Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of erythroleukemia (EL) associated with monosomy 7 is reported. The EL was diagnosed 20 months after the initial diagnosis of monosomy 7 was made. An immunologic study of the blast cells using a monoclonal antibody was positive for glycophorin A, which suggested that they were of erythroid origin; this was confirmed by electron microscopy. Chemotherapy was started with low dose cytarabine. However, the patient had severe bone marrow suppression and died of pneumonia. Our case shows that monosomy 7 is an abnormality of the pluripotential stem cells, including erythroid cells, that resulted in a true erythroid neoplasm.
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PMID:Erythroleukemia in a child associated with monosomy 7. 206 74

A 74-year-old man was admitted to the National Defense Medical College Hospital because of purpura on the extremities. The blood hemoglobin level was 11.5 g/dl, the white blood cell count 7. 3 x 10(9)/l with 3% blastic cells, and the platelet count 4.0 x 10(9)/l. There was leukoerythroblastosis with only mild teardrop appearance of erythrocytes. The blastic cells consisted of two types, megakaryoblast-like cells and myeloblast-like cells. There was a very mild hepatosplenomegaly, but no lymphadenopathies. The bone marrow aspirations yielded dry taps. The marrow biopsy specimen revealed myelofibrosis associated with trilineage hyperplasia, but no apparent infiltration of leukemic cells. Platelet-associated IgG (PAIgG) had a high titer and the response to platelet transfusions was poor. On prednisolone and colchicine, the blastic cells in the peripheral blood disappeared and the platelet count increased. He died of pneumonia. The autopsy showed myelofibrosis with hyperplasia of myeloid and erythroid lineage in the bone marrow. Megakaryocytes were relatively few and there was no infiltration of leukemic cells.
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PMID:[Myelofibrosis associated with immunological abnormalities]. 221 80

Sphha/sphha anemic mice have an abnormality in the erythroid membrane protein, alpha spectrin, and exhibit multiple related clinical abnormalities, including spherocytosis, shortened red cell survival, chronic hemolysis, hemosiderosis, and extramedullary hematopoiesis. In addition, these mutant mice exhibit a granulocytosis and lymphocytosis, lymph node hyperplasia, elevated serum immunoglobulins, membranoproliferative glomerulonephritis, and decreased lifespan--abnormalities that are less clearly attributable to a spectrin defect. In order to further elucidate the mechanisms of disease in these animals, we undertook a series of bone marrow transplantation experiments. Transplantation of anemic marrow into lethally irradiated congenic +/+ mice resulted in chronic spherocytosis, hemolytic anemia, peripheral leukocytosis, and extramedullary hematopoiesis. Additionally, transplant recipients of anemic marrow which had received a higher radiation dose (12 Gy) had increased numbers of peripheral blood CD4+ and CD8+ lymphocytes, a hypocellcular thymus, and a severe pneumonitis characterized by nodular areas of consolidation and edema. Mice receiving congenic +/+ marrow and irradiated with the same radiation dose exhibited minimal pulmonary abnormalities. Anemic mice transplanted with congenic +/+ marrow usually died, but the survivors exhibited reversal of some clinicopathological changes. These results would suggest that the clinical abnormalities of sphha/sphha mice are in part attributable to abnormalities of hematopoietic stem cells but may also involve defects in other cell types. The pathogenesis of the accompanying lymphoid abnormalities observed in this mutant anemic mouse and any correlation with the erythroid spectrin defect are presently unknown. The pulmonary disease that develops in the transplant recipients of anemic marrow needs to be characterized further but may represent a unique model of lung injury.
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PMID:Transplantation studies in mice with congenital hemolytic anemia. 234 Jun 52

