Gregory M. Ledet

Today started off horribly.  The doorbell rang at 10:30 and I was still sleeping, seeing as I didn’t go to bed until 4am.  I knew my wife was downstairs, but I still wanted to see what was going on.  I made the first step and my feet slipped out from under me.  Down the stairs I went.

Not a good pic, but click for larger image

I screwed up my arms pretty good, but that’s just the part I can show you here.  My lower back and and tail bone are destroyed.  My neck is killing me.  It hurt like hell when it happened, and now it’s getting worse as everything tightens up.  I only thought that I wasn’t doing good with the treatment, now I have this to contend with.  Trust me when I tell you… I’m in a shitload of pain.  The best part about it?  The doorbell was UPS delivering more Pegasys.  I went through pain to take delivery of pain.  It was so loud when I fell down the stairs that the neighbors came running over to see if I needed help.  I couldn’t move for about 10 minutes.

While I was sitting here in pain I tried to get some things done knowing that I have company arriving tomorrow and I had a doctor’s appointment today at 3 and it was going to take an hour and a half to get to the doctor’s office.  This is where to good day comes into play.  The doctor’s appointment was my first meeting with the PA that will be taking care of me during my Hepatitis treatment.  It was also my first look at the blood work I’ve had done since I started treatment.  We got to the office and everything went OK at first.  We went over the CBC and CMP info and I was informed that my white count was a little low, but my AST and ALT were looking better!

Click the image for full spreadsheet containing values

For those of you that don’t know, the AST and ALT are liver enzymes. Liver enzymes allow doctors to learn about the health of your liver. There are thousands of these enzymes in the liver and blood stream, but two of them — known as AST and ALT — are especially useful for determining the severity of liver disease.  When liver cells are damaged, AST and ALT are “leaked” into the blood stream.  The amount of these enzymes give the doctor an idea of just how screwed up your liver is.  When the levels are high it causes concern because the liver isn’t functioning the way it should.  In simple terms: if AST and ALT are high, that’s BAD.  Liver enzymes are like golf scores.  By looking at the teal and orange lines in the chart above, you’ll get an idea of what my liver enzymes have been doing this year.  I started treatment on Nov. 20th, so they have gone down since then.  Click that chart and bring up the full numbers and the spreadsheet.  Lots of info in there, including the numbers that you need to make that chart look right.

So, now we know that my liver is working a little better because they’ve gone down since my last test.  This is a GOOD thing, but it isn’t what I wanted to know.  I wanted to know my Viral Load.  That’s the test that I needed.  It’s going to give me a number and that number is the amount of virus found within a given volume of blood.  My last test, in September, gave me a viral load of 1,720,000 IU/mL.  That mean there’s 1.7 million of those little viruses swimming around in that vial of blood.  I had the viral load done again on the 21st and, I’m happy to say, it came back UNDETECTABLE!  That’s right!  The HCV RNA was not detectable in a range of 43 IU/mL to 69,000,000 IU/mL.  It could still be there, but it’s less than 43 IU/mL.  The next test I’m going to have done will be able to detect it down to 10 IU/mL.  If it’s not detected there, then it’ll be save to say that I’m kicking it’s ASS.  Or at least, I’ve kicked at least 1,719,957 of their asses so far.

5 more months of treatment and it’ll be looking VERY good for me attaining SVR.  This is what this treatment is all about.  It’s about it working.  It’s about me beating it and not letting it beat me.  And this is also help for all of you out there that are looking into starting treatment.  There is hope!  I’m a guy that started treatment before and stopped after 4 weeks.  I had well over a year to let the virus mutate on me and build an immunity to the treatment, but it didn’t.  It’s still getting it’s ass kicked, and as am I.

Speaking of getting my ass kicked, falling down the stairs this morning really sucked.  My body is really starting to tense up and hurt like hell.  I’m eating pain pills right now like mentos just trying to take the edge off.  I mean hell… I sat on my nuts when I fell.  Yes, my full 240 lbs of weight landed on my testicles as I was dropping down the stairs. It still really hurts…  Not to mention that I popped a cyst on my kidneys when I fell (I have Polycystic Kidney Disease too) and I’ve been pissing blood all afternoon.

I’m still going to keep updating this blog, especially with info on my blood tests and everything.  But the question still remains… How do you feel my day went.  Was it a good day?  Was it a bad day?  Or, was it just Tuesday?

Last night I felt a lump at the injection site. It kinda worried me that maybe the medication didn’t make it’s way entirely into my body, so I’m going to do things a little differently on this coming Friday’s injection.  Well, that’s neither here nor there, so here’s today’s video!

Ok, now that we got that out the way, let’s talk about genotypes.  It is much easier to talk of the Hepatitis C virus as if it is a single organism but in fact it is a range of viruses, similar enough to be called Hepatitis C virus, yet different enough to be classified into subgroups. Consequently, a better way to understand the terms HCV ‘genotypes’ and ‘subtypes’ is to compare them to things that we can more readily relate to.

The group of birds we call ‘raptors’ (birds of prey) have evolved into different main types. Imagining raptors as being Hepatitis C viruses, you could take one major raptor type, such as eagles, and imagine these as being one of HCV’s main types (genotypes). But eagles as a group are made up of different sub types such as the Bald Eagle and the Golden Eagle. You could imagine each of these as being one of the HCV subtypes that make up an HCV genotype.

