title: [Splenic rupture associated with aggressive conversion of indolent T-cell prolymphocytic leukemia].
abstract: A 65-year-old man was diagnosed with leukocytosis in a routine medical examination. Further laboratory examinations showed increased LDH and sIL-2R levels in the serum. There was no evidence of infiltrative lesions or organomegaly. Bone marrow aspiration revealed many atypical small-sized lymphocytes without apparent nucleoli. Flow cytometric analysis of atypical lymphocytes was positive for T-cell markers, and chromosome analysis showed a normal karyotype. He was diagnosed with the small cell variant of T-PLL. Approximately 34 months later, having received no treatment, his cervical lymph nodes increased in size and number, and his white blood cell count, LDH and sIL-2R levels also rapidly increased. He was then admitted to our hospital. Bone marrow aspiration and cervical lymph node biopsy revealed complex chromosome abnormalities including inv(14)(q11;q32). Computed tomography showed swollen lymph nodes all over his body and hepatosplenomegaly. On the fourth hospital day, spontaneous splenic rupture occurred. Transcatheter arterial embolization was unsuccessful and the patient died. We report this case with rare autopsy findings.
authors.affiliation: Department of Hematology, Showa General Hospital, Japan.
authors.forename: Sachie
authors.initials: S
authors.lastname: Wada
authors.forename: Koichi
authors.initials: K
authors.lastname: Kitazume
authors.forename: Takayuki
authors.initials: T
authors.lastname: Suzuki
authors.forename: Akira
authors.initials: A
authors.lastname: Fujita
authors.forename: Seiichiro
authors.initials: S
authors.lastname: Shimizu
mesh_terms: D000368:Aged; D001706:Biopsy / Q000379:methods; D002869:Chromosome Aberrations; D017809:Fatal Outcome; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D006801:Humans; D015461:Leukemia, Prolymphocytic, T-Cell / Q000150:complications / Q000235:genetics* / Q000473:pathology; D008297:Male; D013161:Splenic Rupture / Q000209:etiology*