Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027947 (neutropenia)
 17,527 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Zidovudine was used in an open uncontrolled study for treatment of 145 human immunodeficiency virus (HIV) patients, 102 with acquired immune deficiency syndrome (AIDS) and 43 with symptomatic HIV disease (acquired immune deficiency syndrome related-complex, ARC). The mean period of follow-up was 6 +/- 2.5 months. The median survival time of AIDS patients on zidovudine was 4.5 times longer when compared to a historical zidovudine untreated AIDS group (1657 vs. 370 days). This should be interpreted with reserve regarding improvements in treatment of all aspects of HIV infection and heightened awareness of AIDS which may have led to earlier diagnosis in the zidovudine treated groups. Pneumocystis carinii pneumonia (PCP) was very rarely a cause of death in zidovudine-treated patients (4.8%), while it was responsible for the death in 46.2% of historical controls (P less than 0.001). Extensive Kaposi's sarcoma was equally the cause of death in treated as well as in historical patients. Median T4 cell counts increased on zidovudine reaching a peak at the end of the fourth month of therapy in the ARC group and at the end of the first month in the AIDS group with a subsequent fall. Sixty per cent (53 of 87) patients were p24 viral antigen positive at the start of treatment and 19% of them had a fall of more than 50% in antigen level in three months while 32% became antigen negative within 2.5 months. Survival in patients where the antigen disappeared or in whom there was a major (greater than 50%) fall in antigen level was significantly higher than in those for whom there was no change in antigen level or in whom the antigen was negative at the start of the study (P less than 0.05). Forty-seven of the 145 zidovudine treated patients needed to be transfused because of anaemia. The mortality was significantly higher in this group of patients, particularly in those transfused prior to zidovudine therapy. Neutropenia occurred in four subjects. Platelets rose after the start of zidovudine but subsequently fell to thrombocytopenic levels in eight patients.
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PMID:Zidovudine treatment of patients with acquired immune deficiency syndrome and acquired immune deficiency syndrome-related complex: St Stephen's Hospital experience. 249 85

Eighteen asymptomatic men with persistent human immunodeficiency virus type I (HIV-I) p24 antigenaemia were treated with zidovudine 250-500 mg (+/- acyclovir 800 mg) 6-hourly for 4-12 weeks, and subsequently with zidovudine 500 mg (+/- acyclovir 1600 mg) 12-hourly for 36 weeks. After 24 weeks six additional HIV antigenaemic subjects were entered and treated directly with zidovudine 500 mg 12-hourly. Over the treatment period serum HIV-I p24 (HIV-Ag) levels declined in all 24 subjects; significantly so in 17, and to below cut-off values in five. Mean serum HIV-Ag levels in different treatment groups declined in 68-78%. Initial increases in CD4+ cell counts were not sustained. Over 48 weeks serum HIV-Ag levels rose in three out of five non-treated men with persistent HIV antigenaemia, and they slightly declined in two; the mean serum HIV-Ag level in this group rose 67%. Regression of enlarged lymph nodes was seen in 19 out of 19 of the zidovudine-treated subjects. In the 24 zidovudine-treated subjects no disease progression occurred during follow-up, whereas two out of five non-treated men went on to develop CDC group IV A, and IV C-2 disease, respectively. Adverse reactions to the study drugs were infrequent and mild. Anaemia caused symptoms in two, but serious leucopenia or neutropenia was not observed. An initial positive effect on thrombocyte numbers was not sustained. These data demonstrate that in asymptomatic HIV-infected subjects zidovudine 500 mg 12-hourly is well tolerated and has a persistent inhibitory effect on viral replication.
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PMID:Markers for progression to acquired immune deficiency syndrome and zidovudine treatment of asymptomatic patients. 249 86

Leukopenia attributable to lymphopenia and neutropenia was detected over a 28-week period in a 12-year-old domestic cat infected with feline immunodeficiency virus (FIV). Mild normocytic, normochronic anemia also was evident. Platelet counts were normal, and serum biochemical values were unremarkable. Antibodies to FIV were detected in serum by use of immunofluorescence and immunoblot electrophoresis assays. Cytologic evaluation of bone marrow aspirates revealed normal cellular morphologic features, maturation, and myeloid-to-erythroid ratio. Normal marrow cellularity was determined histologically. There was, however, a significant (P less than 0.01) inhibition of colony-forming unit granulocyte/macrophage-derived progenitors when marrow cells were cultured in the presence of autologous serum, compared with that when marrow cells were cultured in the presence of serum obtained from clinically normal cats, thus suggesting the presence of a humoral inhibitory substance directed specifically at the granulocyte/macrophage lineage. These cell culture results were consistent with those reported for human beings with acquired immunodeficiency syndrome and neutropenia. Thus, FIV infection may be an excellent animal model in which to study human immunodeficiency virus and should be considered in the differential diagnosis of cats with chronic leukopenia.
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PMID:Chronic leukopenia associated with feline immunodeficiency virus infection in a cat. 253 75

