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Suffering from Cirrhosis, want to gain weight and live healthy
I was diagnosed with Pernicious Anemia in 2012, and was advised by the Dr. to take VitB12 shots. ( As Ive deficiency of it) I had lost weight from 85kg to 78kg during that, with platelets down to 35k only and hemoglobin to 4. I recovered with 5 shots ( each shot in alternate day)
In 2014, I vomitted blood due to upper GI bleeding. Endoscopy was done and banding was done (3). I was off alcohol for 1 month post this, but continued post that ( though medication was on, Ciplar LA,Actibile300) Was 88 kg, reduced to 80 kgs recovered the weight in 8 -9 months.
In 2017 Feb, again had Upper GI bleeding and banding was done.(23.02.2017) Again vomitted blood on 24.02.2017 and Dr. did the glu in stomach. with 3 pints of blood transfusion.
Off liquor since 2 months and will continue with the abstinence. Was 85kg when admitted. Within a week was reduced to 70Kg.
No ascites though.
HOw can I recover this lost weight? In the earlier episodes I continued alcohol. But now I have discontinued.
Also is this the end stage of liver disease? HOw much time I might have?. I m 35 years old
In 2014, I vomitted blood due to upper GI bleeding. Endoscopy was done and banding was done (3). I was off alcohol for 1 month post this, but continued post that ( though medication was on, Ciplar LA,Actibile300) Was 88 kg, reduced to 80 kgs recovered the weight in 8 -9 months.
In 2017 Feb, again had Upper GI bleeding and banding was done.(23.02.2017) Again vomitted blood on 24.02.2017 and Dr. did the glu in stomach. with 3 pints of blood transfusion.
Off liquor since 2 months and will continue with the abstinence. Was 85kg when admitted. Within a week was reduced to 70Kg.
No ascites though.
HOw can I recover this lost weight? In the earlier episodes I continued alcohol. But now I have discontinued.
Also is this the end stage of liver disease? HOw much time I might have?. I m 35 years old
Hi
Sorry to hear of your illness.
When you get to the stage of Varices its almost certainly very advanced scarring of the Liver. Cirrhosis is the end stage of the disease, not your life, although obviously there is a link.
You are still pretty young and if you stay sober and look after yourself you may get some Liver function back and have many years left.
Sorry to hear of your illness.
When you get to the stage of Varices its almost certainly very advanced scarring of the Liver. Cirrhosis is the end stage of the disease, not your life, although obviously there is a link.
You are still pretty young and if you stay sober and look after yourself you may get some Liver function back and have many years left.
All cirrhosis in considered to be end stage liver disease.
This is further defined as compensated cirrhosis where the liver can still perform it daily functions and decompensated cirrhosis where the liver is no longer able to keep up.
Decompensated cirrhosis is defined by the development of jaundice, ascites, variceal hemorrhage, or hepatic encephalopathy. Survival is poor in patients with decompensated cirrhosis and they should be considered for liver transplantation.
Unfortunately there is no going back from decompensated cirrhosis the only way to improve your health will be to have a liver transplant.
Of course this is up to your doctor to determine if you still have enough function remaining that discontinuation of consumption of alcohol will be enough in your case.
The loss of weight could be caused by loss of muscle mass as this is another symptom of decompensated cirrhosis.
"Muscle wasting is defined as the progressive and generalized loss of muscle mass. Muscle depletion is a common feature of chronic liver disease found in approximately 40% of patients with cirrhosis."
Here is a good article from the U.S. Veterans administration about decompensated cirrhosis.
https://www.hepatitis.va.gov/patient/complications/cirrhosis/decompensated.asp
If you do need a liver transplant to survive you will need to have a documented period of abstinence from alcohol. You will need to qualify to be on the transplant list based on you medical condition and other factors. You should discuss your eligibility to be listed with your liver specialist.
Has your doctor discussed the option of liver transplantation? Are you seeing a hepatologist associated with a liver transplant center?
Do you know your MELD score? The MELD is how patients are ranked on the transplant list based on severity of illness.
Know one can say how much time you have. If you stay away from alcohol it will slow or stop you progression you may even be able to improve with time.
Really the choice is up to you.
Best of luck
This is further defined as compensated cirrhosis where the liver can still perform it daily functions and decompensated cirrhosis where the liver is no longer able to keep up.
Decompensated cirrhosis is defined by the development of jaundice, ascites, variceal hemorrhage, or hepatic encephalopathy. Survival is poor in patients with decompensated cirrhosis and they should be considered for liver transplantation.
Unfortunately there is no going back from decompensated cirrhosis the only way to improve your health will be to have a liver transplant.
Of course this is up to your doctor to determine if you still have enough function remaining that discontinuation of consumption of alcohol will be enough in your case.
