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)

A case of chronic benign neutropenia in a 7-year-old Caucasian male is reported. The predominant clinical symptoms were persistent gingivitis and periodontitis. The clinical, hematological, oral radiographical, histological, and therapeutical features of this uncommon disease are discussed.
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PMID:Gingivo-periodontal manifestations in chronic benign neutropenia. 27 30

The role of neutrophilic granulocytes in the loss of gingival collagen has been studied by inducing experimental neutropenia during initial gingivitis in beagle dogs. Neutropenia was induced for 4 d in three animals with normal gingiva by repeated injections of rabbit anti-neutrophil serum. During neutropenia microbial plaque was allowed to form on the teeth. Samples of junctional (crevicular) leukocytes and gingival fluid were taken on days 0 and 4. Block biopsies of buccal gingiva were obtained on day 4. Stained semi- and ultrathin sections were used for histometric and stereologic tissue analysis. Gingival fluid flow increased from day 0 to day 4 in all dogs while junctional leukocytes increased in one dog only. Subgingival plaque had formed in most biopsies, and in the junctional epithelium very few neutrophilic granulocytes were present. In the coronal connective tissue subjacent to the junctional epithelium lymphoid cells, structurally abnormal neutrophilic granulocytes and monocytes/macrophages were diffusely scattered. The gingival collagen appeared mainly displaced by the inflammatory cells rather than dissolved. The data suggest that neutrophilic granulocytes may contribute to the loss of gingival collagen during initial gingivitis in dogs. The neutrophils also seem to be of importance for the limitation of subgingival plaque growth along the tooth surface.
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PMID:Effect of experimental neutropenia on initial gingivitis in dogs. 37 Sep 65

Feline immunodeficiency virus (FIV) has morphological, physical and biochemical characteristics similar to human immunodeficiency virus (HIV), the cause of AIDS in man. However, it is antigenically and genetically distinct from HIV; an antigenic relatedness with equine infectious anaemia virus has been demonstrated. FIV has been molecularly cloned and sequenced. Diagnostic tests are commercially available and attempts at preparing inactivated, subunit and molecularly engineered vaccines are being made in different laboratories. During FIV infection a transient primary illness can be recognized, with fever, neutropenia and lymphadenopathy. After a long period of clinical normalcy a secondary stage is distinguished with signs of an immunodeficiency-like syndrome. The incubation period for this stage can be as long as 5 years, during which gradual impairment of immune function develops. Many FIV-infected cats are presented for the first time showing vague signs of illness: recurrent fevers, emaciation, lack of appetite, lymphadenopathy, anaemia, leucopenia and behavioural changes. Later, the predominant clinical signs observed are chronic stomatitis/gingivitis, enteritis, upper respiratory tract infections, and infections of the skin. Neoplasias, neurological, immunological and haematological disorder are seen in a smaller proportion. The immunodeficiency-like syndrome is progressive over a period of months to years. Concomitant infection with feline leukaemia virus has been shown to accelerate the progression of disease. In vitro, phenotypic mixing between FIV and an endogenous feline oncovirus (RD114) has been demonstrated which leads to a broadening of the cell spectrum of the lentivirus. Bovine immunodeficiency virus (BIV) has been isolated only once, and all attempts to obtain additional isolates have failed; it has been recovered from the leucocytes of cattle with persistent lymphocytosis, lymphadenopathy, lesions in the central nervous system, progressive weakness and emaciation. As with the feline representative, BIV also was found to possess a lentivirus morphology and to encode a reverse transcriptase with Mg++ preference; it replicates and induces syncytia in a variety of embryonic bovine tissues in vitro. Antigenic analyses have demonstrated a conservation of epitopes between the major core protein of BIV and HIV. The original isolate has been molecularly cloned and sequenced. Besides the three large open reading frames (ORFs) comprising the gag, pol, and env genes common to all replication-competent retroviruses, five additional small ORFs were found. Numerous point mutations and deletions were found, mostly in the env-encoding ORF. These data suggest that, within a single virus isolate, BIV displays extensive genomic variation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Animal immunodeficiency viruses. 133 43

