Malcolm Needs

You would need to know the number of platelets in your apheresis unit, which must be at least 3x10 to the 11 per litre. Then you need to know your patient's surface area in metres squared and weight in kilograms. So for a standard unit (3x10 to the 11), with a standard person (1.7 metres squared and 70 kilograms) the corrected increment would be; 44x10 to the 9 per litre x 1.7/0.7 = approximate rise of 108x10 to the 9. I thought everyone knew that:sarcasm::sarcasm: ! ACTUALLY, I HAD TO COMBINE THE FIGURES FROM TWO DIFFERENT TEXT BOOKS FOR THIS, AND THEN JUGGLE THE NUMBERS, SO I WOULD TREAT THIS THEORETICAL FIGURE WITH A VERY LARGE DOSE OF SALT. There is one thing worse than my spelling - and that is my maths!!!!!!!!!! :eek::eek::eek::eek:

I think your last sentence was the best thing to do; far better than the ravings of a Croydon-based lunatic!!!!!!!! :D:D:D:D:D

I'm sorry Fluffy agglutinates, but you are incorrect on both counts! Individuals with Weak D can and do make alloanti-D (Joyce has verified this at the IBGRL), and some partial D phenotypes give a very weak reaction with anti-D reagents (although not as weak as does a Del). You will also find that some hospital laboratories test cord red cells with an anti-D that will detect partial DVI and will give anti-D immunoglobulin prophylaxis if this test is positive (although they do not necessarily type the mum with this anti-D first to see if the baby inherited it from her)! :redface::redface:

Thanks for that. You would be a bit unlucky if your donors were C+, E+ or K+, given that they would also have to come from the Black population (not impossible, I know, but much less likely), but there is still a good chance of encountering a Jk(a+b+) donor. :)

I'm not advocating that you do this for one moment (particularly as it would not be a validated test), but there is a possibility (not a probability) that you could have done this. If you had "dissolved" the blood stain in a tiny bit of saline, then you would have also have "dissolved" some plasma. The resultant liquid could then be centrifuged to get rid of any cell debris. This liquid could then be used to inhibit anti-human globulin, used with red cells known to be coated with an IgG. If the AHG did not cause agglutination, then the plasma was from a human. If it did cause agglutination, then the plasma came from the meat. This test would be extremely difficult to control, and would presuppose that the family were not cannibals!!!!!!!!!!!!!!! :D:D:D

I agree entirely (why I asked the series of questions in my earlier post). For one thing, if it is a genuine Bhm, it could be that any B antigen on the red cells comes from adsorption of small amounts of B substance from the plasma (Type I chains), rather than being an integral part of the red cell membrane (Type II chains). Murine monoclonal antibody may not "recognize" these Type I chains as well as it does Type II chains, and these Type II chains are more easily "washed off" during the initial washing stages of the elution (depending on what elution technique was used. :confused:

As a matter of interest, what is her Rh and K type, and which antigens are you ignoring? An exchange every 6 to 8 weeks with anti-U! Lucky U! I bet that's fun finding blood for her that often. :)

Welcome Mary Ann.

Thanks. To be honest, that's what I thought myself. :)

Thanks Fluffy, but I'm actually off on certified sickness leave; I'm a poorly boy!

Thanks Fluffy. I'm off until Monday, but will certainly talk to "The Egg" on my return. I await Joyce's findings with a great deal of interest. When she gives her verdict, will you post the result please? :confused:

No. To be honest, I doubt if I would have worried much about the anti-Lea when it was detectable. Lewis antibodies (and antigens come to that) are strange in that they change over time, and this is because Lewis antigens are really plasma antigens that are adsorbed onto the surface of the red cell, rather than being an integral part of the red cell membrane. A baby usually starts off as an Le(a-b-) and then, if they are eventually to become an Le(a-b+), will go through the stages of Le(a+b-), Le(a+b+) and then Le(a-b+) as the fucosyl transferase enzymes mature. However, an individual may not remain as an Le(a-b+) throughout their lives. A pregnant lady, who is usually Le(a-b+) can become Le(a-b-) during her pregnancy, and even produce anti-Lea and/or anti-Leb, but will lose the antibody after childbirth and revert to being Le(a-b+). I certainly would not go hunting for E-, Le(a-b-) blood if the anti-Lea is no longer detectable (remember, Le(a-b+) blood has a little bit of Le(a+b-) or Le(a+b+) in it). On the other hand, if the anti-E were to disappear, I would most certainly continue to give E- blood. :)

Mission accomplished Marilyn! I am extremely jealous!!!!!!!!!!!!!! :(:(

Very expensive though.

What blood group are you going to give if the patient requires a red cell transfusion?

It could be, but it is unlikely on two counts. Firstly, the anti-C titre is lower than the anti-D titre, and you would expect the opposite for an anti-G. Secondly, although there are some partial D types that are G-, most are G+, which would mean it would be an auto-antibody, and so you would expect a positive DAT and reaction between the patient's own red cells and their own plasma in the auto control.

Gosh, I wish I had that quickness of wit. Mind you, the "Bedpan" obviously knew to whom your coworker was talking! Quite right too! :D:D:D:D

Love it!!!!!!!!!!!!!!!

By the way, what is the lady's Lewis type? I am intrigued by this one!

But does this mean that protein no longer adsorbs to the surface of these newer plastics? Don't know; just asking. :confused:

Hi Fluffy agglutinates, The result with the anti-H is the really puzzling one for me. Yes, the ethnicity "fits" for a sub-group of B, but even with a group A1 or a group A1B you would expect some sort of weak reaction with anti-H. Could you tell me at what temperature the patient's red cells were incubated with the anti-B and anti-A,B, whether the anti-A,B was a genuine anti-A,B, or was it a mixture of monoclonal anti-A and monoclonal anti-B, were the patient's red cells enzyme-treated and the tests repeated and what method was used for the elution (heat, acid, alkaline, Lui)? Lots of questions I know, but the answers will all give clues. ...but I am puzzled by the reaction with the anti-H. Could be your suspicion of a Bmh is correct! HIGHLY unusual! By the way, do you know the answer, and has the sample been sent to Joyce? :confused::confused:

What worries me a little about your proposal (although I can quite see from where you are coming dcharland) is that, very often the units transfused to neonates have their haematocrits artificially increased by disposing of the some of the plasma. Will not the adult units have a "normal" haematocrit and, therefore, the neonates could be in danger of ending up with a form of iatrogenic anaemia or worse, if the anaesthetists adjust the haematocrit in an uncontrolled way, circulatory overload? I don't know, I am only asking. :confused::confused::confused:

Amen to that. :)

No, no, they should be allowed to go on holiday, and, of course, some of the money we pay towards the reagents must pay towards these holidays (reasonble profits). There is a difference between them selling excellent reagents and reagents that are just a mixture of others, on the mis-guided premise that we actually need them. The difference between a 5 star hotel and a 4 star hotel!!!!!!!!!!!

Now that idea I could live with!