The loss of weight could be caused by loss of muscle mass as this is another symptom of decompensated cirrhosis.
"Muscle wasting is defined as the progressive and generalized loss of muscle mass. Muscle depletion is a common feature of chronic liver disease found in approximately 40% of patients with cirrhosis."
Here is a good article from the U.S. Veterans administration about decompensated cirrhosis.
https://www.hepatitis.va.gov/patient/complications/cirrhosis/decompensated.asp
If you do need a liver transplant to survive you will need to have a documented period of abstinence from alcohol. You will need to qualify to be on the transplant list based on you medical condition and other factors. You should discuss your eligibility to be listed with your liver specialist.
Has your doctor discussed the option of liver transplantation? Are you seeing a hepatologist associated with a liver transplant center?
Do you know your MELD score? The MELD is how patients are ranked on the transplant list based on severity of illness.
Know one can say how much time you have. If you stay away from alcohol it will slow or stop you progression you may even be able to improve with time.
Really the choice is up to you.
Best of luck
1 Comments
Gene Variant Predicts Liver Recovery After HCV Cure
May 08, 2017
CHICAGO -- Genetic variation can help predict which patients with decompensated cirrhosis will recover liver function after treatment for hepatitis C (HCV), a researcher said here.
The new direct-acting agents (DAAs) against HCV lead to viral cures in most cases, and the liver recovers some of its lost function even when liver damage has been extensive, noted Winston Dunn, MD, of the University of Kansas Medical Center in Kansas City, Kan.
But some patients with decompensated cirrhosis do not recover liver function and still are candidates for transplant -- but it is difficult to pick them out before treatment, Dunn said at Digestive Disease Week 2017.
In a prospective cohort study, Dunn's group showed that a single nucleotide polymorphism (SNP) in the gene -- dubbed Patatin-like Phospholipase Domain Containing 3 (PNPLA3) -- helped predict recovery.
It's the first time a genetic variant has been observed to be associated with recovery after successful HCV therapy, Dunn told MedPage Today.
The gene has been studied in steatosis, fatty liver disease, and fibrosis, commented Norah Terrault, MD, of the University of California San Francisco, "but nobody has looked at it as a marker for recovery."
"This is sort of the flip side, and I think there's some reason to think that it could be a relevant marker," she told MedPage Today.
But she cautioned that the study is small, so the data have to be regarded as preliminary.
If the data are confirmed, they could have an important clinical application -- helping doctors decide whether to treat HCV patients with advanced liver disease who are waiting for a transplant.
"We have been concerned that, for some of these patients, we could actually be doing them harm by curing their HCV," Terrault said, and thereby making them less eligible for transplant, which is the "definitive treatment" for cirrhosis.
"So far, we really haven't been able to identify any [variables] that could help us pick out who's going to get better and who's not after we cure their HCV," she said.
After successful DAA treatment, Dunn said, "half to two-thirds of patients will get better clinically but the remaining patients will struggle along and may get worse."
The PNPLA3 gene plays a role in the risk for fatty liver; people with two copies of the C allele at the SNP Rs738409 have a lower chance of developing steatosis, while one or two copies of the G allele yield an increased risk.
"We thought that patients with decompensated cirrhosis might suffer injury from hepatitis C or they might have a synergistic effect of hepatitis C and fatty liver," Dunn said.
To test the idea, they enrolled 35 patients with Child-Pugh Class B or C cirrhosis because of HCV infection who were going to have interferon-free therapy with DAAs.
They excluded people with active alcohol consumption, HIV or hepatitis B co-infection, other causes of cirrhosis, a history of hepatocellular carcinoma, a previous liver transplant, or unsuccessful HCV treatment with an interferon-containing regimen.
Dunn's group collected DNA from each patient using a cheek swab and sequenced it to determine the allelic status of PNPLA3 -- CC, CG, or GG.
The primary outcome of the analysis was changes in Child-Pugh score and Model for End-Stage Liver Disease (MELD) score after DAA treatment, Dunn said.
Thirty patients were cured of HCV by the treatment, where cure was defined in the usual way as no detectable HCV virus 12 weeks after the end of therapy (SVR12).
Two patients initially responded but relapsed, one with two copies of the C allele and one with a C and a G, the researchers reported. One patient (CG) had a liver transplant and two (both with CC) died before SVR12.
Of the 30 who were cured, 16 had two copies of the C allele, and the remaining 14 had either one or two copies of the G allele.
At baseline, patients with the CC variant had a significantly higher BMI (35 versus 29, on average) but similar Child-Pugh and MELD scores at 8.6 and 13 versus 7.6 and 14, respectively.
