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

Three children (girls) suffered from neutropenia mediated by anti-neutrophil IgG-Fc receptor type III (Fc gamma RIII) antibodies. The first patient (newborn) had asymptomatic and transient neutropenia caused by maternal Fc gamma RIII iso-antibodies. The second patient (6 months), whose neutropenia was diagnosed as a 'benign neutropenia of childhood' caused by transient anti-NAI autoantibodies, suffered from mild bacterial infections. The third patient (12 years) suffered from serious infections. The anti-Fc gamma RIII autoantibodies showed neither anti-NA1 nor anti-NA2 specificity. She also developed autoimmune thyroiditis (Graves' disease). Both the duration of the neutropenia and the seriousness of the bacterial infection were variable in our patient group. The first two patients both made spontaneous recoveries, while the third patient depended ultimately on granulocyte-colony stimulating factor (G-CSF).
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PMID:[Neutropenia due to antibodies against Type III Fc receptors on neutrophil granulocytes: 3 children with different clinical courses]. 956 43

Previous studies have shown that the plasma level of soluble IgG Fc receptor type III (sFcgammaRIII) is a measure of the total body neutrophil mass. The aim of this study was to determine whether the plasma level sFcgammaRIII is associated with the risk of contracting bacterial infections in patients with neutropenia. We collected blood from 66 patients suffering from acquired idiopathic neutropenia, whose blood was sent to our laboratory for diagnostic evaluation of neutropenia (neutrophil count <1,500 cells/microL). Soluble FcgammaRIII levels were measured in plasma. Genotype distibutions of FcgammaR polymorphisms were determined. Clinical data were obtained from the patient files. Patients were assessed as to whether or not they had suffered from a bacterial infection 3 months before to 3 months after a single sFcgammaRIII measurement. In addition, longitudinal data were obtained from 21 patients. Of the 66 neutropenic patients who were included, 15 had suffered from a bacterial infection in the period 3 months before to 3 months after sFcgammaRIII measurement. The age and sex distribution was equal among the groups with and without infections, as were the genotype frequencies of neutrophil FcgammaR polymorphisms. Both neutrophil count and plasma level sFcgammaRIII were significantly lower in the patient group with infections, compared with the noninfected group (P = .03 and P < .0001, respectively). No infections were reported for patients who had plasma sFcgammaRIII levels above 100 arbitrary units (AU; normal value, 30 to 200). After matching each infected patient with two noninfected patients having the same neutrophil count, sFcgammaRIII plasma levels remained significantly lower in the group with infections (P = . 0001). For the patients who were followed in time, no infections were reported when sFcgammaRIII levels were above 100 AU. In conclusion, our population of patients with chronic idiopathic neutropenia with plasma sFcgammaRIII levels above 100 AU did not show an increased risk of contracting bacterial infections.
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PMID:Clinical value of soluble IgG Fc receptor type III in plasma from patients with chronic idiopathic neutropenia. 957 35

Fever in neutropenic cancer patients is often due to the development of an infection. The standard management of febrile neutropenic patients involves the administration of empiric, hospital-based, parenteral antibiotic therapy. Although this treatment strategy has evolved from experience in high-risk patients with hematological malignancies, in whom bacterial infection can result in substantial morbidity and mortality, it has been adopted for all patients with febrile neutropenia, largely because of the inability of clinicians to reliably distinguish between patients who are at high risk for developing such morbidity/mortality and those who are not. The development of risk-assessment models has facilitated the recognition of high-, moderate-, and low-risk subgroups among febrile neutropenic patients and allows the administration of outpatient antibiotic therapy to the moderate- and low-risk groups, with the same degree of efficacy and safety as hospital-based therapy. Monotherapy with the carbapenems (imipenem/cilastatin and meropenem), with their broad spectrum of activity and established efficacy in high-risk patients, represents realistic options for risk-based treatment of febrile neutropenic patients within and outside the hospital setting.
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PMID:Expanding the options for risk-based therapy in febrile neutropenia. 963 17

