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Sorry guys but you've got it wrong about the witches. she was a witch if she DID NOT drown - in which case she was burned at the stake. whether she had anti-D or not!

Probably not helpful, but there is not a shred of scientific or clinical evidence for the efficacy and safety of this time limit. Totally expert opinion based upon a group of white haired males (like me) sitting around a table eating tuna fish sandwiches 60 years ago :). We document such stuff for the two regulatory agencies and two accreditation groups we are inspected by. How's that for efficiency? Four inspections.

I am going to make myself VERY unpopular here. Firstly, there is no such antigen as Kell (the closest is K5 or Peltz), and there is no such antibody as anti-Kell (the closest is anti-K5 or Anti-Peltz). The blood group system is Kell Blood Group System, but the first antigen within that system is K, and the antibody directed against that antigen is anti-K. The ONLY individuals who can be described as being Kell Negative are those incredibly rare individuals who have the Ko phenotype. Secondly, ONLY genes can be either homozygous or heterozygous (or, in some cases, hemizygous). Antigens CANNOT be described as either homozygous or heterozygous (or, in some cases, hemizygous). As red cells do not contain a nucleus, but merely express antigens, as the result of the individual inheriting certain genes, red cells CANNOT be either homozygous or heterozygous (or, in certain circumstances, hemizygous). The correct way of describing such red cells is to describe them as having either homozygous expression, or heterozygous expression (or, in some cases, hemizygous expression). Having got that off my chest (BUT, IT IS VERY IMPORTANT), I will now address the underlying question of this thread. Without doubt, the reaction between an anti-K and the K antigen CAN show "dosage"; I don't think anyone would dispute that these days. However, the more important question is, over the years and years and years that we have been using antibody screening cells that are K+k+, and have, therefore, NOT detected an anti-K that only reacts with red cells that have (supposed) homozygous expression, and do not forget, some of those cells may actually have come about as the result of a genotype of KE02/KEN, which means that the red cells actually have hemizygous (or "single dose"expression), how many patients have actually suffered a haemolytic transfusion reaction that has been clinically significant, causing morbidity or mortality? I would contend that, having looked through as much of the available literature as I have been able, the answer is zero. Obviously, if there is an anti-K present in the first place, albeit, it is undetectable by routine serological techniques, then transfusing the individual with either K+k+ or K+k- red cells will boost the anti-K, but it has not, as far as I know, resulted in mortality or morbidity, but will, almost certainly, result in an increase in titre and avidity of the antibody (I recognise, of course, that this could have disastrous results in a pregnancy, but only if the pregnancy is not properly monitored). On top of all the above, it is well-known that there are mutations of the KEL1 gene, resulting in "unusual" amino acid substitutions, resulting in weakened expression of the K antigen, are not unknown. It is well known that almost all blood group systems have their "quirks", which means that nobody can rely 100% on their antibody screening cells, BUT WE ALL DO! I would politely suggest that an anti-K that is only detectable with red cells that are (genuinely) K+k- are not that important.

I read on the Internet that if a person sinks in water and drowns, they're proven to be a witch........

I would get back to God (Oh, sorry, I meant the OB) and get him to give the reference. With all the work done by Clarke, Mollison, and the more recent work Urbaniak, all three of whom were professors for good reason, and all three of whose work showed this to be a waste of time, money etc, I have grave doubts that such a citation, by a reliable author/authors, exists (but I will try to contact Stan, because, if he doesn't know, I doubt if anyone else will, just in case).

Reply from Professor Stan Urbaniak. "Hi Malcolm. This does indeed sound like nonsense. The only work I know of trying to reduce the anti-D titre in women was using oral RhD rbc extract (Biermé et al) and that was shown to useless in a clinical trial. Best wishes Stan - from sunny Mallorca!"

As long as idiots exist in the world, they will thwart any solid plan we put in place to mitigate their recklessness.

I have actually seen a number of these beasts - usually as a result of a complaint that cell x did not pick the cell up when cell y did - and cell y just happened to be a K+k-. Usually these were antibodies that were detected years ago and whose levels have now fallen, predictably, with time. The pragmatic point is - you are never going to get every single set of screening cells with a k- cell in them. If you've got one, great - use it! If you haven't I still would not lose any sleep over it. Malcolm's points above are of course totally relevant as usual

I agree entirely with what you posted Ensis01, however, I am prepared to make a small wager that the anti-C and anti-e described in the article, found in a sickle patient, was actually an anti-hrB. Classically, an anti-hrB mimics an anti-C+e (in the same way that anti-hrS classically mimics anti-ce/anti-f). If I did win my wager, the patient would have a mutated RHce gene, and even if he/she had been transfused with Ro red cells from the start (and so probably matching the apparent Rh type), an anti-hrB would probably still have been formed (see, for example, Chou ST, Jackson T, Vege S, Smith-Whitley K, Friedman DF, Westhoff CM. High prevalence of red blood cell alloimmunization in sickle cell disease despite transfusion from Rh-matched minority donors. Blood 2013; 122: 1062-1071; doi: https://doi.org/10.1182/blood-2013-03-490623).

