PMC9085745_01
Patient's bone marrow smear. (Hyperplasia was active in bone marrow, no obvious compensatory hyperplasia and thrombocytopenia were observed in red system.)
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Laboratory examination revealed that hemoglobin 46 g/L, platelets 4x109/L, white blood cells 3.65x109/L, reticulocyte count 11.62%, stool OB (+), urine protein (3+), urine occult blood (4+), D-Dimer 2.99 mg/L, and coagulation function were normal; creatinine 39.2 mumol/L, aspartate aminotransferase (AST) 58U/L, urea, albumin (ALB), and alanine aminotransferase (ALT) were normal; total bilirubin 43.7 mumol/L, indirect bilirubin 30.3 mumol/L, direct bilirubin 13.4 mumol/L, lactate dehydrogenase (LDH) 1,166 U/L; Coombs test (-); Broken red blood cells can indeed be seen on peripheral blood smears; ANA 1:640 granular type, lupus anticoagulant, and anticardiolipin antibody antibodies were negative; complement C3, C4, and anti-dsDNA were normal; G-6-PD was normal; bone marrow smear showed active bone marrow hyperplasia, no obvious compensatory hyperplasia, and thrombocytopenia in the erythroid ( Figure 1 ); no paroxysmal nocturnal hemoglobinuria (PNH) clones were detected in the bone marrow, and no immunophenotypic abnormalities related to acute leukemia and high-risk MDS were detected; infection-related tests were negative.
The result of ADAMTS13 autoantibodies and ADAMTS13 inhibitory autoantibodies.
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On the 7th day of admission, the result of ADAMTS13 autoantibodies (ELISA assay) were 0.84%, and ADAMTS13 inhibitory autoantibodies were positive, confirming our diagnosis ( Figure 2 ).
Changes of hemoglobin and platelets during treatment.
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The above treatment process is shown in  Figure 3 .
The result of ADAMTS13 autoantibodies and ADAMTS13 inhibitory autoantibodies after treatment.
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After a month, the ADAMTS13 autoantibodies rose to 67.14%, and the ADAMTS13 inhibitory autoantibodies were negative ( Figure 4 ).