A 84 years old lady was unwell for a week and upon contact with the health services she was found to have a hemoglobin of 3.6 g%. To the left is her blood picture.
| October 2008 - Clumping blood |
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| Written by Abu Dzarr |
| Saturday, 18 October 2008 15:45 |
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She started having mild lethargy and fever over that one week. There was no dark urine. She was not aware of turning yellow. She had mild cough but no shortness of breadth. On examination, she appeared pale and had tinge of jaundice. Her hemodynamics was normal. Temperature was 37.6C. There was gallop rhythm and flow murmur, Grade 2 ESM over the aortic area. She had coarse crepitations over the left lower zone otherwise there was no other signs of consolidation. There was no hepatosplenomegaly, neither was there any palpable lymphadenopathy. There was consolidative changes over the left lower zones . Her 12-lead ECG showed normal sinus rhythm. Her blood counts were as follow. Hb 3.6g%, MCV 110 fL, MCH 100, TWBC 18.1 x 109/L and Platelet 324 x 109/L. Figure 1. The following photomicrograph showed her peripheral blood smear. Notice that her red blood cells were clumped together. We were not able to assess the morphology of individual red cell.
Figure 2. There was relative neutrophilia with left shift. Majority of the neutrophil show toxic granulation and vacuolation as shown below.
Figure 3. When her slides were prepared at 37oC, we can grossly notice the difference in the degree of clumping on each slides. The lower slide were warmth.
Figure 4. When the warmth slide was observed under x400, noticed that the degree of clumping has remarkably reduced. Compare this photomicrograph with figure 1. The morphology of individual red cells can be clearly visualized and we can see a lot of spherocytes which has lost its central pallor and numerous polychromatic cells (red cells whose cytoplasm appeared bluish) indirectly indicating reticulocytosis.
Figure 5: In fact the clumping can even be observed on the wall of the specimen tube as shown below. If it is immersed in ice water (say for a minute) the clumping will become more pronounced.
Liver function test: TP 60, Alb 33 g/L, Glob 27 g/L, AST 34, ALT 27 IU/L, ALP 102 IU/L, Total Bili 65 μmol/L (D 25 ID 40) Renal function test: BUN 7.1, Na 141, K 4.3 mmol/L, Creat 101 μmol/L, Ca 2.10 mmol/L Lactate Dehydrogenase: 718 IU/L Urine for hemoglobin was negative. Mycoplasma serology was negative
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| Last Updated ( Sunday, 02 November 2008 22:55 ) |






Her direct antiglobulin test (DAT) was positive with strong reaction 3+ for C3d and 1+ for IgG. Her DAT for IgM was negative. Her indirect antiglobulin test was negative.
There are about 30+ more of blood group systems corresponding to either polypeptide (rhesus group one of them) or carbohydrate molecules (the usual ABH as an example) on red cell surface (that was 2 years ago when I last updated myself). Probably a couple more now.
The anti Ii (big I small i) is one of these blood group system. Apparently now the big I and small i has been reclassfied into separate systems. At birth the majority of molecules on the red cell surface from this system if we follow the old classification is the small i, a linear repeats of N-acetylGalactosamine (GalNAc). This is brought about by the sequential action of two enzymes glycosyl transferases; beta-1,3-acetyl glucosaminyl transferase and beta-1,4 galactosyl transferase. In fetus and neonates the molecules in this system are in the small i form.
As we grow older (approximately by 18 months) there is progressive conversion of this molecule from small i antigen to big I antigen. A third enzymes or transferase also known as GCNT2 (beta 1,6 GlnAc T) , lead to addition of branch chains on the original linear i antigen. Hence this new structure is the I antigen. Majority of adults are in the I antigen form.
Cold agglutinin has predominantly anti-I specificity. When we do the cold agglutinin titers we wish to obtain cells which are devoid of big I antigen as a reference. The degree of agglutination using the patients red cells which has big I antigen is compared to cells devoid of this antigen i.e cord blood with predominantly small -i antigen. If there are a difference of more than two folds between these two samples, then we may consider that the cold agglutinin has anti-I specificity.
The reason we pick group O and not A, B or AB is to avoid getting entangled with immune reactions that may occur towards the ABH systems. Group O cells are devoid of the A and B antigens, hence we are better assured of this.
More can be read about blood group I here.
Hope this help