Amphotericin-B liposomal/cefepime/cloxacillin
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Neutropenia: 2 case reports In a case report, a 2-year-old girl developed neutropenia during treatment with cefepime and cloxacillin, and a 4-yearold boy developed neutropenia during treatment with cefepime for cystic fibrosis respiratory exacerbations. Additionally, treatment with amphotericin-B liposomal also contributed to the development of neutropenia in the boy [routes not stated]. Case 1: A 2-year-old girl was diagnosed with cystic fibrosis in her neonatal age. Her medical history was significant for poor weight gain, pancreatic insufficiency and respiratory exacerbations with cultures of bronchial secretion with methicillin-resistant Staphylococcus aureus (MRSA). She was admitted to the hospital due to respiratory exacerbation and started receiving treatment with triasociated antimicrobial therapy with cloxacillin 50 mg/kg/dose every 6h along with amikacin and ceftazidime. On admission, leukocytes was 9 310 cells/mm3 with absolute neutrophil count (ANC) of 5 030 neutrophils/mm3, CRP was 3.8 mg/dL and renal function was normal. Due to lack of availability of ceftazidime in the hospital, her treatment was switched to cefepime 50 mg/kg/dose every 8h. The culture of bronchial secretion was positive for multi-sensitive Staphylococcus aureus and Pseudomonas aeruginosa, however; her triasociated therapy was maintained. After 16 days of treatment, haemogram was performed, which showed a leukocyte count of 1 800 cells/mm3 and ANC of 43 cells/mm3. As a result, neutropenia secondary to cloxacillin and cefepime therapy was considered. Therefore, cloxacillin and cefepime were discontinued, and treatment was switched to levofloxacin. After 2 days, haemogram examination revealed an increase in leukocyte count to 3500 cells/mm3 with an ANC of 165 cells/mm3 and recovered completely on the sixth day of cefepime discontinuation. Case 2: A 4-year-old boy was diagnosed with cystic fibrosis at the age of 2 years after experiencing multiple episodes of pneumonia. His medical history was significant for chronic colonisation due to MRSA, oxygen dependence, neurofibromatosis type 1, pancreatic insufficiency and chronic lung damage including bronchiectasis. He was admitted to the hospital due to increased respiratory secretions and fever. He started receiving treatment with triasociated antimicrobial therapy with ceftazidime, amikacin and cotrimoxazole given a final culture of bronchial secretion with Stenotrophomonas maltophilia. On admission, the culture of bronchial secretion was positive for multi-sensitive Pseudomonas aeruginosa. Due to lack of availability of ceftazidime in the hospital, his treatment was switched to cefepime 50 mg/kg/dose every 8h along with amikacin; however, cotrimoxazole therapy was stopped. Subsequently, amikacin was stopped after completing 14 days of treatment. On cefepime therapy day 16, he presented with a fever of 39°C. Laboratory tests revealed leukocytes of 12 700 cells/mm3 (69% segmented), CRP of 7 mg/dL along with normal renal and hepatic function. An echocardiogram revealed central venous cath
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