After SVR12, the 16 patients with a CC genotype saw both scores improve on average, by 1.7 points on the Child-Pugh score and 1.67 points on the MELD score. Specifically, 13 patients (81 %) improved the Child-Pugh score and eight (50%) had improved MELD score by at least one point. None saw scores worsen.
In contrast, patients with at least one G allele did worse -- only five (36%) had a better Child-Pugh score and just four (29%) improved their MELD score by at least one point, they reported. At the same time, three patients (21%) had a worse Child-Pugh score and 4 (29%) lost at least a point on the MELD score.
https://www.medpagetoday.com/meetingcoverage/ddw/65113
May 08, 2017
CHICAGO -- Genetic variation can help predict which patients with decompensated cirrhosis will recover liver function after treatment for hepatitis C (HCV), a researcher said here.
The new direct-acting agents (DAAs) against HCV lead to viral cures in most cases, and the liver recovers some of its lost function even when liver damage has been extensive, noted Winston Dunn, MD, of the University of Kansas Medical Center in Kansas City, Kan.
But some patients with decompensated cirrhosis do not recover liver function and still are candidates for transplant -- but it is difficult to pick them out before treatment, Dunn said at Digestive Disease Week 2017.
In a prospective cohort study, Dunn's group showed that a single nucleotide polymorphism (SNP) in the gene -- dubbed Patatin-like Phospholipase Domain Containing 3 (PNPLA3) -- helped predict recovery.
It's the first time a genetic variant has been observed to be associated with recovery after successful HCV therapy, Dunn told MedPage Today.
The gene has been studied in steatosis, fatty liver disease, and fibrosis, commented Norah Terrault, MD, of the University of California San Francisco, "but nobody has looked at it as a marker for recovery."
"This is sort of the flip side, and I think there's some reason to think that it could be a relevant marker," she told MedPage Today.
But she cautioned that the study is small, so the data have to be regarded as preliminary.
If the data are confirmed, they could have an important clinical application -- helping doctors decide whether to treat HCV patients with advanced liver disease who are waiting for a transplant.
"We have been concerned that, for some of these patients, we could actually be doing them harm by curing their HCV," Terrault said, and thereby making them less eligible for transplant, which is the "definitive treatment" for cirrhosis.
"So far, we really haven't been able to identify any [variables] that could help us pick out who's going to get better and who's not after we cure their HCV," she said.
After successful DAA treatment, Dunn said, "half to two-thirds of patients will get better clinically but the remaining patients will struggle along and may get worse."
The PNPLA3 gene plays a role in the risk for fatty liver; people with two copies of the C allele at the SNP Rs738409 have a lower chance of developing steatosis, while one or two copies of the G allele yield an increased risk.
"We thought that patients with decompensated cirrhosis might suffer injury from hepatitis C or they might have a synergistic effect of hepatitis C and fatty liver," Dunn said.
To test the idea, they enrolled 35 patients with Child-Pugh Class B or C cirrhosis because of HCV infection who were going to have interferon-free therapy with DAAs.
They excluded people with active alcohol consumption, HIV or hepatitis B co-infection, other causes of cirrhosis, a history of hepatocellular carcinoma, a previous liver transplant, or unsuccessful HCV treatment with an interferon-containing regimen.
Dunn's group collected DNA from each patient using a cheek swab and sequenced it to determine the allelic status of PNPLA3 -- CC, CG, or GG.
The primary outcome of the analysis was changes in Child-Pugh score and Model for End-Stage Liver Disease (MELD) score after DAA treatment, Dunn said.
Thirty patients were cured of HCV by the treatment, where cure was defined in the usual way as no detectable HCV virus 12 weeks after the end of therapy (SVR12).
Two patients initially responded but relapsed, one with two copies of the C allele and one with a C and a G, the researchers reported. One patient (CG) had a liver transplant and two (both with CC) died before SVR12.
Of the 30 who were cured, 16 had two copies of the C allele, and the remaining 14 had either one or two copies of the G allele.
At baseline, patients with the CC variant had a significantly higher BMI (35 versus 29, on average) but similar Child-Pugh and MELD scores at 8.6 and 13 versus 7.6 and 14, respectively.
After SVR12, the 16 patients with a CC genotype saw both scores improve on average, by 1.7 points on the Child-Pugh score and 1.67 points on the MELD score. Specifically, 13 patients (81 %) improved the Child-Pugh score and eight (50%) had improved MELD score by at least one point. None saw scores worsen.
In contrast, patients with at least one G allele did worse -- only five (36%) had a better Child-Pugh score and just four (29%) improved their MELD score by at least one point, they reported. At the same time, three patients (21%) had a worse Child-Pugh score and 4 (29%) lost at least a point on the MELD score.
https://www.medpagetoday.com/meetingcoverage/ddw/65113
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