Malcolm Needs

If your patient is Kell Negative (Ko) you have real problems. If your patient is K Negative, you, and your patient, have more chance!

I have an idea what it might be, but am bound by the rules of the game (fair enough). Please can you remind the likes of me when we can "put our oar in"? Thanks. P.S. It looks really good Bb_in_the_rain!

It is, nevertheless, true. Thorpe SJ, Boult CE, Stevenson FK, Scott ML, Sutherland J, Spellerberg MB, Natvig JB, Thompson KM. Cold agglutinin activity is common among human monoclonal IgM Rh system antibodies using the V4-34 heavy chain variable gene segment. Transfusion 1997; 37: 1111-1116. Thorpe SJ, Ball C, Fox B, Thompson KM, Thorpe R, Bristow A. Anti-D and anti-i activities are inseparable in V4-34-encoded monoclonal anti-D: the same framework 1 residues are required for both activities. Transfusion 2008; 48: 930-940.

Welcome Lily623.

Welcome phelyce.

A few things as far as human reagents. Firstly, you never know what else may be in them in terms of antibodies directed against low prevalence antigens, because there is absolutely no way that the producer has the ability to test for all such specificities (I can remember once a human-derived anti-D reagent produced at one of the places I worked, also had a Gm antibody in it that we didn't know about. It is highly unlikely that this would have caused too many problems, but there is, nevertheless, a small chance that this could have caused a false positive). Secondly, you never know what else may be in them in terms of viruses, some of which may, as yet, be unknown to us (remember, HIV, used not to be known). This is a danger to the producer and the person using the reagent, rather than the patient. Thirdly, the avidity of human reagents is, in general, pretty poor (particularly anti-D). A few things concerning monoclonal reagents. Some of them cross-react with other specificities (although not many), but, famously, monoclonal anti-D reagents will react with the I and i antigens if used straight from the fridge. They have to be blended by experts to ensure that the desired epitopes are detected, but certain Partial D types (e.g. Partial D Type VI) are not detected (unless required). They are very specific and very avid (both of which are greatly to be desired). Virally, they are almost certainly sterile. Hope that helps.

Welcome KLLP.

Welcome juandobermanz.

Well jnadeau, be it on your head! You might receive insulting posts from others on the site now! Unfortunately, the photographs of me actually receiving the gold medal and glass plaque were not of great quality, but this is one taken at the Institute of Biomedical Science soon afterwards. Even here, my hair and beard look a bit like I have just poked my fingers into an electrical socket, my tie has gone awry and, these days, a wide angle lens is required on all occasions, but here it is in all its glory!

Sadly Neil, it is not the case that anti-Inb is wholly or largely IgM; indeed, it is almost always IgG. It is thought that Indian Blood Group System antibodies do not cause HDFN because they bind to CD44 on foetal monocytes and macrophages and, therefore, have a blocking effect on FcγR1. This being so, or likely to be so, plasma exchange is likely to be less effective that might be thought, because of rebound from the extra vascular spaces.

Welcome Chica.

No, it is not just you.

She very possibly can (although two things; it would most certainly depend on the titre of the anti-Inb prior to EACH transfusion [and that would have to be 1) a doctor's decision and 2) a bit of a guess, as anti-Inb is so rare) and also, I would suggest IvIgG, rather than methylprednisolone (or, possibly, both). However, having said all this, there is NO DOUBT that anti-Inb is clinically significant in terms of haemolytic transfusion reactions, although the same is not the same for HDFN.

I pleasure entirely, and thank you too.

No, we didn't, because the controls for electronic issue were controls on how the IT programme works (or doesn't) by testing the programme "to destruction" before it was allowed to "go live". There is no way (that I know of) to control that any antibody can be detected following allo-adsorption (as the adsorption cells will, almost certainly be positive for high prevalence antigens (and so will adsorb out such antibodies such as anti-Lan) and, in any case, no antibody screening cells or panel cells will express every low prevalence antigen. In other words, no transfusion is safe (unless the patient will expire without it, the safest transfusion is that which is never given). I think what I am trying to say is that you can only do your best. No transfusion is ever 100% safe, but you cannot control everything (even the MHRA and UKAS admit that - and that is saying something!), but, unless you can come up with something that many people (including some of the "greats" of blood transfusion) have overlooked for years, then there are some situations where it is impossible to run controls that are not just there as a sop to the person running the tests.

NHSBT certainly uses the "immediate spin" cross-match in cases of AIHA when no atypical allo-antibodies have been detected underneath the auto-antibody. That having been said, particularly with the two sample policy and a robust IT system (and the guarantee by NHSBT that what is printed on the unit label vis-a-vis the unit group, is what is the unit group) an electronic issue (there is no such thing as an electronic cross-match - that is rather like calling the Rh Blood Group System either the Rhesus or rhesus Blood Group System), whereby there is minimal human intervention, I agree that electronic issue is far, far safer than an "immediate-spin" cross-match.

I am not at all surprised at that, as reagents have improved so much in the last two decades.

Essentially, this is because the A1 antigen is qualitatively different from any other A antigen. As a consequence, all individuals with an A subgroup of any kind are capable of producing an anti-A1, which would explain the reaction with A1 cells, but not A2 cells. In addition, the different A types, including, in this case, A1, are, in effect, a continuum from the strongest A1, right down to the weakest, for example, Am, and, in some cases it is impossible to detect any A antigen on the red cells, but it is possible to detect A substance in, for example, saliva, which would explain the results of the adsorption/elution testing. I really would advise against ABO genotyping, unless you are really interested (and I wouldn't blame you if you were), as it is a very expensive technique which won't tell you in which "pool" to put the donor (A or O). This will still be subjective. If it is just that you are concerned that this patient could be "dangerous", in theory they probably could be (although, in practice, probably not so) and I would enthusiastically thank the donor for giving, but with an explanation detailed enough to let them know why (not over-burdening them with science, while also not treating them as an idiot), ask them not to donate again in future.

Could not agree more.

Welcome AYO.

Welcome BruceLyon.

I can see from where you are coming, BUT from where do you get your anti-Weak D? The patient is a Weak D, NOT a Weak D Positive.

Sorry this has taken so long John, but my contact has been on annual leave, followed by a bout of sickness leave (no stamina these youngsters)! He has recommended the following paper. Bawazir WM, Flatt JF, Wallia JP, Rendon A, Cardigan RA, New HV, Wiltshire M, Page Lizanne, Chapman CE, Stewart GW, Bruce LJ. Familial pseudohyperkalemia in blood donors: a novel mutation with implications for transfusion practice. Transfusion 2014; 54: 3043-3050. doi: 10.1111/trf.12757.

Welcome Heyerdahl De Guzman.

Welcome Eric S. Hoy.