Muhammad Awwal

Thank you @Malcolm Needs

Greetings, The Handbook of Transfusion Medicine by Dr Norfolk says that the 1st choice of platelet for a group B patient is group A platelet (HT negative). Is there a scientific basis for this, or is it just down to population frequency and logistics? Thanks

Hi, with my limited knowledge, am I right to assume that the affinity of this antibody should be the same as the previous 2 times that you have tested the patient samples? If affinity doesn't change, and if the methods are consistent, could it be that the pregnant lady's anti-Jra is being 'boosted' by fetal Jra (considering it is a HFA)? Or maybe there is a 'steric-hindrance' sort of thing that is preventing proper adsorption? Thanks

Yes, you are right sir.

Hi all, Considering that recently transfused/pregnant patients may potentially be developing a new antibody which may still be of the IgM type. How important is it to test sample @ RT (or use polysecific AHG reagent) especially for transfusion-dependent patients? Thank you

Hi Malcolm,

What is a 'saline control plasma' please?

Hi all. I acknowledge that most seniors on this platform are aware of this fact. However I thought to share it because I recently attended a 'Training' and this ? could not be answered. I recently read that it's because B-lymphocytes have some receptors that are able to interact with sugar-based antigens without the help of T-helper cells which can directly initiate B-cells production of IgM, and because of lack of the help of the T-helper cells, class switching does not occur. Memory cells are also NOT produced, so antibody production continues only as long as there is antigen exposure. ABO antibodies are an example of T-independent immune response. The IgM antibodies are directed against the bacteria in the gut but cross-react with A & B antigens on RBCs. This is especially for the attention of youngies like me. BUT I am expecting the input from the seniors here. Thank you and have a good day.

Hi all, Regarding by-passing a panel, wouldn't you still need to fulfil the '3and3' or '2and2' rule to definitively identify the known antibody, and would a 3-cell antibody screen panel provide this? I have read somewhere about using cells as a set because they are 'complimentary'.

Thank you, exlimey.

Thank you, Malcolm.

Wow! Malcolm. Congratulations! You have indeed deserved it! From the little I have 'researched' about you. You are an inspiration, but can I achieve what you have? Hmn, maybe in 2 lifetimes. Congratulations once more.

Hi👋 I am solving case study of patient with AIHA (consistent with lab findings). DAT is +ve in IgG only. Antibody screen and panel is pan reactive in AHG (& enzyme-treated RBC) . After auto-adsorption, defined reaction was appeared in AHG but still panreaction in enzyme-treated RBCs. My question is, is the reaction of enzyme-treated RBCs with auto-adsorbed plasma still due to incompletely adsorbed auto-antibody? Is it IgM, since some reactions are absent in AHG? How can this be resolved, please? I have searched the internet without success, and I found this forum during my search. Thank you 👋🙏

Thank you so much. I am a Biomedical Scientist in the UK, and I am very interested in transfusion science and I am currently studying towards a specialist portfolio in Transfusion science. I have come to this forum with an empty 'bowl of knowledge', which I hope you will help me fill. Thank you again