17 August 2026 (Monday) - Sounds Like Sezary's Syndrome...

 The LEAST recommended diagnostic test is option 1. Bone marrow aspirate and biopsy

The patient shows the typical clinical picture of Sézary syndrome (cutaneous T-cell lymphoma, likely stage T4NxB2M0), characterized by erythroderma (erythema involving >80% of the body surface area), generalized lymphadenopathy and lymphocytosis with a TCR rearrangement shared between the skin and the blood. Skin biopsies, PET-CT and lymph node biopsies are indicated for diagnosis and staging. In the absence of unexplained cytopenia, a bone marrow study is generally not necessary. 

First-line therapies include low-dose methotrexate, extracorporeal photopheresis, retinoids and interferon. Mogamulizumab (an anti-CCR4 monoclonal antibody) is the treatment of choice for relapsed/refractory disease. Allogeneic transplantation should be considered in selected cases.

Reference: 

• Dummer R, et al. Cutaneous T cell lymphoma. Nat Rev Dis Primers. 2021;7(1):61. Published 2021 Aug 26. 

• Latzka J, et al. EORTC consensus recommendations for the treatment of mycosis fungoides/Sézary syndrome - Update 2023. Eur J Cancer. 2023;195:113343. 

• Olsen E, et al. Revisions to the staging and classification of mycosis fungoides and Sezary syndrome: a proposal of the International Society for Cutaneous Lymphomas (ISCL) and the cutaneous lymphoma task force of the European Organization of Research and Treatment of Cancer (EORTC). Blood. 2007;110(6):1713-1722. 

3 August 2026 (Monday) - Learning Monday

 The correct answer is option 3. Mixed phenotype acute leukemia with KMT2A rearrangement  

Immunophenotypic properties of MPAL can change over time: both variable proportions of different lineages and phenotypic alterations have been described as lineage switch. Most cases of lineage change involve a switch from ALL to AML. A retrospective review can often reveal the presence of an unrecognized or underappreciated malignant subclonal population present in the initial specimen. This may represent a minor population which displayed more chemoresistance and emerged after eradication of the chemosensitive dominant clone. This kind of lineage switch is most common in MPALs with KMT2A rearrangement where a small myeloid/monocytic population can be difficult to appreciate due to hyperleukocytosis with a dominant B-precursor population at diagnosis.

Reference: 

Weinberg OK, Arber DA, Döhner H, et al. The International Consensus Classification of acute leukemias of ambiguous lineage. Blood. 2023;141(18):2275-2277. 

27 July 2026 (Monday) - Myeloma Treatment

 

I thought option 3 and I said so. I was told: The correct answer is option 3. The patient remains biologically high-risk despite achieving MRD negativity. 

Achieving MRD negativity at a sensitivity of 10⁻⁶ is an excellent treatment outcome and is strongly associated with improved progression-free and overall survival in multiple myeloma. While MRD negativity reflects how effectively treatment has reduced the disease burden, cytogenetic abnormalities provide important information about the underlying biology of the myeloma clone. 

In this patient, the presence of both t(4;14) and gain(1q) identifies biologically aggressive disease. Although deep responses such as MRD negativity can substantially improve outcomes, current evidence suggests that they do not completely eliminate the adverse prognostic impact of multiple high-risk cytogenetic abnormalities. Data from studies have shown that patients with ultra-high-risk disease can achieve high rates of MRD negativity, yet their long-term outcomes remain inferior to those of patients with standard-risk disease achieving the same depth of response. 

Therefore, the most accurate interpretation is that this patient remains at increased risk of relapse despite achieving MRD negativity. 

16 July 2026 (Thursday) - Learning Monday (three days ago...)

 

The correct answer is option 4. Heatstroke 

The cells depicted are neutrophils (A-D), lymphocytes (E) and monocytes (F) with botryoid nuclei, characterized by hypersegmented nuclei with a radial arrangement. These were first seen in 1980 in six patients with heatstroke and were named after the Greek term “botrys,” which translates onto “bunch of grapes” because of their resemblance. Since then, they have been described in other conditions causing severe hyperthermia, such as cocaine and methamphetamine abuse, autoimmune limbic encephalitis, sepsis, drug rash with eosinophilia and systemic symptoms (DRESS) and neuroleptic malignant syndrome. These nuclear changes have been hypothesized to be early stages of oncotic (karyolysis) and apoptotic (karyorhexis and pyknosis) cell death because of extreme heat.

