By August 2025, I’ll be two years on epcoritamab, effective against my CLL but also suppressing my normal T and B cells and increasing my infection risk.
Infections are the leading cause of death in chronic lymphocytic leukemia (CLL), accounting for between one-third and half of all mortality. Patients on treatment are often at even higher risk.
In the case of my trial of epcoritamab, of the four deaths recorded, three were from infection and one was from skin cancer that may well have been related to the immune suppression caused by both the CLL itself and the epcoritamab.
While I have so far dodged any infections or second cancers other than one basal cell carcinoma, easily cured with a Mohs procedure, a specialized method of surgically excising the cancer, I don’t plan to test my luck anymore.
What ultimately convinced me to stop the trial was the results of my T cell subset blood test. I already knew that the bispecific antibody had, for the most part, wiped out all my B cells, the cancerous ones that had mutated to form my clonal CLL, but also all my healthy antibody-producing B cells. Epcoritamab targets the surface marker CD20, which is found on all B lymphocytes, so it’s no surprise there. In this way, it is similar to other monoclonal antibodies used to treat CLL, such as rituximab and obinutuzumab, in that it depletes both normal and cancerous cells. And while not having any antibody-forming B cells is not ideal, it is rarely life-threatening.
Low or no T cells is a whole different story. Think AIDS. Epcoritamab is a bispecific antibody. It works its magic by engaging my healthy T lymphocytes to kill the B lymphocytes, but in doing so, the T lymphocytes exhaust themselves and die.
My T cell counts are low. They weren’t six months ago. My helper CD4 T cell count is 350. Normal is >500. AIDS range in <200. My cytotoxic or CD8 killer T cell count is also low. My total T cell count is low. It might be even lower now as the blood was drawn before I received another and likely last epcoritamab injection. And the T cell counts only address the quantity of cells. Their quality is almost certainly impaired.
Time to quit. The risk-benefit ratio has tilted in the wrong direction. The likelihood of getting much more benefit from one more shot in the belly is small, the chances of a long treatment-free remission are already high if I stop now, and the future looks bright with the number of great new therapeutic options available when the time inevitably comes that I’ll need treatment again, growing every year.
Time to say thanks and move on. In a follow-up post here and on my blog at https://bkoffman.blogspot.com, I’ll talk more about the psychological impact of going off therapy. At least in my case, while it will be wonderful not to have to engage with my cancer so often through all the regular trial visits, there was some real reassurance in checking in monthly with my doctor and knowing all was going well. I will miss that.
10 Responses
Doc,
Sorry to hear about this setback after all the good news prior. I’m hoping that the low T-cell count is temporary and if rebounding is possible, the T-cells will be fruitful and multiply once again.
Hello Dr. Koffmann,
thank you for your blog and for sharing your journey which gives hope to many of us patients. I have a question about the epcoritamab treatment. Was it considered at some point to combine the therapy with another drug instead of continuing as before?
Dr.Koffmann,
I am a physician and I am currently on no treatment.My oncologist is at Emory Winship Cancer Institute and we are at the 1 year mark. I have had 1 episode of enterococcal bacteremia for which I had 6weeks of IV antibiotics.Of course my concern is getting more infections.I am still practicing full time.Have you considered IVIG infusions?Your blog is very informative as I embark on this journey.May God bless you and keep you safe.Continue the good fight.
Alan D Justice M.D FACP
I think the possible choice to stop because of a future infection is a well thought out choice with supporting proof of a possible illness. I also think your concern is an ill affect of the medication? I had always thought medication was suppose to attack “bad” cells? This medication seems to attack “all” cells it is designed to attack. Normally winter is the big sick season so you have time to build some good cells to help prevent a future illness. Your shared information will be helping many people with their future choice. I take Brukinsa and I developed two ill affects (high blood pressure, cough.) I had taken medication for high blood pressure but my blood pressure kept increasing? After 3 weeks off medication my blood pressure returned to normal with new medication. My cough cleared up after 2 weeks. I may begin taking my medication to see if my health issues return? Sharing information with others can be a benefit to others.
Brian – You have always been so smart (and courageous) in navigating your care and treatment. I am confident you are making the right choice for yourself. Onward in good health!
Dear Dr Koffmann,
I hope your immune system to recover soon after stopping the trial!
Thank you for keeping us aware about your health and the evolution of this trial; I am looking forward to hearing good news about your health again, soon..
By the chance, I thank you also so much for your efforts with CLL Society initiatives. You are strong, God will surely bless you!
Dear Dr Koffman,
I hope your immune system to recover soon after stopping the trial!
Thank you for keeping us aware about your health and the evolution of this trial; looking forward to hearing good news about your health again, soon..
By the chance, I thank you also so much for your efforts with CLL Society initiatives. You are strong, God will surely bless you!
Dr Koffman:
I completely understand your dilemma. I have been on cyclosporin now for a second time. The treatment is long due to a slow taper. Given my unusual AIHA, PRCA, ITP and again AIHA; my specialist believes it is time to actually treat the underlying CLL with obin+ven. I’m hoping to have a safe taper off of cyclosporin before beginning the CLL treatment. I had one scare with urosepsis followed with IV antibiotics. I also receive monthly IVIG. Having both B and T cells suppressed is certainly more concerning. I live safe by mostly living an outdoor lifestyle in our RV. I’m otherwise healthy and enjoying life.
I believe you’re making a wise decision. Thank you for sharing!
Geri
Thank you for documenting your treatment journey, Dr. Koffman. Your reports on your treatment, all the work you have done to create the CLL Society, to inform us all about latest developments, and your advocacy are inspirational for us all.
Dr. Koffman,
I cannot tell you how much I appreciate your blogs with this journey. I feel like you’ve been a guinea pig for all of us with CLL, with the catalog of treatments you’ve gone through. By the way, I dislike the term ‘guinea pig’ — because I dislike animal testing! But it was the best analogy I could come up with.
I’ve been in a clinical trial with the BTK inhibitor acalabrutinib (trade name: Calquence) for over 10 years, and I’ve responded extremely well. I’m essentially in remission with uMRD!
Today, my oncologist told me the clinical trial is ending. Calquence was approved by the FDA in November 2019 to treat CLL, but I’ve continued on the trial to (I assume) give the drug-maker further data on long-term use. But now, that’s come to an end.
I, of course, will continue to take the drug as it will be prescribed for me by my oncologist. But it is very strange knowing that the manufacturer will no longer be tracking MY specific progress, no longer asking for blood samples, or scans, or a bone marrow biopsy (which I really will not miss at all). I will very much be interested in your follow-up post about going off therapy and the psychological impact of not checking in monthly with your doctor. God bless you, Dr. Koffman, for everything you’ve done for CLL patients.