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gagpinks

IgG or IgM?

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We have patient who has developed anti-c at 30 weeks gestation.Her  antibody screen was negative at 28 weeks and her bloos group is B RhD positive . Sample sent to reference lab for titre and it was 15 and at 34 weeks her titre gone up do 20 iu/ml. Since she  developed anti-c her her reverse group is reacting  with B cell 2+ or 3+. Do you think it's because of anti-c  is IgM in nature.  If that the case, Will it casues severe HDFN?

Thanks 

 

Edited by gagpinks

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12 minutes ago, gagpinks said:

We have patient who develop anti-c at 30 weeks gestation.Her  antibody screen was negative at 28 weeks and her bloos group is B RhD positive . Sample sent to reference lab for titre and it was 15 and at 34 weeks her titre gone up do 20 iu/ml. Since she  developed anti-c her her reverse group is reacting  with B cell 2+ or 3+. Do you think it's because anti-c IgM in nature.  If that the case, Will it casues severe HDFN?

Thanks 

 

Hi gagpinks,

As a UK Biomedical Scientist, if it is the last thing I do, it will be to teach you to use the correct nomenclature!

I can assure you that NHSBT Reference Laboratories DO NOT perform titres on samples of anti-c (or anti-D) from pregnant women, but, instead, perform quantification, and they are reported as IU/mL, and only because the computer system we use will not allow us to report them in the correct nomenclature (IUmL-1)!  Okay, rant over!

I would say that, without a doubt, there is an element of IgM in this lady's anti-c (unless, of course, there is another, as yet unidentified IgM antibody against another antigen expressed by the reverse grouping B red cells) as the reverse grouping B red cells have the Rh phenotype rr.  This may mean that the quantification results are falsely high, because the rr red cells used to perform the quantification are enzyme treated with bromelin to decrease the zeta potential and allow the red cells to come into closer proximity with each other, and this would enhance a reaction with an IgM anti-c, just as well as it would an IgG anti-c.

That having been said, there is no guarantee (at this time) that there is not an element of IgG anti-c present, and as this situation cannot be guaranteed, the pregnancy should be treated as if the entire anti-c is IgG, and that the quantification results are accurate; in other words, the case should, at least for now, be treated as if severe HDFN is a possibility.

So, what to do?  Well, one thing that you should do is send a sample of maternal peripheral blood to the IBGRL for foetal genotyping, to determine if the foetus carries the RHc gene (it almost certainly will, as the biological father is unlikely to also be c Negative, as the mother must be - although it is possible - but then, why would the mother have made an anti-c).  Assuming, therefore, that the foetus carries the RHc gene, and will express the c antigen on its red cells, then, again, you have to treat the pregnancy as if severe HDFN is a possibility.

The other thing that should be done at this stage, either by your own laboratory (if you have the reagents and the SOP, with staff competent in the technique - UKAS, you understand!), or by the Reference Laboratory (more likely) is to treat the maternal plasma with dithiothreitol (or a similar reducing agent - but please, not 2ME - unless you have lost your sense of smell!) to denature the IgM anti-c molecules, to see if there is an element of IgG anti-c present.  If there is an element of IgG present, then, once again, the pregnancy should be treated as if severe HDFN is a possibility.  This could be an unusual, but not unique case, of an antibody causing clinically significant HDFN, where the antibody has been formed after 28 weeks of gestation.

Come what may, the maternal antibody should be monitored from now until delivery as a minimum every two weeks, and, of course, the foetus should also be monitored by MCA Doppler (or something similar) until delivery, just to be on the safe side.

Sorry I can't give you a more definitive answer, but this is both a rare and interesting case.

One thing that I would ask, and that is, if the antibody screen was negative at 28 weeks of gestation, why were you sent another sample at 30 weeks of gestation?  Did the lady have a potential sensitising event, such as a fall?

Malcolm

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Hi Malcolm 

Sorry about using wrong terminology , and yes I would love to learn from you. We arre monitoring this lady as per guidelines. It was just thought came in mind because she developed anti-c during pregnancy.  We have performed antibody identification at room temperature and it was reacting strongly 4+( anti-c).

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On 28/08/2016 at 8:19 AM, gagpinks said:

Hi Malcolm 

Sorry about using wrong terminology , and yes I would love to learn from you. We arre monitoring this lady as per guidelines. It was just thought came in mind because she developed anti-c during pregnancy.  We have performed antibody identification at room temperature and it was reacting strongly 4+( anti-c).

Lady had delivered the baby and Hb was 198g/dl and required triple phototherapy.  Baby is well and now has been discharged. 

Edited by gagpinks

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Posted (edited)

Another interesting  similar case. In this case antibody screen negative in first pregnancy and also negative at booking blood in second pregnancy.  Repeat antibody screen at 28 weeks found to be positive with anti-c . There is also additional reaction detected in reverse group probably due to Anti- c IgM in nature . Send sample to RCI and quantification level is 37.2 IU/ml and followed repeat testing in 2 weeks went up to 56. Clinician decided to induce her at 36 week. First baby was Rh negative now just waiting for baby to born. Hope baby is not r'r . Otherwise it will be real challenging scenario.  

Edited by gagpinks

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On 6/28/2018 at 11:50 AM, gagpinks said:

Another interesting  similar case. In this case antibody screen negative in first pregnancy and also negative at booking blood in second pregnancy.  Repeat antibody screen at 28 weeks found to be positive with anti-c . There is also additional reaction detected in reverse group probably due to Anti- c IgM in nature . Send sample to RCI and quantification level is 37.2 IU/ml and followed repeat testing in 2 weeks went up to 56. Clinician decided to induce her at 36 week. First baby was Rh negative now just waiting for baby to born. Hope baby is not r'r . Otherwise it will be real challenging scenario.  

Here are my questions regarding this case.

1) Is it acceptable to assume an antibody predominantly IgM if reactive at room temperature, without using DTT or flow cytometry to confirm it? If there are enough IgG, it may agglutinate at room temperature as well. 

2) We often time see problems in ABO plasma type due to anti-c and anti-e. We never questioned whether it is IgM or IgG since they are predominantly IgG in nature. Are we going to be "reinventing the wheel" if we DTT treat an antibody that is known to be predominantly IgG. 

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Well dothandar, the answer to your first question is "YES", because this phenomenon has been seen many times over many years.  In those earlier years, experiments were performed to determine the immunoglobulin molecules present, and in every case there was a mixture of IgM and IgG.  In the end, it was decided that performing such experiments was a waste of time and money, for very little return.  Why reinvent the wheel now?

Turning to question two, all immune antibodies start off as IgM as a result of primary sensitisation, but then quickly change to IgG, even from the primary sensitisation (and almost always from a secondary sensitisation), and, undoubtedly, some IgG antibodies can cause agglutination when no potentiating agents are present (for example, IgG ABO antibodies), however, this is not true of Rh antibodies.  In the case of Rh antibodies, it is not a function of the antibody, so much as a function of the number and proximity of the antigens.  This can be seen with certain examples of human-derived IgG anti-D, which never cause "saline agglutination" at 37oC with red cells of "normal" Rh types, but do so with red cells exhibiting the exulted-D types (such as D--/D--, DCw-/DCw-. etc, because the number of D antigen sites available, particularly towards the outer layer of the sialic acid cloud, allow for Rh IgG immunoglobulins to come close enough between two (or more) different red cells to cause agglutination.  However, even in such a situation, the incubation temperature needs to be 37oC, and not "room/ambient" temperature.

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