Colin Barber

Shily, I am sure Malcolm will also post a reply as I know he has investigated cases of Hyperhaemolysis. I my area of London we have a number of Sickle Cell patients who are treated in our hospital. Within that population of Sickle Cell patients we have at least 4 that I know of who are not able to be transfused.
The reason for this is whenever they have been transfused once they have become sensitised they have a haemolytic transfusion reaction in which they seem to destroy not only the the transfused cells but also some of there own cells as well.
It's very frightening when it happens because as Malcolm says it's potentially fatal. As far as I know there are lots of theories but no one knows the actual mechanism involved in the haemolytic episode, it appears to be an acute onset aggressive haemolytic process triggered by transfusion. Most of the patients have complex serology usually with multiple allo antibodies, the haemolytic reaction occur when phenotyped and crossmatch compatible units are given and post transfusion reaction investigations still show that the units were apparently compatible.
I think there is a PhD for who ever works out exactly what is going on in these patients.
Colin

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:

Malcolm this site would be poorer without your posts and one thing about blood bankers is we all seem to have quite strong views and I am sure we can all verge on the self-opinionated at times, but good thing about a reasoned debate is we can also all still learn something and at times have our views changed by a well formed line of thought. Anyway please keep posting.

Rravkin@aol.com,
I am sorry I don't the exact methodology our colleagues in the Blood Service use to test for the presence of bacteria in the packs. They have recently announced that from next year they will roll out bacterial testing of all platelets they issue. If any of the UK NHSBT staff who subscribe to Blood bank talk pick up on this thread they will I am sure be able to answer. The link to changes to platelets is:http://hospital.blood.co.uk/library/pdf/The_Update_Nov_2010.pdf

From the 2003 BCSH Platelet guidelines:
2. RhD incompatibility
• RhD-negative platelet concentrates should be given, where possible, to RhD-negative patients, particularly to women who have not reached the menopause (grade B recommendation, level III evidence).
• If RhD-positive platelets are transfused to a RhD-negative woman of childbearing potential, it is recommended that anti-D should be given (grade B recommendation, level III evidence). A dose of 250 i.u. anti-D should be sufficient to cover five adult therapeutic doses of RhD-positive platelets within a 6-week period, and it should be given subcuta- neously in thrombocytopenic patients.
• It is not necessary to administer anti-D to RhD-negative men or women without childbearing potential who have haematological disorders and receive platelet concen- trates from donors who are RhD positive.