Malcolm Needs

Cliff,
   The site looks great. I can not change the profile pic yet! Lots of new options...we can change display name that is really great!!
Big Thank you to cliff...

Thanks to all for your thoughts and prayers.....
 
We are strong---BOSTON STRONG!
 
Yes, Cliff and I are BWH'ers (Brigham and Women's Hospital) we had 10 trauma rooms going on Monday evening---an unusual occurrence, to say the least!!!!!
 
----By day I am Blood Bank at a neighboring Boston hospital, by night I am a Chemistry specialist at BWH. We were on lockdown all day Friday----having SWAT teams in your hospital and State Police manning the doors is still surreal to me, but that is what we endured all week last week and culminating Friday night. We are recovering----but it will be a while before we get back to "normal".......we are so fortunate to have had the resources to absorb the influx of injuries. From First responders to the trauma teams to the ancillary services, we pulled together and saved a lot of people.
 
Here's to hoping that no other city goes through anything like what we just did......thanks again for all your support!
 
 

Nope.  We had a few discrepancies with prenatal blood types from other labs.  Weirdly, they were all AB Neg.  Found out the doctor's office staff manually types in all blood types to the prenatal chart report.
 
You guessed it....the lab reports all said "Ab screen Neg"...the secretary thought that meant AB Neg.  You really can't make this stuff up.

Same here. Last year we had a doc send her patient to us 3 times: once for RhoGam work/up, twice to verify her type since we reported it as "Rh positive, not a candidate for RhoGam," while the reference laboratory supposedly reported Rh negative. It appeared that the doc was reading the [negative] result of the patient's antibody screen from the office chart and mentally equating the word "negative" with the need for Rh Immune Globulin.
Also, we draw a Type and Screen on all new OB admissions, then a Verification tube if they have no history in our system. The OB department has been one of the loudest protestors, but they may change their tune after this weekend when one of their nurses drew her own patient but labeled the tube with another patient's name. This was caught by comparison to previous records.
Never a dull moment!

He does that too !!!!!!!!!!!, very skilled, our Lord Needs!!!!!! 

Hello Malcolm,
         Please do not give more work to Cliff! If you have a cell phone you can play games on FB!!!   :)        

Thanks Cliff.
 
Ah well, I'll have to take in a pack of cards to play patience, or something like that when I'm doing multiple alloadsorption incubations when I'm on-call!!!!!!!!!!!!!!!!!

I haven't forgotten you, but I have a LOT of work to do to get the rest of the site live. The Library is going to take a lot longer than I hoped, very tedious manual database updates. I will find you an arcade.  
 
 
 
I'm still learning how to use the system, your usergroup wasn't allowed to use the Like button, you can now.

I am extremely pleased that you agree with my posts, especially the bit about all the best people being Ch-!!!!!!!!!!!!!!!!!!!!!!!!!!!!
:D:D:D:D

"Rhesus" Young Struik! Forsooth!
In most cases, TRALI is caused by donor leucocyte antibodies reacting with alloantigens present on the patient's leucocytes, although patient alloantibodies have been involved in some rare cases. The antibodies concerned are usually HLA class I and II specific, but HNA antibodies have also caused this. I would think that the reason they are saying that SDP is thought of as "risk free" is down, almost entirely, to the dilution factor, as the palsma is pooled, rather than the sovent detergent treatment.

Possibly quicker.


nOften clinically ineffective, asthe transfused donor cells are rapidly haemolysed by active C3b in the plasma,which binds to virgin CR1 sites on transfused red cells.
nThe autologous cells arerelatively resistant to C3b haemolysis, as all CR1 sites are blocked by C3d/g moities.

This sounds like a boast, but it isn't meant like that at all.
We've had some really great samples in in the last month (or just under).
1 x anti-Lan.
1 x anti-k.
1 x Oh.
1 x anti-Gya.
1 x anti-Joa.
Kudos to Joyce Poole and Nicole Thornton (who has taken over from Joyce, since Joyce retired) and their team for identifying the anti-Lan, the anti-Gya and the anti-Joa for us, because they foxed us - although we should have got the anti-Lan ourselves (black mark for me there).
I love working in red cell immunohaematology at NHSBT-Tooting Centre. We have such a great ethnic mix of patients that we see all sorts of antibodies that most people wouldn't see in their entire professional career. I am so lucky.
Right - that's me confirmed as a nerd then, if that fact wasn't already confirmed!!!!!!!!!!!!

