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

Neutropenia may be caused by neutrophil autoantibodies. The detection of such antibodies has always been difficult. Recently, we developed a sensitive indirect immunofluorescence technique applicable to granulocytes which proved to be of value in the detection of granulocyte alloantibodies. We have now used this method to investigate the serum and cells of 29 patients with idiopathic or secondary neutropenia. In four patients neutrophil-antigen-specific autoantibodies were detected in the serum and the patient's own granulocytes showed direct fluorescence. Furthermore, differences in the immunoglobulin composition and the temperature of optimal activity of the autoantibodies were found. Direct fluorescence was also demonstrated with the granulocytes from five other neutropenic patients and with the granulocytes from five non-neutropenic patients mainly with infectious disease. However, no granulocyte antibodies could be eluted or shown to be present in the serum. This indicates that a positive direct granulocyte fluorescence test may not be considered as proof that autoantibodies are present.
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PMID:Autoimmune granulocytopenia: the detection of granulocyte autoantibodies with the immunofluorescence test. 35 31

The activity of cefazolin (CEZ) and cephradine (CED) was studied in experimentally infected neutropenic mice. Neutropenia was induced by 600 rad whole-body irradiation; an infection was induced by the injection of 5 X 10(6) Escherichia coli into the thigh on Day 5 after irradiation. Antibiotics were administered 1 h later, and antibacterial activity was estimated from bacteria counts made in the homogenized individual thighs 3 h after infection. The effect of a low dose of each of the cephalosporins on the infection was significantly lower in the absence of granulocytes than in animals with intact host defence; at higher dosages the effect of both antibiotics on the infection was the same in neutropenic and unirradiated mice. In the neutropenic mice, CEZ was 2.95 times more active than CED against E. coli in vivo, this difference in activity being similar to that found earlier in normal mice.
Infection 1979
PMID:Antibacterial efficacy of cefazolin and cephradine in neutropenic mice. 37 21

Mezlocillin, a new semisynthetic penicillin chemically related to ampicillin which is more active than carbenicillin against Ps. aeruginosa, B. fragilis and Strep. faecalis and which inhibits many Klebsiella, was evaluated in the therapy of 34 episodes of infection in 26 patients. Infection sites included pulmonary, urinary tract and tissue infections, including peritonitis. Seven patients had bacteremia. Clinical cures were achieved in 83 per cent and bacteria cures in 76 per cent of infections. Cure was achieved with mezlocillin in patients with infections caused by carbenicillin-resistant species. Adverse effects of therapy were minimal, one rash and one episode of reversible neutropenia. Serum and body flevels of susceptible organisms.uid levels were easily maintained above the inhibitory levels of susceptible organisms. Mezlocillin was a safe, well tolerated and effective antibiotic in the treatment of infections due to susceptible organisms.
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PMID:Mezlocillin in the therapy of serious infections. 50 86

Spontaneous amyloidosis was found in dogs affected with hereditary cyclic hematopoiesis (CH dogs). Early perifollicular deposits of amyloid were observed in the spleens of 15-week-old CH dogs. By the 24th week, amyloid deposits were also found in the liver, kidneys, pancreas, adrenals, and small intestine; the incidence of the condition rose to more than 90%. The visceral involvement and the histologic characteristics of amyloid deposition closely resemble those of the secondary form in humans. A transient lymphoid hypoplasia was noted in the spleens of neonates and pups. This abnormality did not appear to be related to exogenous conditions. In young adult dogs, the initial hypoplastic characteristics were replaced by enlarged marginal zones in the follicles of the spleen, composed of pyroninophilic cells and, in a later stage, of PAS-positive cells. These cellular changes preceded the amyloid deposition. Due to the characteristic cyclic neutropenia of the hereditarily transmitted hematologic syndrome, most CH dogs experience episodes of infectious diseases, although the episodes of infection may be separated by long periods of relatively good health. This may provide the underlying antigenic stimulation which triggers the process of amyloid deposition. However, the lag period for the onset of amyloidosis is extremely short and the type of infections is not considered a predisposing factor for amyloid deposition. It is possible that a peculiar sensitivity of the lymphoid system in the CH dog would facilitate the development of widespread amyloidosis. Since the sequence of splenic lymphoid hypoplasia, follicular activation, and amyloid deposition associated with age are consistently repeated, the CH dog may be a suitable animal model for the study of the pathogenesis of secondary form of amyloidosis in humans.
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PMID:The cyclic hematopoietic dog: a model for spontaneous secondary amyloidosis. A morphologic study. 68 47

