLA mismatch. In conclusion, HLA matching did not influence graft survival in patients after LT for end-stage HCV infection, however, despite less rejection episodes, the fibrosis progression increased in patients with less HLA mismatches within the first year after LT. Copyright 2006 AASLD
Lots of good information you shared above, thanks so much! -- A bit surprising and disconcerting data -- so counter-intuitive and seemingly paradoxical. It appears to be a trade-off then: better HLA matching means less rejection, but faster progression of fibrosis; poorer HLA matching means slower disease progression, but higher rejection risk. (Damned if you do and damned if you don't, eh?)
Doesn't it also really indirectly point to how important SVR is for HCV transplant patients?
If one were to presume that fibrosis progression would not play into the equation for an SVR patient (can't help but ask: would it?)... I wonder if in such cases better HLA matching would be desired to reduce risk of rejection?
As a new visitor to this community, I am unable to answer your questions, as I am not very knowledgeable about transplants, but I do send you and your family all my best wishes. I hope you are successful in your pursuit of better health.
SVR is very important post transplant. I have read many article which indicate that achieving SVR does halt fibrosis progression and in some cases may improve liver architecture. I juts got my labs back from last Thursday and my ALT is 12, AST 17 and bilirubin 1.0. I know that had I not achieved SVR my labs wouldn't look anything like that.
I am not very familiar with HLA matching but my guess would be that with so few livers available we probably cannot expect to see close matching become a priority in the allocation process. I do not know how matching would affect rejection. I rejected twice and maybe three times early post transplant - but who's counting - and I was treated with Solu-Medrol and everything resolved quickly. This stuff gets too complicated for me a lot of the time.
Gastroenterology. 2006 Jan;130(1):179-87.
Gene expression patterns that correlate with hepatitis C and early progression to fibrosis in liver transplant recipients.
Smith MW, Walters KA, Korth MJ, Fitzgibbon M, Proll S, Thompson JC, Yeh MM, Shuhart MC, Furlong JC, Cox PP, Thomas DL, Phillips JD, Kushner JP, Fausto N, Carithers RL Jr, Katze MG.
Department of Microbiology, School of Medicine, University of Washington, Seattle, Washington 98195-8070, USA.
BACKGROUND & AIMS: Liver transplant recipients infected with hepatitis C virus (HCV) develop recurrent hepatitis soon after transplantation and, in some cases, progress to fibrosis within the first 2 years. Our goals were to identify molecular processes influencing the liver disease progression and to find potential gene markers of early fibrosis. METHODS: We performed gene expression profiling on serial liver biopsy specimens obtained from 13 (11 infected and 2 uninfected) transplant recipients within the first year after transplantation at 0, 3, 6, and 12 months. The data were compared with clinical observations and with a gene expression database obtained for 55 nontransplant HCV-infected and uninfected liver samples. RESULTS: We identified several specific gene expression patterns. The first pattern was unique for the transplant recipients regardless of their infection status. The corresponding genes encoded stress response proteins and blood proteins involved in coagulation that were differentially expressed in response to posttransplantation graft recovery. The second pattern was specific to HCV-infected samples and included up-regulation of genes encoding components of the interferon-mediated antiviral response and immune system (antigen presentation, cytotoxic response). This up-regulation pattern was absent or suppressed in the patients who developed early fibrosis, indicating that the disease progression might result from an impaired liver response to infection. Finally, we identified gene expression patterns that were specific for 12-month biopsy specimens in all 4 HCV-infected patients who developed early fibrosis. CONCLUSIONS: The identified gene expression patterns may prove useful for diagnostic and prognostic applications in HCV-infected patients, including predicting early progression to fibrosis.
High adherence with a low initial ribavirin dose in combination with pegylated-IFN alpha-2a for treatment of recurrent hepatitis C after liver transplantation.
Hörnfeldt E, Gjertsen H, Weiland O.
Department of Medicine, Division of Infectious Diseases, Karolinska University Hospital Huddinge, Karolinska Institute, Stockholm, Sweden.
Patients with recurrent hepatitis C after liver transplantation often cannot tolerate full dose of pegylated interferon (peg-IFN) and ribavirin (RBV) and are often withdrawn prematurely from treatment. We chose a low initial RBV dose, later increased due to tolerance to a mean dose of 600 mg daily (range 200-1000 mg daily) in combination with a peg-IFN alpha-2a 180 mcg weekly in an effort to improve tolerance and minimize withdrawals. 16 patients with hepatitis C recurrence and 1 with de novo HCV infection with a mean age of 54 y (range 43-66 y), 71% males, were treated. All patients completed the intended treatment schedule 24 weeks for genotype 2 and 3 and 48 weeks for genotype 1 and 4. Early viral response was achieved in 12 (71%), non-response in 1 patient with genotype 4, and sustained viral response in 4/5 (80%) patients with genotype 2 or 3 and 3/11 (27%) with genotype 1, p<0.05. To conclude, we found that utilizing a low initial daily RBV dose, later increased due to tolerance in combination with peg-IFN alpha-2a 180 microg weekly, was successful. Hence, all patients completed a full treatment course, which also offered a reasonable efficacy.