Hi Linyuan,
I'm afraid there is no easy way to explain all this without using a lot of jargon that make it difficult to understand, but I will do my best.
Although most people have heard of the ABO and the Rh Blood Group Systems, there are, in fact, 30 different Blood Group Systems. Within most of these systems, there are several antigens (mostly sugars or proteins that are expressed on the surface of the red cell). For example, within the ABO Blood Group System, there are three antigens (A, B and A1 - group O individuals have no ABO antigens), however, within the Rh Blood Group System there are well over 40 different antigens.
The Mi(a) antigen is found within the MNS Blood Group System (it was the 7th antigen found within this system, which also has over 40 different antigens).
Altogether, there have been something over 350 different human red cell antigens described, although, of course, no everyone expresses everyone of these antigens on their red cells.
If you lack a particular antigen, you can make antibodies against this particular antigen (alhtough you do not make antibodies against every antigen that you lack. Very often, although not always, you have to be stimulated to produce these antigens by either having been given blood that expresses an antigen that you lack, or by carrying a baby whose red cells express an antigen that you lack (expressed because the baby inherits a gene from the father that leads to the expression of this antigen). Sometimes, however, the body produces antibodies without any apparent stimulation (such as anti-A and/or anti-, although, in reality, there are stimulants within the environment.
Now, to try to answer your questions.
1) No, there is ABSOLUTELY nothing wrong with your blood, in terms of you producing the anti-Mia. Many millions of people throughout the world produce red cell antibodies, and they are as fit as a fiddle.
2) All antibodies are proteins. There are five basic types of these (IgA, IgD, IgE, IgG and IgM). All of these basic types produce lots of different specific antibodies - in your case, the specificity is anti-Mia.
The two types we are interested in, in the world of transfusion, are IgG (which are a sort of Y shape) and IgM (which are a sort of star shape). What we are looking at, in the laboratory, is the ability for these antibodies to cause clumping (the correct word is actually agglutination) of red cells that express the corresponding antigen. In your case, your anti-Mia will cause Mi(a+) red cells to clump, but not Mi(a-) red cells to clump.
IgM antibodies tend to cause this clumping of red cells without any help.
IgG antibodies, however, are smaller than IgM antibodies, and cannot "reach across" between two red cells to cause this clumping without a "bit of help". All antibodies, as I said are proteins, and all of these are a particular kind of protein called immunoglobulins. In the case of your anti-Mia, it would appear to be an IgG antibody (from the report), and one way that we can "help" the IgG antibodies to "reach across" two red cells to cause the clumping is to perform a particular test called an indirect antiglobulin test (I won't go into details - it is fairly comlpicated to explain, but is a very sensitive test), but for this test we use a particular reagent called anti-human globulin, and this is the AHG to which the report refers. So, if you require a blood transfusion, the laboratory would test (cross-match) the proposed units by this test, using AHG, to ensure that the blood is compatible with your antibody (i.e. your antibody would NOT cause the red blood cells to clump).
If your antibody did cause the red cells to clump, and you were transfused these red cells (don't worry - this blood would NOT be given to you - that is the point of the test), then your antibody could destroy these transfused red cells, and you could become very ill indeed (I STRESS AGAIN, the point of testing the blood to be transfused to you is so that this does not happen).
Haemolytic disease of the newborn happens when you have an IgG antibody of some specificity (in your case anti-Mia) and the foetus's red cells express the corresponding antigen (in your case Mia). The antibody can cross the placenta (IgM antibodies do not) and can destroy the foetuses red cells (haemolyse them). This used to be a real problem, but nowadays, as long as the pregnancy is well-monitored and, if considered necessary for the baby's health and wellbeing, there are such interventions as early delivery or intrauterine transfusions, then the baby will be born with no problems. I must stress, however, that many women have produced red cell antibodies, of many different specificities, and have had babies that are totally unaffected, despite the fact that they express the corresponding red cell antigen on their red cells - so don't worry!
I hope this explanation helps to some degree, but, if not, say so and I, or one of the many really nice people on this site, will try to explain it in a different way.