Reference: 

• Verdú G, Vallvé M, San-José P, Molina A, Merino A. Diagnostic Value of Botryoid Nuclei as a Biomarker of Severe Hyperthermia and  Systemic Inflammation in Heatstroke and Neuroleptic Malignant Syndrome: A Challenge of Climate Change. Int J Lab Hematol. May 2025. doi:10.1111/ijlh.14500 

• Chiriac R, Pourchet V. Noyaux botryoïdes des leucocytes induits par le syndrome de DRESS. Ann Biol Clin (Paris). 2025;83(2):220-222. doi:10.1684/abc.2025.1961 

11 May 2026 (Monday) - Iffy Valves

 

Looks like an iffy heart valve to me. The correct answer was:

 

“The correct answer is option 3. Revision of prosthetic valve. 

Mechanical hemolysis may results from malfunctioning prosthetic valves. Hemolysis is intravascular and may give rise to iron deficiency due to hemoglobinuria. Treatment is by correcting the valve malfunction”. 

 

Go me!!!

2 February 2026 (Monday) - Learning Monday

 

It’s not Immune thrombocytopenia. The platelet count is too high and the patient would have had bruising and other symptoms which would have come to light before any surgery.

It’s not Wiskott-Aldrich syndrome as that has small platelets.

It’s not DIC as the clotting isn’t outside the normal range.

 

Large and pale platelets – grey platelet syndrome…

8 December 2025 (Monday) - Learning Monday

It’s aplastic anaemia…
 
In hypocellular MDS you’d expect to see blasts in the bone marrow.
Mycobacterial infection doesn’t result in hypocellularity.
Haemophagocytosis wasn’t seen.
It’s not pure red cell aplasia as other cell lines are affected. 

1 December 2025 (Monday) - Learning Monday

I won’t lie. I don’t know. It’s AML. Back in the day we’d do a Sudan Black stain and that was good enough.  Things have massively changed in the understanding and diagnosis of leukaemia.

 

Here’s the answer:

 

“Correct answers are A and B. This case illustrates a discrepancy between the two AML classification systems and underscores the complexity of diagnosis in the presence of multiple genetic alterations. An integrated diagnostic approach, including flow cytometry, cytogenetics, and molecular genetics, is necessary to reach a final diagnosis. The patient would be classified as an AML with mutated TP53 according to ICC 2022 and as an AML myelodysplasia-related according to WHO 2022. In the ICC 2022 classification, AML with mutated TP53 is recognized as a separate entity, including Pure Erythroid Leukemia, if morphologic criteria for this entity are respected.  According to WHO 2022, 5q deletion is included in the cytogenetic abnormalities defining AML-MR.  In both systems, the diagnosis of AEL (WHO 2022) or PEL (ICC 2022) requires ≥30% immature erythroid cells (proerythroblasts) and a bone marrow with erythroid predominance (≥80% of cellularity). The case of this patient doesn't comply with the criteria of the >30% proerythroblasts (he does have 45% of erythropoiesis in the BM, but not 30% or proerythroblasts)”.

 

Here’s a link to an article on the matter from an expert panel. I’ll make the observation that it wasn’t that long ago that we were all far more knowledgeable on the matter as we used to do a lot of the testing in-house and not send it off to reference labs…

10 November 2025 (Monday) - Warm AIHA

I got that right…not that I will ever be deciding on the therapies, but it really helps if I know what the drugs are, what conditions they are for, and how they work.

Here’s the first reference, and here’s the second.

3 November 2025 (Monday) - A.P.L.

 

Acute promyelocytic leukaemia…  There’s some pictures here and an article about how the condition is best treated here.

 

Oh… Statements 1, 3, and 4 are correct.

The images given show dumbbell-shaped blasts consistent with acute promyelocytic leukemia (APL), a subtype of AML known for its aggressive presentation and high risk of bleeding and/or thrombosis due to coagulopathy. Unlike other AML variants, APL often leads to disseminated intravascular coagulation (DIC), supported by lab findings such as elevated INR, prolonged aPTT, low fibrinogen, and high D-dimer.

Despite its favorable long-term prognosis, APL is a hematologic emergency requiring urgent treatment.  The coagulopathy in APL is primarily driven by tissue factor (TF) released during promyelocyte destruction, triggering excessive activation of the coagulation cascade. With the advent of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) as frontline therapy, APL has become the most curable AML subtype. APL blasts are typically negative for HLA-DR and CD34, distinguishing them from other AML variants.

20 October 2025 (Monday) - Learning Monday

It’s Learning Monday and the European Hematology Association have a puzzler for us as they so often do on a Monday… 

Looks like a case of TTP to me… 

It was.

Here’s the first of the references, and here’s the second.

