Viral hepatitis G primarily detected in children with malignant tumors. Clinical case

Abstract

Introduction. HVG was first isolated in 1996 from patients with posttransfusion hepatitis and belongs to the Flaviviridae phalimilia, as does HCV. HVG transmission is achieved parenterally, through blood transfusions, drug administration and hemodialysis. HVG induces acute or chronic viral hepatitis, which has a milder course than HCV. The role of HVG in the determination of acute hepatitis is not well defined. It has been established that HBV mainly affects cholangiocyte epithelial cells. 60-70% of patients after healing form anti-HVG. Because the route of transmission is common with liver viruses B and C, HVG-VHB si HVG-VHC,HVHG-HIV coinfection, HBV-H is common: HVG co-infection with HBV -6%, HCV -15% and HIV - 35%. Purpose. To present the diagnostic and therapeutic problems faced by oncopediatricians in the process of diagnosis and treatment of malignant tumors in young children based on this clinical case, which developed the episode of severe acute hepatitis and acute liver failure, caused by VHG. Materials and methods. For the presentation of this case, the data from the inpatient medical file from the oncopediatrics section of the Chisinau Oncology Institute, from the patient's outpatient medical file (F112), the discharge extract from the oncopediatrics department, and from Moscow were used., Russian Federation, the results of additional examinations provided by the patient's parents, with their written and verbal consent. The patient was previously considered healthy, the primary diagnosis of nephroblastoma was confirmed morphologically and immunohistochemically (No. 30276-92 / 19): ,,Nephroblastoma of the right kidney. St III.Nx.M0. Condition after a neoadjuvant PChT treatment (with 70% reduction of the tumor). Radical surgical treatment. R-therapy 12 GY.8 PChT adjuvant. Results. Patient S.D., 2 years, diagnosed with: Giant right kidney nephroblastoma at the age of 13 months. He was repeatedly hospitalized in Pediatric Oncology Department (primary 08.2019; repeated 26.11.19/16.12.2019) for specific PChT 2 adjuvant treatments according to the SIOP Umbrella Protocol. Physiological - weight 9,800g, waist 85cm, BMI – 13,6 (P1, Z – 2,2). He was born from the second pregnancy, at term, with a birth weight of 3,800g, vaccinated according to the vaccination schedule. Unacute hereditary-collateral anamnesis, mother's health-familial renal polycystosis, father-unaccounted. At birth, he was vaccinated against HVB4 and BCG. To IMSC to CT - presence of massive retroperitoneal tumor mass in the region of the right kidney. The anamnesty of the disease. From 15.08.19 a specific neoadjuvant treatment was initiated according to the scheme: Vincristin, Dactinomycin, Doxorubicin. The treatment was relatively satisfactorily supported with tumor regression in 70% with "Right nephrectomy. Cholecisectomy." Histological N30276-92/19 confirmed "nephroblastoma". RT 12 Gy and multiple blood and plasma infusions. The patient was discharged with relative improvement, with the recommendation to continue specific treatment at the place of residence according to the SIOP Umbrella 2016 protocol. On the 10th day of specific PChT treatment (2nd adjuvant treatment) in children appear: To = 39C, repeated vomiting, 2 episodes of diarrhea. In hemogram-agranulocytosis; ECG 200 / min. Detoxification treatment was started, hemostimulator, hepatoprotectors, symptomatic. In the dynamics the patient's condition worsened, with the installation of drowsiness, apathy, the appearance of jaundice. He was consulted by a cardiologist, infectionist, pediatrician, gastroenterologist, hepatologist – IHA and IRA. Toxic hepatitis, possibly medicinal? Toxic nephritis. Thrombocytopenia. CID syndrome. Operated nephroblastoma. Hb 93g / l, PLT 63x10 / 9l, Urea 14 mmol / l, Creatinine116.6 mcmol / l, Total bilirubin 181 mcmol / l), ALT = 567 U / l, AST = 638U / l, hypoproteinemia, hypoalbuminemia, hypoprothrombinemia (IP = 40%). HBsAg-, anti-HCV sum. negative. Transfer to the ATI. The general condition of the patient after 4 days of intensive treatment has improved. He underwent intensive treatment and resuscitation syndrome, symptomatic, with stabilization of general condition and vital signs. After 10 days he was discharged for prolonged treatment, with reduced doses of chemotherapeutic and symptomatic remedies. The third hospitalization in IMSP IO followed on 11.02.20 for the continuation of the specific PChT. Due to the persistence of ALT and AST increased, the child underwent an additional in-depth examination to determine the cause of persistent cytolysis syndrome, including the determination of HBV, HCV, HBV, HAV, EVB and CMV and HBV DNA, HCV RNA (Teal Time). Semiquantitative HBV RNA. HBV “infection-past” status was determined with anti-HBs + anti-HBcor summary +, but with negative HBV DNA, against the background of positive HBV RNA. The doses of the chemotherapeutic preparations were reduced by 20%, hepatoprocytes were administered repeatedly, antivirals resulting from the young age of the child and the morbid condition. On 10.06.20 the patient finished the specific PChT treatment, being monitored in dynamics according to an individual scheme, including the assessment of the status of HBV RNA and HBV RNA, HCV RNA, liver functions. Biochemical indices are presented in the table, have a similar characteristics characteristic of acute toxic hepatitis, pancreatitis. Conlcusion: 1. HBV infection of the 13-month-old child diagnosed primarily with malignant nephroblastoma of the right kidney was performed posttransfusion, during the treatment of vital and important complex radical treatment (chemotherapy, radiotherapy, surgery, hemotransfusion). 2. Acute posttransfusion HVG in the patient has evolved severely being conditioned by toxic hepatitis as a manifestation of the underlying disease and on an asymptomatic background of "infection-past" (occult) HBV, seropositive form, characterized by the presence of anti-HBs +, anti-HBcor sum +, negative HBV DNA.