Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The composition of the hemopoiesis was determined in iliac crest biopsies of 51 patients with polycythaemia vera. There was a good correlation between thrombopoiesis and thrombocytes and, to a minor degree also between erythropoiesis and erythrocytes in untreated patients as well as between granulopoiesis and granulocytes in 32P-treated patients. In patients with normal blood counts there existed no correlation between the bone marrow and the blood counts within smaller limits of the cell count. Histomorphometric analysis shows no difference either between untreated and 32P-treated patients or between patients with and without splenomegaly. This is an argument against a significant intrasplenic hemopoiesis or an intrasplenic cell pooling, or destruction (hypersplenism), respectively. The blood sinusoids are hyperplastic and distended. With increasing hyperplasia of the hemopoiesis the sinusoids become relatively smaller. So changes in vascularisation may be of importance in the infrequent transitions into myelofibrosis and/or leukemia.
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PMID:[Relationships between hemopoiesis and peripheral blood counts in untreated and 32P-treated patients with polycythaemia vera (author's transl)]. 96 31

Foam cells in the spleen, bone marrow, liver and lymph nodes were examined on the 73 reliably recorded and sampled leukemia autopsy cases encountered at Kobe University from 1958 to 1972. Although the substances stored in the foam cells were biochemically unknown, the foam cells in leukemia could be morphologically classified into two types: The one was identified with the Gaucher type, but the other was not identified with the sea-blue type and might be considered as to be the transitional type described in another report. Foam cells could be found in the spleen of 6 out of 12 cases of chronic myeloid leukemia, one out of 2 cases of chronic lymphatic leukemia, one out of 7 cases of leukemic lymphosarcoma, one out of 9 cases of acute lymphatic leukemia, and none in 3 cases of monocytic leukemia. In acute myeloid leukemia, the incidence of foam cells in the spleen was 47.5% in 40 cases, and acquired lipidoses were more frequently seen in cases under 19 years of age, in male cases, in cases with an enlarged spleen over 400 g, and in cases of over 4 months' duration.
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PMID:Secondary lipidosis in leukemia. 99 40

The natural history and haematological features of 18 patients with a chronic form of myelomonocytic leukaemia are described. The majority were elderly and, in this series, females predominated. Haematological prodomata, such as unexplained monocytosis, leucopenia, or thrombocytopenia were common, and the clinical onset was insidious. Splenomegaly was variable but tended to increase as the disease progressed. Anaemia was usually less than in the acute disease, unless compounded by iron deficiency. The blood film typically showed a mixed monocytosis and granulocytosis, cells in both lines showing abnormalities. 'Paramyeloid' cells, appearing in Romanowsky stained films intermediate between myelocytes and monocytes, were characteristic, although cytochemical and electron microscopical analysis suggests that these cells may be allotted to one or other cell line. The marrow aspirate was characteristically hypercellular, showed granulocytic hyperplasia, and, in contrast to the well-differentiated blood picture, the proportion of poorly differentiated cells, including blasts, was high. Serum lysozyme levels were usually raised. Five of the 18 cases survived more than 5 years, while 10 lived 2 years or longer. The morphological and clinical features form part of a spectrum including acute myelomonocytic leukaemia, into which several of the patients transformed. Recognition of the syndrome is important because the patients are probably best managed without intensive chemotherapy.
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PMID:Chronic myelomonocytic leukaemia. 105 74

Portal haemodynamic studies were carried out in 11 subjects, seven with chronic myeloid leukaemia and four with chronic lymphatic leukaemia, and results compared with those obtained in five patients with 'idiopathic' splenomegaly and with control subjects. All 11 patients with chronic leukaemia had intrasplenic pressures above 11 mmHg and of these four had pressures above 20 mmHg. Portosystemic collaterals were seen on splenovenography in four of these patients. Hepatic vein wedge pressure was above 7 mmHg in nine patients and these high levels were a result of increased free hepatic vein pressure. The corrected sinusoidal pressure and post sinusoidal resistance were essentially normal in all patients. Evidence of increased pre-sinusoidal resistance was seen in six patients. Estimated hepatic blood flow above 1500 ml/min was seen in six patients and all had evidence of histological portal or sinusoidal infilatration. Patients with 'idiopathic' splenomegaly regardless of increased liver blood flow did not have a significant increase in intrasplenic pressure and no alteration in other haemodynamic parameters. It appears that increased liver blood flow alone in a normal liver can only minimally elevate intrasplenic pressure but can play a significant part in the pathogenesis of portal hypertension when liver structure is altered.
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PMID:Portal hypertension in chronic leukaemia. 105 78

