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Query: UMLS:C0027947 (neutropenia)
 17,527 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reviewed the clinical and laboratory presentation of Haemophilus species bacteremia at our institution, with special attention to predisposing and prognostic factors. Of 36 cases, 18 presented with pneumonia, 1 with cellulitis, and another with sinusitis. No cases of meningitis or endocarditis were detected. Most episodes were caused by Haemophilus influenzae, and the overall response rate to treatment was 72%. Factors including chronic obstructive pulmonary disease, alcoholism, prior splenectomy, and neutropenia did not play an important role in these patients' infections. Most of the isolates serotyped were found to be nontypable. The occurrence of ampicillin resistance was 6% throughout the study. Ampicillin, chloramphenicol, and second-generation cephalosporins were all effective therapeutic regimens. Bacteremia due to Haemophilus species remains an uncommon infection in patients with cancer, despite the predominance of traditional predisposing factors.
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PMID:Haemophilus species bacteremia in patients with cancer. A 13-year experience. 273 Feb 52

Endotoxin reduces the release among other cytokines of tumor necrosis factor (TNF) and interleukin 1 (IL-1) and causes peripheral lymphopenia and a dose-response-dependent initial neutropenia followed by a monophasic neutrophilia. TNF alone induces lymphopenia and an initial neutropenia followed by a biphasic neutrophilia. IL-1 alone induces lymphopenia and a monophasic neutrophilia. TNF-plus-IL-1 caused a greater lymphopenia than either monokine alone, suggesting that both monokines contribute to LPS-induced lymphopenia. TNF-plus-IL-1 induced neutropenia similar in magnitude to that induced by TNF alone and induced a neutrophilia significantly greater than that induced by either monokine alone, suggesting that LPS-induced neutropenia is caused by TNF, while LPS-induced neutrophilia is due to the combined effects of TNF and II-1. TNF and IL-1 were administered together with LPS to simulate the in vivo condition of endogenous monokine release during gram-negative bacteremia. TNF combined with LPS increased both the duration and magnitude of LPS-induced lymphopenia, LPS-induced neutropenia, and LPS-induced neutrophilia. TNF-plus-LPS treated rats at 2 hours after injection exhibited a striking 93% decrease in bone marrow neutrophils even though no peripheral neutrophilia was yet apparent, suggesting that the subsequent neutrophilia was due to demargination and recirculation of neutrophils sequestered in the peripheral vasculature immediately after their release from the bone marrow. Epinephrine, which causes neutrophilia by demargination but not by release of marrow neutrophils, reversed the initial neutropenia in TNF-plus-LPS-treated rats and increased the neutrophilia. IL-1 combined with LPS increased LPS-induced neutrophilia, suggesting that endogenous IL-1 also contributed to LPS-induced neutrophilia. Corynebacterium parvum-primed rats with hyperplasia of the monocyte-macrophage system and treated with TNF differed from naive rats treated with TNF in that the second peak was as great as the initial peak of neutrophilia, supporting the hypothesis that the second peak of TNF-induced neutrophilia is due to the release of endogenous monokines. In conclusion, exogenous TNF, IL-1, and adrenal hormones affect circulating numbers of lymphocytes and neutrophils in a fashion consistent with their postulated endogenous role in the regulation of leukocyte trafficking during bacterial infection.
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PMID:Hematologic interactions of endotoxin, tumor necrosis factor alpha (TNF alpha), interleukin 1, and adrenal hormones and the hematologic effects of TNF alpha in Corynebacterium parvum-primed rats. 278 48

Pseudomonas putrefaciens is an unusual cause of human disease. Since 1978 only five cases of bacteremia due to this organism have been reported. Within 12 recent months four cases of bacteremia due to P. putrefaciens were seen - two occurred in patients with chronic infections of a lower extremity, one in a patient with neutropenia, and one in a patient with fulminant septicemia and disseminated intravascular coagulation. Two of the patients had prostheses; in neither case did prosthetic infection or prosthetic failure occur. Two syndromes of bacteremic infection with P. putrefaciens are suggested. One syndrome is associated with chronic infection of a lower extremity, is fairly well tolerated, and responds to appropriate antimicrobial agents. The other syndrome is more fulminant and may be associated with severe underlying debility, liver disease, and malignancy. It is not yet known whether this is a meaningful distinction. The significance of the recent increase is the isolation of this organism is not clear at present.
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PMID:Pseudomonas putrefaciens bacteremia. 291

