Q. My mother is 55 years old and suffering from decompensated liver due to hepatitic C virus. she has had 4 episodes of hepatic encephalopathy (3 minor and 1 major due to spontaneous bacterial peritonitis). She has had ascites since that episode. She was diagnosed with Hep C and compensated cirrhosis 2 years ago - she took Interferon but that did not prove effective. Now she has developed caries spine (TB). She is on second line drugs for 4 months which is not proving effective in eradicating the TB virus. Her current results are bilirubin 3.4, ALT 29, PT 14, albumin 1.9, ESR 108, platelets 47.
a) under this condition what would you advise us to do?
b) can she undergo transplant whilst she is on TB (tuberculosis) treatment?
c) would you suggest adding first line drugs for TB (that is rifampicin, pyrazinamide, isoniazid) - she took rifampicin but her bilirubin shot up to 6, so we discontinued.
d) also will hepatitis C re-infect the transplanted liver and if so how long on average does that take? I have heard re-infected hepatitis
C virus is more aggressive and damages the liver causing cirrhosis rapidly
e) I've heard that there are drugs for cirrhosis which are under trials - do you know at what stage these are?
A. a) Your mother has decompensated liver cirrhosis from hepatitis C and requires a liver transplant. Interferon treatment would not be tolerated in this situation. Medical treatment alone would not be adequate in the long run.
b) Yes - she can undergo the transplant on TB treatment if the TB is not active.
c) The use of anti-TB medication is difficult in patients with liver cirrhosis. Do you have the culture results of the TB? This will help the choice of medication. Second line medication may be needed if the first line medication cannot be tolerated.
d) Hepatitis C is likely to re-infect the new liver but treatment can be given after the liver transplant and is usually quite effective. In a very small group of patients, one can have a rapidly recurring form of hepatitis C but this is unusual.
e) There are currently no effective drugs that will treat cirrhosis specifically. Treatment is usually directed at the underlying cause of the liver disease. At the end of the day, we would need to assess the patient before giving you a final result.
Monday, July 06, 2009
Sunday, May 31, 2009
My Mother Was Diagnosed With Hepatocellular Carcinoma
Q. My mother was diagnosed with hepatocellular carcinoma in 2007. This diagnosis was based on a recent MRI scan which revealed a large tumour (around 8cm) that extends from the capsule surface right down to the porta hepatis.
The appearance was typical of HCC and there was also evidence of recent haemorrhage within the tumour. AFT levels exceeded 2000ng/ml. Prior to the diagnosis, her health has deteriorated rapidly; she was experiencing severe right upper quadrant pain which radiated to her back and kept her awake at night.
She was also diagnosed with chronic Hepatitis C in 2001. Although interferon/ ribavirin dual therapy was commenced in 2002, it was ineffective. Cirrhosis was diagnosed after a liver biopsy. There is no concurrent problem to note and her health was good until late August 2007. We were informed that curative treatment was not an option as the tumour did not fulfil the Milan criteria for resection, chemotherapy would not be efficacious, and the tumour was too large for radiofrequency ablation. The last option presented was chemoembolisation.
Unfortunately her liver function was poor, she was in Child Pugh group C, and this treatment can only be given to those in Child Pugh group A or B as the risk of adversity in these groups is low. The only feasible option given was palliation and letting the disease progress and take its natural course but this is not acceptable to us. If there is no evidence of extra-hepatic spread of the cancer, would a transplant be possible?
A. It is an extremely difficult decision to decide on the best treatment for a patient with a large HCC and decompensated liver disease. You are quite right in thinking that currently, there is no curative treatment for such a condition except for liver transplantation which would treat her liver cancer together with her decompensating liver cirrhosis.
