Malcolm Needs

We haven't noticed any problems yet, but I will keep an eye open and also keep you informed.

I presume that this is the titration equivalent of our cut-off point of 0.5 IU/mL for passive anti-D (that amount is brand new, by the way. It used to be 1.0 IU/mL). If the anti-D titre is above 8, or the quant is above 0.5 IU/mL, the anti-D is presumed to be immune.

I would suggest a formal risk assessment. I would, but it would probably be ignored! :rolleyes:

No, you are being perfectly logical. I just thought that I should make the point, otherwise the "science" is not proven.

Our experience during the last several year since switching to plasma has brought me to the conclusion that those strictly "complement-dependent Anti-Kidd antibodies" are far, far less common than I was led to believe during my original training.

A minimum of 2 cell samples expressing presumed homozygosity of the gene, if available. In some cases, of course, this is not possible (for example, we had to group the partner of an Oh pregnant lady the other day. He was H+, but was he HH or Hh? Who knows?). There are also rare occasions when we only have one example of a particularly rare "homozygous" type (such as a Cw+, Cx-, MAR-), but there is nothing else you can do under the circumstances.

In the UK, the Guidelines state that, as long as it is known for certain that a pregnant lady has been given ant-D immunoglobulin, no further antibody testing is required after 28 weeks gestation (unless, of course, she has a fall or something). Similarly though, if we are tracking an antibody, such as anti-c, through a pregnancy, we would only run a mini panel of 6 cells, including one known c+, with the other 5 covering all the other clinically significant antigens (including an R1Rz to cover the E antigen), and would only perform a full panel if the lady's plasma reacted with 1 or more of the 5 cell samples that we would expect to be negative. We would, of course, also quantify they anti-c.

Hi Tim. I have no doubt whatsoever that you are right. The kind of antibody I was talking about in my post above is disappearingly rare, and I would not want to go back to routine tube IAT for all the tea in China. I am a huge fan of gel. On the other hand, for certain specialised tests performed in my laboratory, LISS tube IAT can be an essential tool.

The problem with the investigation of rare Rh antigens (and, come to that, very common Rh antigens, such as HrB) is that approaching the problem from either the antibody or the panel direction is fraught with difficulty due to the paucity of reagents. If you are really talking about rare Rh antigens (such as, for example Cx) the only real way to address the problem is by using rare antisera (such as anti-Cx). On the other hand, if you are also talking about very common Rh antigens, the problem is somewhat easier, because you can use such antibodies as Rh29 to demonstrate that the high incidence antigen is part of the Rh Blood Group System (assuming, of course, that such a reagent is available for your use - a big assumption, I know). Once you have established that the antigen really is part of the Rh Blood Group System, you can either use specific Rh antibodies to determine whether or not the antigen is expressed on the red cells, or nowadays, it is probably just as easy (if not more so) to obtain genomic DNA from the patient and subject it to sequencing of exons 1 to 9 of the RHD and/or RHCE gene. THat having been said, however, this is not as "easy" as it sounds. THere was a paper published earlier this year (Pham B-N, Peyrard T, Juszczak G, Dubeaux I, Gien D, Blancher A, Cartron J-P, Rouger P, Le Pennec P-Y. Heterogeneous molecular background of the weak C, VS+, hrB-, HrB- phenotype in black persons. Transfusion 2009; 49: 495-504) that showed the molecular background of the weak C, VS+, hrB-, HrB- phenotype to be, quite frankly, a bit of a mess!

Actually, many "warm" are complement binding, but the question was about "cold" antibodies.

I agree downloading from PAS to the LIMS cuts the risk of subsequent mistakes. I have no arguement with that. On the other hand, of course, not correcting a mistake that is on PAS perpetuates the mistake. If John Smith (DoB 01.01.59, blood group AB D Pos) is put on as Jon Smith, and then a real Jon Smith (DoB 01.01.59) comes in, and he is group O, D Neg, where are you then? :confused:

The very best of luck Lara, but from your intelligent posts, luck shouldn't come in to it!

In that case, it's unlikely to be a low incidence antigen, assuming they use exactly the same batch in exactly the same way. We get this occasionally with our hospitals using a DiaMed panel, whilst we use our own NBS panel, which, of course, will not express the same antigens. Also, just ocasionally, it could be due to expression of a Bg antigen that can "disappear" by being soluble. If they wash or resuspend their panel in a different suspension medium (we use Diluent2, most of our hospitals use Alseiver's solution) this too can make a difference. :confused:

I, too, get these telephone calls at all times of the day or night and try to point them in the right direction (mind you, if it is a daft telephone call, instead of pointing them in the right direction, I may well tell them exactly where to go!). Seriously though, I do agree with you that it very often is faster, and cheaper, than querying a software program.