Although infection continues to be a major cause of morbidity and mortality in neutropenic patients, newer strategies have resulted in a shorter duration of neutropenia. The prime risk to patients with short-duration neutropenia (defined as neutropenia of less than 14 days) is bacterial infection, which is reduced by the administration of prophylactic antibiotics, and possibly by the use of clean food, sterile water, and protection against transmission of organisms from healthcare workers' hands.
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PMID:Strategies for prevention of infection in short-duration neutropenia. 975 61

Neutropenia and impairment of neutrophil function are commonly observed in patients with human immunodeficiency virus (HIV) infections. The HIV regulatory protein Tat is known to exert immunosuppressive effects. Alcohol is known also to be an immunosuppressive factor, and as alcohol abuse is common among HIV infected hosts, both factors may interact in an additive or synergistic fashion to further impair the host defenses of these patients. In order to test this possibility, endotoxin-induced neutrophil beta2-integrins CD11b and CD18 expression, phagocytosis, and hydrogen peroxide generation were examined in normal and HIV-1 Tat-transgenic mice in the absence and presence of ethanol intoxication. Acute ethanol intoxication was induced in mice (body weight of 25+/-1 g) by an intraperitoneal (ip) injection of ethanol (3 g/kg, 20% in normal saline). Thirty min later, the animals were given an ip injection of endotoxin (20 microg in 0.2 ml of saline/mouse). Vehicle-treated controls received an ip injection of saline without ethanol or endotoxin. Two hr after endotoxin administration, the animals were killed to determine neutrophil functions with flow cytometry. The baseline expression of CD11b and CD18 was similar in normal nontransgenic and Tat-transgenic mice. Endotoxin administration significantly up-regulated CD11b and CD18 expression in normal mice. This up-regulation was suppressed in Tat-transgenic mice. Ethanol intoxication inhibited endotoxin-induced CD11b and CD18 expression in normal mice and totally abolished endotoxin-induced CD11b and CD18 expression in Tat-transgenic mice. Neutrophil phagocytic activity in normal and Tat-transgenic mice was similar. Ethanol intoxication produced a similar inhibition of phagocytosis in both study groups. Endotoxin suppressed phagocytosis in normal mice, and this suppression was more pronounced in Tat-transgenic mice. Spontaneous and phorbol myristate acetate (PMA)-stimulated hydrogen peroxide generation by circulating neutrophils (PMNs) were similar in normal and Tat-transgenic mice. Neither ethanol nor endotoxin affected hydrogen peroxide generation by PMNs. These data show that both Tat and alcohol significantly impair PMN function, and this may be a mechanism leading to the increased susceptibility of the HIV-infected host to bacterial infection.
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PMID:The human immunodeficiency virus type I Tat protein potentiates ethanol-induced neutrophil functional impairment in transgenic mice. 988 49

Use of fluoroquinolones for antimicrobial prophylaxis during neutropenia is often cited as a significant predisposing factor for viridans group streptococcus (VGS) bacteraemia. Newer compounds in this class are reputed to have enhanced activity against Gram-positive bacteria, and we determined the minimal inhibitory concentrations (MICs) for ciprofloxacin and three of the newer compounds: trovafloxacin, fleroxacin and clinafloxacin, against 44 isolates of VGS. On a gravimetric basis, clinafloxacin was most active (MIC90 0.19 mg/l), whereas ciprofloxacin and fleroxacin were the least active (both MIC90 16 mg/l). Clinafloxacin warrants further study as an agent of prophylaxis against bacterial infection in neutropenic patients.
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PMID:Activity of quinolones against viridans group streptococci isolated from blood cultures of patients with haematological malignancy. 992 71

Meropenem and imipenem/cilastatin, currently the only available carbapenem agents in Europe and the United States, are characterised by a broad spectrum of antimicrobial activity and stability to beta-lactamase-mediated resistance mechanisms. A guide to the use of carbapenems in clinical practice is presented; the role of carbapenems in the treatment of several types of serious bacterial infection and an up-to-date account of their clinical efficacy and safety profiles are discussed. The good clinical efficacy and favourable safety profiles of the carbapenems make them valuable as initial empirical therapy in the treatment of ventilator-associated pneumonia, sepsis of unknown origin, post-operative peritonitis, paediatric meningitis, and febrile neutropenia. However, to maintain superior efficacy, the carbapenems should be used appropriately for definitive therapy.
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PMID:Carbapenems in clinical practice: a guide to their use in serious infection. 1022 11