In many centres, due to acute shortage of cadaveric donor livers, patients with liver cancer beyond the Milan criteria are not transplanted. However, there are centres such as ours where living donor liver transplantation (LDLT) is widely practiced and often patients with large tumour, way beyond Milan criteria but with no extra-hepatic metastastes and also no large venous involvement such as the large hepatic veins and the main portal vein, are being transplanted successfully. The majority of patients transplanted in Asia using LDLT are beyond the Milan criteria as there is no other alternative treatment.
The 3 year survival rate for this group has ranged from 25-40% and it is well known that for patients who have survived the 3 years are likely to continue living beyond this period as the recurrence rate decreases markedly after the first 12-18 months. The main constraint to LDLT is, of course, the availability of a suitable donor.
The appearance was typical of HCC and there was also evidence of recent haemorrhage within the tumour. AFT levels exceeded 2000ng/ml. Prior to the diagnosis, her health has deteriorated rapidly; she was experiencing severe right upper quadrant pain which radiated to her back and kept her awake at night.
She was also diagnosed with chronic Hepatitis C in 2001. Although interferon/ ribavirin dual therapy was commenced in 2002, it was ineffective. Cirrhosis was diagnosed after a liver biopsy. There is no concurrent problem to note and her health was good until late August 2007. We were informed that curative treatment was not an option as the tumour did not fulfil the Milan criteria for resection, chemotherapy would not be efficacious, and the tumour was too large for radiofrequency ablation. The last option presented was chemoembolisation.
Unfortunately her liver function was poor, she was in Child Pugh group C, and this treatment can only be given to those in Child Pugh group A or B as the risk of adversity in these groups is low. The only feasible option given was palliation and letting the disease progress and take its natural course but this is not acceptable to us. If there is no evidence of extra-hepatic spread of the cancer, would a transplant be possible?
A. It is an extremely difficult decision to decide on the best treatment for a patient with a large HCC and decompensated liver disease. You are quite right in thinking that currently, there is no curative treatment for such a condition except for liver transplantation which would treat her liver cancer together with her decompensating liver cirrhosis.
In many centres, due to acute shortage of cadaveric donor livers, patients with liver cancer beyond the Milan criteria are not transplanted. However, there are centres such as ours where living donor liver transplantation (LDLT) is widely practiced and often patients with large tumour, way beyond Milan criteria but with no extra-hepatic metastastes and also no large venous involvement such as the large hepatic veins and the main portal vein, are being transplanted successfully. The majority of patients transplanted in Asia using LDLT are beyond the Milan criteria as there is no other alternative treatment.
The 3 year survival rate for this group has ranged from 25-40% and it is well known that for patients who have survived the 3 years are likely to continue living beyond this period as the recurrence rate decreases markedly after the first 12-18 months. The main constraint to LDLT is, of course, the availability of a suitable donor.
Wednesday, May 27, 2009
Hepatitis B Virus (HBV) Testing
HBV is transmitted through infected body fluids, including blood, semen, and vaginal fluids (including menstrual blood). It also can be transmitted from a pregnant woman to her child at or near the time of birth.
There are several different HBV tests. These are the HBV tests most commonly done:
* Hepatitis B surface antigen (HBsAg) is the earliest indicator of an active hepatitis B infection. This antigen may be present before symptoms of an HBV infection are present. If this antigen level remains high for more than 6 months, then you will probably become a carrier of HBV, meaning you can transmit it to others throughout your life.
* Hepatitis B surface antibody (HBsAb) usually appears about 4 weeks after HBsAg disappears. The presence of this antibody means that the infection is at the end of its active stage and you cannot pass the virus to others (you are no longer contagious). This antibody also protects you from getting HBV again in the future. The test is done to determine the need for vaccination—the antibody will be present after receiving the HBV vaccine series, showing that you have protection (immunity) from the virus. Occasionally your test may show that you have both the HBsAb and HBsAg antibodies. In this case, you are still contagious.
* Hepatitis B e-antigen (HBeAg) is an HBV protein that is only present during an active HBV infection. This test determines how contagious you are. Testing for this antigen can also be used to monitor the effectiveness of treatment for HBV.
