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)

Four of 12 Chinese patients receiving BACOP, in combination with recombinant human granulocyte colony-stimulating factor, for aggressive non-Hodgkin's lymphoma developed a rapidly progressive pneumonic illness characterised by diffuse pulmonary infiltrates and hypoxaemia. The condition proved fatal in three, and in none could an infective cause be identified. A retrospective analysis revealed only one episode of pneumonia in the previous 24 patients in whom the same BACOP regimen was administered without granulocyte colony-stimulating factor support. Granulocyte colony-stimulating factor, by augmenting white cell production, pulmonary sequestration and margination and production of toxic oxygen species, may exacerbate underlying subclinical bleomycin pulmonary toxicity. Caution should be exercised before using granulocyte-stimulating factors in bleomycin-containing regimens.
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PMID:Serious pulmonary complications in patients receiving recombinant granulocyte colony-stimulating factor during BACOP chemotherapy for aggressive non-Hodgkin's lymphoma. 752 99

We report a case of aplastic anaemia (AA) treated with granulocyte colony-stimulating factor (G-CSF) terminating as acute myeloblastic leukaemia (AML). Because of severe pneumonia, 250 micrograms of G-CSF was administered for 30 d to promote neutrophil recovery. Following G-CSF therapy, myeoblasts appeared, and the diagnosis of AML was then made. The myeloblasts proliferated in response to G-CSF in vitro and in vivo. In AA, development of AML after treatment with G-CSF is rare. Therefore a careful observation for leukaemic transformation is necessary in long-term administration of G-CSF for AA.
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PMID:Development of acute myeloblastic leukaemia in a case of aplastic anaemia treated with granulocyte colony-stimulating factor. 752 51

We report a patient with refractory anemia with excess blasts who showed a lineage-unrestricted hematologic response to granulocyte colony-stimulating factor (G-CSF). After 17 months of a stable disease state, the patient developed pneumonia, progression of cytopenia, and reduced cellularity and blast mass in the bone marrow. He was given G-CSF to overcome the pneumonia. Not only the neutrophil count, but also the platelet count increased soon after initiation of the G-CSF therapy; both counts became normal on the fifth day of the G-CSF therapy. Additionally, the anemia improved gradually. The neutrophil and platelet counts were maintained in the normal range for 3 months after cessation of the G-CSF. In vitro studies showed that G-CSF alone stimulated megakaryocyte colony formation from bone marrow mononuclear cells (BMMNC), and accessory cells in the BMMNC were necessary for expression of this G-CSF-induced in vitro megakaryocytopoiesis. These results suggest that, in coordination with accessory cells, G-CSF stimulated megakaryocytopoiesis in the patient. This case provides valuable information for understanding the mechanisms of a lineage-unrestricted hematologic response to G-CSF, which is very rarely observed in MDS.
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PMID:Lineage-unrestricted hematologic response to granulocyte colony-stimulating factor in a patient with refractory anemia with excess blasts. 753 78

We monitored the plasma elastase alpha 1-proteinase inhibitor complex levels in 21 patients with primary lung cancer who received combination chemotherapy with or without recombinant human granulocyte colony-stimulating factor (rhG-CSF), and 15 normal nonsmokers as controls. Of the 21 patients, 14 received combination chemotherapy without rhG-CSF (among them, 6 developed pneumonia) and 7 received combination chemotherapy with rhG-CSF (among them, 1 developed pneumonia). We measured peripheral WBC counts, C-reactive protein (CRP) levels, plasma elastase alpha 1-proteinase inhibitor complex (complex) levels, and complex/WBC values during cancer chemotherapy. In patients who received cancer chemotherapy without rhG-CSF and had no complications (n = 8), WBC values decreased after chemotherapy, and then gradually increased. Complex levels also decreased slightly after chemotherapy and gradually recovered. The value obtained from dividing the complex concentration by WBC count (complex/WBC value) remained stable during cancer chemotherapy. In patients who received cancer chemotherapy with rhG-CSF and had no complications (n = 6), WBC values decreased after chemotherapy, and then rapidly increased to abnormally high values. Complex levels also decreased slightly after chemotherapy and rapidly increased to abnormally high values together with the WBC counts. The complex/WBC values remained stable during cancer chemotherapy. In patients who developed pneumonia during cancer chemotherapy with or without rhG-CSF (n = 7), their complex levels, complex/WBC values, and CRP levels were elevated at the onset of pneumonia. The maximum complex levels (the highest levels during chemotherapy) were significantly higher in patients who received cancer chemotherapy with rhG-CSF and did not develop pneumonia (583.1 +/- 114.5 ng/mL) and in patients who developed pneumonia during cancer chemotherapy (516.7 +/- 113.2 ng/mL), compared with normal nonsmokers (130.2 +/- 5.5, p < 0.01) and patients who received cancer chemotherapy without rhG-CSF and did not develop complications (211.5 +/- 23.3, p < 0.01). The maximum complex/WBC values were not increased in patients who received cancer chemotherapy with rhG-CSF (0.08 +/- 0.01) and patients who received cancer chemotherapy without rhG-CSF (0.092 +/- 0.01, p < 0.01). The maximum complex/WBC values were significantly higher in patients with pneumonia (0.56 +/- 0.12) compared with normal nonsmokers (0.026 +/- 0.002, p < 0.01) and patients without complications. These findings suggest that although rhG-CSF increases total plasma elastase burden, increased release of neutrophil elastase from individual neutrophils does not take place in vivo in the absence of pneumonia.
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PMID:Measurements of plasma elastase alpha 1-proteinase inhibitor complexes in patients receiving cancer chemotherapy with granulocyte colony-stimulating factor. 753 56

