A case of acquired hemolytic anemia of 12 years’ duration showing a permanent polyagglutinability for at least 9 years, is presented.

1. Polyagglutinability is due to the presence on the surface of the patient’s erythrocytes of an antigen unknown up to the present time, which is independent of antigens T and H and does not behave like a normal antigen modified by proteolytic enzymes. It has been designated by the letters Tn. The Tn substance is not secreted in saliva. This antigen has not been found on the erythrocytes of 25 members of the patient’s family.

2. The substance which induces agglutination (natural anti-Tn) was found to be present in the serum of 473 white adults and 33 adult Negroes. It was absent or weak in 28 sera from cord’s blood. It acts like a complete antibody, being active in saline at the temperature of laboratory and then inducing massive clumping of Tn red cells. Through absorption and elution studies and through sensitization in rabbits, we have been able to demonstrate that anti-T and anti-Tn are distinct.

3. There are in our patient’s serum: (a) a substance specifically active against Tn erythrocytes treated by trypsin; this may be an immune anti-Tn; (b) a nonspecific incomplete antibody weaker than the anti-Tn and active against all varieties of red cells treated by trypsin; (c) an incomplete anti-E; (d) a cold antiplatelet substance; and (e) an immune antileukocyte antibody.

These three last antibodies are very probably due to transfusions.

4. To explain the combination of an acquired hemolytic anemia and polyagglutinability, two hypotheses are presented: (a) The acquired hemolytic anemia has no relationship to the existence in the patient of a very rare group antigen, perhaps confined to one family. (b) The hemolytic anemia is directly related to the existence of the Tn antigen on our patient’s red cells and is due to the development of an immune anti-Tn antibody against the Tn antigen, this last antigen being either a group antigen or an antigen revealed or modified by the causal agent of the disease.

This content is only available as a PDF.