Menogaril, a semisynthetic derivative of nogalomycin, was brought to phase I clinical testing in patients with refractory solid tumors. Twenty-seven patients received 50 evaluable courses. Menogaril was given as a 1-2-hour iv infusion on 5 consecutive days, with courses repeated every 4 weeks, provided there was reversal of all drug-related toxic effects. The starting dose was 3.5 mg/m2/day X 5, with escalations in subsequent cohorts of patients to 56 mg/m2/day X 5. Neutropenia was dose dependent and dose limiting. At 56 mg/m2/day X 5, the median wbc count nadir was 1100/microliter, and two of four patients were hospitalized for fever and suspected bacteremia. At 50 mg/m2/day X 5, the wbc count nadir was 2300/microliter. Platelet toxicity was less severe. Nonhematologic toxicity consisted primarily of local urticaria and moderate to severe phlebitis at the infusion site, which were dose dependent and lasted up to 6 weeks. For phase II studies, the recommended dose of menogaril is 50 mg/m2/day for 5 consecutive days administered as a 2-hour intermittent infusion, repeated every 28 days.
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PMID:Phase I trial of menogaril administered as an intermittent daily infusion for 5 days. 294 44

The increasing prevalence of bacteremia caused by gram-positive bacteria in granulocytopenic acute leukemia patients prompted us to evaluate, in a prospective randomized trial, the role of teicoplanin, a new glycopeptide antibiotic, when it was added to amikacin plus ceftazidime, as an empiric therapy of fever in these patients. Of 47 evaluable episodes, 22 were treated with the teicoplanin regimen and 25 were treated with the combination of amikacin and ceftazidime. The overall response to therapy of patients treated with teicoplanin was slightly better (82% improvement) than that obtained with amikacin plus ceftazidime (52%). The response rate of patients with gram-positive bacteremias was 80% (4 of 5) to the regimen that included teicoplanin; 25% (1 of 4) of the patients treated with amikacin plus ceftazidime responded to treatment; and for patients with gram-negative bacteremias, the response rates were, respectively, 100% (4 of 4) and 70% (7 of 10). The better results obtained with amikacin-ceftazidime-teicoplanin treatment were most evident in patients with profound (less than 100/mm3) and persistent neutropenia (83 versus 30% improvement). Furthermore, a good response rate of patients with gram-positive bacteremias (seven of eight; 87% improvement) was achieved in a small group of bone marrow transplant patients who were all treated with amikacin-ceftazidime-teicoplanin. No severe side effects were documented in any patient. Teicoplanin, as a drug administered as a single daily dose, seems to be a safe and useful anti-gram-positive agent when used in combination with amikacin-ceftazidime as an empiric therapy of febrile episodes in granulocytopenic acute leukemia patients.
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PMID:Prospective randomized clinical trial of teicoplanin for empiric combined antibiotic therapy in febrile, granulocytopenic acute leukemia patients. 295 98

Cyclic neutropenia is a benign, hematologic disorder characterized by recurrent episodes of severe neutropenia at 21 day intervals. There are associated cyclical variations in other blood cells. Patients with this disease have malaise, stomatitis, cervical lymphadenopathy and fever during the recurrent neutropenic periods. The exact cause of cyclic neutropenia is unknown. About one third of human cases appear to be inherited in an autosomal dominant pattern. In the other cases, the disease appears to arise spontaneously with symptoms usually beginning in infancy or early childhood. In adult patients, the disease may be acquired and occur in association with a clonal proliferation of large granular lymphocytes. Clinical studies in man and investigations in grey collie dogs, which have a very similar disease, strongly suggest that cyclic neutropenia is due to an abnormality in the regulation of early hematopoietic precursor cells. Therapy for cyclic neutropenia involves local and symptomatic therapy for the recurrent mouth ulcers and pharyngitis, and antibiotics for episodes of sinusitis, pneumonia, peritonitis, or bacteremia. Therapy with glucocorticosteroids, androgens, and plasmapheresis has been efficacious in a few adult patients, but no therapy has been proven to alter the cycling of blood counts in children. Despite their repetitive illnesses, patients with cyclic neutropenia grow and develop normally. With the help of attentive physicians and dentists, their quality of life and life expectancy are good. Current research on hematopoietic growth factors offers promise of new approaches to therapy.
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PMID:Cyclic neutropenia: a clinical review. 305 63

We reviewed the hospital course of 35 patients who underwent autologous bone marrow transplantation. Fever and profound neutropenia developed in all. Microbiologically confirmed infection developed in 22 patients, and unconfirmed but clinically evident infection developed in six. A bacterial infection developed in 21 patients (most commonly bacteremia without a detectable focus). Mucocutaneous fungal (12 patients) and viral (13 patients) infections were common, whereas invasive fungal (two patients) and viral (one patient) infections were uncommon. New pulmonary infiltrates developed in seven patients. Six deaths occurred during the initial hospitalization for transplantation, only one of which was directly attributable to infection. Stepwise logistic regression analysis retained male gender, total body irradiation, administration of trimethoprim/sulfamethoxazole, and development of mucositis or diarrhea as predictors of decreased survival, whereas higher pretreatment albumin levels and the administration of oral nonabsorbable antifungals were associated with an increased likelihood of survival. A comparison of these infectious complications with those found in allogeneic bone marrow transplant recipients shows similarities and differences with potentially important implications for patient management.
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PMID:Analysis of early infectious complications after autologous bone marrow transplantation. 305 92