Sepsis is a common cause of morbidity and mortality. Neutrophils are the major defense against bacterial invasion, and granulocyte colony-stimulating factor (G-CSF) augments both neutrophil number and function. In our study, 160 rabbits were inoculated transtracheally with 0.5 mL of a solution containing 10(4) colony forming units per milliliter of Pasteurella multocida. Twenty-four hours later, chest x-rays and quantitative blood cultures demonstrated pneumonia and bacteremia. Therapy was then begun with penicillin G and either recombinant human G-CSF (rG-CSF; 5 to 8 micrograms/kg subcutaneously) or placebo every day for 5 days. Arterial blood gases and 23 other parameters of organ function were performed before inoculation and serially thereafter. All rabbits underwent histologic examination of organs at the time of septic death or when sacrificed on day 6. A total of 149 rabbits survived long enough to initiate therapy. A significant increase in leukocytes by day 4 was found in the rG-CSF-treated group. There was a trend towards improved survival in the rG-CSF group (77% v 67%; P = .13, n = 149). Analysis of pretreatment variables revealed sepsis-induced leukopenia (< or = 2,800/microL) as the only predictor of significantly improved survival with rG-CSF treatment (57% v 39%; P = .04, n = 73). The majority of the survival benefit occurred within the first 24 hours of treatment. This was before the time that a significant difference in mean white blood cell (WBC) count was observed between the study groups, making intravascular leukocytosis an unlikely explanation for the survival advantage in the rG-CSF group. No significant difference in laboratory variables reflecting organ function was demonstrated between the groups. Histologic grading of inflammation (0, normal, to 6, necrosis) in seven organs revealed that the surviving rabbits had mild but statistically significant increased inflammation in the liver, spleen, and noninoculated lung in the rG-CSF versus placebo groups (liver: 2.6 v 1.5, P < or = .0001; spleen: 3.2 v 2.3, P < or = .0001; and noninoculated lung: 2.9 v 2.5, P = .04). Administration of rG-CSF, in addition to penicillin G, in immune competent rabbits with gram-negative sepsis complicated by leukopenia significantly improved survival over antibiotics alone. The administration of rG-CSF in early sepsis for a short therapeutic duration was not associated with any clinically evident toxicity. Clinical trials using rG-CSF in septic patients with leukopenia are indicated.
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PMID:Granulocyte colony-stimulating factor versus placebo in addition to penicillin G in a randomized blinded study of gram-negative pneumonia sepsis: analysis of survival and multisystem organ failure. 754 3

We report a 72-year-old man with refractory anemia with excess of blasts who presented severe pancytopenia and pneumonia and received granulocyte colony-stimulating factor (G-CSF) treatment over a 6-week period. In addition to a dramatic increase in mature neutrophils, platelet count and hemoglobin level, the patient achieved a hematological remission which continued for more than 5 months despite discontinuation of the treatment. This observation confirms that in some cases during G-CSF treatment erythropoiesis and thrombopoiesis may improve in addition to the expected effect on neutrophils. While the patient remained in hematological remission, bone marrow examination revealed trilineage dysplasia. This finding suggests that the hematological remission in this patient may not have resulted from a recovery of non-clonal hematopoiesis of a normal clone, but may have derived instead from the monoclonal hematopoiesis of a neoplastic clone.
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PMID:Trilineage response to granulocyte colony-stimulating factor administration in a patient with myelodysplastic syndrome. 754 37

