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abnormalities of brain tissue with cirrhosis

Cerebral magnetic resonance imaging reveals marked abnormalities of brain tissue density in patients with cirrhosis without overt hepatic encephalopathy.

Liver Unit, Hospital Clínic, University of Barcelona, Barcelona, Spain. ***@****

We applied advanced magnetic resonance imaging and Voxed based Morphometry analysis to assess brain tissue density in patients with cirrhosis.

Forty eight patients with cirrhosis without overt hepatic encephalopathy (17 Child A, 13 Child B, and 18 Child C) and 51 healthy subjects were matched for age and sex. Seventeen patients had history of overt hepatic encephalopathy, eight of them had minimal hepatic encephalopathy at inclusion, 10 other patients had minimal hepatic encephalopathy at inclusion but without history of previous overt hepatic encephalopathy, and 21 patients had none of these features.

Patients with cirrhosis presented decreased brain density in many areas of the grey and white matter. The extension and size of the affected areas were greater in patients with alcoholic cirrhosis than in those with post-hepatitic cirrhosis and correlated directly with the degree of liver failure and cerebral dysfunction (as estimated by neuropsychological tests and the antecedent of overt hepatic encephalopathy). Twelve additional patients with cirrhosis who underwent liver transplantation were explored after a median time of 11months (7-50months) after liver transplant. At the time of liver transplantation, three patients belonged to class A of the Child-Pugh classification, five to class B and four to class C. Compared to healthy subjects, liver transplant patients showed areas of reduced brain density in both grey and white matter.

These results indicate that loss of brain tissue density is common in cirrhosis, progresses during the course of the disease, is greater in patients with history of hepatic encephalopathy, and persists after liver transplantation. The significance, physiopathology, and clinical relevance of this abnormality cannot be ascertained from the current study.

32 Responses
419309 tn?1326506891
I'm probably going against the current here, but I hesitate to attribute the findings to viral infection itself; the article actually doesn't specifically address hcv, just cirrhosis.  It raises questions about brain matter in relation to ammonia and encephalopathy, but really doesn't address the findings in relation to viral infection.  I'm more inclined to suspect that these findings are more likely related to metabolic toxicity/ammonia due to cirrhosis rather than viral infection or liver fibrosis, especially since the article did not point to similar findings in the pre-cirrhotic patients with liver disease. Just my 2 cents. ~eureka
Avatar universal
Very sad.  Don't mean to hijack your thread but here is some positive news about neuro function for  those people who fight the virus successfully.  I don't know if this applies at all with severe cirrhosis but it does apply to others.  

Avatar universal
Don't worry about hijacking the thread. It's just information and yours is welcome. Here is another recent article about SVR and its "impact on cirrhosis-related histopathological features".

A morphometric and immunohistochemical study to assess the benefit of an svr in hcv cirrhotic patients.


Although annular fibrosis is the hallmark of cirrhosis, other microscopic changes impacting on liver function such as sinusoid capillarization or loss of metabolic zonation are common. A sustained virological response (SVR) may halt fibrosis deposition in hepatitis C virus (HCV) infected patients, but its impact on the other cirrhosis-associated lesions is unknown.

To assess the impact of an SVR on cirrhosis-related histopathological features.

Paired pre- and post-treatment liver biopsies from 38 HCV cirrhotics with an SVR were analysed. Fibrosis was staged by METAVIR and the area of fibrosis by morphometry. Ductular proliferation, metabolic zonation, sinusoid capillarization and hepatic stellate cells activation were assessed by anti-cytokeratin7 (CK7), -glutamine synthetase (GS), -cytochrome P4502E1 (CYP2E1), -CD34 and alpha-smooth muscle actine (αSMA).

After 61 months from an SVR, cirrhosis regression was observed in 61%, and the collagen content decreased in 89%. Although periportal and lobular necroinflammation vanished, portal inflammation persisted in 66%. Ductular proliferation decreased in 92%. Before treatment, metabolic zonation was lost, as shown by GS and CYP2E1, in 71% and 88%, respectively, with normalization in 79% and 73%, after an SVR. Conversely, no changes in sinusoidal capillarization were observed after treatment, as assessed by CD34 (p=0.41) and αSMA (p=0.95). Finally, no differences in all the immunohistochemical scores emerged whether or not cirrhosis persisted.

Cirrhosis regression and fibrosis amount decrease are frequently observed among HCV cirrhotic patients with an SVR. Despite ductular proliferation vanishing and lobular zonation restoration, portal inflammation and sinusoidal capillarization may not regress after viral eradication. (HEPATOLOGY 2012.).

1815939 tn?1377995399
It appears to me that both of these articles demonstrate the need for more education concerning HCV, widespread routine diagnostic testing for HCV, and aggressive treatment of people with HCV. It seems the ramifications of the current approach (basically do nothing until a person has liver disease) are broad and potentially affect far more than just the liver of the person if one considers relationships, ability to work and function well, future medical costs, contributions to society, etc.

Thanks for posting the articles, Mike and Curiouslady.
Avatar universal
Since some of the treatments also may affect the cognitive abilities of some people, it is a catch 22 situation.  
1815939 tn?1377995399
Yes, I agree.

However, I still think there should be widespread education about Hep C and routine testing of everyone to ascertain how many people actually have Hep C (not how many they guess might have it based on faulty numbers). I also think that if people are diagnosed with Hep C they should be educated further, followed up for health problems, and offered treatment options. Right now most people discover by accident that they have Hep C (usually after they already have liver damage of varying degrees), not really an ideal method for addressing a serious and potentially fatal disease, an epidemic, especially when there is an easy blood test available that would diagnose those with Hep C.

Perhaps my term "aggressive treatment" is not very clear. I do not mean that people should be pressured into treatment that they do not want. However, I do think everyone should be tested for Hep C and they should also have the opportunity to be treated after being fully informed of the probable consequences of not treating and of the potential consequences of treating. Some doctors figure if you don't have stage 2 or 3 you don't need treatment, but they are not taking into account the numerous other medical problems Hep C may cause (in addition to liver disease), the person's quality of life, the fact that it is easier to treat younger and healthier individuals that have less liver fibrosis than to wait for them to age and have more disease progression and/or other diseases that may complicate successful treatment.

So when I use the term aggressive, I am really referring to agressive education campaigns, aggressive routine testing and diagnosis, and aggressive treatment if the affected person so desires.  

I know I am passionate about education and diagnosis and treatment, but I really think the current ostrich head in the sand approach (by the governemnt and health officials who are supposed to be dealing with health issues and epidemics and who issue guidelines, policies, and standard of care protocols) just isn't enough.

It is nice to see that Berkeley Free Clinic is offering free Hep C testing. That is a major step in the right direction. Thanks for that bit of welcome news Orphanedhawk.
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