* HBV DNA testing checks for genetic material (DNA) from the hepatitis B virus. The HBV DNA tests measure how much genetic material is present. A high level of HBV DNA means that the virus is multiplying in your body and you are very contagious. If you have a chronic HBV, an elevated viral DNA level means you are at an increased risk for liver damage and may want to consider treatment with antiviral medicine. Testing for HBV DNA is also used to monitor the effectiveness of treatment for chronic HBV infection. HBV DNA testing is a more sensitive test than HBeAg (above) for detecting HBV in the blood.
Other HBV tests are not done as often:
* Hepatitis B core antibody (HBcAb) is an antibody to the hepatitis B core antigen that appears about 1 month after an active HBV infection. It can be found in people who had an infection in the past and in those with long-term (chronic) HBV. It usually is present for life. Blood banks test for this antibody when screening donated blood for hepatitis B.
* Hepatitis B core antibody IgM (HBcAbIgM) is another antibody to the hepatitis B core antigen. It indicates an HBV infection that has occurred within the last 6 months.
* Hepatitis B e-antibody (HBeAb) shows that the active stage of an acute HBV infection is almost over, and your risk of being contagious is greatly reduced.
A hepatitis B vaccine is available to prevent an HBV infection.
Hepatitis D virus (HDV) testing
Infection with the hepatitis D virus (HDV), or delta agent, occurs only in people who are already infected with the hepatitis B virus (HBV). Vaccination against hepatitis B will prevent hepatitis D infection. Hepatitis D infection is rare in the United States and Canada, except among people who inject illegal drugs and those who are frequently exposed to blood products. The hepatitis D test detects HDV antibodies. A positive test indicates only that you have been infected with HDV—it cannot distinguish between an acute or chronic infection. Another test, the HDV RNA test, is needed to determine whether you have an active HDV infection. It does not distinguish between an acute or chronic infection. This test currently is not available except in research settings.
Since hepatitis B infections can be spread through sexual contact, practice safe sex until your test results are returned.
There are several different HBV tests. These are the HBV tests most commonly done:
* Hepatitis B surface antigen (HBsAg) is the earliest indicator of an active hepatitis B infection. This antigen may be present before symptoms of an HBV infection are present. If this antigen level remains high for more than 6 months, then you will probably become a carrier of HBV, meaning you can transmit it to others throughout your life.
* Hepatitis B surface antibody (HBsAb) usually appears about 4 weeks after HBsAg disappears. The presence of this antibody means that the infection is at the end of its active stage and you cannot pass the virus to others (you are no longer contagious). This antibody also protects you from getting HBV again in the future. The test is done to determine the need for vaccination—the antibody will be present after receiving the HBV vaccine series, showing that you have protection (immunity) from the virus. Occasionally your test may show that you have both the HBsAb and HBsAg antibodies. In this case, you are still contagious.
* Hepatitis B e-antigen (HBeAg) is an HBV protein that is only present during an active HBV infection. This test determines how contagious you are. Testing for this antigen can also be used to monitor the effectiveness of treatment for HBV.
* HBV DNA testing checks for genetic material (DNA) from the hepatitis B virus. The HBV DNA tests measure how much genetic material is present. A high level of HBV DNA means that the virus is multiplying in your body and you are very contagious. If you have a chronic HBV, an elevated viral DNA level means you are at an increased risk for liver damage and may want to consider treatment with antiviral medicine. Testing for HBV DNA is also used to monitor the effectiveness of treatment for chronic HBV infection. HBV DNA testing is a more sensitive test than HBeAg (above) for detecting HBV in the blood.
Other HBV tests are not done as often:
* Hepatitis B core antibody (HBcAb) is an antibody to the hepatitis B core antigen that appears about 1 month after an active HBV infection. It can be found in people who had an infection in the past and in those with long-term (chronic) HBV. It usually is present for life. Blood banks test for this antibody when screening donated blood for hepatitis B.