Therapy of patients with the acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (ARC) with azidothymidine (AZT) and 2'-3'-dideoxycytidine (ddC) is complicated by severe anemia, neutropenia, and thrombocytopenia, the cause of which is unknown. We therefore tested the effect of AZT, ddC, and an additional 2'-3'-dideoxynucleoside analogue, 2'-3'-dideoxyadenosine (ddA), on the hematopoietic progenitor cells derived from the bone marrow of normal persons and patients with AIDS/ARC. All three substances dose-dependently inhibited the in vitro colony formation of the pluripotent (CFU-GEMM), as well as the erythroid (BFU-E) and granulocyte-macrophage progenitor cells (CFU-GM). The 50% inhibition of normal progenitors by AZT occurred at 0.13 microM for CFU-GEMM, 0.32 microM for BFU-E, and 1.9 microM for CFU-GM, by ddA at 15 microM for CFU-GEMM, 40 microM for BFU-E, and 140 microM for CFU-GM. ddC was the most toxic agent and already inhibited 71% +/- 16% (mean +/- standard error of the mean [SEM]) of CFU-GEMM and 52% +/- 22% of BFU-E at 0.1 microM, whereas the 50% inhibition of CFU-GM was reached at 0.3 microM. Hematotoxicity occurred at concentrations lower than necessary to inhibit the human immunodeficiency virus (HIV), except for ddA, which is 100 times less toxic than AZT whereas its antiviral effect is only 10 times less. The inhibition of progenitor cells from AIDS patients by the 2'-3'-dideoxynucleosides was comparable to normal progenitors, except for a higher sensitivity of AIDS-derived CFU-GEMM and BFU-E to AZT.
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PMID:Inhibitory effect of azidothymidine, 2'-3'-dideoxyadenosine, and 2'-3'-dideoxycytidine on in vitro growth of hematopoietic progenitor cells from normal persons and from patients with AIDS. 254 17

Long-term management of cytomegalovirus (CMV) retinitis by intravitreal injection of ganciclovir was evaluated in ten patients with acquired immune deficiency syndrome (AIDS). Patients were unable to tolerate systemic ganciclovir because of severe neutropenia (8 cases), catheter-induced sepsis (1 case), or the need to continue therapy for human immunodeficiency virus (HIV) with zidovudine (ZDV) (1 case). All patients had a favorable response to initial treatment. Cytomegalovirus retinitis progressed in four fellow eyes in which treatment was deferred. Vision improved or remained stable in all but one eye. Patients were followed for a mean of 4 months and received an average of 16.6 intravitreal injections in each eye. Relapse occurred late in the course while on maintenance treatment in five eyes (33%). There was no evidence of toxicity from repeated intravitreal injections. Treatment was very well tolerated. The only severe complication in a total of 249 injections was a single case of Staphylococcus epidermidis endophthalmitis which responded to intravitreal antibiotic treatment. Intravitreal ganciclovir is an effective alternative to systemic ganciclovir in those patients with severe neutropenia and in those patients who desire to remain on systemic ZDV.
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PMID:Treatment of cytomegalovirus retinitis with intravitreal ganciclovir. Long-term results. 254 Apr 70

Feline immunodeficiency virus (FIV) (formerly feline T-lymphotropic lentivirus or FTLV) was first isolated from a group of cats in Petaluma, California in 1986. The virus is a typical lentivirus in gross and structural morphology. It replicates preferentially but not exclusively in feline T-lymphoblastoid cells, where it causes a characteristic cytopathic effect. The major structural proteins are 10, 17 (small gag), 28 (major core), 31 (endonuclease?), 41 (transmembrane?), 52 (core precursor polyprotein), 54/62 (reverse transcriptase?), and 110/130 (major envelope) kilodaltons in size. The various proteins are antigenically distinguishable from those of other lentiviruses, although serum from EIAV-infected horses will cross-react with some FIV antigens. Kittens experimentally infected with FIV manifest a transient (several days to 2 weeks) fever and neutropenia beginning 4 to 8 weeks after inoculation. This is associated with a generalized lymphadenopathy that persists for up to 9 months. Most cats recover from this initial phase of the disease and become lifelong carriers of the virus. Complete recovery does not occur to any extent in nature or in the laboratory setting. One experimentally infected cat died from a myeloproliferative disorder several months after infection. The terminal AIDS-like phase of the illness has been seen mainly in naturally infected cats. It appears a year or more following the initial infection in an unknown proportion of infected animals. FIV has been identified in cats from all parts of the world. It is most prevalent in high density populations of free roaming cats (feral and pet), and is very uncommon in closed purebred catteries. Male cats are twice as likely to become infected as females. Older male cats adopted as feral or stray animals are at the highest risk of infection, therefore. The infection rate among freely roaming cats rises throughout life, and reaches levels ranging from less than 1% to 12% or more depending on the area. Clinically affected cats tend to be 5 years or older at the time of hospitalization. Experimental and seroepidemiologic studies suggest that FIV is transmitted mainly by bites. Intimate, non-traumatic contact (mutual grooming, shared use of food, water and litter pans) is inefficient in transmitting the infection. In utero and venereal transmission could not be demonstrated in laboratory settings. There is no statistical linkage between FIV and feline leukemia virus (FeLV) infections in nature. The FeLV infection rate in FIV-infected animals is the same as it is for non-FIV-infected cats.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Feline immunodeficiency virus infection. 254 90