Approaches to the diagnosis and classification of preleukemic states involving chronic cytopenias are presented and discussed. Diagnosis of these states is facilitated by the identification of anomalies in all the myeloid cell lines (i.e., those derived from the bone marrow). These cellular anomalies may be morphologic, biochemical, or functional in nature or may affect the quantity of cell in each line in the bone marrow and the peripheral blood. Such anomalies may occur alone or may be associated. A tentative classifiction is proposed which is based on one or several of these anomalies. Among the quantitative criteria of classification is a moderate and static excess of myeloblasts and promyelocytes in the bone marrow. Refractory anemia with an excess of myeloblasts (RAEM) in the most frequent of these states. Its main clinical and hematologic features are described. The disease course is quite typical, the mean survival being 20 months; some patients survive for more than 30 months. Acute myeloid leukemia (AML) was the cause of death in less than 28% of cases. Infection in the absence of severe neutropenia was frequent. The relationship between RAEM and AML is disc,ssed, and the individual characteristics of RAEM are emphasized.
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PMID:Preleukemic states. I. Definition and classification. II. Refractory anemia with an excess of myeloblasts in the bone marrow (smoldering acute leukemia). 100 6

Infection with cytomegalovirus (CMV) continues to be one of the most common complications following allogeneic bone marrow transplantation. A proportion of patients with CMV infection also experience neutropenia. To investigate the possible role of CMV in the suppression of hematopoiesis, we have examined the effect of CMV on the growth of isolated myeloid progenitors and on the production of myeloid cells in the long-term bone marrow culture (LTMC) system. In these studies, various isolates of CMV were added either directly to cultures of progenitors or to LTMC established from normal CMV-seronegative donors. In the first system, myelosuppression is manifested by a reduction in the number of colonies that grow. In the second system, myelosuppression is manifested by a reduction in the number of myeloid cells produced and released into the culture supernatant. Analysis of the data observed indicated that myelosuppression could in some cases be attributed to direct infection of myeloid progenitors. In other cases stromal cells were infected. In the latter cases, myelosuppression was then caused by an alteration in cytokines produced by the stromal cells. These observations made in vitro raise the possibility that comparable mechanisms may be responsible for the myelosuppression observed with CMV infection in vivo. To pursue this possibility we proposed to detect the CMV genome in defined subpopulations of marrow cells isolated from infected patients. Given the technical restrictions imposed by the small sample size available from patient marrow aspirations, our initial attempts to develop on appropriate technique involved isolation of cells from CMV-seropositive normal bone marrow donors. Using the polymerase chain reaction we were able to amplify CMV DNA contained within marrow cells of some healthy CMV-seropositive marrow donors.
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PMID:Cytomegalovirus and marrow function. 132 82

Sixty-four consecutive febrile episodes in 50 consecutive patients with malignancy and neutropenia were empirically treated with a combination of ceftazidime and amikacin. Of 52 analysable episodes, the response rate was 59.6% overall and 26.3% of episodes with microbiologically documented infections with septicaemia. Infection-related death occurred in 10 patients (19.2% of episodes). The response rates were similar in patients with acute leukaemia or other malignancies. Poor response is attributed to increased frequency of infections with Gram-positive and fungal organisms. A modified empiric regimen including cover for Gram-positive and fungal organisms is suggested in similar patient populations.
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PMID:Ceftazidime and amikacin as empiric treatment of febrile episodes in neutropenic patients in Saudi Arabia. 808 23

