Update conference info: Blood-borne (duh), not spread nearly as efficiently by sex as are Hep B and HIV, if the sex partner has it and one is monogamous & hetero, risk of acquiring it per year is about 0.6%. If not monogamous, goes up fairly significantly. If monogamous but Male with male sex, risk is higher, too. Female to female sexual transmission rate is not well defined.
IVDU still most common way of getting infection these days. Health workers have small but significant risk due to blood exposures.
Up to 44% of cases can’t be explained by typical risk factors (IVDU, MSM). But the harder one grills the patients, the smaller that “44%” number becomes. But even the most rigorous screens still have 10% of cases as ‘unexplained’.
20% of cases or less have symptoms during the acute infection. If the virus is treated during the acute infection, up to 98% cure rate is seen. People with symptomatic infections have a higher chance of clearing the virus on their own, too since the symptoms are generally due to a strong immune response.
Anywhere from 15-25% of folks clear it on their own within 6 months, usually in 3 months or less. If not cleared on its own by 6 months, it won’t generally be cleared without treatment.
If not treated, 20-25% will go on to have cirrhosis. Of those with cirrhosis, 4-6% go on to have liver cancer. One doesn’t see liver cancer arising from Hep C unless there is cirrhosis.
How to identify who will have cirrhosis: Tough to do. Some folks are rapid deteriorators (2-6 years), some intermediate (7-20years), some slow (20-50+ years). If one can identify when they got the infection that can help determine which category they are in. If the patient first did IV drugs in 2001 and liver biopsy this year shows bridging fibrosis (stage III), then he’s a rapid deteriorator. If he had a transfusion in 1979, and biopsy shows small portal fibrosis (Stage I), he’s a slow deteriorator, and probably doesn’t merit treatment.
Who to treat? Anyone with Stage II or worse on liver biopsy. Degree of inflammation (or Grade) doesn’t matter nearly as much. Except: Don’t treat chronic lung disease people, folks with decompensated cirrhosis, severe mental illness (they will get worse!), and be real careful with folks with significant cardiac dysfunction. Plus be ware of treating anyone else with a wide range of less common disease states.
Does genotype matter? Only in deciding what treatment to use. 1 and 4 get 48 weeks of pegylated interferon along with ribavirin, and 2 & 3 (more readily cureable) get interferon (pegylated or otherwise) and ribaviring for 24 weeks. Cure rate for genotype 2 is about 90%, for 3 it’s 80%. For type 1 it’s around 40-45%.
Genotype has no bearing on severity of disease or its course.
Genotype 1 and response to treatment: Need to see a 2 log drop after 12 weeks of treatment. Don’t get it, stop treatment! Need to see viral load drop to zero at 24 weeks also. If virus persists at all at 24 weeks, chance of cure very very low.
Goal of treatment: Viral elimination! Check for virus at end of treatment, and 6 months later. If not present 6 months later, consider a cure.
Treatment failure: Virus appears to be all gone at 48 weeks, but same infection back 6 months later. Consider retreatment, for longer period of time. How long? Good question. Perhaps 18 months to 2 years.
Seeing many folks now coming down with new Hep C infections after successful treatment for first infection! Frustrating!!! Usually IVDU’s who have not found recovery. Sometimes new infections from different sex partners.
A role for viral suppression? Some type 1s get viral reduction but not viral elimination by treatment. Is this desirable? Some think so, for folks with compensated cirrhosis. May keep them out of terminal liver failure and reduce chance of cancer. A study should be out in 18 months which may show if just suppressing the virus long-term (think years, with low dose peg-intron weekly but no ribavirin after the 48 weeks of treatment) reduces the risk of cirrhosis and/or liver cancer.
Consumption of alcohol or use of illicit drugs forbidden during active treatment, and failure to abide by this should be grounds to terminate treatment, because it lowers the effectiveness so much.
Treatment is still rough. Up to 30% dropout rate due to unacceptable side-effects. This drop-out rate can be decreased with vigorous use of meds to combat side-effects (erythropoeitin to fight anemia, neupogen to fight low white blood counts, analgesics for headaches, anti-depressants for depression, antinauseants for well, you know).
New therapies? Nothing to replace interferon yet. New classes of meds, protease, polymerase, synthetase inhibitors, are in clinical trials and look promising. They may end up being added as 3rd agents to interferon and ribavirin. Could end up replacing ribavirin. time will tell.
Hep C vaccine? Not on the horizon yet. Very difficult, same degree of difficulty as HIV vaccine. Prevention prevention prevention!!!
Now, ask me about chronic Hep B! (or better yet, wait a while before asking). We covered that today too. Far more complicated, yet simpler. Can’t cure it, not sure if suppressing virus is more helpful than harmful.