Neutropenic individuals are at high risk for bacterial and fungal infections. Filgrastim (r-metHuG-CSF, NEUPOGEN) has been shown to improve chemotherapy-induced neutropenia significantly. Because a high incidence of HIV-infected patients have neutropenia, often associated with myelosuppressive antiretroviral medication, Filgrastim is frequently used as a treatment strategy for this HIV-associated neutropenia. This review summarizes published work related to the use of Filgrastim in HIV-infected patients. Literature bases (EMBASE, MEDLINE, Int. Pharm. Abs., SciSearch, and Aidsline) from 1970 to 1998 were searched for articles describing the relationship of Filgrastim and ANC to bacterial infection rates, bacterial infection outcome, and overall survival. Thirty-five related articles were identified during this search. Filgrastim appears to have a significant role in increasing peripheral ANC and enhancing neutrophil function in patients with HIV infection and AIDS. This may translate into a clinical benefit of delivery of full-dose myelosuppressive antiretroviral therapy and decreased susceptibility to infections and increased survival in this patient population.
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PMID:The use of Filgrastim in AIDS-related neutropenia. 1059 30

Neutropenia frequently complicates infection due to human immunodeficiency virus (HIV). The etiology of neutropenia in this setting includes bone marrow infection or infiltration, myelosuppressive therapies, the presence of antibodies to HIV, and accelerated apoptosis. Protection against microbial invaders by neutrophils is further compromised by impaired chemotaxis and phagocytosis, production of toxic oxygen species, and expression of cellular adhesion molecules. Neutropenia is a significant risk factor for bacterial infection in HIV-infected patients. Endogenous cytokines, such as granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor, regulate neutrophil count and function. Treatment with recombinant human methionyl G-CSF (filgrastim) has lessened neutropenia in patients with HIV infection. Clinical trials have shown that the incidence of bacterial infections and the number of consequent days of hospitalization for HIV-infected patients receiving filgrastim therapy are lower. Filgrastim treatment also allows administration of larger doses of myelosuppressive agents.
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PMID:Neutropenia, neutrophil dysfunction, and bacterial infection in patients with human immunodeficiency virus disease: the role of granulocyte colony-stimulating factor. 1067 24

Sepsis and its complications are severe clinical syndrome that is caused by systemic inflammatory response of the host to infection. Despite the use of common and numerous new therapeutic protocols, mortality from this severe disease is still very high. In the study are presented 155 patients (111 males, 44 females) of average age 49.6 years with mean septic score 12.9 (2-40). Mortality in our patients was 20.6%, septic shock developed in 31.6%, ARF in 20.0%, DIC in 12.9%, and MODS in 25.8% of patients. Positive correlation existed between initial sepsis score and mortality. Older age and the presence of primary diseases (34.2% of patients) were associated with significantly higher septic score and were good prognostic factor for the poor outcome of sepsis. Between mean arterial pressure in the first 24 h after the admission and mortality existed negative correlation (p < 0.05). Positive hemocultures were found in 69.7%, and bacterial infection in 78.7% of patients. GP bacteremia was found in 55.6% of patients and GN in 45.4% of all positive hemocultures. Confirmed bacteremia and bacteremia caused by GPB were associated with the higher mortality rate compared to the patients with negative hemocultures and GN bacteremia (p < 0.05). Concentrations of fibrinogen and urea in the blood at the admission in the patients with sepsis were very good prognostic factors of the disease outcome, and leukopenia, leukocytosis and neutropenia were associated with the increased mortality. Negative correlation existed between fibrinogen concentration and mortality (p < 0.001), while positive correlation (p < 0.001) existed between urea concentration and mortality. In the absence of more efficacious therapeutic protocols, fast recognition of the sepsis, evaluation of its severity, knowledge of the risk factors for its poor outcome and aggressive use of antibiotic and existing supportive therapy can significantly decrease high mortality of this too severe clinical syndrome.
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PMID:[Significance of determination of certain clinical and laboratory parameters in the evaluation of severity and outcome in sepsis]. 1070 10


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