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.)
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.
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.
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.
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.
* 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 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."
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.
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.
A prospective evaluation of fibrosis progression in patients with recurrent hepatitis C virus following liver transplantation.
Yilmaz N, Shiffman ML, Stravitz RT, Sterling RK, Luketic VA, Sanyal AJ, Mills AS, Contos MJ, Coterell A, Maluf D, Posner MP, Fisher RA.
Hepatology Section, Virginia Commonwealth University Medical Center, Richmond, VA 23298, USA.
Recurrence of hepatitis C virus (HCV) following liver transplantation (LT) is universal. A subset of these patients develop advanced fibrosis and cirrhosis and it is believed that this leads to increased posttransplantation mortality. The specific aims of this study were to determine the incidence of advanced fibrosis and those factors associated with this process, and to evaluate causes for mortality in patients with recurrent HCV. A total of 227 patients who underwent LT with chronic HCV were monitored prospectively. The mean age of this group at LT was 49.5 yr; 76% were male and 85% were Caucasian. Fibrosis progression was monitored by protocol liver biopsy, initially performed 6 months after LT and then at 6- to 24-month intervals. Advanced fibrosis, defined as the bridging fibrosis or cirrhosis, developed in 1%, 11%, 25%, and 41% of patients after 1, 3, 5, and 6-10 yr, respectively. Acute cellular rejection hepatic steatosis, a persistent elevation in serum alanine aminotransferase and donor-race were associated with the development of advanced fibrosis. In contrast, the development of advanced fibrosis was not affected by the use of interferon prior to undergoing LT, cytomegalovirus disease, or donor age. A total of 60 patients (26%) died over 15 yr of follow-up. Although graft failure accounted for 45% of deaths in patients with advanced fibrosis, this represented only 8% of all deaths in patients with recurrent HCV. Sepsis was the most common cause of death and this was observed with similar frequency in patients who developed advanced fibrosis (45%) and in those with less advanced fibrosis (47%). In conclusion, approximately 41% of patients with recurrent HCV developed advanced fibrosis 6-10 yr after LT. However, complications associated with sepsis, not recurrent cirrhosis, was the most common cause of death in patients with recurrent HCV and this was similar in patients with or without advanced fibrosis.
Here is a portion of an article co-authored by our new Expert Physician:
In liver transplant (LT) recipients, persistence of hepatitis C (HCV) infection in viremic recipients almost always leads to graft reinfection. In fact, serum viral titers may reach pre-transplant levels within the first few days post-operatively. Serum levels of HCV RNA peak 1-3 months post-transplant, reaching titers many fold higher than pre-transplant levels 4,6. Furthermore, histological evidence of HCV recurrence occurs in over 90% of patients within 5 years of the transplant and has a variable clinical course 1,6. Histological progression of HCV is accelerated after LT and can result in the fairly rapid development of graft failure and cirrhosis 7,8,9. Several studies have shown that as many as 20% of HCV patients undergoing liver transplant may develop cirrhosis within 5 years, with almost 50% developing cirrhosis within a decade. Once patients develop cirrhosis from recurrent HCV, they are at risk for the same complications as other patients including variceal bleeding, ascites and hepatocellular carcinoma. Berenguer and colleagues observed rapid hepatic decompensation in LT recipients with graft cirrhosis due to recurrent HCV 1,4,10.
Recent studies looking at large numbers of patients with adequate long-term follow-up have confirmed that patients with HCV undergoing liver transplantation have increased morbidity and mortality and have lower 5 and 10 year survival rates when compared to patients undergoing liver transplantation for other etiologies of cirrhosis 1,8,9. HCV is the most frequent indication for LT in the United States and in Europe. By the year 2020 the proportion of untreated HCV patients developing cirrhosis is expected to increase by 30%, the number of cirrhotic patients with HCV to increase by 100%, and the number of HCV cirrhotic patients developing hepatocellular carcinoma by 80% 2. With the anticipated increase in patients requiring LT for HCV related liver disease, development of effective strategies to reduce graft failure due to HCV recurrence is essential.