* Hepatitis B core antibody IgM (HBcAbIgM) is another antibody to the hepatitis B core antigen. It indicates an HBV infection that has occurred within the last 6 months.
* Hepatitis B e-antibody (HBeAb) shows that the active stage of an acute HBV infection is almost over, and your risk of being contagious is greatly reduced.
A hepatitis B vaccine is available to prevent an HBV infection.
Hepatitis D virus (HDV) testing
Infection with the hepatitis D virus (HDV), or delta agent, occurs only in people who are already infected with the hepatitis B virus (HBV). Vaccination against hepatitis B will prevent hepatitis D infection. Hepatitis D infection is rare in the United States and Canada, except among people who inject illegal drugs and those who are frequently exposed to blood products. The hepatitis D test detects HDV antibodies. A positive test indicates only that you have been infected with HDV—it cannot distinguish between an acute or chronic infection. Another test, the HDV RNA test, is needed to determine whether you have an active HDV infection. It does not distinguish between an acute or chronic infection. This test currently is not available except in research settings.
Since hepatitis B infections can be spread through sexual contact, practice safe sex until your test results are returned.
Saturday, May 16, 2009
Decompensated Liver Due To Hepatitic C Virus
Q. My mother is 55 years old and suffering from decompensated liver due to hepatitic C virus. she has had 4 episodes of hepatic encephalopathy (3 minor and 1 major due to spontaneous bacterial peritonitis). She has had ascites since that episode. She was diagnosed with Hep C and compensated cirrhosis 2 years ago - she took Interferon but that did not prove effective. Now she has developed caries spine (TB). She is on second line drugs for 4 months which is not proving effective in eradicating the TB virus. Her current results are bilirubin 3.4, ALT 29, PT 14, albumin 1.9, ESR 108, platelets 47.
a) under this condition what would you advise us to do?
b) can she undergo transplant whilst she is on TB (tuberculosis) treatment?
c) would you suggest adding first line drugs for TB (that is rifampicin, pyrazinamide, isoniazid) - she took rifampicin but her bilirubin shot up to 6, so we discontinued.
d) also will hepatitis C re-infect the transplanted liver and if so how long on average does that take? I have heard re-infected hepatitis
C virus is more aggressive and damages the liver causing cirrhosis rapidly
e) I've heard that there are drugs for cirrhosis which are under trials - do you know at what stage these are?
A. a) Your mother has decompensated liver cirrhosis from hepatitis C and requires a liver transplant. Interferon treatment would not be tolerated in this situation. Medical treatment alone would not be adequate in the long run.
b) Yes - she can undergo the transplant on TB treatment if the TB is not active.
c) The use of anti-TB medication is difficult in patients with liver cirrhosis. Do you have the culture results of the TB? This will help the choice of medication. Second line medication may be needed if the first line medication cannot be tolerated.
d) Hepatitis C is likely to re-infect the new liver but treatment can be given after the liver transplant and is usually quite effective. In a very small group of patients, one can have a rapidly recurring form of hepatitis C but this is unusual.
e) There are currently no effective drugs that will treat cirrhosis specifically. Treatment is usually directed at the underlying cause of the liver disease. At the end of the day, we would need to assess the patient before giving you a final result.
a) under this condition what would you advise us to do?
b) can she undergo transplant whilst she is on TB (tuberculosis) treatment?
c) would you suggest adding first line drugs for TB (that is rifampicin, pyrazinamide, isoniazid) - she took rifampicin but her bilirubin shot up to 6, so we discontinued.
d) also will hepatitis C re-infect the transplanted liver and if so how long on average does that take? I have heard re-infected hepatitis
C virus is more aggressive and damages the liver causing cirrhosis rapidly
e) I've heard that there are drugs for cirrhosis which are under trials - do you know at what stage these are?
