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)

Type C RNA viruses can be induced by certain chemicals from cells of many mouse strains. Both C58 and BALB/c cells have been shown to contain endogenous viruses that are designated N-tropic because they grow preferentially in cells of NIH Swiss mouse origin. While demonstrating many similar biological and immunological properties, the C58-induced virus is around 10-fold more infectious per physical particle than the N-tropic virus of BALB/c cells. In the present studies, inoculation of these viruses into newborn NIH Swiss mice led to the development of diseases associated with splenomegaly and lymphadenopathy at similar frequency in each group. The disease induced by C58-MuLV was histophathologically diagnosed as lymphoblastic leukemia and was highly malignant following transplantation into newborn mice. The histopathological appearance of spleens from BALB/c virus-affected animals was distinguishable, demonstrating instead myeloid metaplasia or myelogenous leukemia. These findings provide evidence that different endogenous mouse type C viruses can induce distinct diseases in the same mouse strain. Furthermore, they implicate the N-tropic virus endogenous to C58 cells as a major factor in the development of lymphoblastic leukemia that occurs at high frequency in that strain.
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PMID:Different hematological diseases induced by type C viruses chemically activated from embryo cells of different mouse strains. 4 91

In general, megakaryocytic myelosis is nowadays considered to be a separate disease entity, one of the myeloproliferative syndromes. Morphologically there are localised or diffuse proliferations of usually large pleomorphic megakaryocytes and immature atypical megakaryocytes up to megakaryoblasts in the bone marrow, in the sense of a haemoblastosis. In the course of the disease megakaryocytic splenomegaly develops. A sarcomatous form (megakaryoblastoma, megakaryo-sarcoma) is rare. Megakaryocytic myelosis may arise from chronic meyloid leukaemia or polycythaemia vera, rarely as a transitional stage to an acute myeloblastic leukaemia or megakaryoblastic leukemia in the sense of a blast crisis. The mature form of the disease, which has an age peak at 59 years and is not sex-linked, often takes a course over years with increasing splenomegaly, anaemia, moderate leucocytosis and usually marked thrombocytosis (average value of 720 X 10(9)/1). Life threatening complications are haemorrhages, thromboembolism and increased frequency of infections due to antibody deficiency in the advanced stage.
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PMID:[Megakaryocytic myelosis: clinical and morphological features (author's transl)]. 26 86

The pathophysiology of serially passaged myeloid leukemia of the RFM mouse was studied. The disease was characterized by progressive splenomegaly and infiltration of both marrow and spleen by myeloblasts. The animals became anemic and there was an associated erythroid hyperplasia in the spleen. Leukemic spleen cells obtained from animals early in the course of the leukemia were less malignant than those obtained from preterminal mice. The leukemia is most sensitive to alkylating agents but is also responsive to antimetabolites.
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PMID:Murine myeloid leukemia: I. Pathophysiology and drug sensitivity. 27 Oct 44

Chronic lymphocytic leukemia and chronic granulocytic leukemia vary considerably in their clinical features, laboratory findings, and therapy, but both generally have an ominous prognosis. Chemotherapy remains the mainstay of treatment in both disorders, with adjunctive measures to control complications such as anemia and splenomegaly. Immunotherapy for granulocytic leukemia is still under study but appears promising.
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PMID:Managing chronic leukemias. 29 42

From 1969--1975 patients with predominantly megakaryocytic myelosis were observed. Diagnosis was made up after histologic examination of iliac crest bone biopsy specimens embedded in methacrylate. From 6 patients rebiopsies and from further eleven ones the removed spleens were available. Autopsy was performed in 12 cases. In our material predominantly megakaryocytic myelosis was especially observed in male patients of advanced ages. The course of the disease was rarely acute, most often chronic and associated with the development of an extreme splenomegaly. Transition into osteomyelofibrosis or osteomyelosclerosis was frequent, the latter condition tended to develop a so-called myelosarcoma. The cause of death often was a generalized hemorrhagic diathesis with gastrointestinal hemorrhage or an fatal infection.
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PMID:[Pathologc findings in megakaryocytic myelosis (author's transl)]. 89 19

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

To understand further the hematopoietic dyscrasias induced by a variant (a) of Rauscher leukemia virus (RLV), we used Escherichia coli endotoxin to stress the hematopoietic system of control and RLV/a-infected BALB/c mice. During the preleukemic stages of virus infection, there was slight splenomegaly without peripheral blood erythroblastosis. Granulocyte release and tissue mobilization mechanisms appeared unaffected by the RLV/a infection. Both RLV/a-infected and control mice reacted to endotoxin with peripheral granulocytosis and peritoneal granulocyte mobilization, though the circulating granulocyte levels in RLV/a-treated mice initially were lower than those in controls. Spleen of RLV/a-infected animals were larger than those of controls, but both responded to endotoxin with elevated numbers of granulocytes and erythroblasts. Since numbers of bone marrow erythroblasts in both groups of mice were decreased after endotoxin, stem cell competition and/or shunting of stem cells from marrow to spleen may have been involved. Endotoxin also induced rapid falls in hematocrit levels in both groups. These studies suggested that RLV/a-infected mice can be a model to study 1) erythropoietic dysfunction uncomplicated by defective granulopoietic release and tissue mobilization control mechanisms, and 2) progression of evolving granulocytic leukemia.
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PMID:Granulopoiesis in "preleukemic" mice with anemia induced by Rauscher leukemia virus, variant a. 110 69