Studies were conducted in guinea pigs, myelosuppressed by cyclophosphamide, for determination of whether passive immune therapy for Pseudomonas aeruginosa pneumonia would be useful in the setting of neutropenia. Groups of infected animals (14 per group) were treated with a single intravenous infusion of hyperimmune IgG antibody to P. aeruginosa (PA-IGIV; 500 mg/kg), tobramycin (1.7 mg/kg per 8 hr), ticarcillin (120 mg/kg per 6 hr), or combinations of these regimens. Control groups received intravenous albumin solution. Survival rates were 0% with albumin only, 0% with PA-IGIV, 43% with tobramycin (P less than .05), 86% with tobramycin plus PA-IGIV (P less than .05 vs. tobramycin alone), 7% with ticarcillin, and 43% with ticarcillin plus PA-IGIV (.05 less than P less than .10 vs. ticarcillin alone). Additive intrapulmonary killing of P. aeruginosa and prevention of bacteremia were observed in animals treated with tobramycin plus PA-IGIV compared with either treatment alone. Thus, passive immune therapy for P. aeruginosa pneumonia may be useful in the neutropenic host, but only when used in conjunction with antimicrobial agents.
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PMID:Passive immune therapy for experimental Pseudomonas aeruginosa pneumonia in the neutropenic host. 310 84

The clinical records of all patients with blood cultures positive for a bacterial pathogen were retrospectively examined during an 11-year period to determine the rate of and clinical features associated with polymicrobial bacteremia. During this period, bacteria were isolated in 6302 blood cultures. Of these cultures, 38 instances (0.6%) of polymicrobial bacteremia occurred in 38 patients. In 37 patients (97%), an underlying condition was identified that was considered a predisposing factor for polymicrobial bacteremia--18 patients (42%) had lesions of the gastrointestinal tract, 13 patients (34%) had an indwelling central venous catheter, nine patients (24%) had a malignant neoplasm or were receiving chemotherapy, and nine patients (24%) had neutropenia. A total of 98 pathogenic organisms were isolated; 52 were gram-negative and 46 were gram-positive, and 18 patients (47%) had more than two organisms isolated. Polymicrobial bacteremia was usually clinically indistinguishable from monomicrobial septicemia. Overall mortality was 32%. Polymicrobial bacteremia continues to be a rare, but serious, infectious disease that usually affects children with underlying medical problems and is associated with a high rate of mortality.
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PMID:Polymicrobial bacteremia in children. An 11-year experience. 317 21

Leukopenic, immunosuppressed recipients of solid organ allografts are at high risk for gram-negative bacterial sepsis, and mortality remains unacceptably high (greater than 30%). The purpose of this study was to determine whether murine monoclonal antibody (MAb) directed against lipopolysaccharide (LPS, endotoxin) would reduce lethality caused by a septic insult in immunosuppressed mice, and to determine if a specific antibody class would prove more efficacious in this setting. Two MAbs (3-H9, IgG3; 7-B5, IgM) were selected that reacted by ELISA, immunodot blot, and Western blot analysis against the O antigen polysaccharide portion of Escherichia coli 0111:B4 LPS. The 3-H9 MAb, 7B-5 MAb, or sterile saline was administered i.v. to normal or neutropenic Swiss-Webster mice immediately prior to an E coli 0111:B4 bacterial (i.v. or i.p. plus hemoglobin) or LPS (i.v.) challenge. In normal mice, administration of 3-H9 MAb or 7-B5 MAb i.v. immediately prior to a bacterial or endotoxin challenge resulted in a significant increase in the LD50. Neutropenia lowered the LD50 by nearly one log10 in both the bacteremia and peritonitis models. Both MAbs provided similar protection, raising the LD50 one log10 in neutropenic mice. Thus neutropenic animals receiving either MAb had a mortality nearly identical to that of normal animals receiving saline. No significant difference between the protective capacity of these MAbs was noted in any of the three models. These studies demonstrate that MAbs directed against LPS exert protection during gram-negative bacterial sepsis in either normal or neutropenic animals. In addition, the particular IgG and IgM MAbs examined provided similar protective capacity. Antibody directed against LPS may provide an additive form of therapy that may serve to decrease lethality during clinical gram-negative sepsis in immunosuppressed patients.
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PMID:Antibody immunotherapy of gram-negative bacterial sepsis in an immunosuppressed animal model. 327 38


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