13 October 2025 (Monday) - Unexplained Erythrocytosis

Well… presumably the chap is not unwell? The Hb of 18.4 isn’t especially high…

The JAK2 being negative pretty much rules out polycythaemia rubra vera (or polycythaemia Rupert Bear as I once heard it called).

Erythropoetin receptor mutations usually result in low levels of EPO so that is pretty much ruled out too.

EPO levels are typically higher in individuals with pulmonary diseases.

My gut feeling is that this would be a relative erythrocytosis until I saw the P50 was low.

 

This might be a haemoglobinopathy with a high affinity haemoglobin…  A haemoglobinopathy was the correct answer. I got it right... but this would be *very* obscure.

 

Here’s an article on erythrocytosis with several useful links.

29 September 2025 (Monday) - Platelets...

Big platelets… not many of them… is this Bernard Soulier Syndrome? Or Von WIllebrands?

The other day I mentioned that I need to refresh myself on specialist leukaemia testing. It would seem that whilst I wasn’t looking there’s been great strides made in the genetics of platelet diseases.

There’s a list here which at first sight meant absolutely nothing to me. But half the battle of CPD is realizing what I need to develop…

3 February 2025 (Monday) - Stopping Vitamin B12 Injections?

Monday - #LearningMonday.  I got it right – answer three.

 

“Tina has not consumed her vitamin B12 reserves built up by injections over the years. 

Large quantities of cobalamin are retained in the liver after absorption, as a result, any decline in the intake of cobalamin may take five to ten years to show clinically.  

Even if intake would stop altogether, normal liver supplies account for approximately two years of normal cobalamin consumption.  

Although sporadic reports of spontaneous remission of pernicious anemia are present in the literature, such events are very rare.    

Reference:

Jajoo SS et al. Etiology, Clinical Manifestations, Diagnosis, and Treatment of Cobalamin (Vitamin B12) Deficiency. Cureus. 2024 Jan 12;16(1):e52153.”   

16 December 2024 (Monday) - Learning Monday

Learning Monday – how best to assess the progression of myeloma? Back in the day it was by bone marrow aspirate, and it still is. Admittedly these days we do different things with the marrow once it’s aspirated though.

9 December 2024 (Monday) - Learning Monday

Bone marrow transplantation… who would be the best donor? I was right in choosing option 2.

Back in the day bone marrow was the future for the lab in the district general hospital. We did autologous transplants for a few years, but allogenic transplantation would be in our remit. HLA typing and all the testing…

Didn’t turn out that way, did it?

11November 2024 (Monday) - T.T.P.

“The correct answer is plasma exchange (PE). 

The treatment of choice for patients with thrombotic thrombocytopenic purpura (TTP) is plasma exchange. 

Although fresh frozen plasma infusion might be of limited impact, it is not the definitive treatment since it does not help removing the autontibodies from circulation. 

Platelets are thought to be contraindicated in TTP because of the theoretical possibility of worsening the TTP. 

Gamma globulin is ineffective in increasing the platelet count in TTP. 

Caplacizimab is an adjunct to PE but cannot replace it.”   

Reference:  Scully M, et al. Caplacizumab Treatment for Acquired Thrombotic Thrombocytopenic Purpura. N Engl J Med. 2019;380:335-346.

 

Plasma exchange? Haven’t done one of those for years…

28 October 2024 (Monday) - Learning Monday

A normocytic anaemia with incredibly low ferritin? But stomach cancer… this is an anaemia due to a deficiency of both iron and vitamin B12.
 
I got it right.

21 October 2024 (Monday) - Learning Monday

I wasn’t sure but wondered if it was Sezary syndrome. 

It wasn’t.

"The clinical presentation, the morphology, the immunophenotype and the positive finding for HTLV-1 were all consistent with adult T-cell leukemia lymphoma. 

All the other T-cell disorders are HTLV-1 negative.  

In addition, the patient was of African descent and central and West Africa have been shown to be endemic for the virus and the associated diseases". 

Reference:  Cook LB, Phillips AA.  How I treat adult T-cell leukemia/lymphoma. Blood. 2021;137:459-470.

 

Well – I learned something there…

7 October 2024 (Monday) - Learning Monday

It’s Monday – time to turn to the European Hematology Association’s “Learning Monday”.

Perhaps the start of learning is finding out what you don’t know.

 

Apparently Ruxolitinib is indicated in patients with symptomatic splenomegaly and/or constitutional symptoms due to IM-2 and HR PMF. Bearing in mind I don’t know what Ruxolitinib IM-2 or HR PMF are, there’s the start of today’s CPD…