In DIN, antibody binding to a target cell usually requires the presence of the causative drug and the complement is often consumed (9). associated with DIN are antithyroidal medicines, anticonvulsants, and antibiotics such as cephalosporins, penicillins, sulfonamides, and chloramphenicol, even though pathogenesis of DIN is definitely poorly understood (3). Here, we describe the brief history of a child with pneumococcal pneumonia, who experienced severe neutropenia during antibiotic treatment and in whom we recognized 4 kinds of antibiotic-dependent antineutrophil antibodies. == CASE Statement == A 22-month-old son presented to another hospital with fever and cough for 3 days. On admission to our institution, he was irritable and dyspneic. Physical examinations exposed markedly decreased breathing sounds on the remaining lung fields. The radiologic findings showed diffuse infiltration in the remaining lower lung fields without shifting of pleural fluid. Laboratory studies on admission disclosed the following ideals: hemoglobin 11.2 gm/dL, white blood cell (WBC) 9,800/L (differential count; segmented neutrophil 82.6%, lymphocyte 14.8%, monocyte 2.6%), platelet 281,000/L, erythrocyte sedimentation rate (ESR) 55 mm/hr, C-reactive protein (CRP) 32.2 mg/dL. We started antibiotics with augmentin (100 mg/kg/day time, intravenously) and tobramycin (5 mg/kg/day time, intravenously) as well as intravenous immunoglobulin (IVIG, 1 gm/kg) after SCH58261 septic workup including blood cultures. Three days later, we switched antibiotics to vancomycin (50 mg/kg/day time, intravenously), cefotaxim (200 mg/kg/day time, intravenously), and roxithromycin (8 mg/kg/day time, orally) because the blood tradition revealedStreptococcus pneumoniaebeing sensitive to vancomycin and the antibody titer forMycoplasma pneumoniaewas 1:160 even with a negative chilly agglutinin test. His medical condition became well without fever after 8 days of antibiotic therapy. On hospital day time 12, before which it was not evident, fluid shifting on a chest radiography was recognized and also confirmed by chest computed tomograohy (CT) scans. A chest tube was put and pleural fluid analysis showed compatible findings with transudate, probably due to earlier antibiotic therapy. Furthermore, polymerase chain reactions forMycobacterium tuberculosisandMycoplasma pneumoniaein pleural fluid were also bad. The serologic test forMycoplasma pneumoniaeantibody was 1:160 and chilly agglutinin test was bad. The blood checks disclosed hemoglobin 6.2 g/dL, WBC 18,500/L (differential count; segmented SCH58261 neutrophil 62%, lymphocyte 35%, monocyte 3%), platelet 979,000/L, reticulocyte 2.3%, ESR 68 mm/hr, CRP 4.32 mg/dL. He did not receive packed reddish blood cells (RBC) because of a positive direct Coombs test and warm antibody within the screening test. He received aspirin because of a high platelet count. On hospital day time 15, fever developed again and persisted until hospital day time 18, when progressive, generalized, erythematous maculopapular rashes also appeared and a complete blood count (CBC) exposed hemoglobin 7.8 g/dL, WBC 4,200/L (differential count; segmented neutrophil 29%, lymphocyte 59%, monocyte 9%, eosinophil 1%, atypical lymphocyte 1%, myelocyte 1%), platelet 224,000/L, and reticulocyte 7.3%. Generalized pores and skin rashes and edema were aggravated until hospital day time 22, SCH58261 when IVIG and solumedrol was administered with replacement of vancomycin by same doses of augmentin and tobramycin after removal of the chest tube. Thereafter, the fever and skin rashes disappeared, even the CBC findings on hospital day 26 showed severe neutropenia (complete neutrophil count: 492/L). On hospital day SCH58261 32, the fever developed again without any significant symptoms or indicators. CBC findings on next day disclosed severe neutropenia with WBC 3,700/L (differential count; segmented neutrophil 1%, lymphocyte 91%, monocyte 8%). Severe neutropenia persisted until withdrawal Rabbit Polyclonal to NFE2L3 of augmentin and tobramycin as well as administration of granulocyte colony-stimulating factor (G-CSF, 5 mcg/kg/day, subcutaneously) for 3 days from hospital day 36 when the blood samples for antineutrophil antibodies were collected. The brief clinical course as well as the changing pattern of complete neutrophil counts is usually offered inFig. 1. == Fig. 1. == The clinical course and changing pattern of complete neutrophil counts according to antibiotic treatment. Aug, Augmentin; Tobra, Tobramycin; IVIG, intravenous immunoglobulin; G-CSF, granulocyte-colony stimulating factor; WBC, white blood cell count; ANC, complete neutrophil count. To detect neutrophil antibody, we used the mixed passive hemagglutination assay (MPHA), using extracted.