Hi there, I am new to this site, so I hope I am posting this in the right place. I guess I am looking for some insight. A few weeks ago, in the blood bank which I work, we recieved a type and screen on a labor and delivery patient. The patients type was A negative, and the antibody screen was positive, both cells 1&2 reacting weak 1+. The tech set up an ortho panel C ficin treated and untreated. The untreated panel reacted weak 1+ for anti-D (which was rhogam), but the ficin panel reacted 4+ with all cells, except the auto control which was negative. When a DAT was performed, that was negative as well. After conferring with the lead tech and the supervisor, it was decided that this patient had a cold autoantibody. This sort of puzzles me, as I thought that in a cold autoantibody situation, the autocontrol will be positive, as will the DAT for compliment. I understand that ficin can enhance colds, but I guess I am just not totally convinced that this was in fact a cold. Has anybody ever come across anything like this? I would really appreciate some helpful input! Thanks so much!

Hi there, I am new to this site, so I hope I am posting this in the right place. I guess I am looking for some insight. A few weeks ago, in the blood bank which I work, we recieved a type and screen on a labor and delivery patient. The patients type was A negative, and the antibody screen was positive, both cells 1&2 reacting weak 1+. The tech set up an ortho panel C ficin treated and untreated. The untreated panel reacted weak 1+ for anti-D (which was rhogam), but the ficin panel reacted 4+ with all cells, except the auto control which was negative. When a DAT was performed, that was negative as well. After conferring with the lead tech and the supervisor, it was decided that this patient had a cold autoantibody. This sort of puzzles me, as I thought that in a cold autoantibody situation, the autocontrol will be positive, as will the DAT for compliment. I understand that ficin can enhance colds, but I guess I am just not totally convinced that this was in fact a cold. Has anybody ever come across anything like this? I would really appreciate some helpful input! Thanks so much!

Hi klsmith,

Actually, this is not that an unusual situation in a group A patient (reactions with all enzyme-treated red cells, DAT negative and auto negative) and the key to it is in the ABO group of the patient and the ABO group of your screening and panel cells.

The patient, being group A, will have most of her H antigen (L-fucose) "hidden" by her A antigen (N-acetyl-D-galactosamine), whilst the screening and panel cells, being group O, will have all of their H antigen exposed.

The patient can, therefore, make an anti-H or anti-HI that will appear to be an alloantibody (although it is actually an auto-antibody) that will react very much more strongly with group O red cells (particularly those that have been enzyme-treated) than group A red cells.

Hope that helps.

Malcolm

:):)

Dear KlSmith and Malcolm,

Thank you for this interesting case and responce. As I have worked at several BB's I find the practice of running a selected cell panel (a D rule out panel) a much more efficient way of utilizing tech time, reagents, and overall expence. But I see that this practice takes away the experience of the situation that you present today. Question is, what is the clinical relevance of the Anti-H or Anti- HI in generating compatible blood products if this patient should have a need? Would your facility now be compelled to perform prewarm crossmatches as it has ID'ed a "Cold Agglutinin?" My concern is simply that you need only experience once an L&D patient going bad to realize how important it is to have the ablity to produce compatible products at a very fast pace. The practice at your facility, a practice that I have engaged as well, although thorough, is questionable when considering it's impact on our our ability to readily generate products for this patient if the need arises.

Dear KlSmith and Malcolm,

Thank you for this interesting case and responce. As I have worked at several BB's I find the practice of running a selected cell panel (a D rule out panel) a much more efficient way of utilizing tech time, reagents, and overall expence. But I see that this practice takes away the experience of the situation that you present today. Question is, what is the clinical relevance of the Anti-H or Anti- HI in generating compatible blood products if this patient should have a need? Would your facility now be compelled to perform prewarm crossmatches as it has ID'ed a "Cold Agglutinin?" My concern is simply that you need only experience once an L&D patient going bad to realize how important it is to have the ablity to produce compatible products at a very fast pace. The practice at your facility, a practice that I have engaged as well, although thorough, is questionable when considering it's impact on our our ability to readily generate products for this patient if the need arises.

Well, the point is, in this case, that it would be a good idea to "prove" the specificity before things get out of hand, but this is very easily done by using several samples of group A1 red cells, treated with a proteolytic enzyme. Assuming that I am correct (that the specificity is either anti-H or anti-HI), then all of these should be compatible.

In such a case, therefore, all group A units of blood would be compatible, and providing blood would be simple (i.e. group A). That having been said, however, unless the patient were to undergo profound temperature loss ( and I can't see any reason why she should) group O blood would be perfectly okay for transfusion, because:

1. the transfused blood would soon reach body temperature (and so the anti-H or anti-HI would be irrelevant, and

2. do not forget that the "main" incompatibility was detected with enzyme-treated red cells and, of course, the red cells being transfused have not been enzyme-treated.

This antibody would be clinically insignificant.

:D

Malcolm Needs,

Thanks so much for your answer, it was very helpful!

Malcolm Needs,

Thanks so much for your answer, it was very helpful!

My pleasure.

:D:D:D:D

We call an antibody cold antibody, it must react strongly in 4 degree C ,weaker in room temperature and 37 degree C.

The case KLSMITH described maybe a cold antibody and maybe an enzyme only antibody.

We see klsmith's pattern fairly frequently, and Malcolm gave a good explanation. When we through a saline antibody screen and auto control in the refrigerator for 15 minutes, all of the cells will usually react 3+ or 4+ positive.

How common is the practice of routinely running both a regular and ficin-treated panel? It seems that such a practice (like routinely reading tubes at IS, which has somewhat gone out of practice) just leads to unnecessary complications and lots of time & energy chasing clinically insignificant antibodies.

We do it with every single sample submitted to us (except we use papain), except for second and subsequent samples from pregnant ladies with a known antibody, but then we are a Reference Laboratory.

That having been said, it is advised in the BCSH Guidelines for Hospital Laboratories to do this too.

How common is the practice of routinely running both a regular and ficin-treated panel? It seems that such a practice (like routinely reading tubes at IS, which has somewhat gone out of practice) just leads to unnecessary complications and lots of time & energy chasing clinically insignificant antibodies.

Like Malcolm we do the same thing for all antibody id workups except we use PEG instead of Ficin or Papain, and unlike Malcolm we are a hospital based transfusion service.:D

We use solid phase first, then proceed from there. I do not see the value of doing both regular and ficin or PEG panels at the same time on a routine basis in a hospital lab. Many of the patients hospital labs have will have simple antibodies that do not require that much workup. We see more complicated ones because we function as a reference lab for the local hosptial community. But even knowing that, we start with a basic panel and go from there.

I am one to go with the simplest thing first and not muddy the water with too many panels at first. I have not found many that I think the combination of the ABO, screen cells, and history information is not enough to decide what to do with the specimen. We do just the gel panel A. I look at the screen results and the panel, if things look squirrly, we send it out. Much more time and cost effective for us.

Would it be protocol to report this "auto-antibody" on the patient's clinical test results? It has been my expierence that enzyme treated cells do enhance reactivity of non-significant auto antibodies.

Yes.

It is still an auto-antibody whether it is clinically significant or not.

Most people, if you look hard enough, have an auto-anti-I. This is an auto-antibody, but rarely is it clinically significant, except in certain pathological states or conditions.