A number of reports have described accelerated fibrosis progression post-liver transplantation and this may in part be due to the age of the donor liver allograft 10. The median rate of fibrosis progression is between 0.3 and 0.6 stage per year post-transplant compared to 0.1 to 0.2 stage per year in immunocompetent HCV patients. Various risk factors for poor outcomes post-LT for HCV have been described. Berenguer et al have shown that the use of liver allografts from deceased donors older than age 60 is associated with a more severe recurrence of HCV as well as a more rapid progression to cirrhosis when compared to LT recipients receiving allografts from younger donors 10. Once patients develop cirrhosis post-transplant, the 1 and 3 year actuarial risks of decompensation are 42% and 62%, respectively, vs. less than 5% by 1 year and less than 20% by 5 years in immunocompetent patients with chronic HCV infection 1,4,5. A subset of patients develop a severe cholestatic form of HCV that rapidly progresses to graft failure, similar to the fibrosing cholestatic hepatitis that originally described in patients with recurrent hepatitis B post-transplant. Characteristically, there is a very high HCV serum RNA level, profound hyperbilirubinemia and high levels of alkaline phosphatase and gamma-glutamyl transferase, and liver biopsy reveals feathery degeneration predominantly in the perivenular area (Figure 1), portal tracts showing chronic inflammation ranging from mild-severe with occasional lymphoid aggregates (Figure 2) 4,11. Actively proliferating bile ductiles are often seen. Risk factors for severe recurrent HCV include advanced donor age, HCV genotype 1, high HCV RNA levels before and after transplant, early histological recurrence of HCV, concomitant cytomegaloviral infection, the use of T lymphocyte-depleting immunosuppressive agents such as OKT3, and treatment of presumed acute cellular rejection with pulse corticosteroids. Data are conflicting as to whether recipient age, warm or cold ischemia times, gender, HLA mismatch, ethnicity or pre-transplant severity of illness influence the rate of recurrent HCV and its severity 1,4,5,12,13,14.
I think most centers try to either minimize or eliminate steroids in liver transplant patients with HCV because of the increase in viral activity. I seem to recall that steroids are still commonly used with heart transplant recipients and perhaps with other organ transplants as well but I am not sure about that. I was on steroids immediately post transplant but the dose was tapered and discontinued within 6 months
Here is a quick overview from:
Steroid versus steroid-free protocols
The known toxicity of long-term steroid exposure has prompted the development of steroid-free immunosuppressive regimens. Benefits of the withdrawal or avoidance of steroids include normal growth in children, improved lipid profiles, improved blood pressures, better glycemic control, and lower risk of bone disease.
The development of cyclosporine prompted attempts to develop steroid-free protocols. Initially, patients were doing well with cyclosporine monotherapy. Over time, 50% of these patients required steroids, usually for acute rejection. More recently, a follow-up study of 100 patients in Denmark who underwent transplantation on steroid-free protocols showed a 1-year graft survival rate of 97% and a 4-year rate of 82%. Strong randomized studies are undoubtedly needed to prove both efficacy and safety of these protocols.9
Steroid withdrawal has been used as a strategy to avoid adverse steroid effects in transplantation patients. Recent data show the risk of rejection is higher in patients withdrawn from steroids on a cyclosporine-based protocol. After tacrolimus became available, protocols with this drug showed that withdrawal of steroids after 6 months was successful 80% of the time. More recently, studies involving rapid steroid withdrawal (over 1-2 wk) in patients taking tacrolimus show similar graft survival rates compared with patients withdrawn after 3-6 months.
In African American patients, the risk of acute rejection is high; therefore, steroid-tapering regimens are prohibited. The use of sirolimus with tacrolimus followed by a steroid taper at 3 months has resulted in acceptable rejection rates in African Americans in one early study.10 The role of sirolimus and mycophenolate mofetil in steroid-free protocols has yet to be definitively determined, although the future looks promising for greater use of steroid-free protocols.
QUESTION: I received my liver transplant from Dr. Starzl in Pittsburgh in 1984. Can you provide me with some statistics on survival rates, etc.? I am enjoying a relatively normal and healthful life since then - I am a 56-year-old female. However, I had to undergo a kidney transplant a year ago, from my brother. My sole kidney was failing due to the anti-rejection medication that I have been taking for all of these years. Do you also have any statistical information on survival rates regarding patients who have received a kidney following a liver transplant?
