{"title":"Adverse Course of Listeria monocytogenes Infection in Pediatric Patient with T-Cell Acute Lymphoblastic Leukemia","authors":"A. Płotka","doi":"10.26420/ANNHEMATOLONCOL.2019.1240","DOIUrl":null,"url":null,"abstract":"Oncological patients are at an increased risk of an opportunistic infection caused by Listeria monocytogenes . Listeriosis remains infrequent in oncological patients. This article describes a case report of a 15-year old boy diagnosed with T-ALL, who developed L.monocytogenes infection during an intensive cancer treatment. The patient’s treatment proceeded with numerous complications. Impaired coagulation led to genetic examination and factor V Leiden and heterozygotic C667T and A1298C mutations of MTHFR detection. Corticosteroid therapy resulted in insulin resistance and hyperbilirubinemia with normal hepatic enzymes level. Gilbert’s syndrome was confirmed. CT evaluating remission revealed asymptomatic invasive pulmonary aspergillosis. After finishing Protocol II the rise in CRP was observed with decreased number of WBC. Patient was feverish and complained of nonspecific abdominal pain and dysuria. USG detected fluid in right iliac fossa. A few hours later boy’s neurological state dramatically worsened. CT revealed acute hydrocephalus, which needed immediate drainage. Listeria monocytogenes was isolated from CSF. Despite intensive antibiotic therapy, infection caused boy’s death. On clinical examination massive submandibular and cervical lymphadenopathy, petechiae all over the body, especially severe in pelvic girdle, splenomegaly (spleen reaching lower quadrant) and hepatomegaly (3cm above subcostal arch), tachycardia (150/min), on auscultation diminished vesicular murmur paraspinal on both sides were noticed. Blood tests revealed leukocytosis (104 ths./µl), III grade thrombocytopenia (22ths/µl) and hyperuricemia (27mg/dl), high level of creatinine (1,18mg/dl) and urea (75mg/dl). Boy presented with, both laboratorary and clinically, renal insufficiency in 4 th stage (GFR-22ml/min). Intravenous rehydration, rasburicase and diuretics were administered resulting in gradual decrease and normalisation of uric acid. RTG and CT examinations revealed widened mediastinum (implying tumour), pleural and pericardial effusion. Due to clinical presentation and laboratory findings, the initial diagnosis of T-cell acute lymphoblastic leukemia was made and confirmed by myelogram and immunological examination of bone marrow. Treatment according to ALL IC BFM 2009 for intermediate-risk ALL was immediately administered. During induction phase clinical and biochemical signs of renal insufficiency occurred. Patient required hemodialysis with calcium supplementation (Ca-0,81 mmol/L) and hyperphosphatemia management at the same time (P-12,42mmol/L). Boy developed symptoms of tetany, which disappeared after normalisation of calcium","PeriodicalId":72219,"journal":{"name":"Annals of hematology & oncology","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2019-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annals of hematology & oncology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.26420/ANNHEMATOLONCOL.2019.1240","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
Oncological patients are at an increased risk of an opportunistic infection caused by Listeria monocytogenes . Listeriosis remains infrequent in oncological patients. This article describes a case report of a 15-year old boy diagnosed with T-ALL, who developed L.monocytogenes infection during an intensive cancer treatment. The patient’s treatment proceeded with numerous complications. Impaired coagulation led to genetic examination and factor V Leiden and heterozygotic C667T and A1298C mutations of MTHFR detection. Corticosteroid therapy resulted in insulin resistance and hyperbilirubinemia with normal hepatic enzymes level. Gilbert’s syndrome was confirmed. CT evaluating remission revealed asymptomatic invasive pulmonary aspergillosis. After finishing Protocol II the rise in CRP was observed with decreased number of WBC. Patient was feverish and complained of nonspecific abdominal pain and dysuria. USG detected fluid in right iliac fossa. A few hours later boy’s neurological state dramatically worsened. CT revealed acute hydrocephalus, which needed immediate drainage. Listeria monocytogenes was isolated from CSF. Despite intensive antibiotic therapy, infection caused boy’s death. On clinical examination massive submandibular and cervical lymphadenopathy, petechiae all over the body, especially severe in pelvic girdle, splenomegaly (spleen reaching lower quadrant) and hepatomegaly (3cm above subcostal arch), tachycardia (150/min), on auscultation diminished vesicular murmur paraspinal on both sides were noticed. Blood tests revealed leukocytosis (104 ths./µl), III grade thrombocytopenia (22ths/µl) and hyperuricemia (27mg/dl), high level of creatinine (1,18mg/dl) and urea (75mg/dl). Boy presented with, both laboratorary and clinically, renal insufficiency in 4 th stage (GFR-22ml/min). Intravenous rehydration, rasburicase and diuretics were administered resulting in gradual decrease and normalisation of uric acid. RTG and CT examinations revealed widened mediastinum (implying tumour), pleural and pericardial effusion. Due to clinical presentation and laboratory findings, the initial diagnosis of T-cell acute lymphoblastic leukemia was made and confirmed by myelogram and immunological examination of bone marrow. Treatment according to ALL IC BFM 2009 for intermediate-risk ALL was immediately administered. During induction phase clinical and biochemical signs of renal insufficiency occurred. Patient required hemodialysis with calcium supplementation (Ca-0,81 mmol/L) and hyperphosphatemia management at the same time (P-12,42mmol/L). Boy developed symptoms of tetany, which disappeared after normalisation of calcium