Megakaryocyte morphology was studied quantitatively in primary thrombocythaemia (PT) and in chronic myelogenous leukaemia (CML). The relation of thrombokinetics to megakaryocyte quantifications was evaluated in PT and compared to previously obtained results in polycythaemia vera (PV) and idiopathic thrombocytopenic purpura (ITP). Megakaryocyte area, number and volume per mul bone marrow were significantly higher in PT as compared to controls. The nuclear lobe number was significantly increased and the megakaryocytes were shifted towards more mature forms, suggesting a prolonged megakaryocyte generation time. In CML the megakaryocyte number and volume per mul bone marrow were also significantly above normal, but the megakaryocyte area, number of lobes and degree of megakaryocytic maturation were significantly below normal. Platelet production was in PT 6.2 times normal and proportional to the increase in megakaryocyte volume which was 6.8 times normal. In PV with major splenomegaly the mean platelet production rate was higher (9.5 times normal) although their peripheral platelet count was lower than in PT. This discrepancy is explained by the greatly enlarged splenic platelet pool in the PV patients. In ITP the mean platelet production rate was 2.2 to 3 times normal and was significantly lower than in PT and PV.
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PMID:Megakaryocyte quantifications in relation to thrombokinetics in primary thrombocythaemia and allied diseases. 106 Jan 75

We have studied immunologic reactivity to leukemia-associated antigens in patients with chronic myelocytic leukemia (CML) treated with chemotherapy and adjunctive immunotherapy. All patients were immunologically competent as measured by skin test reactivity to dinitrochlorobenzene. Immunotherapy consisted of allogeneic irradiated leukemic myeloblasts injected intradermally, with BCG vaccine (Research Foundation, Chicago, Ill.) given by multiple puncture at the same site. 10(9) cells plus BCG were given weekly for 4 wk, and 10(8) cells plus BCG were given at monthly intervals thereafter. Eight patients judged clinically to be in the stable phase of their disease developed circulating antibody against the immunizing blast cells demonstrable by cytotoxicity and immunofluorescence assays. The antibody also showed reactivity against a panel of myeloblasts (12 paients) but not against the corresponding remission lymphocytes (five patients) or normal lymphocytes (20 donors). In two cases the antibody showed reactivity against the patient's own leukemic blasts. Seven of these eight patients have maintained a steady clinical course ranging from 20 to 40 mo, while one entered the blastic phase and died. Six patients were judged to be in the aggressive phase of CML because of progressive leukocytosis and splenomegaly or increasing myeloblastosis; five died an average of 16 mo after diagnosis. Humoral antibodies were not detected in these patients after repeated courses of BCG and allogeneic leukemic cells. We conclude that specific active immunotherapy of patients with CML can abet the production of humoral antibody against blast cell antigens and that this response may be impaired during the aggressive phase of the disease.
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PMID:Antibody responses to leukemia-associated antigens during immunotherapy of chronic myelocytic leukemia. 106 Apr 71

Pretreatment characteristics of 48 infants (under 2 years of age) with leukemia treated over a period of 18 years at a single institution were studied in relation to response to therapy, extramedullary involvement, and survival. In order to provide a basis of comparison, 45 of the infants were each paired with an older (2-9 years of age) leukemic child, who had the same race, and disease type, who was treated within the same period of time and received similar suportive care and chemotherapy, and when possible, was of the same sex. The overall median survival times of infants and their pairmates were 211 days and 445 days, respectively. Initial status of the spleen was the single significant factor in relation to the length of survival. Median survival time for infants with splenomegaly was 186 days compared to a median survival time of 414 days for infants without splenomegaly. The complete response rate was 75% for infants and 80% for the pairmates. Median duration of remission was 84 days for infants and 280 days for their pairmates. Initial peripheral leucocyte count was significantly related to the duration of remission; patients with very high leucocyte counts had the shortest remissions. The duration of remission increased throughout the period covered by this study, however, prognosis relative to pairmates remained poor. Central nervous system leukemia occurred in 44% of infants and 40% of the pairmates; incidence of CNS leukemia was much higher (70%) in infants under one year of age than in infants one year old (37%). Extramedullary leukemia occurred at other sites in 46% of the infants and 31% of the pairmates. The only pretreatment characteristic of prognostic importance for predicting extramedullary involvement was the patient's age at diagnosis.
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PMID:Unfavorable prognosis of acute leukemia in infancy. 106 May 4