We have studied the hematopoietic system of the immunodeficient mouse mutant, viable motheaten (mev/mev). These mice usually die by 9 weeks of age from severe pneumonitis. The lungs at that time are infiltrated with granulocytes, macrophages, and lymphocytes. Granulocyte and macrophage precursor cells (CFU-GM) are dramatically increased in the spleens of mev/mev mice, whereas the bone marrow population of these precursors is decreased when compared with littermate control animals. The CFU-GM population retained its normal dependence on granulocyte-macrophage colony-stimulating factor (GM-CSF) for proliferation and differentiation. In contrast, the frequency of an erythroid precursor (CFU-E) was dramatically increased in spleen and showed increased sensitivity to erythropoietin (Epo). Moreover, a splenic CFU-E subpopulation formed normally appearing erythroid colonies in the absence of exogenous Epo. The bone marrow CFU-E population was significantly diminished in size when compared with either wildtype C57BL/6J mice or mice heterozygous for the mev allele. Unlike the CFU-E population, erythroid burst-forming unit (BFU-E) frequency in mev/mev mice was diminished both in bone marrow and in spleen, although the total number of splenic BFU-E was increased because of splenomegaly in these animals. BFU-E retained their dependence on the presence of both Epo and a source of interleukin 3 (IL-3) for proliferation and differentiation into erythroid bursts. Spleen cells from mev/mev mice, when stimulated in vitro with pokeweed mitogen, failed to produce significant quantities of IL-3. Comparison with medium or +/mev heterozygotes revealed that mev/mev spleen cell-conditioned medium showed a 40-fold reduction in burst-promoting activity. Thus, in viable motheaten mice, there is a major shift in hematopoiesis from bone marrow to spleen, which is accompanied by a diminished capacity of spleen cells to produce burst-promoting activity. These data and those from other studies suggest that the hematopoietic microenvironment of marrow may be impaired in this mutant.
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PMID:Hematologic abnormalities of the immunodeficient mouse mutant, viable motheaten (mev). 278 74

The interrelationships between various components of the non-immune inflammatory response (white cell count, plasma lactoferrin, C-reactive protein, ferritin, iron and iron-binding capacity), were studied serially in a variety of inflammatory conditions including acute lobar pneumonia, active pulmonary tuberculosis, rheumatoid arthritis on gold therapy and sepsis in the face of marrow hypoplasia induced by chemotherapy. Lactoferrin concentrations paralleled the white count in all groups. They were highest in pneumonia and tuberculosis, mildly elevated in rheumatoid arthritis and markedly decreased in neutropenic sepsis. Very high initial lactoferrin concentrations were associated with a poor prognosis in acute pneumonia. C-reactive protein and ferritin concentrations remained elevated through the period of study in acute pneumonia and neutropenic sepsis, while they gradually normalised over weeks in subjects with tuberculosis or rheumatoid arthritis on therapy. In pneumonia and tuberculosis moderate hypoferraemia and a reduced iron-binding capacity were evident. In contrast, a raised percentage saturation was present in neutropenic sepsis, probably related to erythroid marrow suppression. Comparisons between ferritin, lactoferrin and C-reactive protein in the various groups supported the concept that ferritin behaves in part as an acute phase reactant and that hypoferraemia in inflammation is due to deviation of iron into ferritin stores. The suggestion that lactoferrin is responsible for the hypoferraemia and hyperferritinaemia was not supported by the present data. Iron deficiency appeared to limit the hyperferritinaemic response in rheumatoid arthritis, while erythropoietic inhibition by chemotherapy dampened the hypoferraemic response in neutropenic sepsis.
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PMID:The non-immune inflammatory response: serial changes in plasma iron, iron-binding capacity, lactoferrin, ferritin and C-reactive protein. 378 68

A nine year old quarter horse exhibited progressive weight loss and inappetance over a 47 day period. There was clinical evidence of pleuritis and pneumonia substantiated by leukocytosis and elevated protein in pleural fluid. Over the entire period the horse was neutropenic and had circulating abnormal immature granulocytes and low numbers of blast cells. Anemia and thrombocytopenia progressively worsened. Bone marrow examination revealed very few mature granulocytes but large numbers of immature cells of the granulocytic series and marked megaloblastic transformation of erythroid cells. These findings were consistent with chronic granulocytic leukemia.
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PMID:Chronic granulocytic leukemia in a horse. 694 47

