Hematology
Clinical discussions on blood disorders, coagulation, transfusion medicine, and hematologic malignancies.
Recent Discussions
For early stage indolent NHL (low grade follicular, MALT) involving midline structures of the head and neck (ie base of tongue, soft palate) how do you apply the concepts of ISRT?
@Dr. First Last,I think your question is a good one and probably not one answerable by definitive data. However, the recent publication of the ILROG guidelines on extranodal disease (Yahalom et al, https://www.ncbi.nlm.nih.gov/pubmed/25863750) and bulk of available data I believe suggest that it’s o...
Would you consider a patient with DLBCL to have CNS involvement if no brain lesion is seen on imaging, CSF flow cytometry is negative, but PCR is positive for MYD88 and KMT2D mutations?
Cerebrospinal fluid (CSF) is an ultrafiltrate of plasma contained within the ventricles of the brain and the subarachnoid spaces of the cranium and spine. It is possible that cfDNA fragments containing MYD88 and KMT2D mutations may have found their way into the CSF and thereby detected by PCR techni...
What dose and fractionation would you deliver to the sole of the foot in a patient with multifocal cutaneous DLBCL that is resistant to systemic therapy?
We need some more information here. Does multifocal mean the patient has multiple skin lesions? The diagnosis of cutaneous DLBCL is also somewhat ambiguous. Is this cutaneous DLBCL leg type, a specific entity in the WHO pathology classification, or perhaps the older WHO classification is being used ...
How do you differentiate atopic dermatitis from mycosis fungoides histologically?
Differentiating mycosis fungoides from any spongiotic process (atopic dermatitis, allergic contact dermatitis, etc.) is extremely difficult and typically requires correlation with clinical features and sometimes molecular findings. Some features that favor mycosis fungoides are: Lymphocytic exocyto...
What is your practice regarding giving G-CSF to patients with ALL during initial induction?
My colleagues and I do not use G-CSF in either ALL or AML unless the neutropenia is unusual and prolonged and associated with infection. The use of G-CSF has been shown to shorten neutropenia by a few days but does not prevent the drop and theoretically, at least it may prolong thrombocytopenia by p...
What is your approach to treatment of relapsed, high-risk MDS with TP53 mutation in a patient that is not considered a transplant candidate?
I don't think that there is a particular answer for those with TP53 mutation with the exception of poor prognosis with whatever will be offered to them. I suggest azacitidine-based therapy based on improved overall survival (OS) compared with other approaches. Azacitidine is the treatment of choice ...
How do you address logistic barriers related to blinatumomab when treating relapsed B-ALL?
This is a very challenging issue that speaks to an incredibly important aspect of delivering not only this drug but others like it. Despite the strong evidence that supports the use of blinatumomab in a variety of clinical scenarios for patients with B-cell ALL [e.g., Gökbuget et al., PMID 29358182;...
How would you manage a patient with morbid obesity who presents with new symptomatic pulmonary embolism a few days after he was started on DOAC for DVT?
There are guidelines from the American Society of Hematology and The International Society of Hemostasis and Thrombosis as well as expert opinions recommending either apixaban or rivaroxaban for venous thromboembolism or pulmonary embolism in patients with BMI >40. In addition, this includes use as ...
How do you assess whether an early-stage Hodgkin's patient is unfavorable?
I personally utilize the GHSG criteria for most patients. To review, a patient has "favorable" disease if they meet all of the following criteria: 1. 1-2 involved sites 2. No bulky disease 3. No extranodal disease (which is rare in early-stage HL) 4. Favorable ESR/B-symptoms profile (ESR < 30 with B...
What additional testing is recommended with heterozygous HFE C282Y mutation whose ferritin is elevated and transferrin saturation percentage is at baseline?
Here, both serum ferritin and transferrin saturation are significantly elevated. Assuming the patient is asymptomatic and LFTs are normal, this profile is suggestive of iron overload. I assume Hb is normal? Would do MRI to look for hepatic iron overload.