Objective We aimed to summarize the laboratory findings and clinical features of hemolytic disease of the fetus and newborn (HDFN). Methods We retrospectively analyzed the data for 17 infants with anti‐M‐induced HDFN (anti‐M‐HDFN) diagnosed between June 2013 and May 2019. Their maternal history, neonatal diagnosis on admission, and laboratory test results were compared with those of 15 infants with HDFN involving the ABO blood group system, 15 infants with HDFN involving the Rh system, and 15 premature infants. Results In the anti‐M‐HDFN group, 94.12% (16/17), 35.29% (6/17), and 17.65% (3/17) had free antibodies in plasma, a positive direct antiglobulin test, and a positive elution test, respectively. In 12 infants, free antibody reactions were stronger at 4°C than at 37°C, and the antibody titer at 4°C ranged from 1 to 512. All 17 infants with anti‐M‐HDFN developed anemia: 14 were treated with blood transfusion and 1 with neonatal exchange transfusion. Sixteen infants improved, and one died. Anti‐M‐HDFN had a higher rate of maternal stillbirth, lower gestational age, lower birthweight, and higher incidence of respiratory distress than other HDFN types. Conclusion Anti‐M may cause HDFN. It may present with varying degrees of anemia, low regenerative anemia, and low bilirubin levels. In addition, infants with anti‐M‐HDFN may have a negative elution test and direct antiglobulin test. These tests are helpful in examining antibody responses at a low temperature of 4°C.

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Background: A neonatal with severe anemia（HB:48g/L）was detected before blood transfusion. A major crossmatch-incompatible result was found with a AB donor and the further some of random 8 donors. To diagnosis the reason of anemia and the mismatched, a series serological tests were detected. Case presentation: The AB positive neonatal was born by B positive mother and AB dad. The neonatal DAT was negative, but the elution was positive with A1 cell and negative with A2 cell. In his mother serum, titer 1024 anti-A were checked out in saline tube, after treated by DTT, titer 64 anti-A1 and 2 anti-A were checked out. The neonatal was diagnosis with Hemolytic disease of the newborn (HDFN). His mother red cell showed a weak agglutinated with anti-A under microscopy. Then was diagnosis as fetomaternal hemorrhage (FMH) through the Kleihauer-Betke test and flow cytometry. A2B red blood were given combine with phototherapy, the neonatal HB was 108g/L on the day 11 before discharged. Conclusions: This is a rare case concurrent FMH and HDFN. The massive red cell of fetus entried maternal blood because of FMH, and then AB fetus red blood tiggered the high titer anti-A1 IgG and caused HDFN.

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