Post date: Mar 9, 2010 5:14:13 PM
Back to my real hobby, doggie medical research!
When I learned that Trevor had prcd-PRA in the fall of 2008, the conventional wisdom said that PRA was an inexorable disease whose course could not be changed in any way. You could find a few websites hinting at the possibility that antioxidants might slow progression. But there were no details. So like other PRA moms and dads who found themselves in a similar situation, I had to put together my own program and hope for the best.
Today, only 18 months later, the picture is entirely different. I have to admit that I'm amazed by how much things have evolved in such a short period of time. There is now compelling evidence that diet and supplements can in fact make a difference in the progression of retinal degeneration.
Here are some recent developments:
In the placebo group the Multi focal ERG readings taken at the beginning of the study showed a statistically significant difference to those taken at the end of the 12 month period. Patients receiving Retina Complex showed no statistically significant difference between the two sets of data. This confirms that there is a SLOWER progression of disease in the treated subjects compared with those getting only placebo.
Professor Jonathon Stone of The Vision Centre, an Australian research organisation, said, "The outcome of this experiment was remarkable – significant improvement in vision after several weeks of taking saffron in pill form, which reversed when the patients were taken off it.
"This is very encouraging for a non-invasive way to treat certain important eye diseases."
The effects of green tea catechins in reducing harmful oxidative stress in the eye lasted for up to 20 hours, the study says.
Of course it's hard to say what any of this means. None of these things constitutes a cure. Even if these supplements do delay progression by a "statistically significant" amount, does that make a quantifiable difference from the patient's perspective? No one knows. On the other hand, it seems obvious that preserving your dog's eyesight for as long as possible is a good thing. There is also the chance that a real treatment will become available (i.e., gene therapy) if you can preserve viable photoreceptor cells for long enough.
In July 2009, my lab Rowan was diagnosed with masticatory muscle myositis (negative on titer test, diagnosis was made through muscle biopsy). We have been treating him with prednisone. This past week (March 10, 2010) we tapered him all the way back to a schedule of 10mg/5mg on alternating days. If this goes well, in a month we'll taper back further to 10mg every other day. Fingers crossed that Rowan doesn't relapse as we taper his dosage back. It's been a long road. If you've ever had a dog on a high dose of prednisone, you know what I mean!
Here is a summary of his prednisone treatment:
August 8, 2009: Started 20mg/day.
August 21, 2009: 40mg/day.
September 9, 2009: 60mg/day.
September 30, 2009: 50mg/day.
October 14, 2009: 40mg/day.
October 28, 2009: 30mg/day.
November 17, 2009: 20mg/day.
December 18, 2009: 15mg/day.
January 8, 2010: 10mg/day.
March 10, 2010: Switched to a month of alternating days of 10mg/5mg. Will continue for a month, then switch to 10mg every other day.
Rowan is doing well. The frustrating thing about prednisone is that its side effects are so severe that once you start giving it, it's hard to distinguish the pred side effects from the disease itself. But in summary: