OBJECTIVE: We report a rare case of acute hemolytic reactions caused by immunoglobulin (Ig)M anti-M antibody and present a literature review.
METHODS: A 61-year-old male patient who underwent blood transfusion developed fever, chills, soy sauce-colored urine, and changes in laboratory test results, including persistently decreased hemoglobin levels, neutrophilia, elevated lactate dehydrogenase level, acute kidney injury, mild acute liver injury, and activation of the coagulation system, indicating acute hemolytic transfusion reaction (AHTR). Antibody screening and major crossmatching results indicated weak positive at 37°C for both posttransfusion and pretransfusion sample. Subsequent serological examinations indicated the presence of IgM anti-M antibodies in plasma but the direct antiglobulin and elution tests were negative. Antibody hemolytic activity assay confirmed AHTR caused by anti-M. The transfused red blood cells were MM and the patient is NN. These signs and symptoms disappeared rapidly and required no additional interventions before discharge.
CONCLUSIONS: The accurate diagnosis of anti-M antibody-mediated acute hemolysis is essential for guiding treatment decisions.

BACKGROUND: Minor ABO-incompatible apheresis platelet transfusion poses a risk of hemolytic transfusion reactions in non-Group O recipients when donor\'s plasma possesses unusual high titers for anti-A and anti-B. The aim was to determine whether the hemolysin test can be used as a screening tool to predict high-titer Group O platelet apheresis donors.
METHODS: A prospective study, with Group O platelet donor\'s samples, was tested for hemolysin test and antibody titration test in parallel. Antibody titration was also performed on products suspended in platelet additive solution (PAS). Hemolysin test was assessed for diagnostic accuracy against antibody titration. Chi-square test and Mann-Whitney U-test were used to determine the relationship between the hemolysin test and antibody titration.
RESULTS: Among 107 Group O platelet donations, median anti-A and anti-B titers in donors were 32 (8-128) and 32 (4-256), respectively. High titer (≥128) for ABO antibodies was seen in 18% of donations, whereas hemolysin test was positive in 69% of donations. Hemolysin test results differ significantly with antibody titration results (P = 0.03). Hemolysin test had higher sensitivity (89%) with a strong negative predictive value (94%). None of the products suspended in PAS had high-titer antibodies.
CONCLUSIONS: Adopting hemolysin test as a screening tool may label a large number of units (69%) unsuitable for ABO-incompatible platelet transfusion. Alternatively identifying donors with high antibody titer or positive hemolysin test and selectively suspending their product in PAS may be a cost-effective approach and certainly prevent high-titer antibodies in the product.

暂无摘要。

Bombay blood group is a rare type that was initially identified in the city of Bombay, India. It is characterized by the presence of serum antibodies anti-A, anti-B, and anti-H, which can cause agglutination in all blood groups within the ABO system. The clinical importance of the Bombay blood group lies in its inability to receive transfusions from other blood groups. In this case report, we present a case of a young male who was initially misdiagnosed as having an O phenotype, resulting in a hemolytic transfusion reaction. This case highlights the diagnostic and therapeutic challenges associated with rare blood phenotypes.

OBJECTIVE: Acute hemolytic transfusion reaction (AHTR) due to ABO-incompatible erythrocyte concentrate (EC) is one of the most catastrophic complications of transfusion. Since the hemolysis is intravascular; hemoglobinemia and hemoglobinuria result in disseminated intravascular coagulation (DIC), acute renal failure, shock, and sometimes death.
BACKGROUND: Treatment of AHTR is mostly supportive measures. Today there are no clear suggestions about plasma exchange (PE) in these patients.
METHODS: Here we report our experience with six patients diagnosed with AHTR due to ABO-incompatible EC transfusion.
RESULTS: We performed PE in 5 of these patients. Although all of our patients were geriatric and most of them had significant comorbidities four out of five patients recovered without an incident.
CONCLUSIONS: Although PE is considered a last-chance treatment when other measures fail in the literature, our experience above indicates that it must be evaluated in every patient with AHTR early in the course. If the patient has cardiac and renal comorbidities, large volume EC is transfused, DAT is negative, plasma color is red and there is macroscopic hemoglobinuria, we suggest performing PE.

BACKGROUND: The Yt system consists of five antigens: antithetical Yta /Ytb and the high-prevalence antigens YTEG, YTLI, and YTOT. We investigated a sample from a Native American (NA) female with post-operative anemia and an unidentified antibody who developed rigors, tachycardia, and hypotension on transfusion of incompatible RBCs.
METHODS: Serologic testing methods included LISS, PEG, and IgG gel. Test RBCs were treated with papain, trypsin, alpha-chymotrypsin, 2-amino-ethylisothiouronium, and dithiothreitol. Rare RBCs were tested, and inhibition studies were performed. DNA extracted from WBCs was used for Sanger sequencing.
RESULTS: Initial testing showed strong 3-4+ plasma reactivity with all panel cells at LISS IAT; auto control was negative. Positive reactions were observed with numerous rare RBCs except for PNH-III, which lack GPI-linked DO, Yt, CROM, JMH, and Emm. Enzyme sensitivity patterns suggest Yt specificity, and soluble recombinant srYt neutralized reactivity. ACHE sequencing revealed YT*A/A genotype but with a homozygous change in exon 2, c.290A>G (p.Gln97Arg). Antibody reactivity was reminiscent of that seen in an unrelated NA male investigated previously. His RBCs were nonreactive with her plasma. ACHE carried the same c.290G/G change.
CONCLUSIONS: Two unrelated NA patients were found to have an antibody to a new high-prevalence Yt antigen, designated YTGT (YT6), associated with a clinically significant transfusion reaction. Identification of the specificity relied on enzyme sensitivity, use of PNH-III RBCs, neutralization using soluble recombinant Yt, and the finding of a novel change in ACHE, c.290A>G (p.Gln97Arg), designated YT*01.-06. IVIG and steroids were used to mitigate further reactions to transfusion.

BACKGROUND: Anti-M antibodies are usually inactive at physiologic temperatures (37 °C). Rarely, these antibodies have been reported to react at physiologic temperatures, resulting in clinically significant hemolytic transfusion reactions or hemolytic disease of the fetus and newborn.
METHODS: We describe a case of an acute hemolytic transfusion reaction due to an anti-M alloantibody reacting at physiologic temperatures in a critically ill patient.
RESULTS: Proper identification and management of anti-M antibody-mediated acute hemolysis rapidly improved and stabilized her hemoglobin.
CONCLUSIONS: Differentiation between anti-M antibody-mediated acute hemolysis and its differential diagnoses is of critical importance to guide therapeutic decisions in these rare clinical scenarios.

BACKGROUND: The identification of alloantibodies to high-frequency antigens (HFA) and subsequent transfusion management can be challenging and often poses a problem in finding the compatible blood for transfusion. The aim of this study was to investigate the specificity of the antibody to the HFA causing a hemolytic transfusion reaction (HTR) and procure the compatible blood unit for future transfusion.
METHODS: A 4-year-old female met with a head injury that led to intracranial bleeding and surgical intervention was required to remove blood clots. In the face of anemia, blood transfusion was planned. The pretransfusion tests on her blood sample revealed the presence of a pan-reactive alloantibody with hemolytic properties. She was transfused with 10 mL of the least incompatible red blood cells (RBCs) to which she reacted with signs of clinical hemolysis, i.e., chill, rigor, fever, and hemoglobinuria, on 3 different occasions. Despite her anemia, she was managed by medical intervention only. Her antibody reacted with all RBCs tested, except autologous and P-null (p phenotype) cells. Her RBCs did not react with anti-PP1Pk, which corroborated her phenotype as P-null. The genomic study revealed she was hemi- or homozygous or for a deletion of 26-bp in A4GALTexon 3, previously reported as causing the P-null phenotype and designated A4GALT*01N.019.
CONCLUSIONS: This report documents a rare case of the P-null phenotype with an alloanti-PP1Pk causing a severe HTR to transfusion of the trial dose of the least incompatible blood. The case is the first example of this specific A4GALTmutation found in India.

OBJECTIVE: Blood transfusion is a key intervention for decreasing morbidity and mortality in many cases and, besides its importance, potentially fatal consequences of incompatible transfusion are a great risk to patients. This study evaluated the incidence and specificity of erythrocyte alloantibodies in multi-transfused patients enrolled at an important Regional Blood Center.
METHODS: This was a single-center retrospective cohort study that eveluated patients enrolled at a Regional Blood Center in a period of four years. A total of 29,128 patient samples were screened, out of which 79 (0.27%) were multiple-transfused patients with alloantibodies identified.
RESULTS: The most common alloantibody found was anti-E (22.55%) followed by anti-D (14.71%), anti-C (5.88%), anti-c (5.88%), anti-e (1.96%) and anti-Cw (0.98%). We also identified combinations of alloantibodies (25.32%), 5.88% of which showed an IgG autoantibody isolated or combined with alloantibodies. The most frequent reason for the need of blood transfusion included cases of surgery, emergency and urgency (36.71%).
CONCLUSIONS: A low rate of development of alloantibodies in multi-transfused patients was found, which could be a consequence of the implementation of red blood cell phenotyping for patients who may receive frequent transfusions, as in the case of some hematological neoplasms and hemoglobinopathies. However, the most common alloantibodies identified were against the Rh and/or Kell systems, with high clinical significance since both can cause delayed hemolytic transfusion reactions. Thus, the implementation of reliable antibody screening tests and the transfusion of phenotyped units for selected patients in all transfusion services represent important measures to increase transfusion safety.

Herein, we report a case of naturally occurring anti-Leb alloantibody identified in the plasma of a first time voluntary blood donor. The immunohematology workup was done on the pilot sample tubes collected during blood donation by the conventional tube technique and using ID-Micro Column System Glass Beads card (anti-IgG, C3d; Ortho-Clinical Diagnostics, Raritan, New Jersey, USA). Blood group of the donor was confirmed to be B RhD positive, and the alloantibody in his plasma was identified as anti-Leb, having clinically significant characteristics. Since in this particular case, anti-Leb was IgM and IgG in nature, it was clinically significant and can lead to hemolytic transfusion reaction, especially if such fresh frozen plasma unit is transfused to Leb negative patients.