Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three patients with amyloidosis in whom hepatomegaly was the main sign ara presented. In all cases jaundice coexisted which is regarded as a rare sign in amyloidosis. Attention is called to the diagnostic difficulties of amyloidosis especially without a preceding clinically overt disease process. The presence of a particularly high activity of alkaline phosphatase in the serum, and focal absence of 99Tc uptake by the hepatic macrophage system in liver scintigram suggested liver tumour. However, demonstration of monoclonal protein in blood, urine or ascitic fluid, or raised level of alpha 2 globulin, should call attention to the possibility of liver amyloidosis. The authors stress the usefulness of the method of preincubation of tissue biopsy specimens in potassium hypermanganate during routine staining with Congo red for differentiation of amyloid AA from amyloid AL.
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PMID:[Diagnostic difficulties in hepatic amyloidosis--clinical analysis and autopsy data of 3 cases]. 226 76

Flow cytometry using a DNA label can quantitate aneuploid clones in malignant tissue. We illustrated the clinical value of this technique in a 71-year-old woman with acute megakaryocytic leukemia, which was diagnosed by staining of the blasts with factor VIII antigen and their morphologic resemblance to megakaryoblasts. Marrow cells were removed from needle biopsies by vortexing in RPMI medium, centrifuged in Ficoll-Hypaque, stained with a propidium-iodide/NP-40 mixture, and analyzed at 488 nm using an argon laser. During 3 weeks of low-dose cytosine arabinoside (ara-c) infusion therapy, hyperdiploid peak A dropped from 35% (day 0) to 2.3% (day 14) to 0% (day 21), with development of marrow hypoplasia. Similarly, hyperdiploid peak B, went from 7.6% to 9.1% to 3.5%. Subsequently, her marrow recovered normal morphology and lost the aneuploid peaks. Her blood counts recovered to near normal. Four months later, she relapsed and had a return of the day-21, incompletely eradicated peak B. There was no evidence of peak A. Repeated treatment with ara-c resulted in temporary suppression of the disease, but she died 3 months later with progressive hepatosplenomegaly. Analysis of cells from her enlarged liver, heavily infiltrated with blasts, showed a large hyperdiploid peak B. In this patient, ara-c therapy induced a remission with permanent eradication of one clone, but incomplete eradication of a second clone, which ultimately led to her relapse and death.
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PMID:Flow cytometry shows recurrent aneuploid clone after remission in megakaryocytic leukemia. 319 26

The present study was carried out to establish a human chronic lymphocytic leukemia (CLL) mouse model by transplantation of a JOK-1 human CLL cell line into SCID (severe combined immunodeficient) mice and to examine anti-leukemic effects of fludarabine phosphate, a prodrug of 9-beta-D-arabinofuranosyl-2-fluoroadenine (2F-ara-A). In vitro cytotoxic screening pattern of 2F-ara-A differed from those of other anticancer agents. Intraperitoneal inoculation with JOK-1 cells in SCID mice allowed the cells to infiltrate into a variety of organs including the liver and thymus, and resulted in the death of the mice with a median survival time of 29.5 days, associated with hepatomegaly, splenomegaly and enlarged lymph nodes. The ascitic cells expressing the human B-lymphocytic cell surface antigen CD19 actually grew after a latent period of 15 days. In this model, twice daily administration of fludarabine phosphate at a dose of 135 mg/kg for 5 days prolonged the survival time of the mice for considerably longer period than once-a-day treatment. Fludarabine phosphate in the doubled course of twice daily increased life span of 32.9%, which was in a similar range to that of doxorubicin. Thus, intraperitoneal inoculation of the human JOK-1 CLL cells into SCID mice seems to serve as an animal model potentially for human leukemia, suggesting that transplantation and subsequent infiltration processes of human CLL cells is useful measures to explore mechanistic aspects for drug-induced modulation of the tumor progression.
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PMID:A human B-cell CLL model established by transplantation of JOK-1 cells into SCID mice and an anti-leukemia efficacy of fludarabine phosphate. 1060 87