We report a case of lymphocyte apheresis failure due to platelet aggregation. A 74-year-old woman with diffuse large B cell lymphoma was admitted to our hospital for the collection of lymphocytes for Kymriah^® therapy. Lymphocytes were harvested using Spectra Optia in CMNC mode. After 1 hour of collection, we observed that the product's lymphocyte count was extremely low. We later recognized that platelet aggregates had obstructed the inlet of the collection port of the intermediate layer. During lymphocyte apheresis, careful observation of the interface is needed. If aggregate formation is suspected, the AC ratio of the blood should be adjusted immediately. The complete blood count of the intermediate product will be helpful in confirming if collection is proceeding under appropriate conditions.

We experienced a case of hemolytic anemia in a baby at late onset from a pregnant woman with anti-E titer, 128 times. Red blood cell (RBC) transfusion performed on day 11 after birth resulted in an improvement in hemoglobin, but anemia recurred 51 days later. We measured the IgG subclass and conducted a Monocyte Monolayer Assay (MMA) over time, and then analyzed the association of the condition of the mother and the child's RBC ratio post-transfusion.

Anti-E of the mother and the baby were of the IgG1 type, and MMA rates were low in both.

The delayed progression and recurrence of hemolysis in this case were due to the low MMA, resulting from the anti-E derived from IgG1 type, and because the remaining anti-E reacted with the baby's RBCs that were regenerated after transfusion.

Neonatal hemolytic disease caused by anti-E, high-titer IgG1 requires long-term follow-up. Analysis of IgG subclasses of irregular antibodies in pregnant women may help predict the pathology of Hemolytic Disease of the Fetus and Newborn (HDFN).

Immune-mediated platelet transfusion refractoriness (PTR) is mainly caused by alloantibodies against human leukocyte antigen (HLA), and rarely by human platelet-specific antigen (HPA). Here, we report a case of acute myeloid leukemia (AML) associated with PTR caused by anti-HPA-5a antibody. The patient was a 38-year-old female who responded poorly to platelet transfusion since the initial transfusion. Only anti-HPA-5a antibody was detected, without any anti-HLA antibodies, leading to the diagnosis of PTR caused by anti-HPA-5a antibody. Patients with hematologic malignancy with PTR have a poor prognosis. HPA antigen testing revealed the patient to be HPA-5b/b, while the HLA-matched sibling was HPA-5a/a. Therefore, hematopoietic stem cell transplantation was not performed during the first remission setting. Complete remission was achieved after two cycles of induction therapy and managed with HPA-matched platelet transfusions and intravenous gammaglobulin without any bleeding complications.

In patients with PTR caused by rare antibodies, finding compatible platelet transfusions can be very challenging and could potentially impact treatment decisions. Future development of HPA-matched platelet products derived from induced pluripotent stem (iPS) cells is desirable.