Hi LaraT23, Are you absolutely certain there is nothing in the plasma? The reason I ask is that, very often, if the cell expresses a low incidence antigen (known or unknown to the producer) you will get quite a few apparently spurious positive results. Antibodies directed against low incidence antigens are quite common amongst the general population, more often than not as a "soup" of many specificities. We had an Lu:14 cell on one of our panels not too long ago (we knew about this one) and detected 2 anti-Lu:14's in 2 weeks. I had never detected one before, and have not since. If the Ortho screen cell and cell #2 are expressing low incidence antigens (not necessarily the same low incidence antigen, by the way) this may explain the problem. On the other hand, of course, it may not!

Is that the one that goes: 1. Use a team approach. 2. Describe the problem. 3. Implement and verify interim containment actions 4. Define and verify root causes. 5. Verify the corrective action(s). 6. Implement permanent corrective actions. 7. Prevent problem recurrence. 8. Congratulate the team. ??????? No, never heard of it! Yes, we do use a version of this, but I always get stuck at 7. I can never bring myself to go on to 8!!!!!!!!!!!!!! :rolleyes:

I didn't know ***** was a swear word in the USA????!!!!!!!!!! :redface::redface:

I couldn't agree more with you LIMPER55. There are Health and Safety Regulations for good reasons, and Health and Safety Regulations for the sake of regulations (and these latter regulations bring the former into disrepute). :mad:

Oh, I know what it means, it's just that the first question drives all the others out of my mind!

I already regard you as an absolute asset Brenda. WELCOME!

I must admit that I have had trouble with the "5 whys" technique - not least trying to think of 5 questions beginning "why?". I can usually get one question in my mind that drives out all the others, namely, "Why did we ***** up?". :confused::confused:

"Unvelievable". I love it! As it intimated, I am a great fan of gel, but, in the right hands, I am a great fan of pre-warmed, warm-washed, tube IAT, using either a broad-spectrum HAG or a monospecific anti-IgG. I had the huge honour (and luck) of being trained in red cell serology by both Dr. Carolyn Giles, when she was in charge of the Red Cell Reference Department of the WHO International Blood Group Reference Laboratory (when Joyce Poole was a Senior Medical Laboratory Technician in her Department) and, of course course, by Joyce Poole herself (who is now Head of this Department). Both taught me how to perform these tests, and, in Carolyn's case, not that she ever did swear, she swore by the technique. In Joyce's case, I know that she still uses the test in her Department on a regular basis. I honestly don't think that this technique is intrinsically insensitive; I think that it is the way people are taught how to perform the technique, and in particular, how they are taught to read the results that is wrong (that and trying to perform a test that is, essentially, unfamiliar to them through lack of practice. I have seen people bash the living daylights out of the tubes are gently spinning them to make the red cell button after addition of the AHG; so much so that they could make a strong anti-D negative! THey are not taught the gentle "tip and roll" required for this technique, with the emphasis onnthe word "gentle". I further think that they are so used to the robustness of the CAT that they do not realise just how gentle the resuspension has to be, and just how weak a positive reaction can be, and still be clinically significant. Without doubt though, it is a technique that needs practice, practice, practice, and performing it once in a blue moon is NOT sufficient to maintain competence. We use it in the Reference Laboratory that I manage quite a lot, but I make sure that my staff/colleagues are well and truely competent in the technique before I let them loose anywhere near a patient's sample. I do agree wholeheartedly with you though about the fact that, what goes on out there is scary! AS the saying goes: "Be afraid, be very afraid!". :eek::eek:

A good point, well made Brenda. We see quite a few of these too. It is probably because, although it is always quoted that there are about 14, 000 Kidd antigen sites per red cell, this is, of course, an average. Some cell samples will have more (the ones that you see reacting) and some less (the ones that you don't see reacting). I totally agree with you that anti-Jka is not an antibody that you want to miss. You only need to look at the antibodies that have caused most clinically significant delayed haemolytic transfusion reactions in any haemovigilance schemes around the world, and anti-Jka always seems to come out on top. We now always run a panel of enzyme-treated red cells by IAT, as well as our normal untreated panel by IAT, and we find that this is much more sensitive than running just the normal IAT panel with an enzyme panel (i.e. we didn't used to take the enzyme panel on to IAT). We get some cracking reactions like that. The problem comes, however, in two ways. Firstly, if the anti-Jka is not detected in the screen (which, in the UK, you only need to do by IAT). Secondly, if there is an "enzyme-auto" pan-reacting antibody present too, as, of course, this masks the anti-Jka (mind you, you soon pick it up by IAT after the transfusion - especially in the eluate!). I think this is the one drawback with using plasma, rather than serum. You do not have the complement system around to help you detect complement binding antibodies. We had a fatal case of anti-Vel in the UK only about 5 years ago, where the anti-Vel could only be detected in serum; but too late I'm afraid. That having been said, I wouldn't want to go back to clotted samples (except for certain specific tests) and I wouldn't want to go away from gel; I think it is a fantastic system too. Like you, I can't recall having seen a case of anti-Jkb reacting in a similar way, but, also as you say, they are considerably more rare in any case. :)

I'm extremely sorry Brenda. I think waht happened was that we were posting almost together, and you just won! As a result, your post appeared just above mine, and NO, it most certainly was NOT aimed at your post.