Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with polymyalgia rheumatica (PMR) is reported in whom, at the time of diagnosis, the number of lymphocytes in peripheral blood and bone marrow was normal. Lymphocytic infiltration typical of PMR was detected in renal and muscle biopsy specimens, and a liver fine-needle aspirate contained an abnormal lymphocytic infiltration, probably leukaemic. The number of lymphocytes gradually increased in bone marrow and peripheral blood until, almost 5 years after PMR had been diagnosed, a typical picture of chronic lymphatic leukaemia (CLL) was observable. The significance of the reported combination is discussed. The possibility is pointed out that a CLL in progress must be suspected when persistent lymphocytosis occurs in a patient with typical PMR, even if initially the response to treatment with corticosteroids suggests that PMR is the sole disorder.
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PMID:Polymyalgia rheumatica and chronic lymphatic leukaemia. 92 20

HAM (HTLV-I-associated myelopathy) rat disease, HAM/TSP (HTLV-I-associated myelopathy/tropical spastic paraparesis)-like myelopathy in rats, occurred in 8 of 8 HTLV-I (Human T cell leukemia virus type I) carrier rats of WKAH strain inoculated with MT-2 cells at either neonates or 4 to 6 months of age. We report here ultrastructural findings of the affected spinal cords and the peripheral nerves of perfusion-fixed HAM rats. They were infected at the age of 4 to 6 months old and showed gait disturbance and hind leg paraparesis 15 months after infection. Pathological alterations of HAM rat disease were mainly confined to marginal areas of white matter of the spinal cord. The affected lesion was rather symmetrical and distributed in the anterior and the lateral columns. A prominent ultrastructural change in the spinal cord was separation of myelin lamellae at the intraperiod line and vacuolation of myelin sheath. Many myelin-debris-filled macrophages and a marked astrogliosis were also observed. In the gliotic areas, lots of demyelinated and remyelinated axons were intermingled. Axons were relatively preserved, however, some of them had tubulo-reticular inclusions. Astrocytes appeared ultrastructurally normal. Lymphocytic infiltration was virtually absent. Ultrastructural alterations of the peripheral nerve were basically similar to those of the spinal cord. Separation of myelin lamellae, macrophages infiltration, demyelination, and remyelination were observed. Schwann cells had also alterations. We observed some apoptotic cell death of the oligodendrocytes and Schwann cells with condensed nucleus and phagocytosis of apoptotic bodies by macrophages. Collective evidence suggests that a series of demyelinating process described above may be caused by apoptosis. No virus particles were seen in the spinal cord and peripheral nerve. Although the precise mechanism of apoptosis is not known at present, possible pathogenetic pathway involving apoptosis in HAM rat disease may contribute greatly to a better understanding of mechanisms implicated in the pathogenesis of HAM/TSP in humans.
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PMID:[Rat model of HTLV-I infection--ultrastructural study of HAM rat disease]. 770 50

Human T cell leukemia virus type I (HTLV-I) can be transmitted into several inbred strains of rats. Adult rats inoculated with HTLV-I immortalized human T cell line MT-2 at 8-37 weeks of age become seropositive HTLV-I carrier rats. Seropositive HTLV-I carrier rats of WKAH strain developed myelopathy similar to HAM/TSP (HTLV-I associated myelopathy/Tropical spastic paraparesis), designated as HAM rat disease. Neuropathological and immunohistochemical features of the affected spinal cord showed symmetrical white matter degeneration characterized by loss of myelin, vacuolar degeneration, infiltration with foamy macrophages and astrocytic gliosis. Lymphocytic infiltration was virtually absent throughout the disease process, and apoptotic cells were observed in the affected spinal cord. Clinical findings and pathological changes in seropositive HAM rats were, in general, milder than findings in seronegative HAM rats as previously described. Provirus genome in the affected spinal cord was evident in 1 of 2 seropositive HAM rats by polymerase chain reaction, but localization of HTLV-I antigen could not be detected by immunohistochemical staining. The collective evidence suggests that development of HAM rat disease is under strict genetic restriction of the host strain, and the primary cause is not mediated by immunological process with effector T cells as suggested in human HAM/TSP, and there seems to be a direct or indirect neurotoxicity for oligodendrocytes mediated by HTLV-I infection.
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PMID:[Analysis of HAM rat disease developed in HTLV-I carrier rat as an animal model of HAM/TSP in human]. 795 97