From time-to-time there are some interesting threads on this site concerning how long a unit can be out of a fridge and then returned to the Blood Bank. Although I am fully aware that we all have to follow Guidelines and Regulations, there is, nevertheless, an interesting areticle that has just been published in Transfusion Medicine Reviews (I haven't had time to read it all yet myself) on this very subject for those who are interested. It is:
Brunskill S, Thomas S, Whitmore E, McDonald CP, Doree C, Hopewell S, Staves J, Cardigan R, Murphy MF. What is the maximum time that a unit of red blood cells can be safely left out of controlled temperature storage? Transfusion Medicine Reviews 2012; 26(3): 209-223.e3.

Well, that one is fairly easy.
Whereas anti-D can cause problems cross-matching in the future, or cause delayed or immediate transfusion reactions if further D Positive blood is transfused for a trauma, to a large extent, the latter can be seen when the first unit is transfused, and can be dealt with by various means (albeit, it is a real pain for the doctors should it happen during a trauma crisis).
Anti-D in pregnancy, however, causes major problems. It can result in the requirement for multiple intrauterine foetal transfusions and extrauterine exchange transfusions and, of course, if not recognised early enough in pregnancy, intrauterine death. Even in these days of fantastic Foetal Medicine Units, ultrasound/Doppler guided IUTs, there is a significant danger to the foetus.
Firstly, the foetus has to be immobilised with a fairly strong muscle relaxant, but, even then, there is a high risk of foeto-maternal haemorrage, the risk of foetal exsangunation and, although the risks are coming down, there is still approximately a 2% risk of foetal death each time an IUT is administered.
For this reason, we would also ensure that our O, D Negative blood for trauma, used for females of child-bearing potential are also K-. We do not want these individuals to make anti-K either, because it can cause such nasty HDFN.
One of your comments was though, that we do not want people given blood in the trauma situation to make Rh antibodies. If you are giving O, rr blood in all cases to try to stop this happening, how do you square the circle with your R1R1 patients making anti-c (another Rh antibody that can cause severe transfusion reactions and HDFN)?
The reason the Guidelines in the UK say what they do is because there has been a high level risk assessment performed, with Level 1 evidence taken into account, and the risk benefit analysis has shown that giving O D positive blood to males and women over 60 (soon to be over 50) is almost as safe as giving O D negative blood to alol patients in the trauma area.
Incidentally, although I now work as the manager in a Reference Laboratory, in another life I worked in Hospital Blood Transfusion Departments, and was the lead Biomedical Scientist when we dealt with three different IRA bombs in London (Chelsea Barracks, Hyde Park Corner and Harrods) and two major train crashes, so I have had experience of working during major incidents requiring mass transfusions for trauma.

Careful John TVC15 was only being sarcastic (see above)!

