Meanwhile incubation of the patient’s fresh serum and his own RBCs with cefoperazone at 37C, gave rise to moderate haemolysis, and the results of DAT for both anti-IgG and anti-C3d were positive. to the discontinuation of cefoperazone treatment, the patient showed strong positive (4+) results for both anti-IgG and anti-C3d direct antiglobulin test (DAT), while cefoperazone-dependent IgM and IgG antibodies were detected. The patient’s plasma and O-type RBCs were incubated with tazobactam or sulbactam answer at 37C for 3 h, the results of DAT for anti-IgG and anti-C3d were both positive. Forty-three days after the discontinuation of cefoperazone, the results of DAT for anti-IgG DP2.5 and anti-C3d were unfavorable. Meanwhile incubation of the patient’s fresh serum and his own RBCs with cefoperazone at 37C, gave rise to mild haemolysis, and the results of DAT for both anti-IgG and anti-C3d were positive. It is suggested that cefoperazone-dependent antibodies can activate complement, and the Vanoxerine 2HCl (GBR-12909) non-immunologic protein adsorption effect of tazobactam or sulbactam can enhance IgG and complement binding to RBCs. This may Vanoxerine 2HCl (GBR-12909) promote the formation of immunocomplexes and complement activation, thereby Vanoxerine 2HCl (GBR-12909) aggravating haemolysis. findings suggesting that this NIPA effect of tazobactam and sulbactam may promote the formation of immune complexes of cefoperazone-dependent antibodies with cefoperazone-coated RBCs experiments were conducted to verify the complement activation effect of drug-dependent antibodies, and the NIPA effect of tazobactam and sulbactam. The results of irregular RBC antibody screening of plasma and acid eluates from the blood samples collected on days 67, 69 (cefoperazone treatment was discontinued), 71, 73, 75, 78, 85, 93, 104, 112, and 123 after hospitalization were all unfavorable. DAT for anti-IgG and anti-C3d of the blood sample collected 2 days prior to the discontinuation of cefoperazone were strongly positive (4+), and gradually weakened for blood samples collected after cefoperazone discontinuation. The results of DAT for anti-IgG and anti-C3d became unfavorable 43 and 16 days after the discontinuation of cefoperazone, respectively. Cefoperazone answer (1C10 mg/mL) were incubated with O-type WRBCs and plasma collected on days 67, 69 (cefoperazone discontinued), 71, 73, 75, 78, 85, 93, 104, 112, and 123 after the patient’s admission, cefoperazone-dependent antibodies were detected in every plasma sample, with the highest titre of 32. While the patient’s plasma was incubated with cefoperazone-coated RBCs at 37C for 1 h, cefoperazone-dependent antibodies were also detected, but the highest titre was only 1 1. Therefore, cefoperazone-coated RBCs are not suitable for the detection of cefoperazone-dependent antibodies. Tazobactam- or sulbactam-related drug-dependent antibodies were not detected in any of the blood samples. Details of drug-dependent antibody testing of the patient’s blood sample collected around the 67th day of admission (2 days prior to the cessation of cefoperazone treatment) are shown in Table 1. Table 1 Results of drug-dependent antibody assessments of blood samples collected 2 days prior to the discontinuation of cefoperazone treatment. control assessments are shown in Table 3. Table 3 validation Vanoxerine 2HCl (GBR-12909) of non-immunologic protein adsorption caused by tazobactam and sulbactam. control test are shown in Table 4. Table 4 testing of blood samples collected after negative direct antiglobulin test results for complement activation and non-immunologic protein adsorption. thead th valign=”top” align=”left” rowspan=”1″ colspan=”1″ NO. /th th valign=”top” align=”left” colspan=”6″ style=”border-bottom: thin solid #000000;” rowspan=”1″ Reactive materials /th th valign=”top” align=”left” colspan=”3″ style=”border-bottom: thin solid #000000;” rowspan=”1″ Incubate at 37 C for 0.5 h /th th valign=”top” align=”left” colspan=”3″ style=”border-bottom: thin solid #000000;” rowspan=”1″ Incubate at 37 C for 1 h /th th valign=”top” align=”left” colspan=”3″ style=”border-bottom: thin solid #000000;” rowspan=”1″ Incubate at 37 C for 2 h /th th valign=”top” align=”left” colspan=”3″ style=”border-bottom: thin solid #000000;” rowspan=”1″ Incubate at 37 C for 3 h /th th rowspan=”1″ colspan=”1″ /th th valign=”top” align=”center” rowspan=”1″ colspan=”1″ P-WRBCs br / (L) /th th valign=”top” align=”center” rowspan=”1″ colspan=”1″ P-S br / (L) /th th valign=”top” align=”center” rowspan=”1″ colspan=”1″ AB-S br / (L) /th th valign=”top” align=”center” rowspan=”1″ colspan=”1″ 40 mg/mL CPZ br / (L) /th th valign=”top” align=”center” rowspan=”1″ colspan=”1″ 40 mg/mL TBT br / (L) /th th valign=”top” align=”center” rowspan=”1″ colspan=”1″ 40 mg/mL SBT br / (L) /th th valign=”top” align=”center” Vanoxerine 2HCl (GBR-12909) rowspan=”1″ colspan=”1″ Agglutination or haemolysis /th th.