Sorry Malcolm, I was distracted by a problem that I was having with a computer crossmatch whilst posting last... Scott

I see from where you are coming Scott, but you would have to perform a cost/benefit analysis on whether or not it is worth including an "enzyme screen" (and I doubt if things have changed since this was last done, because, if anything, indirect antiglobulin techniques, with untreated red cells, have become more and more sensitive) it is not worth it. On the other hand, as far as panels are concerned, I have never understood why people would "drop" this test. It is such a useful test, particularly when there is a mixture of antibody specificities. One thing that is definitely TREASONABLE is having patients, commonly, who are either Ko or Jk;-3!!!!! I TRUST you mean K- and/or Jk(a-)? Come on my friend - you KNOW I am a pedant!!!!!

The word 'significant' is interesting in this context. In most of -Europe antibodies that are detected only in enzymes, including the enzyme-only anti-Es and -Cws would NOT be considered significant and most of the time would not be detected in the first place. Nor would the numerous anti-Lea, -Leb and -P1 that you would pick up. Always assuming that you are working with a sensitive IAT in the first place, of course.

This is me going back to the early 1970s, when I was first working at the International Blood Group Reference Laboratory (IBGRL) when it was still in London, and so my memory might not be 100% reliable, but I'll have a go. Obviously, in those days we used to use polyclonal anti-A or anti-B that was derived from human donors, rather than monoclonal antibodies (essentially, there were no such things in those days). We did know enough, however, not to use anti-A,B from group O donors, because of the chance of cross-reaction. We incubated the red cells against the antibodies at 4oC for about an hour, and then washed them at least six times in normal saline (we didn't even use buffered saline in those days). The last wash was kept as a negative control. Next comes the clever bit. We used heat elution at 56oC, as did many people, but the really clever bit was the way we kept the supernatant at 56oC during the centrifugation stage, so that the antibodies would not go back onto the antigens as the tests cooled down. The Director of the IBGRL at the time was the late, GREAT Dr Kenneth Goldsmith (I use the term "great" advisedly). He built a wooden box that contained the centrifuge, but also had a common light bulb in it that heated the entire contraption when turned on (we had to turn it on a good half an hour before we used it, to allow it all to come to temperature), but the whole contained a thermostat, so that the temperature as close to 56oC, so that a higher temperature did not denature the antibody, and a lower temperature did not allow the antibody to go back on to the antigens (he really was an amazing person - a doctor who was also an expert scientist). The eluate and the last wash were then tested against A1, B and O red cells at room temperature (23oC incubator), which, of course, all acted as internal controls. Later, we realised that the Lui elution technique (using melting ice) was a more efficient technique for eluting ABO antibodies, but everything else (barring the heated centrifuge) was the same. Nowadays, we hardly ever bother. It is very time consuming for virtually no return. If the subject is a patient, we would transfused group O red cells, and if the subject is a donor, it is cheaper and simpler to exclude them, as long as they are counselled, to ensure that they do not feel "stigmatised".

People can be quite creative when it comes to finding an "easier" way to do their job. That is one of the reasons I have always been a firm believer that complicating a process never makes it better or safer. I know the rational behind the 2 types being required but I personally never bought into it being a practical solution the potential problems it is trying to solve because of the many more problems is has seemed to cause for the staff resulting in all the work arounds they manage to come up with. For it to really work you would have to have 2 separate draws performed by two different people at different times. (Both phlebotomists in the room drawing one immediately after the other defeats the purpose.) Then you need to have two different techs perform the testing, one for each sample. This would be impossible in many smaller facilities, especially on evening and night shifts. Of course the requirement came from people based in large, well staffed facilities. I'm starting to ramble so I'll stop here for now. I have one question, in the past the AABB rule was written that you had to have 2 sets of test results, the one you are currently performing and one on file to compare the current one to and if you did not have one on file then you needed the second test performed prior to issuing RBCs. It that still the case?

Testing the same blood sample twice will not detect WBIT. That is why we draw a second blood sample from a different venipuncture from patients who initially type not group O. We are not AABB accredited.

