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when to start treatment

I think I've had HCV for 30 years. At 18 I was diagnosed with nonA nonB hep, now nonA nonB is HepC - I had 3 biopsy's and all results mild stage 1. I have type 1a - I am confused when you should start treatment. Early or late stage.  
3 Responses
408795 tn?1324939275
That's a question you need to talk over with your doctor, your wife or someone who is close to you.  Nobody on this forum, even if they're a doctor can tell you when to treat.   Or they shouldn't tell you, there's tons of information in the archives and all the posts that are on this forum.  The bottom line is you need to decide when to treat on your own b/c it's a personal decision, and that's the answer.  I will leave you with something off of a link, but the link will most likely be zapped off.  Forum guidelines are sometimes violated for whatever reason.  Good luck with your decision.

http://digestive.niddk.nih.gov/ddiseases/pubs/chronichepc/#g

Who should be treated?
Patients with anti-HCV, HCV RNA, elevated serum aminotransferase levels, and evidence of chronic hepatitis on liver biopsy, and with no contraindications, should be offered therapy with the combination of peginterferon and ribavirin. The National Institutes of Health Consensus Development Conference Panel recommended that therapy for hepatitis C be limited to those patients who have histological evidence of progressive disease. Thus, the panel recommended that all patients with fibrosis or moderate to severe degrees of inflammation and necrosis on liver biopsy should be treated and that patients with less severe histological disease be managed on an individual basis. Patient selection should not be based on the presence or absence of symptoms, the mode of acquisition, the genotype of HCV RNA, or serum HCV RNA levels.

Between 30 and 40 percent of patients with chronic hepatitis C have normal serum aminotransferase levels. These patients usually have mild disease that is unlikely to progress. Nevertheless, such patients may wish to be treated and, indeed, response rates to peginterferon and ribavirin appear to be independent of serum aminotransferase levels. Patients who prefer not to be treated at present should be monitored as advances in the field may ultimately lead to more effective and better tolerated therapies. When questions arise regarding treatment, liver biopsy can be helpful in documenting the level of disease activity and liver fibrosis and thus the advisability of waiting for future improvements in therapy.

Patients with cirrhosis can be offered therapy if they do not have signs of decompensation, such as ascites, persistent jaundice, wasting, variceal hemorrhage, or hepatic encephalopathy. However, combination therapy has not been shown to improve survival or the ultimate outcome in patients with pre-existing cirrhosis.

The role of peginterferon and ribavirin therapy in children with hepatitis C remains uncertain. Ribavirin has yet to be evaluated adequately in children, and pediatric doses and safety have not been established. Thus, if children with hepatitis C are treated, monotherapy is recommended, and ribavirin should not be used outside of controlled clinical trials.

People with both HCV and HIV infection should be offered therapy for hepatitis C as long as there are no contraindications. Indeed, hepatitis C tends to be more rapidly progressive in patients with HIV co-infection, and end-stage liver disease has become an increasingly common cause of death in HIV-positive persons. For these reasons, therapy for hepatitis C should be recommended even in HIV-infected patients with early and mild disease. Once HIV infection becomes advanced, complications of therapy are more difficult and response rates are less. The decision to treat people co-infected with HIV must take into consideration the concurrent medications and medical conditions. In particular, ribavirin may have significant interactions with anti-retroviral drugs used to treat HIV infection. In patients with co-infection, control of the HIV infection should be the first priority; in persons who are inadequately treated for HIV or who have low CD4 counts, therapy of concurrent HCV is unlikely to be successful and may have serious complications.

In many of these indefinite situations, the indications for therapy should be reassessed at regular intervals. In view of the rapid developments in hepatitis C today, better therapies may become available within the next few years, at which point expanded indications for therapy would be appropriate.