A. a) Your mother has decompensated liver cirrhosis from hepatitis C and requires a liver transplant. Interferon treatment would not be tolerated in this situation. Medical treatment alone would not be adequate in the long run.
b) Yes - she can undergo the transplant on TB treatment if the TB is not active.
c) The use of anti-TB medication is difficult in patients with liver cirrhosis. Do you have the culture results of the TB? This will help the choice of medication. Second line medication may be needed if the first line medication cannot be tolerated.
d) Hepatitis C is likely to re-infect the new liver but treatment can be given after the liver transplant and is usually quite effective. In a very small group of patients, one can have a rapidly recurring form of hepatitis C but this is unusual.
e) There are currently no effective drugs that will treat cirrhosis specifically. Treatment is usually directed at the underlying cause of the liver disease. At the end of the day, we would need to assess the patient before giving you a final result.
Saturday, April 12, 2008
Liver cancer
Liver cancer is the uncontrolled growth of abnormal cells in the liver. The liver:
* Produces elements that help blood to clot
* Removes or neutralizes poisons, drugs and alcohol
* Manufactures bile, which helps the body to absorb fats and cholesterol
* Helps to maintain normal blood sugar levels
* Regulates several hormones
Cancer in the liver either starts in the liver (primary liver cancer) or spreads to the liver from other places in the body (secondary liver cancer). Primary liver cancer is the most common solid tumor worldwide, with more than one million cases diagnosed each year. However, it is relatively rare in the United States and Europe. The American Cancer Society estimates that more than 17,000 people are diagnosed with primary liver cancer each year. Most of them are over age 40, and more than 15,000 will die of the disease. In the United States, liver cancer is about twice as common in men as in women.
Most liver tumors in the United States have spread (metastasized) to the liver from other organs, most commonly from the colon, rectum, lung, breast, pancreas and stomach. When a cancer spreads to the liver from somewhere else, the cancer cells are the same in both places. For example, if lung cancer spreads to the liver, the cancerous cells in the liver are the same as the cancerous cells in the lung. For that reason, the person is treated for lung cancer, not liver cancer. Doctors would call the cancer in the liver "metastatic lung cancer." The liver is the most common place for cancer to spread.
Only primary liver cancer is treated as liver cancer. There are four main types of primary liver cancer:
1) Hepatocellular carcinoma (hepatoma or HCC) — This cancer accounts for about 84% of primary liver cancers in the United States. It behaves aggressively.
2) Cholangiocarcinoma (bile duct cancer) — This cancer accounts for about 13% of primary liver cancer in the United States. Several conditions increase the risk of developing this cancer, including gallstones, gallbladder inflammation and, sometimes, chronic ulcerative colitis (an inflammation of the large bowel).
3) Angiosarcoma (hemangiosarcoma) — This is a very rare form of liver cancer.
4) Hepatoblastoma — This is a rare type of liver cancer usually found in children younger than age 4.
* Produces elements that help blood to clot
* Removes or neutralizes poisons, drugs and alcohol
* Manufactures bile, which helps the body to absorb fats and cholesterol
* Helps to maintain normal blood sugar levels
* Regulates several hormones
Cancer in the liver either starts in the liver (primary liver cancer) or spreads to the liver from other places in the body (secondary liver cancer). Primary liver cancer is the most common solid tumor worldwide, with more than one million cases diagnosed each year. However, it is relatively rare in the United States and Europe. The American Cancer Society estimates that more than 17,000 people are diagnosed with primary liver cancer each year. Most of them are over age 40, and more than 15,000 will die of the disease. In the United States, liver cancer is about twice as common in men as in women.
Most liver tumors in the United States have spread (metastasized) to the liver from other organs, most commonly from the colon, rectum, lung, breast, pancreas and stomach. When a cancer spreads to the liver from somewhere else, the cancer cells are the same in both places. For example, if lung cancer spreads to the liver, the cancerous cells in the liver are the same as the cancerous cells in the lung. For that reason, the person is treated for lung cancer, not liver cancer. Doctors would call the cancer in the liver "metastatic lung cancer." The liver is the most common place for cancer to spread.