For some years now in the UK (at least since the 1996 BCSH pre-transfusion testing guidelines), it has been common practice in the UK that no K- female below the age of 60 is transfused with K+k+ or K+k- blood, unless they are exsanguinating, and there is no alternative.
As I said in a different post, it used to be common practice to advise Obstetricians to perform MCA DOppler/ultrasound (or whatever was around before these were available!) to monitor all anti-K pregnancies, although these are less predictive in early, rather than late pregnancy in cases of anti-K, and to consider referral to a Specialist Foetal Medicine Unit, depending upon the results. With the inprovement in the competency of individuals to carry out titrations, culminating in greater precision (if not accuracy) with results, we are less cautious, but still worry about an anti-K with a titre anything around 16 to 32.
Not all high-titre anti-K's seem to cause severe HDNF, whilst others with comparatively low levels sometimes cause extremely severe HDNF. It is not known why. Caine and Mueller-Heubach suggested that this may be due to how the K- lady was sensitised to produce anti-K in the first place (Caine ME, Mueller-Heubach E. Kell sensitization in pregnancy. Am J Obstet Gynecol 1986; 154: 85-90) suggested that, if the anti-K was produced as a result of a transfusion, HDNF tended to be less severe than if it was produced as a result of a previous pregnancy, but Leggat et al disputed these findings (Leggat HM, Gibson JM, Barron SL, Reid MM. Anti-Kell in pregnancy. Br J Obstet Gynecol 1991; 93: 667-673.
In 2005, a paper published by Chiaroni et al showed that that there is an association between HLA-DRB1 polymorphism and the production of anti-K. (Chiaroni J, Dettori I, Ferrera V, Legrand D, Touinssi M, Mercier P, de Micco P, Reviron D. HLA-DRB1 polymorphism is associated with Kell immunisation. Brit J Haematol 2005; 132: 374-378). They showed that the combined frequencies of the two HLA-DRB1 alleles (HLA-DRB1*11 and HLA-DRB1*13) was 83% in K immuniaed patients, when compared with 52% in healthy controls (Pc<0.001). One of my own staff members, who is taking an MSc, is going to do her project on the HLA-DRB1 types of lady's with anti-K in pregnancy, to see if there is an association between this polymorphism and the severity of HDNF with K+ babies.
At one time it was thought that anti-K interfered with foetal erythroiesis (Vaughan JI, Warwick R, Letsky E, Nicolini U, Rodeck CH, Fisk NM. Erythropietic suppression in fetal anemia because of Kell alloimmunization. Am J Obstet Gynecol 1994; 171(1): 247-252, and Vaughan JI, Manning M, Warwick RM, Letsky EA, Murray NA, Roberts IAG. Inhibition of erythroid progenitor cells by anti-Kell antibodies in fetal alloaimmune anemia. 1998; 338: 798-803), because the K/anti-K combination interfered with zinc ion transport across the cell membrane, but Daniels et al (Daniels GL, Hadley AG, Green CA. Fetal anaemia due to anti-K may result from immune destruction of early erythroid progenitors [Abstract]. Transf Med 1999; 9 (Suppl.): 16.) showed this not to be the case.
Hope this helps a bit.
:blahblah::blahblah:

For some years now in the UK (at least since the 1996 BCSH pre-transfusion testing guidelines), it has been common practice in the UK that no K- female below the age of 60 is transfused with K+k+ or K+k- blood, unless they are exsanguinating, and there is no alternative.
As I said in a different post, it used to be common practice to advise Obstetricians to perform MCA DOppler/ultrasound (or whatever was around before these were available!) to monitor all anti-K pregnancies, although these are less predictive in early, rather than late pregnancy in cases of anti-K, and to consider referral to a Specialist Foetal Medicine Unit, depending upon the results. With the inprovement in the competency of individuals to carry out titrations, culminating in greater precision (if not accuracy) with results, we are less cautious, but still worry about an anti-K with a titre anything around 16 to 32.
Not all high-titre anti-K's seem to cause severe HDNF, whilst others with comparatively low levels sometimes cause extremely severe HDNF. It is not known why. Caine and Mueller-Heubach suggested that this may be due to how the K- lady was sensitised to produce anti-K in the first place (Caine ME, Mueller-Heubach E. Kell sensitization in pregnancy. Am J Obstet Gynecol 1986; 154: 85-90) suggested that, if the anti-K was produced as a result of a transfusion, HDNF tended to be less severe than if it was produced as a result of a previous pregnancy, but Leggat et al disputed these findings (Leggat HM, Gibson JM, Barron SL, Reid MM. Anti-Kell in pregnancy. Br J Obstet Gynecol 1991; 93: 667-673.
In 2005, a paper published by Chiaroni et al showed that that there is an association between HLA-DRB1 polymorphism and the production of anti-K. (Chiaroni J, Dettori I, Ferrera V, Legrand D, Touinssi M, Mercier P, de Micco P, Reviron D. HLA-DRB1 polymorphism is associated with Kell immunisation. Brit J Haematol 2005; 132: 374-378). They showed that the combined frequencies of the two HLA-DRB1 alleles (HLA-DRB1*11 and HLA-DRB1*13) was 83% in K immuniaed patients, when compared with 52% in healthy controls (Pc<0.001). One of my own staff members, who is taking an MSc, is going to do her project on the HLA-DRB1 types of lady's with anti-K in pregnancy, to see if there is an association between this polymorphism and the severity of HDNF with K+ babies.
At one time it was thought that anti-K interfered with foetal erythroiesis (Vaughan JI, Warwick R, Letsky E, Nicolini U, Rodeck CH, Fisk NM. Erythropietic suppression in fetal anemia because of Kell alloimmunization. Am J Obstet Gynecol 1994; 171(1): 247-252, and Vaughan JI, Manning M, Warwick RM, Letsky EA, Murray NA, Roberts IAG. Inhibition of erythroid progenitor cells by anti-Kell antibodies in fetal alloaimmune anemia. 1998; 338: 798-803), because the K/anti-K combination interfered with zinc ion transport across the cell membrane, but Daniels et al (Daniels GL, Hadley AG, Green CA. Fetal anaemia due to anti-K may result from immune destruction of early erythroid progenitors [Abstract]. Transf Med 1999; 9 (Suppl.): 16.) showed this not to be the case.
Hope this helps a bit.
:blahblah::blahblah:

Hi Liz,
It is in Petz LD, Garratty G. Immune Hemolytic Anemias. 2004 (2nd ed). Churchill Livingstone; one of my favourite books. Specifically, it is Chapter 10, Blood Transfusion in Autoimmune Hemolytic Anemia, and, even more specifically, they discuss this on pages 388 and 389.
Table 10.10 on page 388 is quite revealing (particularly with regard to the top 3 alloantibody specificities in WAIHA).

Anti-A,B tends to be more avid than does either anti-A or anti-B, or a mixture of the two, even in these days of monoclonal antibodies. Thus, you are more likely to detect A and B subgroups, such as a very weak Ax, and this is important if an anti-A1 is present, so that the reverse group using just A1 and B cells, looks like a group O. This is probably more important on the donor side of things, than on the patient side of things, although Martin Olsson tells me that a weak Ax, transfused to a group O patient, tends to only raise the titre of the recipient's anti-A, rather than cause an acute HTR.
I wouldn't do this as an experiment!!!!!!

The above all seems good to me.
I would just add though, that everyone seems to be talking about auto-adsorption. It must be remembered that, if the patient has been transfused within the last three months, or, in the unlikely event that they are, or have been recently pregnant, then an alloadsorption must be performed, rather than an auto-adsorption.

I, too, am making the assumption that the lady is of White ethnicity, from what you post, but it must be remembered that, although Ro is far more common amongst the Black population than the White, it is not unknown for White individuals to be Ro (about 2%), so it is possible that the baby has inherited the Dce haplotype from the father.
:devilish::devilish:

With the advent of molecular testing, the area between Weak and Partial D has become more than a little muddied.
Originally, it was thought that, if the amino acid substitution was within the cytosol or intramembranous, the resultant D antigen would be Weak, but if the amino acid substitution was extracellular, the resultant D antigen would be Partial.
This has proved not to be so, as some of the individuals with "Weak D" ("proven" by molecular testing) have produced alloanti-D.
This is why the term "D variant" is far better to describe all such substitutions, rather than the two, somewhat nebulous, terms above.
It is safe to say that the three most common forms of Weak D, Weak D 1, 2 and 3, only form alloanti-D on very, very rare occasions (and, even then, the anti-D formed tends to be extremely weak), but anything "weaker" than these should most definitely be regarded as capable of forming alloanti-D, and treated as such.

Thanks Deny, and not at all - that's what they are there for.
Remember though - this work is not yet finished. There are still quite a few others to do.

Personally I prefer dealing with the physicians who failed the "God 101 class" . This group is at least more apt to listen and then decide ranther than to assume they know everything. I think I am beginning to see a trend of the younger docs listening more to the "specialist" front line workers. Some are actually rather down-to-earth. Hang in there and keep chipping away at the block of arrogance a little at a time. I try really hard to kill them with kindness and refuse to lower myself to the bad attitudes experienced from some quarters.