Hematology
Clinical discussions on blood disorders, coagulation, transfusion medicine, and hematologic malignancies.
Recent Discussions
How do you monitor and manage minimal residual disease (MRD) in patients with core-binding factor (CBF) AML who are in remission post-induction and consolidation therapy?
For the purposes of this question, we will presume this refers to patients who are MRD-negative by a PCR-based methodology and have completed induction chemotherapy and consolidation.Puckrin et al., PMID 31896684 reported on 114 patients with CBF-AML who were treated with intensive chemotherapy and ...
How frequently would you consider IV iron treatment for ongoing iron loss and severe iron deficiency anemia?
Absolutely. You first want to estimate and replace their iron deficit. For patients who are very anemic, they can start at 2-3 grams deficit. I usually don’t give more than 1500 g of iron dextran at one time, but I will have no concern about doing 1000 or 1500 mg weekly until I have replaced their d...
What is your preferred first line treatment for patients with high risk MDS who are not candidates for transplant?
My choice of first-line therapy for high-risk MDS patients that are not transplant candidates tends to still be a hypomethylating agent (HMA). I send a myeloid molecular profile on all my MDS patients and use the p53 mutation status to make a decision regarding azacitidine vs. decitabine use. For pa...
How would you manage LPL with associated AL amyloidosis?
My approach here would depend upon the nature, impact, and severity of the amyloid. Is the LPL IgG or IgM secreting? Is the amyloid causing immediate physiologic harm (renal, cardiac) or asymptomatic radiographic deposits? How much lymphoma and amyloid, respectively? Treatment options include Benda,...
For a relapsed AML patient who has previously received 7+3 followed by HIDAC consolidation, how do you choose between FLAG-IDA or MEC re-induction?
In general, there is no "optimal" intensive salvage regimen for relapsed/refractory AML failing prior 7+3 and HIDAC consolidation. Prior comparisons of cytotoxic regimens have demonstrated no clear "winner" so it is based partly on clinical experience. At our center, I tend to prefer adding cladribi...
Do you recommend treatment for CLL patients with biopsy proven infiltrative lesions in the liver without hepatic dysfunction or hepatomegaly?
This is a very difficult question without context of why the biopsy of the liver was done. In general, for virtually all body sites, when CLL is found as an asymptomatic surprise finding, I continue observation. This is particularly true when it is an area of high disease presence at the time of aut...
Do you routinely evaluate for PE if a DVT is found?
I would not routinely evaluate for PE in a patient with new DVT, unless they had symptoms or signs suggestive of PE diagnosis. But I would usually evaluate for DVT in a new PE patient. This is in case the patient develops leg swelling or pain in the future and DVT is found then. It's difficult, oc...
Does anything need to be done if hyperlymphocytosis (i.e. ALC > 300K) develops in a CLL patient just starting ibrutinib?
Leukostasis is a feared complication of acute myeloid leukemia (AML) in patients developing peripheral WBC counts >100,000. The cells in AML are large, sticky, and invasive. By contrast, the lymphocytes in chronic lymphocytic leukemia are small (10 microns or so; not much larger than red blood cells...
What hypofractionated radiotherapy dose regimen is acceptable for plasmacytoma?
At the end of the day, it all comes down to delivering a reasonable BED in the range of +/- 50 Gy in fractions of 2 Gy. The type of fractionation chosen is a question of the treatment volume, location, and adjacent OARs. I have treated a few plasmacytomas with SBRT (for instance in the ribs) with 3-...
Do you routinely genotype adult beta thalassemia patients?
Yes, this is recommended by the American College of Medical Genetics and Genomics and is helpful for prognosis and complications. I also test for alpha gene duplication or triplication if there is a mismatch between the beta thalassemia genotype and the phenotype.