12 November 2026 (Thursday) - BTLP-TACT Exercise

Can you believe it – the nice computer at BTLP-TACT have told me I’m not doing enough. I had a look at my individual dashboard which said I’m supposed to have done four cases in the last month and I’ve actually done nine. Bearing in mind the thing clearly can’t count to four, I have to question those antibody identifications it says I missed antibodies in.
But whilst I’m at it I might as well do another case. It gave me two…
 
91653 – a thirty-two year-old woman in theatre needing group and save.
She grouped as A Rh(D) Positive… was that supposed to be a weak reaction? I called the Rh group indeterminate event though it wasn’t.
The antibody screen was positive in cells 1 & 3 so I performed antibody panels.
The IAT panel was positive in cells 1, 3, 6, 9 & 10 corresponding with anti-Fy(a)
The enzyme panel was negative throughout.
 
12769 – a fifty-five year-old chap in A&E with epistaxis.
He grouped as B Rh(D) Positive with antibody screen positive in cells 2 & 3 so I performed antibody panels.
The IAT and enzyme panels were positive in cells 3, 4, 5, 6, 7, 8, 9 and 10 corresponding with anti-c but not excluding anti-E, anti-Lu(a) or anti-Kp(a)
 
I got the thumbs-up…

12 November 2026 (Thursday) - Horiba Update

The nice people at Horiba sent their update today. You can read it by clicking here.
There was a very good review of the diagnosis of AML… and then a frankly wrong bit of advice about dealing with platelet clumping.
Given a numerically very low platelet count and a blood film showing a normal platelet count albeit with platelets appearing clumped you should not report the numerically very low platelet count. There’s two reasons for this. The numerically very low platelet count is clearly wrong and misleading, and the numerically very low platelet count is clearly wrong and misleading. OK, that’s the same reason, but it is so important I thought I should say it twice.
Given platelet clumping with what can clearly be seen to be an adequate platelet count one should report it as “platelets are clumped but appear to be present in normal numbers” (or something along those lines) and then ask for a sample collected into a different anticoagulant. Reporting a frankly wrong platelet count can easily lead to unnecessary, unwarranted (and potentially dangerous) outcomes.
 
There’s a lesson to be learned here… This is from an official update from a respected source. Even the best of us can make mistakes.

 

10 November 2026 (Tuesday) - Back In The Day

Back in the day I used to go to the haematology clinic in Folkestone on a Friday morning where I would perform manual platelet counts using one of these. That was forty years ago... the things are still in use in some labs...


9 November 2026 (Monday) - BTLP-TACT Exercise

Can you believe it - I got yet another snarky email saying I’m not doing enough BTLP-TACT exercises so here we go again…
I was presented with two cases:
 
86241 – a seventy-three year-old chap with alcoholic liver disease needing group and save.
He grouped as O Rh(D) Positive with antibody screen positive in all three cells. I performed antibody screens. The enzyme screen was positive in cells 3 and 5 corresponding with anti-E, and the IAT screen was positive in cells 1, 3, 5, 6, 9 & 10 corresponding with anti Fy(a).
 
76686 – a forty-one year-old chap with sepsis also needing group and save.
He grouped as Rh(D) Positive but the ABO group was indeterminate. With a cell group of A but a reverse group of O, this is one for NHSBT.
His antibody screen was negative though.
 
I got the thumbs-up…

 

9 November 2026 (Monday) - PNH (?)


Well, let’s apply a process of elimination…
The patient is older than me (and I’m ancient) so any condition is unlikely to be a hereditary one.
Having a bone marrow aspiration is traumatic (I’ve seen it done)
So that leaves flow cytometry and cytogenetics.
Bearing in mind from the symptoms it looks like the patient has PNH, the standard test would be flow cytometry to evaluate CD55 and CD59 levels…

The correct answer is 2
Paroxysmal nocturnal hemoglobinuria is an acquired clonal disorder caused by somatic mutations of the PIGA gene that result in impaired production of the glycosylphosphatidylinositol (GPI) anchor on blood cells. The resulting GPI-anchor deficiency can affect multiple haematopoietic lineages. Clinically, patients present with complement-mediated intravascular hemolysis, thrombosis, and bone marrow failure. Diagnosis is established by flow cytometry demonstrating populations of GPI-deficient blood cells.  

Reference:
Fattizzo B, Marchetti M, Cannizzo E, et al. Expert Consensus on the Diagnosis and Monitoring of Paroxysmal Nocturnal Hemoglobinuria (PNH): An Algorithmic Approach in an Era of New Treatments. European Journal of Haematology. 2026.
 

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8 November 2026 (Sunday) - Slide Saturday Challenge

 They are hairy cells... aren't they?
(Apparently not called that any more in the twenty-first century!!!)


7 November 2026 (Saturday) - Neutropenic?

For a long time it has been common knowledge that “people of African origin” have lower neutrophil counts than the general UK public. It would seem that this isn’t strictly true… it is actually people with the Duffy-null phenotype.
New reference ranges have been drawn up for neutrophil counts for these people. There’s an article on it here.
However this begs the question of how do we know where and when to apply this reference range? Should we be performing Duffy phenotyping as part of a chronic neutropenia screen?