Latest update
Noticed that there haven't been many posts recently and don't know how informed everyone is. Chris went back in the hospital on Tuesday (I think) because of a fever. They started him on IV antibiotics and told him he had to stay until he had been without a fever for 24 hours. This is not unexpected since the chemo is making him neutropenic (low white blood cell count which is your immune system). Ryan talked to him again yesterday (Thursday) and apparently he has developed a blood clot (a DVT or deep venous thrombosis) which I believe is in his inferior vena cava (IVC)(the really large vein that returns all the blood from the lower portion of your body back to the right side of the heart). Cancer can make you prone to clots so this is not entirely unusual either. The tricky part is that he is also prone to bleeding (seems counter-intuitive I know) because the chemo is killing his platelets that are responsible for starting the body's clotting mechanism so they have to put him on anti-coagulant medicine (heparin) but not too much or there is serious risk of bleeding. Hopefully, his body will chew through the clot and it will be no big deal. The concern is if a large chunk of the clot were to break off, travel to his heart and then to his lungs where it would occlude small ( or large depending on the size of the chunk) vessels and cause problems with oxygen exchange. That is the danger of a DVT.
There was also some talk about elevated liver enzymes again which Ryan thought was related to the DVT but I think is probably related to the Myelotarg because he had elevated liver enzymes when he got it in St. Louis which is why they only gave him one round of it instead of two. Wow, that was a tremendously long sentence (my former English teachers would be having a cow). Also, for a DVT in the IVC to cause hepatic congestion and damage, it would have to be like completely obstructing the vessel and he would have bigger problems than just elevated liver enzymes.
As you can see, I've gotten most of my information second-hand from Ryan because I was at work yesterday but this is my best interpretation of what is going on. We will keep you posted when we hear more.
Ryan's better, I'm sicker, and Trevor is still doing fine. It seems he isn't just getting some of my antibodies from the breast milk, he is commandeering all of them!
Christy
3 Comments:
Christy, thanks so much for the update, we get bits and pieces but it's a little like the game you play around the campfire,,,where you tell someone something and see how it turns out once everyone re tells the story.
You made the issues and locations very clear. Babies seem to take it off the top, don't they ;)
well, have fun, take lots of photos, and let us know if there is anything we can do. Connie
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New Leukemia Drugs Work Better, Studies Show
December 5, 2004 05:20:41 PM PST , Reuters
Next-generation leukemia pills, designed to help patients not cured by the successful drug Gleevec, work even better than doctors had hoped, researchers said on Sunday.
One new drug, made by Bristol-Myers Squibb, put 86 percent of patients who tried it into remission -- meaning signs of their cancer disappeared, the researchers said.
Although they were only Phase I trials, meant to show the drug was safe, the effects were dramatic, the doctors told a meeting in San Diego of the American Society of Hematology.
"Certainly it is wonderful. It will save lives," said Dr. Alan Kinniburgh, senior vice president of research for The Leukemia and Lymphoma Society.
Oncologists hope the approach may work in many other cancers, too.
Kinniburgh said it is likely that the new pills will be used in combination, like old-fashioned chemotherapy.
"I know of no cancer where one single drug has ever cured the cancer," he said.
The new drugs are being tested in patients with chronic myeloid leukemia (CML), which affects about 4,400 Americans a year and 10,000 people around the world.
HIGH REMISSION RATE
The Bristol drug is known by its experimental name BMS-354825. During the trial, also financed by Bristol-Myers, 31 of 36 patients with advanced CML, who had not been helped by Gleevec, had a complete hematologic response, meaning their bodies stopped producing leukemia cells.
This translates to an 86 percent remission rate, said Dr. Charles Sawyers, a Howard Hughes Medical Institute investigator at the University of California Los Angeles, who is helping test the drug.
Gleevec, made by Swiss drug company Novartis, targets an enzyme called BCR-ABL that leukemia cells use to proliferate. It attaches to the cancerous cells and stops them from growing and spreading.
Sold in Europe under the name Glivec, it was the first "targeted" cancer drug. It made headlines when it was approved in 2001 because never before had a simple pill shown such dramatic effects in cancer.
Gleevec, or imatinib, is Novartis's second-biggest product, with sales in the first nine months of this year of $1.1 billion.
But in a few patients, perhaps 12 percent, the cancer cells mutate just enough to slip out of Gleevec's grip. The cancer comes back.
NEW PILL SEEMS SAFE
So some of the researchers who worked on Gleevec teamed with Bristol-Myers Squibb to develop the new pill, which is less picky about how it grabs onto a cancer cell to deactivate it.
The Bristol-Myers drug affects a different enzyme called SRC, pronounced "sark."
Sawyers said he and colleagues worried that there could be unforeseen side-effects in patients, as no one had ever tested a SRC inhibitor in people. But so far it seems safe, he said.
Novartis also designed its own new compound, AMN107, dubbed "super Glivec," to overcome the weaknesses in Gleevec. It is in phase I safety tests in 76 patients with advanced leukemia and has shown a strong response in half of them, said Dr. Francis Giles of the M.D Anderson Cancer Center in Houston.
"The response rates were dramatic," Giles said in a telephone interview after presenting his findings to the hematology meeting. Giles and colleagues started patients on very low doses of AMN107, but he believes higher doses will show even better responses.
AMN107 is up to 30 times more potent than Gleevec because it was designed to more efficiently bind to the BCR-ABL enzyme, Giles said. "Clearly, we have a decent shot at a cure," he said.
found this, thought I'd post it, I know Chris is on blood thinners and this may not be applicable, but I'd at least thought I'd see if anyone had info on it. Connie
Regarding the article on new chemo-therapeutics, those are drugs that treat a different type of leukemia (CHRONIC myelogenous leukemia or CML) from what Chris has (acute myelogenous leukemia or AML). Totally different disease with totally different treatment.
Christy
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