Congratulations on being 16 years out after liver transplantation. Your question about survival rates in patients as far out as you is not something that there is a lot of information about since the number of patients who received transplants that long ago are relatively few. However, we have analyzed the data from our own program and have the following conclusions. The risk of graft loss or death is greatest in the first year, less in the second year, and essentially after the third year, the risk of dying for a person in your age group is about 2-3% per year (this is only slightly higher than age-adjusted risk of death in non-transplanted patients). Therefore, you might say that your chances of living to 70 (14 years from now) are about 70%. The fact that you had a kidney transplant shouldn't alter your life expectancy much. However the saying goes: you are either alive or dead, you can't be 30% dead or 70% alive!
I suspect that the kidney that your brother gave you will last a while. In general, living related kidney transplants last longer than for cadaveric kidneys. You can expect that the chance of your kidney working until you are age 70 is about 50% (i.e., the half-life of a living donor kidney is about 14 years). If it were a perfect match (i.e., 6 antigen match) then the half-life rises to 25 years.
Don't be too concerned about how much time if left - just enjoy it.
Women Fare Better After Liver Transplant
THURSDAY, Sept. 28 (HealthDay News) -- Women may have an edge on men when it comes to surviving liver transplant, a new British study finds.
The study of over 2,700 patients who received a liver transplant between 1985 and 2003 found that female patients live an average of 4.5 years longer than their male counterparts.
According to researchers at Queen Elizabeth Hospital, Birmingham, average survival time for the patients in the study was 22 years, compared with 29 years for a comparison group of healthy people of similar age.
Average life expectancy for female liver transplant patients was 26 years, compared with 18 for males. The average life expectancy for the general population was 31 years for women and 27 years for men.
Liver transplant patients ages 17 to 34 had an average life expectancy of 28 years. While this was the highest among the transplant patients, it fell far short of the average life expectancy of 51 years for people ages 17 to 34 in the general population.
Overall, patients who required a liver transplant due to primary liver disease had significantly longer survival times than those who had transplants due to hepatitis C, cirrhosis, or cancer.
The findings were published in the journal Gut.
I believe that complications probably vary to some degree according with the underlying disease which necessitated transplantation. Of course, organ rejection is one possible complication with all organ transplants. Recurrence of HCV is another obvious issue post transplant. Autoimmune hepatitis has a different set of issues as do Primary Biliary Cirrhosis and Primary Sclerosing Cholangitis. And some issues arise as a result of the anti-rejection regimen. This is way too complex for me to say anything more about this subject. Suffice it to say that when you're at the point where liver transplantation is the only option the possible complications are not significant at all - in the big picture anyway.
It's like life - we cross those bridges, if and when, we get to them.
I was having my LFT levels higher last month. and i was feeling very strained and had some headache issues. he asked me to increase the Prednisone dosage back to 30 MG and taper it to 15 MG. and he asked me to visit him after a month.
Met him yesterday and said him that i still had the same issues regarding strain and i ve put up a lot of weight as well in the last 2 months. He was suggesting that i may need to plan for a transplant. I have given my blood for tests and had a Ultrasound of obdamen. Need to go back to him after 2 days for reports.
Please suggest me what all i need to ask him in case he refers for a transplant? I am really tensed..Please help.
If he sends you to be evaluated for liver transplant the transplant doctors will be able to answer your questions. Stress is common in these types of situations and everyone deals with it differently. It's not easy for anyone to deal with.
During this appointment I would want to know the specifics of the ultrasound and the lab results. If he doesn't think you need to be evaluated you can ask him for his prognosis and his treatment plan for you. I'd want him to be specific here and tell you what the frequency of labs test and appointments would be (follow up) and what symptoms or test results would trigger a change in treatment. I would start out listening carefully to everything he said and then go from there. I don't have a list of questions I would ask but, questions would probably occur to me during the appointment as I listened to him speak.
Good luck, Mike
My relative in Gurgaon has been suffering from lever Cirrosis since last two years and was in hospitals for six months in 2 years and now admitted in Medanta the Medicity, the doctors advised Lever Transplant as last option in Gangaram delhi, The blood group of none of the close family members is B+ to donate Lever.
I came to know from Dr. Soin site that Braindead people or Accidental victims dying in ICU can donate Lever for transplant. But how can we get this information that anybody with B+ blood group in any NCR Delhi hospital may donate lever to save life of my relative ? Is there any information centre or site where organ donars can be contacted ?
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