Patients with chronic hepatitis C should be advised on the likelihood of a beneficial outcome to antiviral therapy. For patients with genotypes 2 and 3, the likelihood of a sustained virological response is 70 to 80 percent. In patients with genotype 1, the likelihood of a sustained virological response is between 40 and 55 percent, but the individual likelihood correlates with several viral and patient factors. The major predictive factor for a response is the level of HCV RNA in serum: response rates being higher if HCV RNA levels are lower—levels less than 800,000 IU/ml generally being considered low. Furthermore, response rates are higher in women than men, in younger than older persons, in persons with normal body weight compared with those who are overweight or obese, and in persons with lesser degrees of fibrosis on liver biopsy. Strikingly, response rates are also higher among Caucasian Americans and Asian Americans than among African American patients. Thus, average overall response rates in persons with HCV genotype 1 infection are 50 to 60 percent among Caucasian Americans, but only 25 to 30 percent among African American patients. The reasons for these racial differences are not known.

Patients with acute hepatitis C are a major challenge to management and therapy. Because such a high proportion of patients with acute infection develop chronic hepatitis C, prevention of chronicity has become a focus of attention. In small studies, 83 to 100 percent of persons treated within 1 to 4 months of onset have had resolution of the infection. What is unclear is when to initiate treatment, at what dose, for what duration, and with which regimen. A practical but rigorous approach is to start peginterferon (in usual doses) and ribavirin (800 mg daily) for 24 weeks if HCV RNA is still detected 3 months after onset of infection. The role of ribavirin and the use of shorter courses of therapy are currently under evaluation.

In patients with clinically significant extrahepatic manifestations, such as cryoglobulinemia and glomerulonephritis, therapy with interferon can result in remission of the clinical symptoms and signs. However, relapse after stopping therapy is common. In some patients, long-term or maintenance peginterferon therapy can be used despite persistence of HCV RNA in serum if clinical symptoms and signs resolve on therapy.

476246 tn?1418874514
Like fretboard pointed out, it is most ideal to have good support around you. You might not be able to work during treatment and you might have to have someone take care of you at times. So one needs to be well prepared.

According to Dr. Dieterich of Mount Sinai, NYC, one should treat now. There is an interesting video on    hcvsupport.org  called something like  Why I should treat my hep c now! It's on the left hand side under video presentations. The other videos are also quite interesting.

Marcia
Avatar universal
"Patients with cirrhosis can be offered therapy if they do not have signs of decompensation, such as ascites, persistent jaundice, wasting, variceal hemorrhage, or hepatic encephalopathy. However, combination therapy has not been shown to improve survival or the ultimate outcome in patients with pre-existing cirrhosis."

Well that is something you don't hear everyday. It seems that statement should be qualified somehow. I would imagine that people who have SVR'd here on our very own board would beg to differ.

Otherwise what is the point for all of us at stage 4 and beyond? To buy the amount of time you are miserable on treatment?

One thing I will repeat rsl1959, is "PUSH PUSH PUSH" for explanations and info from your docs, PAs, NPs whoever. I had labs and imaging that contradicted each other and didn't really know what was going on.

People here constantly advised me to do more tests, get another opinion, be aggressive and I wimped along at my own little pace (I didn't want to hurt my docs feelings--I figured what if the next guy is worse than who I have now--the hassle with insurance and time--Hep Docs are few and far between, blah, blah, blah).

When the NP would say stuff like, "Even though you have cirrhosis, you can wait for the new drugs." Which of course I wanted to hear.

Now TWO YEARS after that comment, I just had my first endocsopy which revealed varicies. I have no idea if I had them two years ago. I just watched a video posted by Hector and see that having varicies-portal hypertension is another hit for a cirrhotics chances of SVR. If my doc had said, you are stage 4, let's do an endocscopy because it will help us stage you, and this is why we need to do it, you can bet I would have done it. ARRRRRGGGGHHH!

Thank god for the info here, but I never came across that tidbit until seeing Hectors post the other day. I just wish my doc/np had thought of this. If I had changed doc's immediately, possibly I would be done with treatment by now and SVR at this point.

So anyway, just make sure you're ABSOLUTELY clear on where you are at. That those biopsies are good and jive with labs. If you truly are a stage 1, I would imagine hanging on for the new stuff makes sense. But such a tough decision not knowing exactly when that will be.

I made a mistake. I should have had more tests immediately and changed docs.

Foo
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