Thirty-two cats referred to the Feline Studies Centre between June 1987 and October 1988, and 14 in-contact cats, were found to be infected with feline immunodeficiency virus. Most of the 46 cats were non-pedigree and free ranging; 27 were male (19 neutered) and 19 were female (18 neutered). Their ages ranged from one to 17 years and the average age was 5.8 years. The most common clinical signs were lethargy, inappetence, weight loss, pyrexia and lymphadenopathy; most cases had multiple abnormalities. Other common signs were gingivitis, diarrhoea, rhinitis and ocular discharge. Eight cats had neoplasia. The commonest haematological abnormalities were anaemia, neutropenia, lymphopenia and monocytosis. Eight cats had lymphocytosis; seven of these were in a single house-hold. Several cats had high serum globulin levels and half of those tested had high IgG levels. Seven cats had no detectable antibody to feline immunodeficiency virus even though the virus was cultured from the peripheral blood lymphocytes. During follow-up for up to 60 weeks one cat died and 23 were destroyed on humane grounds.
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PMID:Clinical and laboratory findings in cats infected with feline immunodeficiency virus. 255 57

Neonatal host defense simulates a clinical state of immunodeficiency that predisposes the preterm and term newborn to overwhelming bacterial sepsis. There are various immunologic components that are deficient in the newborn and new methods to enhance their function. Defects in both the quantitative and qualitative aspects of the neonatal phagocyte contribute substantially to the immaturity of neonates' immune systems. The neonate lacks an adequate number of granulocyte bone marrow progenitor cells, and has a decreased neutrophil storage pool and an increased tendency to peripheral neutropenia during neonatal sepsis. Additionally, the neonatal granulocyte demonstrates altered physiologic function compared with that found in the adult with respect to chemotaxis, phagocytosis, oxidative metabolism, and bacterial killing. Some recent clinical studies have suggested the benefit of using adult neutrophil transfusions as adjuvant treatment during neonatal bacterial sepsis, yet other studies have found the use of polymorphonuclear neutrophil leukocyte transfusions to be inconclusive. Reduced circulating immunoglobulins and impaired production of specific antibody have also led to recent trials in the use of prophylactic intravenous immunoglobulin in preterm infants predisposed to sepsis. Recently, hematopoietic colony-stimulating factors have been demonstrated to improve in vitro neonatal neutrophil physiologic activity. Future therapy of neonatal sepsis will depend on new nontoxic methods for enhancing neonatal host defense.
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PMID:Neonatal neutrophil host defense. Prospects for immunologic enhancement during neonatal sepsis. 264 45

A boy with combined immunodeficiency having low natural killer (NK)-cell activity received thymopoietin pentapeptide (TP-5) treatment, transplanted with T cell-depleted HLA-haploidentical bone marrow (BMT) cells from his father and with thymus tissue from an infant at different times during the first year of life. He showed a marked increase in large granular lymphocytes (LGL) both during the treatment with TP-5 and after BMT. The LGL generated following TP-5 injection had a T3+Leu11- surface phenotype and low NK activity. In contrast, the LGL appearing after BMT showed T3-, Leu7+, and/or Leu11+ surface phenotypes, had high NK- and K-cell activities, and were lymphokine-activated killer (LAK)-cell precursors. These killer activities were assigned to the Leu7-Leu11+ subset and proved to be of recipient origin. LGL proliferation following BMT was accompanied by neutropenia, which was improved in association with a reduction in the number of LGL and the appearance of T cells of BMT donor origin following thymus transplantation. This suggested the inhibition of granulopoiesis by the LGL and an in vitro study revealed that the Leu7+Leu11- subset of LGL suppressed the growth of granulocyte/macrophage colony-forming units. These results indicated that phenotypically different LGL could be generated by different treatments and that the LGL showing NK activity were distinct from those regulating granulopoiesis. It was also suggested that the generation of LGL was controlled by T cells.
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PMID:Phenotypical and functional heterogeneity of the large granular lymphocytes increased after various treatments in a patient with combined immunodeficiency. 264 8

Zidovudine (azidothymidine) is a thymidine analogue antiretroviral drug active against human immunodeficiency virus (HIV). In acquired immunodeficiency syndrome (AIDS) and AIDS-related complex (ARC) patients, orally and intravenously administered zidovudine is effective in reducing the incidence of opportunistic infections and neoplasms, increasing helper T lymphocyte numbers, and improving survival rates and quality of life. Adverse effects include serious haematological abnormalities and severe headache, abdominal discomfort, nausea, myalgia and insomnia. In addition, neutropenia and other anaemias frequently limit zidovudine therapy and may result in a need for multiple blood transfusions, dose reductions or withdrawal of the drug. However, despite these problems and the lack of information about some aspects of zidovudine use, zidovudine provides a major hope for HIV-infected patients, and it has rapidly become the standard therapy for improving the quality and duration of the lives of AIDS and ARC patients.
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PMID:Zidovudine. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy. 266 Nov 94


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