Hematology
Clinical discussions on blood disorders, coagulation, transfusion medicine, and hematologic malignancies.
Recent Discussions
For patients with microcytosis MCV 75-79 and normal Hb, low TIBC, and normal ferritin do you always rule out thalassemia?
Microcytosis is typical in thalassemia. With a normal ferritin and hemoglobin concentration, I would start screening by measuring HPLC, HbA2 levels that are high in beta-thalassemia carriers. (HbA2 can be normal with “mild” thalassemia alleles and for several other reasons.) Microcytosis without iro...
How do you manage anemia in a patient with myelofibrosis and hemochromatosis?
It is a good question. There isn’t much more you can do. There are new targeted therapies for myelofibrosis which are best answered by an MPD specialist. As for the hemochromatosis, you should still check iron parameters, because if deficiency is present it SHOULD be treated, in this case with IV ir...
What is the target ferritin level for patients with hereditary hemochromatosis and signs of end-organ damage?
I believe the best marker to guide phlebotomy therapy for iron overload is the serum ferritin concentration. I use a target ferritin level of approximately 50 ng/ml. However, one could justify a ferritin level of <200 ng/ml from the literature of serum ferritin compared to body iron stores in HFE he...
In patients who relapse during a treatment-free period after achieving remission on prior 1st/2nd generation TKI, what factors should be taken into consideration when restarting treatment?
I would usually restart therapy in patients who lose MMR after a failed TFR attempt. I would usually use the same TKI they were using before stopping, unless part of the reason for stopping was toxicity, in which case I would consider an alternative TKI that may have a lower probability of having a ...
What front line therapy would you recommend for a patient with CLL on chronic dual antiplatelet therapy?
Given the bleeding risks associated with BTKi, I personally may prefer venetoclax-based therapy if feasible, in treating patients who require dual antiplatelet therapy (DAPT). This is based on safety considerations. I consider both BTKi-based therapy and venetoclax-based therapy great options for fr...
What factors do you take into account for recommending venetoclax/obtinutuzumab vs BTK inhibitors vs chemotherapy in front line therapy for CLL?
For most patients, either BTK inhibitor or venetoclax/obinutuzumab would be appropriate therapies. I would only consider chemotherapy (fludarabine/cyclophosphamide/rituximab) for those <65 years old with IGHV mutated disease and no high risk genetic markers. And even in these patients, I almost alwa...
For CLL patients with high-risk cytogenetics on ibrutinib who develop a cardiac event such as an MI, would you continue ibrutinib?
It depends on the cardiac event (and the CLL status). After any serious event, if the CLL is under good control (clinical CR), I think it is very acceptable to stop the ibrutinib and wait until clinical progression occurs - which can be a while for some patients (median 2 years from the E1912 study)...
Would you ever consider using ibrutinib in CLL patients who have received first line acalabrutinib and then progressed?
There is no benefit of switching between covalent BTKi (Acalabrutinib, zanubrutinib, or ibrutinib) especially in CLL which, in most cases, is driven by a C481S which renders all three ineffective. The only rationale situation to switch between the three would be intolerance. In this situation, switc...
How do you approach treatment for a fit patient with unmutated CLL who has progressed after BTKi and venetoclax containing regimens in the first and second line?
Original answer: February 10, 2023 This is a tough situation and we are seeing increasing number of patients who have failed both BTKi and BCL2i. Clinical trial enrollment with non covalent BTKi, or other novel strategies including CAR T cell therapy should be considered. PI3K inhibitors are also ap...
Do complex cytogenetics have any therapeutic or prognostic relevance in CLL?
In this patient, the finding of a TP53 mutation trumps all, including complex karyotype. In the absence of TP53 mutation or deletion of 17p13.1 (the TP53 locus) on FISH, complex karyotype of 5 or greater abnormalities is generally associated with shorter time to treatment and PFS on both chemoimmuno...