I am all better now, but yesterday after finally catching up on some desperately needed sleep in my Chicago hotel, in the bathroom in the morning, I had a nasty sudden bloody nose that wouldn't stop until I applied 20 minutes of direct pressure with both hands.
It was reassuring to know that my platelets had just been checked the day before at OSU in Columbus and were nearly 400,000 so I knew it wasn't my ITP returning, but could it be some platelet dysfunction related to one of the many meds that I was taking? Use of coumadin excludes you from an ibrutinib trial due to possible increased bleeding risks, but was there a concern if you weren't on a blood thinner? Aspirin and other anti-platelet drugs are OK so the concern may be very specific. Being the information hound that I am, I reviewed some old articles on the subject. A study in Blood (2000) looked at the platelets in patients with XLA (an X linked congenital lack of BTK) suggested "These results suggest either that the
Btk/Tec family kinase activity is dispensable to platelet function or
that there is sufficient Btk/Tec kinase functional redundancy to
rescue signaling in specific receptor pathways.
" In other words, BTK inhibition may have some effect on platelet function, but it is not critical. Another article in the same journal (2006) states: "In summary, the data presented here demonstrate the previously
undocumented and critical role of Btk in bt/VWF-induced signaling in vitro and
GPIb-dependent stable thrombus formation in vivo." This seems to suggest BTK may play a significant role in proper platelet function. Current Biology in 1998 concludes: "Our
results demonstrate that Btk is important for collagen signaling via GPVI, but is not essential for
thrombin-mediated platelet activation." I don't pretend to understand all the nuances of these reports, all of which are several years old and predate the era of BTK inhibitors and none of which were studying ibrutinib or any other BTK inhibitors. Rather, they were looking at the platelets of patients born without BTK. Still the data seems to suggest there is a definite role for BTK in clot formation. However, I am not sure that it is clinically important as there are also clearly redundant pathways and signaling to get a healthy thrombus going in response to an arterial injury.
Every trial visit I am asked about nosebleeds and bruising, so there must a need for some vigilance. But then again I am also asked about a myriad of other possible problems. That's why we do trials, to find out the benefits, and the risks.
I had no other worrisome bruising or bleeding issues, so I practiced my own advice and tried to under react.
After the bleeding finally slowed down, I needed to rush to clean up, shower and dress in a a blood red sweater and black jeans to give my CME lecture on MDS (myelodysplastic syndrome) to about 250 primary care providers in Chicago.
It all went well, but I had to fight the urge to sneeze more than once while on the stage.
My day wasn't done. The next speaker in the line-up, a good friend who is an expert in dementia wasn't feeling that well with stomach issues and asked if I could hang around and perhaps switch times with him and go on in his slot. As it worked out, he spoke as planned, so I went upstairs to my hotel room to rest and to quickly email Dr. Byrd who quite sensibly blamed the dry air of the plane and the hotel heating system and not the meds. He did not think it was a significant issue. Further reassured, I took a very short power nap, woke up early for my CLL lecture with a second milder more easily controlled bloody nose and just made it down to the stage for my final 90 minute presentation.
Ironically, the lecturer-friend on dementia who was at the podium between my two talks had to briefly leave the stage because of his gut issues and the moderator needed to jump in with the save. Fortunately Alzheimer's Dementia was one of her areas of expertise. She however warned me I was on my own, as she was not prepared to talk on CLL if I exited the stage with a Kleenex pressed against my nose.
The lecture was uneventful and well received and I hung around to answer questions including one from a doctor whose husband is enrolling in an ibrutinib trial. Today I am feeling fine. A tender mysterious rash came and went on my nose last night (maybe from all that pinching to control the bleeding), but I have had no other issues.
A bloody nose can be a harbinger of trouble or a false alarm, but in either case, it is startling, annoying, messy and inconvenient. It all made for a dramatic and stressful day, but all's well that ends well and it was ultimately of no consequence. If Dr. Byrd isn't worried about a bleeding issue, either am I.
Still I will be glad to be home tomorrow.
Labs were just great at OSU. My counts are all essentially normal on ibrutinib. No nodes to be felt. Anywhere. Like the vast majority of patients, I am responding well. Without a CT scan or bone marrow biopsy, you could not tell that I have CLL. And maybe soon, even those won't show any evidence of my evil clone.
I will soon be reporting on important issues from the Lymphoma Research Foundation Meeting that took place in Manhattan Beach last week, and I will be going to ASH this year, so watch for some newsy posts soon.
Labels: Bloody nose, CLL MDS. CME, ibrutinib, platelets, Rash