Treatment of myelodysplastic syndromes (MDS) with recombinant human erythropoietin (Epo) is successful in only 10% to 25% of patients. We performed a pilot study in 10 anaemic patients with MDS to examine whether sequentially applied recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF) and Epo improves haemoglobin levels and/or reduces red blood cell transfusion requirements. Morphological diagnoses of patients were refractory anaemia (RA) in 3 cases, RA with ring sideroblasts in 3 cases and RA with excess blasts in 4 cases. GM-CSF was given subcutaneously at a dose of 150 micrograms/m2/d during the initial 10 days. From day 11, Epo was administered by subcutaneous injections for 8 weeks at a dose of 100 U/kg/d and subsequently at an escalated dose of 200 U/kg/d in 3 patients. Changes in reticulocyte counts, haemoglobin levels, RBC support and ferrokinetic parameters were compared with pretreatment values. Two out of 8 evaluable patients showed a rise in haemoglobin levels at week 8 and 10, respectively, and lost their transfusion dependency for a period of 13 and 27 weeks. In 1 patient, haemoglobin level increased only after dose escalation of Epo (200 U/kg/d). Leukocyte counts remained uneffected by treatment with Epo, while 1 patient showed a 4-fold increase in platelet numbers. Toxicity was mild. Two patients died of pneumonia and global heart failure, respectively, unrelated to growth factor therapy. Based on this pilot study, we conclude that sequential treatment with GM-CSF and Epo does not increase erythroid responses in anaemic patients with MDS. Because of the delayed increase in haemoglobin in both responders, we surmise that the beneficial effects were induced by Epo alone.
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PMID:Sequential administration of recombinant human granulocyte-macrophage colony-stimulating factor and human erythropoietin for treatment of myelodysplastic syndromes. 785 74

A 84-year-old man was treated with antibiotics including erythromycin and a diuretic (furosemide) because of acute heart failure and pneumonia. During the treatment, he developed moderate anemia (Hb 8.7g/dl). His anemia improved after the treatment. He again developed marked anemia (Hb 6.3g/dl) during the second treatment with erythromycin and furosemide and received blood transfusions. Bone marrow aspiration study revealed severe erythroid hypoplasia (0.2%). He was referred to our hospital, but he was not treated because his hemoglobin levels and reticulocyte count increased (80%) and his bone marrow showed increased erythroblasts (41.5%). His anemia gradually improved without any treatment. We diagnosed the case as drug-induced pure red cell aplasia (PRCA). We cultured bone marrow cells obtained from the present case and four normal healthy volunteers by a plasma clot method to determine the effects of two drugs on the number of erythroid colony forming unit (CFU-E). Furosemide strongly inhibited the CFU-E colony formation in the patient, but the inhibition effect of erythromycin was moderate. Furthermore, CFU-E was markedly suppressed by a combination of erythromycin and furosemide in both patient and control materials. These results indicate that both furosemide and erythromycin were related to the occurrence of PRCA in this patient.
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PMID:[Pure red cell aplasia induced by erythromycin and furosemide effects on in vitro erythroid colony forming unit (CFU-E)]. 806 24

The article is based on the data obtained in the result of examination of 53 wounded with closed cranial injuries (slight and middle gravity cases), and 34 wounded with spine injuries, but without spinal marrow traumas. The activity of fibroblasts of spinal marrow was studied, as well as the functional activity of peripheral blood monocytes during a ten-day posttraumatic period. It was found out that patients had refractory anemia with a diminishing number of erythroid cells, and also initial infectious complications, such as pneumonia or wound suppuration.
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PMID:[The therapeutic aspects of the treatment and rehabilitation of minor casualties in neurosurgery]. 824 43

Two familial cases of myelodysplastic syndrome (MDS) are reported, one of whom had an abnormal karyotype of 45, XY, -7 (monosomy 7). Case 1 was a 60-year-old woman developed dizziness and nasal bleeding. She was treated with blood transfusion alone. About 11 months after diagnosis, she died of pneumonia. Case 2 was a 22 year-old man, who was the son of case 1, developed febrile disease because of recurrent skin and oral mucosa infections. He had a partial response to low-dose of cytarabine. Thirteen months after diagnosis, he died of severe pneumonia. Both cases were diagnosed as having refractory anemia with excess of blasts due to peripheral blood and bone marrow findings. Both patients had pancytopenia, erythroid hyperplasia in bone marrow, marked dyserythropoiesis, recurrent infectious diseases and severe pneumonia that resulted in death. These symptoms resembled to those reported for monosomy 7 syndrome. Familial MDS with monosomy 7 is rarely reported. These cases are of interest to investigate hereditary factors of MDS.
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PMID:[Myelodysplastic syndrome developed in a mother and her son whose bone marrow karyotype showed monosomy 7]. 884 1


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