Aa
Lack of brain function
I finished my 48 weeks of tx on March 18, 2011. Thankfully all of my sx have gone away except one. This one has me kind of scared that it won't go away. I have lost the ability to take in very much information. I get totally confused. By not being able to take in much info, I mean that when I watch TV on my small screen TV, I can't see the details like what the people are wearing. It is all I can do to get the story line. If there are any words on the screen that need to be read, I'm in big trouble because I am never able to read all of the words before they change screens. I used to be very quick witted, which was great fun in conversations, but now it takes me so long to come up with a response to people that I prefer to stay away from people because it is so frustrating.
Has anybody else experienced this after tx, and how long did it take to go away if ever?
Has anybody else experienced this after tx, and how long did it take to go away if ever?
thank your for the informative link.
if i thought that i could remain in compensated cirrhosis for the next 5 to 7 years without decompensation, i might try to wait for the interferon sparing treatment. i slipped into cirrhosis after about 25 years with the infection. i believe antibiotics caused a rapid progression into cirrhosis.
i am very aware of the dangers of these drugs and i expect to feel much worse after i treat than prior to treatment, but the prospect of a slow miserable death as a result of end stage liver disease is not something i care to experience.
blessings
eric
if i thought that i could remain in compensated cirrhosis for the next 5 to 7 years without decompensation, i might try to wait for the interferon sparing treatment. i slipped into cirrhosis after about 25 years with the infection. i believe antibiotics caused a rapid progression into cirrhosis.
i am very aware of the dangers of these drugs and i expect to feel much worse after i treat than prior to treatment, but the prospect of a slow miserable death as a result of end stage liver disease is not something i care to experience.
blessings
eric
I found an article this morning about interferon treatment and it's affects on the brain. I posted the link so that everyone could read it. Personally, I feel that the risks are much greater than we have been told. Please check it out and let me know what you think.
here is the introduction for the results section of the article i posted above.
Progression to Cirrhosis in Hepatitis C Patients: An Age-dependent Process
Pierre Pradat; Nicolas Voirin; Hans Ludger Tillmann; Michèle Chevallier; Christian Trépo
Authors and Disclosures
Posted: 04/23/2007; Liver International. 2007;27(3):335-339. © 2007 Blackwell Publishing
Abstract and Introduction
Abstract
Background: Age at infection is known to be associated with disease progression rate in hepatitis C virus (HCV) infected patients. The aim of this study was to assess when cirrhosis is expected to occur according to host and viral factors.
Methods: Fibrosis progression was studied in 247 naive HCV patients using multiple regression analysis. The expected age at cirrhosis was calculated for each patient.
Results: Progression rate was 0.13, 0.14, 0.27, and 0.36 U of fibrosis/year for patients with age at infection ≤19, 20–24, 25–36 and ≥37 years, respectively. Age at infection above 37 years was independently associated with fast progression (rate>0.13; P=0.001). Body mass index >25 kg/m2 and alanine aminotransferase>3 × ULN are also possibly associated with faster progression. Based on progression rates, the expected age at cirrhosis is 65.4, 64.6, 64.8 and 69.4 years for age at infection ≤19, 20–24, 25–36, ≥37 years, respectively.
Conclusion: Most HCV patients, if untreated, are expected to develop cirrhosis at about 65 years, irrespective of the age at infection. Thus, age itself seems even more important than age at infection for predicting the occurrence of liver cirrhosis. A specific active monitoring and therapeutic approach should be adopted in older patients to prevent progression to cirrhosis and its complications.
Progression to Cirrhosis in Hepatitis C Patients: An Age-dependent Process
Pierre Pradat; Nicolas Voirin; Hans Ludger Tillmann; Michèle Chevallier; Christian Trépo
Authors and Disclosures
Posted: 04/23/2007; Liver International. 2007;27(3):335-339. © 2007 Blackwell Publishing
Abstract and Introduction
Abstract
Background: Age at infection is known to be associated with disease progression rate in hepatitis C virus (HCV) infected patients. The aim of this study was to assess when cirrhosis is expected to occur according to host and viral factors.
Methods: Fibrosis progression was studied in 247 naive HCV patients using multiple regression analysis. The expected age at cirrhosis was calculated for each patient.
Results: Progression rate was 0.13, 0.14, 0.27, and 0.36 U of fibrosis/year for patients with age at infection ≤19, 20–24, 25–36 and ≥37 years, respectively. Age at infection above 37 years was independently associated with fast progression (rate>0.13; P=0.001). Body mass index >25 kg/m2 and alanine aminotransferase>3 × ULN are also possibly associated with faster progression. Based on progression rates, the expected age at cirrhosis is 65.4, 64.6, 64.8 and 69.4 years for age at infection ≤19, 20–24, 25–36, ≥37 years, respectively.