Only primary liver cancer is treated as liver cancer. There are four main types of primary liver cancer:
1) Hepatocellular carcinoma (hepatoma or HCC) — This cancer accounts for about 84% of primary liver cancers in the United States. It behaves aggressively.
2) Cholangiocarcinoma (bile duct cancer) — This cancer accounts for about 13% of primary liver cancer in the United States. Several conditions increase the risk of developing this cancer, including gallstones, gallbladder inflammation and, sometimes, chronic ulcerative colitis (an inflammation of the large bowel).
3) Angiosarcoma (hemangiosarcoma) — This is a very rare form of liver cancer.
4) Hepatoblastoma — This is a rare type of liver cancer usually found in children younger than age 4.
Sunday, February 17, 2008
Fatty liver, Alcoholic hepatitis and Cirrhosis
Fatty liver (steatosis) is the initial and most common consequence of excessive alcohol ingestion. It is potentially reversible. Fatty liver is the accumulation of fat as large droplets of triglyceride. The liver usually enlarges.
Alcoholic hepatitis (steatohepatitis) is a combination of fatty liver, diffuse liver inflammation, and liver necrosis (often focal), all in various degrees of severity. Cirrhosis may be present as well.
Cirrhosis is advanced liver disease characterized by extensive fibrosis that disrupts the normal liver architecture. The amount of fat present varies. Alcoholic hepatitis may coexist.
Iron accumulation in the liver occurs in up to 10% of alcoholics with normal, fatty, or cirrhotic livers. Accumulation is not predicted by iron intake or body iron stores.
Symptoms and Signs
Symptoms match the stage and severity of disease. Symptoms generally become apparent in patients during their 30s; severe problems appear about a decade later.
Fatty liver usually causes no symptoms. In 1⁄3 of patients, the liver is enlarged, smooth, and occasionally tender.
Alcoholic hepatitis ranges from a mild, reversible illness to a life-threatening disease. In moderate cases, patients usually are malnourished and present with fatigue, fever, jaundice, right upper quadrant pain and tenderness. Their condition often deteriorates in the first few weeks of hospitalization.
Severe cases may involve jaundice, ascites, hypoglycemia, electrolyte abnormalities, hepatic insufficiency. Cirrhosis may cause symptoms ranging from minimal to those of alcoholic hepatitis or the complications of end-stage liver disease.
Commonly, portal hypertension (often with esophageal varices and upper GI bleeding, ascites, portal-systemic encephalopathy)
Alcoholic hepatitis (steatohepatitis) is a combination of fatty liver, diffuse liver inflammation, and liver necrosis (often focal), all in various degrees of severity. Cirrhosis may be present as well.
Cirrhosis is advanced liver disease characterized by extensive fibrosis that disrupts the normal liver architecture. The amount of fat present varies. Alcoholic hepatitis may coexist.
Iron accumulation in the liver occurs in up to 10% of alcoholics with normal, fatty, or cirrhotic livers. Accumulation is not predicted by iron intake or body iron stores.
Symptoms and Signs
Symptoms match the stage and severity of disease. Symptoms generally become apparent in patients during their 30s; severe problems appear about a decade later.
Fatty liver usually causes no symptoms. In 1⁄3 of patients, the liver is enlarged, smooth, and occasionally tender.
Alcoholic hepatitis ranges from a mild, reversible illness to a life-threatening disease. In moderate cases, patients usually are malnourished and present with fatigue, fever, jaundice, right upper quadrant pain and tenderness. Their condition often deteriorates in the first few weeks of hospitalization.
Severe cases may involve jaundice, ascites, hypoglycemia, electrolyte abnormalities, hepatic insufficiency. Cirrhosis may cause symptoms ranging from minimal to those of alcoholic hepatitis or the complications of end-stage liver disease.
Commonly, portal hypertension (often with esophageal varices and upper GI bleeding, ascites, portal-systemic encephalopathy)
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