Suggest Treatment For Chronic Hepatitis C Infection
Here’s what the tests did show: I had blood work, liver biopsy, ultra sound scan of liver and spleen, that I have Hepatitis C type 1A and a 6.7 viral load. It also showed low blood platelets (123), and high iron and ferretin levels, which the doctor believes could be hemochromatosis. The ultra sound and a physical exam indicated a slight enlargement of my spleen. I have lost 20 to 25 pounds in the past 6 months to a year which is the main reason for all the tests.
The first infectious disease specialist locally in Saginaw Michigan said 80% of my liver has cirrhosis and is irreversible, and the other 20% is fibrosis the progression of which can be halted. He wants to put me on medication which has a 92% cure rate i.e., peg interferon, ribavirin, and one of the brand new medications, sofosbuvir. Being confused by the cirrhosis vs fibrosis issue and not wanting to endure the interferon and ribavirin side effects, or potential health risks, I sought a second opinion from the XXXXXXX Clinic in Ohio. When I told the specialist at the XXXXXXX Clinic what the Saginaw physician had said in terms of 80% cirrhosis and 20% fibrosis he said he doesn’t even know what that means. He said once you are diagnosed with cirrhosis, you have cirrhosis. It is never cirrhosis with a small percentage of fibrosis, its just cirrhosis. As far as the prescribed drug regime he said there is no longer a need for Interferon and ribavirin and is going to put me on a combination of Sofosbuvir and Simeprevir which have essentially no side effects and also a 92% cure rate.
What I am wondering is if you could comment on what I have told you in terms of my symptoms and whether or not you think it sounds like stage three liver disease. The Saginaw specialist said I am stage three moving towards stage four. Personally I doubt the disease is all that advanced because I feel fine and I don’t have many symptoms that would confirm this diagnosis. What do you think?
Also, what do you think about the two different med regimes? Do you think what I have described sounds consistent with late stage 3 liver disease? The XXXXXXX specialist says with liver biopsies you don’t always see what you think you see. He eventually wants to do another biopsy which will be originated from my neck. I presume this is to compare with the other horizontal sample which was taken from my side. This would give him a better look at whether there is some bridging or if the bridges are starting to connect, or whatever. What do you think? I realize this is a lot of information but I am wondering if you concur with one physician or the other in terms of diagnosis and prescribed med regime.
explained
Detailed Answer:
Hello and Welcome
I appreciate your concern.
The histologic features of chronic HCV infection are well defined. Two components are considered: activity and fibrosis.
Activity (grade). Activity is gauged by the number of mononuclear inflammatory cells present in and around the portal areas, and by the number of dead or dying hepatocytes. Changes in activity do not imply progressive disease.
Fibrosis (stage). The fibrotic response to HCV infection is variable. Fibrosis implies possible progression to cirrhosis. In mild cases, fibrosis is limited to the portal and peri portal areas. More advanced changes are defined by fibrosis that extends from one portal area to another. The term for this is "bridging fibrosis." In some, this reaction evolves into cirrhosis.
Lack of Specific Findings on Liver biopsy is a problem in many situations. All histologic abnormalities in HCV infection—individually and collectively—are seen in other viral and non viral liver diseases. Even interpretation of fibrosis requires caution. A previous heavy user of alcohol, even though abstinent for several months prior to liver biopsy, may have significant hepatic fibrosis. Without concurrent changes of steato hepatitis, the fibrosis might be erroneously ascribed to HCV when, in fact, alcohol may have been more important in the activation of stellate cells and consequent fibrosis.
The classification you are being provided is confusing.
you have chronic hepatitis C with cirrhosis. Now the cirrhosis needs to be assessed whether its compensated or decompensated and in which class i.e based on bilirubin, albumin, pro thrombin, encephalopathy a score called CHILD PUGH score is calculated to assess the severity of the chronic liver diseases.
Spleen enlargement is a sign of portal hypertension , though it can occur independently. weight loss can occur simultaneously in CLD.
For Hemochromatosis the most accurate test is a liver biopsy, get it done in consult with your doctor.
The combination of sofosbuvir plus simeprivir is an option but simeprivir is not recommended or used with great caution in cirrhosis. Ribavirin can be an alternative for simeprivir , please consult a consultant hepatologist to tailor the treatment accordingly.
Let me know if you have any query
wishing you best of health
Thanks
However, the XXXXXXX Clinic seems to be saying that I am at stage 3 possibly even 2, and that what I have is liver Fibrosis. According to them (if I am understanding correctly) if you have Cirrhosis you are in stage 4. Is my confusion just a matter of terminology? When does Fibrosis start being called Cirrhosis?
Thanks again.
explained
Detailed Answer:
hello again, hope you are fine
Let me make it more clear.
Anything that damages the liver over many years can lead the liver to form scar tissue. Fibrosis is the first stage of liver scarring.
When scar tissue builds up and takes over most of the liver, this is a more serious problem called cirrhosis.
compensation or de compensation depends upon bilirubin, albumin, pro thrombin, encephalopathy (CHILD PUGH score ), to see if synthetic functions are intact or not.
In August 2014, the Infectious Diseases Society of XXXXXXX and the XXXXXXX Associations for the Study of Liver Diseases, in collaboration with the International Antiviral Society-USA, released a new section to their online guidelines (hcvguidelines.org) to cover information on when to begin therapy and in which patients with chronic hepatitis C virus (HCV) infection. The new section is intended to aid clinicians in prioritizing treatment to patients who will benefit most.
The guidelines propose that because all patients cannot receive treatment immediately upon the approval of new agents, priority should be given to those with the most urgent need. The recommendations include the following
•Patients with advanced fibrosis, those with compensated cirrhosis, liver transplant recipients, and those with severe extraheptic hepatitis are to be given the highest priority for treatment
•Based on available resources, patients at high risk for liver-related complications and severe extrahepatic hepatitis C complications should be given high priority for treatment
•Treatment decisions should balance the anticipated reduction in transmission versus the likelihood of reinfection in patients whose risk of HCV transmission is high and in whom HCV treatment may result in a reduction in transmission (eg, men who have high-risk sex with men, active injection drug users, incarcerated persons, and those on hemodialysis)
Thanks