RESUMEN
We report the first case of immune mediated thrombocytopenia and concurrent hemolytic anemia (Evans syndrome) that developed during valproic acid (VPA) therapy. The 6 years-old girl had been stable with VPA therapy for seizure disorder for 5 years. She was admitted due to purpura and petechiae on both legs. Her blood test was only significant for thrombocytopenia with normal hemoglobin level. Her thrombocytopenia was not caused by VPA toxicity, because of positive anti-platelet antibody. Thrombocytopenia was improved after steroid and intravenous globulin. However, hemoglobin was shown gradual drop with increased reticulocytes counts, high level of lactic dehydrogenase, and a positive direct Coombs test. She had a complete clinical recovery with negative anti-platelet antibody and direct Coombs test after discontinuation of VPA. VPA has a lot of side effects including hematologic toxicity, although this drug is used for seizure disorders. This report is the first Evans syndrome due to VPA, even though VPA induced pure red cell aplasia with positive anti-nuclear antibody or thrombocytopenia by direct toxicity.
Asunto(s)
Niño , Femenino , Humanos , Anemia Hemolítica , Prueba de Coombs , Epilepsia , Pruebas Hematológicas , Pierna , Oxidorreductasas , Púrpura , Aplasia Pura de Células Rojas , Reticulocitos , Trombocitopenia , Ácido ValproicoRESUMEN
Advances for the treatment of childhood cancer in several decades have remarkably improved long-term survival. Anticancer therapy is capable of causing a variety of delayed toxicities including secondary malignant neoplasm. Therefore close follow-up for secondary malignant neoplasm is important for surviving patients from cancer. Renal cell carcinoma is a rare tumor in childhood and has been reported previously to occur after treatment of a few solid tumors, including neuroblastoma. This report represents the first documented case of renal cell carcinoma arising as a secondary malignant neoplasm in a pediatric patient who previously was treated for germ cell tumor.
Asunto(s)
Niño , Humanos , Carcinoma de Células Renales , Estudios de Seguimiento , Células Germinativas , Neoplasias de Células Germinales y Embrionarias , NeuroblastomaRESUMEN
Acute sensorineural hearing loss is unusual as initial manifestations in a child with acute lymphoblastic leukemia (ALL), even though facial or oculomotor nerve palsy as early finding of leukemia was reported. The pathology of sensorineural hearing loss in leukemia showed as leukemic cell infiltration, hemorrhage, infection, and local ischemia due to hyperviscosity. A 12-year-old boy with ALL was admitted due to multiple cervical lymphadenopathy with left sided sensorineural deafness. He complained gross hematuria and purpura on whole body. His initial complete blood cell counts were hemoglobin 11.9 g/dL, hematocrit 34.3%, white blood cells 164,000/muL (segmented neutrophils 3%, lymphocytes 11%, monocytes 2%, immature blast 84%), and platelet 28,000/muL. Pure tone audiogram revealed profound sensorineural hearing loss of the left ear at all frequencies. His brain MRI showed no definite abnormal findings without hemorrhage or infarction in inner ear or temporal lobe. He received induction chemotherapy and total 4 times of transtympanic steroid injection with 1 week interval. His hearing power at complete remission was more improved than admission, but not completely recovered until 5 months. We proposed that hearing impairment might be an initial manifestation in acute leukemia with hyperleukocytosis.