Immunotherapy can be defined as treatment directed at augmenting host immune defence mechanisms. Non-antimicrobial therapies and immunoprophylaxis in bone marrow transplantation (BMT) can be subdivided into three broad categories: passive immunotherapy with intravenous immunoglobulin (IVIG); cytokine therapy; and anti-endotoxin-directed treatments. Most studies using IVIG in BMT are prophylactic and suffer from variability in study design, type of IVIG and dosing regimens. Various effects on viral and bacterial infections and graft-versus-host disease (GVHD) have been reported but few if any have shown benefit in terms of improved patient survival. Moreover the immunomodulatory effect of immunoglobulin G preparations is frequently overlooked. With the exception of cytomegalovirus (CMV) pneumonitis, there is little evidence of benefit in the treatment of established infections and the relative benefits of hyperimmune preparations are poorly established. The development of haemopoietic growth factors has led to the widespread use of cytokines in BMT. The benefits of these agents both in the prevention of fever and infection and as adjuvants to standard antimicrobial therapy in established infection (e.g. invasive mycoses) are rapidly becoming apparent. Both human recombinant granulocyte-macrophage colony-stimulating factor (rhGM-CSF) and granulocyte colony-stimulating factor (rhG-CSF) have been shown to accelerate granulocyte recovery following BMT and reduce fever days, antibiotic usage and hospitalization. RhGM-CSF appears superior in these respects. The roles of interleukin 1 (IL1), IL3, IL6 and interferons are also under evaluation. As with the much publicised studies using anti-endotoxin antibodies as therapy in sepsis, there is little evidence of benefit in the few studies performed in BMT patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunotherapy and immunoprophylaxis in bone marrow transplantation. 756 Sep 54

We determined the effective method of administration of recombinant human granulocyte colony-stimulating factor (rhG-CSF) in patients with transitional cell carcinoma of the urothelium receiving methotrexate, etoposide and cisplatinum (MEC) therapy. Recombinant human G-CSF was administered at 2 micrograms/kg subcutaneously starting after the white blood cell count was less than 3,000/mm3 (short administration) or starting immediately after finishing MEC therapy (prophylactic administration). The median white blood cell nadir for the control group, short administration group and prophylactic administration group, was 275 +/- 77, 250 +/- 317 and 2,066 +/- 47/mm3, respectively. The number of days with a white blood count of less than 1,000/mm3 for the control group, short administration group and prophylactic administration group was 6.6 +/- 0.6, 4 +/- 2 and 0.9 +/- 0.5 days, respectively. The difference between the control group and prophylactic administration group was statistically significant (p < 0.01). These findings indicated that the prophylactic administration of rhG-CSF following MEC therapy was effective for preventing leukopenia. Other side effects of stomatitis, diarrhea and pneumonia were also decreased using rhG-CSF after MEC therapy.
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PMID:[Effect of recombinant human granulocyte colony stimulating factor in patients with transitional cell carcinoma of the urothelium receiving methotrexate, etoposide and cisplatinum combination chemotherapy]. 768 38

A model of chronic ethanol ingestion was used to study the effects of granulocyte colony-stimulating factor (G-CSF) on the pathogenesis of pneumococcal pneumonia in intoxicated rats. G-CSF or 5% dextrose in water (D5W) was administered subcutaneously to ethanol-fed and pair-fed control rats on days 6 and 7 of pair feeding. Rats were infected transtracheally with type 3 Streptococcus pneumoniae on day 8. In pair-fed control rats, G-CSF significantly increased the total number and percentage of polymorphonuclear leukocytes (PMNL) in the peripheral blood (P < .001), augmented PMNL recruitment to infected lungs (P < .01), and significantly increased survival from pneumococcal pneumonia (P = .01). In contrast, treatment of ethanol-fed rats with G-CSF did not enhance pulmonary PMNL delivery and did not increase survival following experimental pneumococcal pneumonia, despite a significant increase in the total number and percentage of circulating PMNL (P < .001). These data suggest that despite increasing the numbers of circulating PMNL, G-CSF is unable to provide protection against fatal pneumococcal pneumonia in ethanol-fed rats.
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PMID:Granulocyte colony-stimulating factor protects control rats but not ethanol-fed rats from fatal pneumococcal pneumonia. 769 Aug 25

A 66-year-old man was treated for IgD (lambda) multiple myeloma with 2mg/day melphalan and 20mg/day prednisolone. Subsequently, he developed pneumonia for which he received antibiotics, an antifungal agent and granulocyte colony-stimulating factor (G-CSF) twice. Myeloma cells appeared in the peripheral blood 10 days after the second G-CSF course. In addition, skin tumors developed on his extremities and chest 14 days after the second use of G-CSF. The skin tumors consisted of immunohistochemically IgD (lambda)-positive myeloma cells. The skin tumors may have been formed from the bone marrow by metastasis, a very rare occurrence in multiple myeloma. Before the development of the tumors we administered G-CSF, which may also have been related to the formation of the skin tumors.
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PMID:[IgD myeloma with skin tumor]. 782 97


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