The neutropenia often seen in infants of hypertensive mothers (IHMs) at < 12 hours of age has been associated with nosocomial infection in the first 18 days of life. To assess maternal hypertension as an independent factor for nosocomial infection, we compared 101 low birth weight (< or = 2.00 kg) IHMs to a concurrent birth weight-matched group of infants of normotensive mothers (INMs). Infants without differential leukocyte counts at < 12 hours of age were excluded, leaving 93 IHMs and 98 INMs. The incidence of neutropenia at < 12 hours among IHMs was not significantly different from that among INMs (42/92 (45%) vs 37/98 (38%)). Nosocomial infection was more frequent in neutropenic IHMs than in neutropenic INMs (12/42 vs 2/37; p = 0.007). Infection in IHMs included omphalitis (2 infants), pneumonia (4), and sepsis with or without meningitis (6); INMs had cellulitis (1) and sepsis (1). The underlying mechanism(s) for this predisposition remains to be elucidated, although limited data suggest that neutropenia may be more severe and prolonged among IHMs.
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PMID:Increased nosocomial infection in neutropenic low birth weight (2000 grams or less) infants of hypertensive mothers. 144 66

We evaluated the efficacy and safety of piperacillin-pefloxacin potentially associated to vancomycin as a non nephrotoxic antimicrobial therapy in febrile neutropenic cancer patients, treated with nephrotoxic chemotherapy. Fifty-seven patients: 49 with solid tumors and 8 non-Hodgkin lymphomas, were treated during 85 episodes with: piperacillin 4 g IV every 8 h pefloxacin 400 mg IV every 12 h. If the patient remained febrile after 72 h, 1 g of vancomycin IV was added every 12 h. The mean duration of neutropenia was 7 days (3-14 days). In 44 episodes, the granulocyte nadir was < 100/mm3. Infection was microbiologically documented in 17 episodes (20%) with ten Gram-positive cocci and 11 Gram-negative bacilli. There were 64 apyrexia with piperacillin-pefloxacin (75%) and further 14 were resolved by the addition of vancomycin (total success = 92%); three early changes because of clinical deterioration (two episodes) or germ resistance (one episode); three protocol violations, and one apyrexia by addition of amphotericin. Neither septic death nor toxicity were observed. We conclude that this empirical treatment is active and safe and avoids nephrotoxicity in cancer patients heavily treated with nephrotoxic chemotherapy.
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PMID:[Value of the combination of piperacillin and pefloxacin possibly followed by vancomycin in the treatment of febrile neutropenia in nephrotoxic chemotherapy]. 146 96

Tumour necrosis factor (TNF), a polypeptide produced by mononuclear phagocytes, has been implicated as an important mediator of inflammatory processes and of clinical manifestations in acute infectious diseases. To study further the potential role of TNF in infectious diseases, recombinant Escherichia coli (E. coli) derived human (r.HuTNF-alpha) and bovine TNF (r.BoTNF-alpha) were intravenously (i.v.) administered in dwarf goats. Rectal temperature, heart rate, rumen motility, plasma zinc and iron concentrations, and certain other blood biochemical and haematological values were studied and compared with the changes seen after E. coli endotoxin (LPS) was administered (dose: 0.1 microgram/kg i.v.). Following a single injection of 4 micrograms/kg of r.BoTNF-alpha, shivering and biphasic febrile response were observed, accompanied by tachycardia, inhibition of rumen contractions, drop in plasma zinc and iron concentrations, lymphopenia, and neutropenia followed by neutrophilia. The i.v. administration of a single injection of 4 micrograms/kg r.HuTNF-alpha induced shivering and biphasic febrile responses, accompanied by anorexia and a similar drop in plasma trace metal concentrations when compared with r.BoTNF-alpha-treated goats. The TNF-alpha-induced symptoms were essentially the same as those that occurred after LPS administration. However, the time of onset of these changes after the injection of TNF-alpha was significantly shorter than after LPS. Moreover, the r.BoTNF-alpha induced a longer lasting neutrophilic leucopenia, less neutrophilia, and a more persistent lymphopenia than after LPS injection. Neither r.BoTNF-alpha nor LPS caused severe haemo-concentration. Furthermore, no cross-tolerance between r.BoTNF-alpha and LPS could be demonstrated. We conclude that both r.BoTNF-alpha and r.HuTNF-alpha induce many of the physiologic, haematologic and metabolic changes that characterize the acute phase response to LPS. The overlapping biological activities of r.BoTNF-alpha, r.HuTNF-alpha and LPS in dwarf goats may indicate that both recombinant tumour necrosis factors have some homology with caprine TNF-alpha.
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PMID:Fever and acute phase response induced in dwarf goats by endotoxin and bovine and human recombinant tumour necrosis factor alpha. 148 32


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