I realized it was time for another drug shakeup: My T-cell count (an immune measurement) kept falling. They'd been doing a pretty steady decline for 4 1/2 years. It wasn't particularly alarming until recently: New drugs were coming on the market, and I still had some leeway. But then I started on the most effective antiretroviral combination (AZT+3tc) in late August 1995. My viral load dipped immediately. And, after a couple month delay, my T-count took a slight upswing. Both of these were good. And short-lived.
By May of this year, my viral load was back up to what it was before adding 3tc, and -- for the first time -- my T-count fell below 200.
Below 200 is the arbitrary point at which someone who is HIV positive is automatically considered to have AIDS, whether or not one has had opportunistic infections. (I had fallen into the AIDS category years back when I was diagnosed with "AIDS encephalopathy," which is where the brain starts changing size and/or shape. Of course, a friend suggested maybe I was just showering with too hot or cold of water.) So, despite having had the diagnosis previously, the new number was still a psychological barrier -- kind of like how some people feel when turning 40. And with my viral load going back up, I knew what was going on: I was "failing" my current drugs and needed to make a change.
I should back up a bit and give a short drug history to put the drug failure into perspective. Early on, when AZT alone was considered the standard of care, Project Inform made a convincing case that AZT alone was not enough: Combinations of drugs would be more effective. If one anti-HIV drug worked somewhat, two drugs working at different points of the virus would be even better. The goal was to reduce the amount of HIV as much as possible. (Studies published since then have proven that combination therapies are indeed more effective.) So, with this concept mind, here is my anti-HIV drug history:
Well, I've known for years that HIV begins to become resistant to AZT within a year or 18 months. So, for the last couple of years, the chances of it being effective for me were not great. But, when 3tc studies were done, they found that 3tc would re-sensitize HIV to AZT. In fact, the combination of 3tc+AZT was shown to suppress HIV more than any previous combination. So it was with great hopes that I added 3tc to my regimin in August, even before it was FDA approved. And, as I noted above, I did get a short-lived benefit. I believe it was so short lived because of my previous long-term AZT usage. I don't regret that usage, though, as it could be why I'm still here.
- Began AZT January 1992.
- Added ddC July 1992 (so I was on AZT+ddC).
- Stopped ddC and began ddI January 1993 (then I was on AZT+ddI). (As a sidenote, the only reason I changed from ddC to ddI was that ddC made me an awful bitch. I was anxious and gnarly. ddI was much kinder to me -- and those around me!)
- Added 3tc in August 1995 (so then I was on AZT+ddI+3tc).
Nonetheless, it was time for action. If my current drugs weren't working, I needed a change. Since I'd already been on four of the five antiretrovirals, I only had one left there. But there was also the whole new class of drugs called protease inhibitors. These are the drugs you may have heard about -- they made big headlines when they became the fastest FDA-approved drugs in history in early 1996.
There were reasons why I had not chosen to start a protease inhibitor yet. The first one approved was called saquinavir (Invirasetm). I knew from the studies that it had almost no side effects. But it did have a major problem: Almost none of it (around 3%) got absorbed into the bloodstream. The second one approved was called ritonavir (Norvirtm). It was just the opposite: It got absorbed much better, but had a lot of side effects -- and over 200 documented drug interactions. Not pretty.
The third protease inhibitor approved was indinavir (Crixivantm). I read good things about it and heard good things from friends on it. But, around the same time, I was hearing something else in addition: Studies were showing that whatever protease inhibitor you started on was what you would probably need to remain on: Once on a protease inhibitor, you often got resistant to the other protease inhibitors. (This does not seem to be the case with saquinavir/Invirasetm, however. There is speculation that is because of its current low absorption. [A new formulation is in the works]) So, I needed to make my choice wisely. Since there was a fourth protease inhibitor in the pipeline, I was in no hurry to make a decision.
Then things changed. As I mentioned, my viral load started going back up. My T-count started dropping to record lows. I got pneumonia -- twice. (Part of that's my own doing -- I smoke.) I started to have an outbreak of shingles. And it seemed I may have picked up cyclospora. (If you hadn't read about it, there was a June 1996 outbreak in Houston and other cities.)
So, I popped onto Project Inform's Web site and started reading up on the protease inhibitors. My impression was confirmed: It appeared Crixivantm was the current protease inhibitor of choice. (As of this writing, ritonavir appears about as effective, but the drug interactions concerned me.) But, I learned something else: It seems that you get a more effective result from a protease inhibitor if you also change your antiretrovirals at the same time. What would I do?
Now I had my tentative drug combinations:
- AZT+3tc was the most effective antiretroviral combination. I didn't want to drop either one. So, I would remain on both. But I could double my AZT dose and remain within normal limits. (Sidenote: AZT is the only antiretroviral documented to cross the blood-brain barrier -- helpful for dementia.)
- I should probably add d4T, since it was the only antiretroviral I've never been on. Plus, it had the added benefit of working on the same enzyme that AZT does. Maybe it would add a little oomph to my waning AZT effects.
- With three other antiretrovirals, my chances of developing peripheral neuropathy (painful tingling and numbness in the extremities) was growing. I should drop ddI -- which I'd been on for 3 1/2 years anyway -- as it is the primary culprit for peripheral neuropathy.
But that wasn't enough. Would my proposed combination have any bad drug interactions with what I was already on? I made a list of my other prescribed drugs:
- Crixivan
- 3tc
- AZT
- d4T
What | How much | Why am I on it? |
---|---|---|
B-12 injection | 1 cc 3x/week | Increases B cells, which I'm low in. Neurologic & brain function. May prevent OIs. |
Bactrim D.S. 800/160 | 1 tablet QD | PCP prophylaxis & toxoplasmosis of the brain prophylaxis |
Beconase AQ | 2 sprays BID | Nasal steroids to reduce allergies |
Cipro 500 mg | 1 tablet BID | Trying to fully clear up sinus infection. (Stopped shortly afterward.) |
Effexor 37.5mg | 1 tablet BID | Antidepressant |
Humibid L.A. tab 600 mg | 2 tablets BID | Contains guafinisen, a mucous thinner to keep sinusses clear. |
Prosom 2 mg | 1 tablet QD | Sleeping pill. |
Zantac tab 150 mg | 1 tablet BID | Reduces production of stomach acid. I had a burning stomach before I started it. May increase T-cells with AZT. |
Zovirax tab 400mg | 1 tablet BID | Herpes prophylaxis, may be synergistic with AZT. May prophylax against CMV at higher doses. Also, triggers production of "cyclovir phosphate," an anti-HIV agent, in the body. |
Now I popped back onto Project Inform's web site and found their handy drug interaction chart. I did a search on each of my proposed drugs and saved that drug's section to a word processing file. None of my proposed drugs had known interactions with my other drugs.
Armed with all my information, I went to see my doctor. She had a couple dosing suggestions that were slightly different than what I'd come up with, but we were in basic agreement. My decision was medically sound.
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