No more than 150 cases of neonatal leukemia had been reported in the literature. Seven additional cases are reported herein. The incidence of neonatal leukemia has been of one in 50,000. Its incidence among the group of neonates requiring hospitalization has been of 0.075%. The seven neonates with leukemia consist of five males and two females. Two of them had an associated Down's syndrome. Abdominal distension, hepatomegaly, splenomegaly, cutaneous manifestations and purpura were the most frequent clinical findings in our patients. Severe anemia was present in only three patients. Thrombocytopenia was recognized in six of them. A high white blood cell count was present in five patients. The number of blast cells in their peripheral blood smear ranged between 16 and 100%. A remarkable myeloid dominance was observed. One patient died two hours after birth and his diagnosis was made at autopsy. Three patients were diagnosed before the age of three weeks. The three patients with myeloid leukemia were treated with DNR and Ara-C. A complete hematological remission was achieved in two of them. One patient died of a Pn. carinii pneumonia one month after the remission was induced. The remainder patient of this group had a Down's syndrome and the leukemia had been confirmed by hepatic biopsy. After two years of maintenance with Ara-C and Thioguanine he is alive and both, peripheral blood and bone marrow, remains normal. A lymphocitic leukemia was seen in only two patients. One was treated with prednisolone and VCR, and the other with prednisolone, VR and L-Asp. In both cases a good response to the chemotherapy was observed. Autopsy was performed in all patients who died but one. The pathological findings are analyzed. The low survival among patients with neonatal leukemia may be influenced by the toxic side effects of the used chemotherapy. All aspects of the medical treatment including drugs of choice and the usefullness of isolation devices are further discussed.
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PMID:[Neonatal leukemia. Report of seven cases (author's transl)]. 106 63

A study on 25 South African Black patients with chronic myelogenous leukaemia (CML), who were followed for 3 1/2 years, is reported. The Ph chromosome was found in 19 of 20 patients studied. Males predominated in a ratio of 2,5:1. Several unusual clinical features were encountered: significant lymphadenopathy, congestive cardiac failure and skin lesions. Patients with lymphadenopathy responded to busulphan therapy no differently from patients without lymphadenopathy. Nine patients had congestive cardiac failure, and in 7 of these a cause could not be found. Three untreated patients became pregnant, indicating that CML per se does not cause infertility. The haematological measurements were similar to those of previous reports; however, the marked splenomegaly suggests that South African Black patients present themselves for treatment rather late in the disease. The median survival time of 34 months is similar to that of previous reports of larger series from other parts of the world.
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PMID:Chronic myeloid leukaemia in South African blacks. 107 Jan 65

To evaluate the role of immune response in regression of leukemia, we studied the effect of immunosuppression on the spontaneous regression of a leukemia induced by a specific strain of Friend murine leukemia virus complex (RFV). Thymectomy of newborn but not adult outbred Swiss mice markedly inhibited regression. The effect of antithymocyte serum (ATS) on regression depended on the timing of ATS treatment. Regression was markedly inhibited in leukemic mice given ATS just before the start of regression. During leukemia development, ATS treatment but not thymectomy potentiated splenomegaly and delayed the start of regression. Both ATS treatment and neonatal thymectomy increased mortality as a function of the decrease in disease regression. Treatment with normal rabbit serum also inhibited regression but, when given during leukemia development, affected neither the splenomegalic response to RFV nor the number of deaths. The data demonstrated that an intact immune system was required for leukemia regression and suggested that some thymus-dependent parameter of immune response was a major factor in regression.
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PMID:Effects of thymectomy and antithymocyte serum on spontaneous regression of Friend virus-induced erythroleukemia. 108 46


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