Pakming Wong

Transformation of inferior vena caval thrombosis to membranous obstruction in a patient with the lupus anticoagulant

A 24-yr-old woman with hemolytic anemia developed multiple thrombosis of the hepatic vein and inferior vena cava. She was found to have circulating lupus anticoagulant that could have been causally related to the thrombosis and hence the Budd-Chiari syndrome. On her first admission to the hospital vena cava and hepatic vein catheterizations revealed partial thrombotic occlusion of the cava at the level of the diaphragm, which was subsequently transformed into complete membranous obstruction. The right hepatic vein, which was patent on the first admission, was also completely occluded. These observations support the theory that membranous obstruction of the inferior vena cava is a sequela to inferior vena caval thrombosis rather than a congenital anomaly.

Heritable rare fragile sites in patients with leukemia and other hematologic disorders

Fragile site studies were performed on a total of 126 patients with leukemia and other hematologic disorders including myelodysplastic syndrome (MDS) and polycythemia vera (PV). Compared with an incidence (6.0%) of heritable rare fragile sites in the healthy population, the frequency was not higher in the patient group (3.2%), as a whole. However, two cases of fra(17)(p12) in MDS appeared fourfold larger than expected for this group of patients. In one case, a homozygous carrier of fra(17)(p12) in PV was also very rarely expected from its population incidence. These findings suggested a possible role of rare fragile sites, at least in the etiology of these preleukemic or myeloproliferative disorders.

VINBLASTINE-LOADED PLATELET TRANSFUSION IN AN ALLOIMMUNIZED PATIENT

Department of Haematology, JEAN-PIERRE N c Stobhill General Hospital, Clasgow G21 3 U W R. L. C. CUMMINC E. H. HORN R. B. HOGC Lefrere. J.J.. Courouche, A.M.. Girot. R. . Bertrand. Y. & Soulier. J.P. (1986) Six cases of hereditary spherocytosis revealed by human parvovirus infection. British journal ojHaernatolog!l. 62 ,65 3-658. Mortimer. P.P. (1983) Hypothesis: The aplastic crisis of hereditary spherocytosis is due to a single transmissible agent. journal oJ Clinical Pathology. 36, 4 4 5 4 4 8 . Mortimer. P.P.. Humphries. R.K.. Moore, J.G.. Purcell. R.H. & Young. N.S. ( 1 983) A human parvovirus-like virus inhibits haematopoietic colony formation in vitro. Nature. 302, 4 2 6 4 2 9 . REFERENCES Cossart. Y.E.. Field, A.M.. Cant, B. & Widdons, D. (1975) Parvoviruslike particles in human sera. Lancet. i, 72-73.

DECREASED SERUM 1α,25-DIHYDROXYVITAMIN D3 LEVELS IN LEUKAEMIA

istics of our case deserve additional comments. The myelodysplastic changes seen in apparently non-leukaemic bone marrow cells and the hypoplastic presentation coupled with pancytopenia suggest that AML might have followed a preleukaemic state. Cases of AML following myelodysplastic syndromes (MDS) have been recently recognized (Hehlmann et al, 1981; Eridani et d, 1985; Neame et al, 1985). This, like other evidences (Editorial, 1983), may indicate that some cases of MDS are the result of a defect of the pluripotential stem cell. A hypoplastic presentation has been reported in both AML (Howe et al, 1982) and common ALL (Breatnach et al, 198 1). Hypocellular acute and leukaemia and monosomy 7 are regarded as bad prognostic characteristics in AML (Borgstrom et al, 1980; Howe et ul, 1982). The excellent response to therapy in this patient suggests that intensive post-remission chemotherapy schemes designed for AML might be of value in these cases.