My doctor would like to start me on maintenance treatment with Rituximab. I would have an infusion every two months for two years. I had 3 treatments of bendamustine and rituximab (Oct, Nov and Dec 2015, followed by 3 treatments of rituximab only Jan, Feb, and March 2016.) Prior to treatment I was in Watch & Wait from November 2012-September 2015. Where should look to learn more about the use of maintenance therapy rituximab?
There are no good phase 3 data available for the use of rituximab maintenance therapy. Most of the studies show that with continued rituximab therapy you can lengthen a remission, but this is really meaningless. None of the studies looked to just administering rituximab at the time of relapse. We do see complications of long-term rituximab treatment as well, and it is therefore hard to justify the benefits. It would be particular important to remember that when you relapse, you should be treated with ibrutinib, acalabrutinib, or venetoclax, all with excellent response rates and progression free survival, and better tolerability than rituximab.
I am still treatment-naive for CLL. I know many doctors have negative responses to us who are juicing and taking supplements. However, I’m wondering in my case if something is going on concerning cell apoptosis. I have added Ashwagandha and Graviola (Sour Sop) to my vitamins for over a year. Since doing so, my WBC has remained stable and the rest of my blood work looks good. However, during my last two physicals I am showing a trace of blood in my urine. My doctor had me come back a couple of times before referring me to a urologist. Neither physician can see any blood in my urine under a microscope. The urologist said there was nothing to worry about. Both have a list of my supplements. SO…since the two supplements above have claims to causing cell apoptosis in SOME cancers, is it possible these urine tests are detecting broken down proteins from apostatized cells? AND, for those who are on medications such as Ibrutinib do they also show traces of blood since this is how CLL cells are eliminated from the body?
When cancer cells are broken down, their byproducts should not be seen as blood in the urine. Blood in the urine can result from being “dip positive”, which would indicate hemoglobin or myoglobin, or “microscopic positive”, which means red blood cells were seen. Several substances can cause the dip stick to be falsely positive, but microscopic review of the urine would be confirmation of whether red blood cells are really there.
My husband was in an ACP 196 trial starting in December 2015. He presented to the trial with weight loss, night sweats, afternoon fevers, itching, and extreme fatigue. He had been in a 2 year CLL partial remission after 2 treatments of FCO. WBCs were 18,000. Scant peripheral lymphadenopathy, but large abdominal nodes, some as large as 10cm. He started ACP 196 on Dec 5, 2015 and started to feel better by mid-January.
In April, his ANC went to 0.3, so they took him off the drug. Two and a half weeks later, his bone marrow biopsy showed Hodgkin’s lymphoma. We were told that he has Richter’s Transformation, and needs to seek treatment. What I read is not reassuring. He is 67 years old with 11q del, ZAP70+, CD38+. Can you point me in the direction of recent research so that we can be better informed?
Hodgkin’s disease can be seen as a type of Richter’s transformation. Overall, Hodgkin’s disease represents <5% of the cases of Richter’s transformation. Fortunately, they are not as resistant to treatment as the large cell type of Richter’s transformations. At this time, the data supports treating patients with the standard Hodgkin’s disease regimens.
I am on my third treatment of obinutuzumab without chlorambucil. During the second two treatments, I had excruciating pain in the left calf. An MRI showed that the bone and muscle in the left calf had infiltration. I am wondering if anyone has experienced this. Treatment with prednisone stopped the pain. I am having a PET scan as my first course of action. Has anyone heard of this?
This is not a common phenomenon seen with obinutuzumab (Gazyva). It is unusual for the bone and muscle to be infiltrated by the same process and needs to be fully evaluated.
For some reason, SLL is combined with CLL even though one is termed a lymphoma and the other leukemia. Much of the literature never even discusses how the staging considerations may be different and the determination of whether or not to treat it may differ. I was able to locate one article by Dr. Terry Hamblin, http://updates.clltopics.org/1993-sll-versus-cll-how-different-are-they; although it was dated back in 2008 and so I’m not sure it is still relevant or not. Can you please shed some light on SLL?
CLL and SLL really are the same disease. There is always variability in the propensity of the CLL/SLL cells to circulate, with SLL representing one extreme. Prior to 1993, a lymph node biopsy from a CLL patient would be reported out as SLL. Now everything is CLL/SLL.
Staging for SLL, in my opinion, should be based upon the Rai stage, with an exception for the lack of lymphocytosis. There have been many SLL patients included in indolent lymphoma trials and treated as “stage IV” patients using the Ann Arbor staging system. Staging is meant to act as an indicator of prognosis and being SLL and stage IV, which is almost always the rule due to some bone marrow involvement, does not indicate anything regarding prognosis.
Richard Furman, MD is Director of the CLL Research Center at Weill Cornell Medical College and a member of the Lymphoma/Myeloma Service in the Division of Hematology/Oncology. He is a member of the Medical Advisory Board for the CLL Society.
Originally published in The CLL Tribune Q2 2016.