Within each of above particular types of eagles, there are further differences. All Bald Eagles, for example, differ from each other in regard to wing span, weight, color, beak size, etc. Similarly, within a Hepatitis C sub-type, individual viruses differ from each other ever so slightly. Such viral differences are not significant enough to form another sub-type but instead form what’s known as quasi-species. It is believed that within an HCV sub-type, several million quasispecies may exist. Scientists predict that people who have Hepatitis C, have billions of actual viruses circulating within their body. Although there may be one or two predominant sub-types, the infection as a whole is not a single entity and is composed of many different quasispecies.

Biologists are generally not known for creativity when it comes to naming things – hence Hepatitis C virus. The most commonly used classification of Hepatitis C virus has HCV divided into the following genotypes (main types): 1, 2, 3, 4, 5, 6, 7, 8, 9, 10 and 11. As we’ve highlighted, HCV genotypes can be broken down into sub-types, some of which include:

1a, 1b, 1c
2a, 2b, 2c
3a, 3b
4a, 4b, 4c, 4d, 4e
5a
6a
7a, 7b
8a, 8b
9a
10a
11a

It is believed that the Hepatitis C virus has evolved over a period of several thousand years. This would explain the current general global patterns of genotypes and subtypes:

1a – mostly found in North & South America
1b – mostly found in Europe and Asia.
2a – is the most common genotype 2 in Japan and China.
2b – is the most common genotype 2 in the U.S. and Northern Europe.
2c – the most common genotype 2 in Western and Southern Europe.
3a – highly prevalent in Australia and South Asia.
4a – highly prevalent in Egypt
4c – highly prevalent in Central Africa
5a – highly prevalent only in South Africa
6a – restricted to Hong Kong, Macau and Vietnam
7a & 7b – common in Thailand
8a, 8b & 9a – prevalent in Vietnam
10a & 11a – found in Indonesia

Here’s a little graphic that will show how the different genotypes are distributed across the globe:

Current scientific belief is that factors such as duration of a person’s HCV infection, their HCV viral load, age, grade of liver inflammation or stage of fibrosis may play an important role in determining response to interferon treatment. Recent studies have suggested that a person’s HCV subtype (or subtypes) may influence their possible response to interferon, or interferon-ribavirin combination treatment.

I have genotype 2a. With this genotype, there’s around an 70% chance that I will achieve SVR after 24 weeks of treatment, and that’s good news. I don’t know how I ended up getting a rare genotype to the US, but it happened and I’m glad that it did.  Genotype 1 as a much lower chance (around 40%) of achieving SVR after 24 weeks of treatment and most people have to go 48 weeks.  Combine that with the fact that we caught it early and the chances of me getting through this without major liver damage are pretty high.

Well, that’s just about everything I can tell you about HCV genotypes. If you have any questions, do not hesitate to use the new comment system I put in place last night. You can login with your facebook, twitter, yahoo, or openID accounts so you don’t have to register for this site to post a comment.  Thanks again for reading and I’ll see you guys tomorrow!

-Greg

Things are a little better today.  I’ll go ahead and get the video out of the way now, then we’ll talk about SVR.

Yeah, that rash is still aggravating me, as is the injection site.  Muscle aches are coming on a little stronger as I type this, but nowhere near what they were Saturday morning.  Now, let’s talk about Sustained Virologic Response (SVR).

SVR is the closest I’ll get to “a cure” for hepatitis. Sustained virologic response, or SVR, is the goal of this peginterferon/ribavirin treatment. This treatment I’m on doesn’t necessarily eliminate the hep C virus from my liver. It can, however, suppress the virus to undetectable levels for an extended period of time. In clinical language, this is called a “sustained virologic response,” or sustained response. It means that during the six months after I complete treatment, there is no detectable hepatitis C virus in my blood.

SVR is a good thing. Studies have shown that with a six-month SVR (which means no detectable virus in your blood for six months after finishing treatment), relapse occurred in only 1-2% of patients. So, for every 100 people who finished treatment and attained SVR, the virus will return in only 2 of them. However, for these people, the virus never really left. The medicine was able to eliminate most of the virus (so much that medical tests couldn’t detect it), but after treatment ended, for whatever reason the virus was able to continue replicating itself.

Early SVR is beneficial. Since the liver has incredible regenerative ability, achieving SVR as quickly as possible is important. This is important because some liver damage can be reversed if the cause of the damage is removed. After SVR is reached and depending on the degree of damage from the virus, the risk of hepatocellular cancer is reduced and about 25% of people see an improvement in fibrosis.

SVR compares one treatment to another. For those of us in treatment, SVR is the goal. However, for physicians and scientists researching new hepatitis treatments, SVR is also used to evaluate new medicines and compare them with proven therapies. For example, depending on the genotype, treatment with interferon alone usually achieves SVR in 15% of the patients. When interferon is combined with ribavirin in the same genotype, SVR is increased to 70% in some people.

Tomorrow I’m going to try to get into genotypes as well as the genotype that I have and what my chances at SVR is.

-Greg

References: About.com and hivandhepatitis.com