In the UK, where this "rule" originated (I think!), our Guidelines do not "allow" the grouping of the same sample twice (what is the point of that, if the sample was taken from the wrong patient in the first place? It would mean that, for example, the sample would be grouped twice as group A, and would be found to be serologically compatible with group A units, even if the patient was actually group O - and so, dead!). We have to have two samples taken at different times (preferentially by a different person). Of course, we would certainly NOT stop blood being given in a situation where the patient is bleeding to death - but we WOULD only give group O blood until the second sample is received and typed (and the Rh type would depend upon sex and age) wherever we can (obviously, in the case of a major incident, we may have to modify this, but the Guidelines allow for such a situation). A VERY intelligent gentleman (Dr. Brian McClelland MB, ChB, ND Linden, FRCP(E), FRCPath), former Consultant Haematologist to the Scottish National Blood Transfusion Service, Edinburgh, UK) once wrote, "Transfusion has risks, but bleeding to death is fatal."

Thanks all. He seemed so convinced that there was an article and he is a respected practitioner. It could be the article was something he remembered from 1985 and he hasn't had a case in recent years.

From the transfusion article "WB offers several benefits over component therapy including providing simultaneous treatment for both oxygen debt and the coagulopathy of trauma; it is a more concentrated product compared to reconstituting WB using component therapy; and cold-stored WB contains PLTs that appear to have equivalent or better hemostatic effect in both in vitro tests and in clinical trials, compared to PLTs that have been stored under conventional room temperature conditions. Another benefit of WB that is perhaps harder to quantify is the simplification of the resuscitation effort with its use, especially in the prehospital environment. In such settings, where the clinical staff are task saturated, patient intravenous access is limited, and storage space in helicopters and ambulances is very limited, having the ability to provide a balanced resuscitation fluid in one bag instead of up to four bags is valuable. This is important because any delay in the provision of blood products in hemorrhagic shock can be lethal; mortality is increased by 5% for each minute there is a delay in the delivery of blood products."

Our ARC is starting to offer these products. They are using a titer cut-off of 200. The whole blood units will cost 3 times the price of a RBC. It's good for 21 days. Oregon Health Sciences University will be stocking them for traumas. They are the 4th hospital in the country supplied by ARC to use WB in their trauma program. Our ARC is the Pacific Northwest region in Portland.

In our case (the UK) it is from the moment the blood is issued from a controlled fridge.

I think one would have to realise that VERY few examples of "enzyme-only" antibodies recorded in the literature that have proved to be clinically significant, which is why, as Anna says, in most countries, it is no longer a requirement to use enzyme-treated red cells in the antibody screen. Of MUCH more importance are any clinically significant antibodies directed against antigens that are denatured by certain enzymes (for example, the Fya antigen being denatured by either of the two most commonly used proteolytic enzymes in transfusion laboratories; namely ficin and papain), and which may be "masked" by the antibody being described in this thread (i.e. antibodies of undetermined significance, AUS's, non-specific reactions). Most clinically significant antibodies are either quite avid, or have a high titre, and so one way of ruling them out is to titrate the plasma until the known (but unidentified) antibody is either no longer detected, or is only detected very weakly, and then test it for the presence of clinically significant antibodies. I know of some laboratories that do this, but it is certainly not a technique that I would recommend under any, but the most urgent circumstances. If, for example, I had an anti-Inb in my circulation, in addition to the sort of antibody being described in this thread (seriously unlikely, as, not only am I of White European ethnicity, rather than of South Asian, Iranian or Arab ethnicity - and I also happen to know that I am In(a-b+), as my blood has been tested - by Joyce Poole, and I am quite prepared to believe her results!!!!!), and this clinically significant specificity was missed because of using the "titration technique", assuming that I survived, I would be straight down to my legal representative at the earliest opportunity! Therefore, I would recommend that, in all cases, a sample is sent to the reference laboratory (and this opinion is NOT formed by the fact that I used to work in a reference laboratory, but is an honestly held view).

I think the more important question would be, how many facilities not doing this are seeing significant negative outcomes because they failed to detect those antibodies this technique would have potentially identified?

Not to my knowledge. Indeed, I don't believe free standing EDs should have blood available, unless there is no hospital within 20-30 miles and no helicopters are available for transport. I would want patients with life threatening bleeding or anemia to be taken only to a facility with on-site surgical facilities, surgeons, interventional radiology, etc. which are generally not available in free standing EDs. In other words, a fully staffed hospital. I would advocate taking such critically ill patients to the nearest level 1 or 2 trauma center, whenever one can, and bypass the free standing ED.

Prof. Theirry Burnouf, Prof. Axel Seltsam, Sue Johnson and some English guy ay Cressier in 2015.

I contact with ortho about this and they reply : " I assume you are doing your crossmatch in gel. If you see any agglutination above the negative red cell button the result is positive. And NO – you cannot respin the card and re-read it. Additional spin time can make a true positive become negative. Hope this helps. Regards, Dee Landers Technical Specialist III Ortho Care Technical Solutions Center "