Conclusion: Most HCV patients, if untreated, are expected to develop cirrhosis at about 65 years, irrespective of the age at infection. Thus, age itself seems even more important than age at infection for predicting the occurrence of liver cirrhosis. A specific active monitoring and therapeutic approach should be adopted in older patients to prevent progression to cirrhosis and its complications.
i am sorry you had a hard time with post treatment side effects. please take a look at the following information. the median age for progression to cirrhosis is 60-65. your information is out of date.
http://www.medscape.com/viewarticle/554637_3
Patients' characteristics are given in Table 1 . The median age at infection was 25 years (25% quartile= 19 years; 75% quartile=37 years), and the median disease duration was 14.5 years (25% quartile=10.2 years; 75% quartile=19.4 years).
The median rate of progression for all 247 patients was 0.13 U of fibrosis/year which gives an estimated time to cirrhosis of 30.8 years. This rate of fibrosis progression varied according to age at infection (Fig. 1) and was 0.13 for patients infected before 20 years of age, 0.14 for 20–24 years, 0.27 for 25–36 years and 0.36 for patients with an age at infection above 36 years (Kruskal–Wallis test gives P25 kg/m2 had a significantly higher progression rate than patients below this threshold. ALT level was also associated with fibrosis progression with a faster rate when ALT>3 × ULN. However, there was no association between the rate of progression and gender or genotype ( Table 2 ).
(Enlarge Image)
Figure 1.
(a) Rate of fibrosis progression according to age at infection given in quartiles. (b) Time to cirrhosis according to age at infection given in quartiles.
Based on the median rate of progression, patients were then classified as fast progressors (progression rate above 0.13 U of fibrosis/year) and slow progressors (progression rate below 0.13) and univariate and multivariate analysis were conducted to detect factors possibly associated with a fast progression. Table 3 indicates that only age at infection above 36 years seems to be associated with fast fibrosis progression. However, as BMI information was only available for a limited number of cases (n=25), this variable was excluded from the multivariate model.
Based on each individual rate of progression, the estimated age at cirrhosis in the absence of treatment was then calculated for all patients according to disease duration. The estimated age at cirrhosis was 65.4, 64.6, 64.8 and 69.4 years for patients with an age at infection ≤19, 20–24, 25–36 and ≥37 years, respectively (P=0.004). Thus, except for the latter group, all patients were calculated to develop liver cirrhosis at the age of approximately 65 years.
To see whether age at cirrhosis varied according to particular patients' profiles, the estimated age at cirrhosis was presented according to three parameters: age at infection, gender and genotype (Fig. 2). Although the number of patients in each category is rather small, this figure indicates that only women with an age at infection below 37 years and infected by a genotype non-1 have a much higher estimated age at cirrhosis (89 years). In all other groups, age at cirrhosis is quite homogeneous and around 60–65 years (P=0.11).
(Enlarge Image)
Fgure 2.
Estimated age at cirrhosis (in years) according to age at infection, gender and genotype (n=137).
http://www.medscape.com/viewarticle/554637_3
Patients' characteristics are given in Table 1 . The median age at infection was 25 years (25% quartile= 19 years; 75% quartile=37 years), and the median disease duration was 14.5 years (25% quartile=10.2 years; 75% quartile=19.4 years).
The median rate of progression for all 247 patients was 0.13 U of fibrosis/year which gives an estimated time to cirrhosis of 30.8 years. This rate of fibrosis progression varied according to age at infection (Fig. 1) and was 0.13 for patients infected before 20 years of age, 0.14 for 20–24 years, 0.27 for 25–36 years and 0.36 for patients with an age at infection above 36 years (Kruskal–Wallis test gives P25 kg/m2 had a significantly higher progression rate than patients below this threshold. ALT level was also associated with fibrosis progression with a faster rate when ALT>3 × ULN. However, there was no association between the rate of progression and gender or genotype ( Table 2 ).
(Enlarge Image)
Figure 1.
(a) Rate of fibrosis progression according to age at infection given in quartiles. (b) Time to cirrhosis according to age at infection given in quartiles.
Based on the median rate of progression, patients were then classified as fast progressors (progression rate above 0.13 U of fibrosis/year) and slow progressors (progression rate below 0.13) and univariate and multivariate analysis were conducted to detect factors possibly associated with a fast progression. Table 3 indicates that only age at infection above 36 years seems to be associated with fast fibrosis progression. However, as BMI information was only available for a limited number of cases (n=25), this variable was excluded from the multivariate model.
Based on each individual rate of progression, the estimated age at cirrhosis in the absence of treatment was then calculated for all patients according to disease duration. The estimated age at cirrhosis was 65.4, 64.6, 64.8 and 69.4 years for patients with an age at infection ≤19, 20–24, 25–36 and ≥37 years, respectively (P=0.004). Thus, except for the latter group, all patients were calculated to develop liver cirrhosis at the age of approximately 65 years.
To see whether age at cirrhosis varied according to particular patients' profiles, the estimated age at cirrhosis was presented according to three parameters: age at infection, gender and genotype (Fig. 2). Although the number of patients in each category is rather small, this figure indicates that only women with an age at infection below 37 years and infected by a genotype non-1 have a much higher estimated age at cirrhosis (89 years). In all other groups, age at cirrhosis is quite homogeneous and around 60–65 years (P=0.11).
(Enlarge Image)
Fgure 2.
Estimated age at cirrhosis (in years) according to age at infection, gender and genotype (n=137).