The term "plasmacytoid T-zone cells" has been used to describe distinctive cells that occur in clusters in the paracortex of some reactive lymph nodes. Recently, tumorous proliferations of these cells have been described in several patients with myelomonocytic leukemias. Neither the nature of these cells nor their relationship to myeloid leukemia has been conclusively established. We report the case of a 64-year-old woman with chronic myelomonocytic leukemia who developed lymphadenopathy that proved to be due to tumorous accumulation of plasmacytoid T-zone cells in the interfollicular regions of the lymph nodes. She underwent splenectomy because of symptomatic splenomegaly; the resected spleen also contained aggregates of plasmacytoid T-zone cells, in addition to extramedullary hematopoiesis. On treatment with busulphan and prednisone, the lymphadenopathy resolved and did not recur. The patient died 7 years later with blast transformation of her myelomonocytic leukemia and no recurrence of lymphadenopathy. The aggregates of plasmacytoid T-zone cells were architecturally and cytologically distinct from the leukemic infiltrates of myeloid cells in the spleen, and there was no evidence of differentiation of these cells into myeloid or monocytic cells. A panel of monoclonal antibodies on paraffin sections revealed no lineage-specific T- or B-cell markers (UCHL1-, L26-), and the plasmacytoid cells were positive for CD68 (KP1) and L60 (CD43), as well as faintly positive for 4KB5 (CD45RA) and MB1 (CD45R). They did not stain with antibodies to myeloid lineage antigens CD15, lysozyme, or myeloperoxidase. The combination of clinical, morphologic, and immunologic features of plasmacytoid T-zone cells in this case suggests that these cells may be of monocytic lineage but are not direct precursors of mature monocytic or granulocytic cells, and may not be part of the neoplastic clone in patients with myelomonocytic leukemia.
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PMID:Plasmacytoid T-zone cell proliferation in a patient with chronic myelomonocytic leukemia. Histologic and immunohistologic characterization. 184 25

The authors discuss diagnostic difficulties that may occur in the interpretation of splenomegaly. In some cases, other tumorous formations, palpable in the left hypochondrium (renal tumor and retroperitoneal fibroma in cases demonstrated) may be taken for splenomegaly. In other cases, diagnostic difficulties may be related to establishing the cause of genuine splenomegaly. Out of 10 patients with genuine splenomegaly, the cause of which could not be ascertained at the prehospital stage, the enlargement of the spleen in 2 was due to liver cirrhosis, in 3, to subleukemic myelosis, in 1, to splenic tuberculosis, in 2, to multiple capillary angiomas of the spleen, in 1, to chronic monocytic leukemia, and in 1 patient, to splenic echinococcosis. In 3 patients out of the 10, the diagnosis was verified by surgery followed by histological examination of the spleen. The conclusion is made about the necessity of the use of clinical and laboratory examinations, of patients with obscure "splenomegaly" together with the use of x-ray and ultrasonography of the spleen, kidneys, gastrointestinal tract, puncture of the bone marrow and spleen. In some cases, splenectomy may be performed along with histological examination of the spleen as the final stage of differential diagnosis of splenomegalies.
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PMID:[Difficulties in the differential diagnosis of splenomegaly]. 204 7

Sixty-one patients with essential thrombocythemia (ET) were followed from 1974 through 1987 at the Medizinische Poliklinik. Fifty-one patients (84%) presented with thromboembolic complications, and eight patients (13%) with hemorrhages. In seven patients (12%), a thrombocytosis was detected accidentally. Disturbances of the microcirculation (67%), mainly of the fingers and toes (53%), were the most frequent thromboembolic symptoms. The mean age of all patients was 58 years (male patients, 61 years; female patients, 56 years). The average platelet count at diagnosis was 897,000/microliter. The average maximal platelet count was 1.231 X 10(6)/microliter (range, 500,000/microliter to 4 X 10(6)/microliter). Seventy-two percent had a moderate leukocytosis (average, 12,400/microliter), 34% a splenomegaly, 29% a hepatomegaly. Signs of hypermetabolism were infrequent, lactate dehydrogenase (LDH) and uric acid elevations, if present, were moderate. Bleeding time and viscosity were normal in most patients. Spontaneous platelet aggregation was increased in 81% of patients (n = 40). Platelet aggregation studies with the aggregation inducing substances adenosine diphosphonate (ADP), platelet activating factor (PAF), thrombin, collagen, and adrenalin showed hypoaggregation in most patients. Adrenalin-induced aggregation distinguished best between ET-patients and reactive thrombocytosis showing hypoaggregation in all ET-patients tested (n = 16) and in none of 22 controls. Bone marrow studies were performed in 57 patients. The histologic studies (done in 49 patients) were consistent with a chronic myeloproliferative disorder in all cases. In 41 cases (84%) the picture of a megakaryocytic myelosis was found, in 12 of these a granulocyte-rich form of megakaryocytic myelosis. Cytologic studies only (eight patients) did not differentiate ET well from reactive thrombocytosis. Platelet aggregation studies and bone marrow histology may be of help in the diagnosis of difficult cases of thrombocytosis. The Philadelphia status was negative in all cases studied (14 patients). Fourteen patients died. The causes of death were thromboembolic complications in probably 11 and acute leukemia in two patients. The probability of 10-year survival is 64% after a mean follow-up time of approximately 5 years. It appears that considering the average age of ET patients at diagnosis, life expectancy is close to normal.
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PMID:Essential thrombocythemia. Clinical characteristics and course of 61 cases. 336 70


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