I believe you have misinterpreted what I wrote. I also think you have misinterpreted some of the other information available to you. I am sorry that you are one of the unfortunate few who have developed awful symptoms as a result of treatment and very sorry if I have offended you in some way. However, if this were such a benign virus than why would everyone be so concerned about getting rid of it? Actually, there are other diseases that can be stimulated through Hep C infection and not just liver failure but I think the rate of never developing cirrhosis is more like 70% rather than 80 to 90%. I recall a poster indicating that she was stage 0 for more than 20 years and then within a few more went into stage 2 to 3 with some bridging. The court is still out on the actual incidence of decompensation because people are still alive. Hopefully, you will find a way to live a good life despite all. You probably made a good decision with what you knew at the time but were terribly unlucky.
In response to your post about "natural progression" ... I was there. You are 100% wrong. Ou rlocal Hep C specialist also attributes it all to interferon / ribavirin.
What I have is not "natural progression." Upon cessation of interferon, I had an explosion of bizarre symptoms in my body that have not until recently "plateaued" (all of my nails have gone icky - it's horrifying). My nether regions have psoriasis. Some days I fear I will lose the ability to ambulate - other days are good. I have mental lability - way up, way down - recognized neurological side-effect. It's easing as time passes.
my ankles, feet, knees, hips, wrists, fingers, palms, right elbow. all have developed arthritis in the last two years, all starting about two months cessation of treatment and steadily getting worse. If i can't stop it, it will kill me because i won't live as a cripple in pain.
I am getting through all this. I have no choice. I pray and meditate every day. I try not to be angry. Anger just ruins and hurts me.
But I am telling you that I was counseled by the doctors that I would have "fatigue and flu like symptoms." I read the literature and warnings that accomapnied the drugs. "Psoriasis" went right over my head - i had no idea that would mean that I might wind up socially isolated due to plaques where the sun doesn't shine. Psoriatic arthritis was not mentioned.
Neurological brain damage was not mentioned.
I informed my doctor of the "serious side effect" of skin rashes as the literature told me to do - he just shrugged. At the end of treatment when I asked him about the skin rashes, he said, "Oh, they'll go away"
One month post-treatment to 3 months post treatment, I could not eat any even moderately spicy food - it burnt my mouth so bad. That is not natural progression. That is bizarre, "you have whacked out my body" stuff.
The worst side effects may come after treatment is stopped.
The following is from 2002, so it may be dated and one may want to look at more recent statistics.
"Seventy-five to 85 percent of those exposed to the virus develop chronic infection. But if you are chronically infected, there is an 80 to 90 percent chance that you will never develop cirrhosis, and a 95 to 99 percent chance that you will not die from chronic liver disease."
http://www.hepcprimer.com/patient/book_excerpt.html
I have lost my physical powers from interferon / ribavirin. I had no idea it was possible. I wake up most mornings feeling like I have been in a bar fight, i hurt so bad. It is hard, because if one is in a fight or an accident, one recovers. Inteferon / ribavirin kicks my butt every day and will do so for the rest of my life.
What I have is not "natural progression." Upon cessation of interferon, I had an explosion of bizarre symptoms in my body that have not until recently "plateaued" (all of my nails have gone icky - it's horrifying). My nether regions have psoriasis. Some days I fear I will lose the ability to ambulate - other days are good. I have mental lability - way up, way down - recognized neurological side-effect. It's easing as time passes.
my ankles, feet, knees, hips, wrists, fingers, palms, right elbow. all have developed arthritis in the last two years, all starting about two months cessation of treatment and steadily getting worse. If i can't stop it, it will kill me because i won't live as a cripple in pain.
I am getting through all this. I have no choice. I pray and meditate every day. I try not to be angry. Anger just ruins and hurts me.
But I am telling you that I was counseled by the doctors that I would have "fatigue and flu like symptoms." I read the literature and warnings that accomapnied the drugs. "Psoriasis" went right over my head - i had no idea that would mean that I might wind up socially isolated due to plaques where the sun doesn't shine. Psoriatic arthritis was not mentioned.
Neurological brain damage was not mentioned.
I informed my doctor of the "serious side effect" of skin rashes as the literature told me to do - he just shrugged. At the end of treatment when I asked him about the skin rashes, he said, "Oh, they'll go away"
One month post-treatment to 3 months post treatment, I could not eat any even moderately spicy food - it burnt my mouth so bad. That is not natural progression. That is bizarre, "you have whacked out my body" stuff.
The worst side effects may come after treatment is stopped.
The following is from 2002, so it may be dated and one may want to look at more recent statistics.
"Seventy-five to 85 percent of those exposed to the virus develop chronic infection. But if you are chronically infected, there is an 80 to 90 percent chance that you will never develop cirrhosis, and a 95 to 99 percent chance that you will not die from chronic liver disease."
http://www.hepcprimer.com/patient/book_excerpt.html
I have lost my physical powers from interferon / ribavirin. I had no idea it was possible. I wake up most mornings feeling like I have been in a bar fight, i hurt so bad. It is hard, because if one is in a fight or an accident, one recovers. Inteferon / ribavirin kicks my butt every day and will do so for the rest of my life.
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