The results of an open-label, randomized, Phase III trial of r-methionyl human granulocyte-colony-stimulating factor (r-metHuG-CSF) in 41 patients with severe chronic neutropenia (SCN) are reported. Patients with diagnoses of congenital, cyclic, and idiopathic neutropenia, with histories of recurrent infections, were evaluated. The primary objective of the trial was to evaluate the ability of r-metHuG-CSF to increase the ANC to greater than 1500/mm3. A secondary objective was to evaluate variables associated with infection-related morbidity in SCN. r-metHuG-CSF treatment consisted of 1 month of dose titration followed by 4 months of treatment at an optimal dose. Patients were randomized to either immediate treatment with r-metHuG-CSF (Group A) or four months of observation followed by r-metHuG-CSF treatment (Group B). r-metHuG-CSF was administered by daily, subcutaneous injection with initial doses of 3 to 10 micrograms/kg/day. Forty of 41 patients who received r-metHuG-CSF had a complete response (median ANC greater than 1500/mm3 during 4 months of r-metHuG-CSF treatment). All cases of gingivitis and severe mouth ulcers resolved upon treatment with r-metHuG-CSF. Serious infections were also eliminated. Only one patient failed to show clinical improvement in response to r-metHuG-CSF treatment. Adverse reactions during the first 5 months of treatment were mild. Splenomegaly (mild) was noted in some patients. The administration of r-metHuG-CSF in patients with SCN significantly increased the ANC (P less than 0.001) and was accompanied by a marked reduction in infectious complications.
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PMID:Recombinant human granulocyte-colony-stimulating factor in the treatment of patients with neutropenia. 137 Feb 64

A 55-year-old man was admitted to our hospital for the evaluation of neutropenia. On physical examination, he had apthae and splenomegaly. CBC showed 1,000/microliter WBC with 5% neutrophils, and microcytic anemia consistent with iron deficiency. Bone marrow examination revealed a marked decrease of mature neutrophils, but normal percentage of immature myeloid cells. There was no morphological abnormality in the hemopoietic cells. He had no drug or family history responsible for the neutropenia. Anti-neutrophil auto-antibody was negative. Hence, a diagnosis of chronic idiopathic neutropenia (CIN) was made. He developed frequent episodes of infection such as balanitis, peri-anal infection, gingivitis, and pharyngitis. He was treated with steroid pulse therapy, anabolic hormone, and high dose gamma-globulin infusion, but no significant improvement occurred. Then, recombinant granulocyte-colony stimulating factor (rG-CSF) was started. The neutrophil count was normalized by the 7th day of 5 micrograms/kg/day rG-CSF administration. The administration of G-CSF was discontinued after a 14-day course. Thereafter, the neutrophil count remained at near normal level (approximately 1,500/microliter) and there have been no episodes of infection in the last 5 months. However this cannot be explained simply by the direct effect of rG-CSF on the myeloid precursors; rather, it suggests some unknown effect of G-CSF on the bone marrow microenvironment regulating myeloid hemopoiesis. We consider this to be a rare case of CIN with frequent episodes of infection, which was successfully treated with G-CSF.
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PMID:[Chronic idiopathic neutropenia improved by recombinant granulocyte colony stimulating factor]. 169 94

A moderate gingivitis was produced in 3 groups of 10 adult Wistar rats with diet 2000 of Keyes and Jordan (1964) delivered for 30 days with a controlled feeding unit. The first group served as untreated control. The second group received 5 intraperitoneal injections of cyclosporine A (15 mg/kg body weight) from day 20 to 30 to interfere with the activation of T lymphocytes and interleukin synthesis. The third group received 2 intraperitoneal injections of cyclophosphamide (100 mg/kg on day 20 and 25) which induced a severe neutropenia. The gingival areas between the upper molar regions were prepared for light and transmission electron microscopy. In the untreated control group, a layer of polymorphonuclear neutrophils (PMN) was observed between the dental plaque and the junctional epithelium with a round cell infiltration in the superficial connective tissue. No bacterial invasion was observed. In the cyclosporine group, despite the action on T lymphocytes, no bacterial invasion occurred, but a differentiated PMN layer was present between the apical dental plaque and the junctional epithelium. In the cyclophosphamide group an important bacterial invasion was observed in the interdental epithelium as well as in the underlying connective tissue. In the local absence of PMNs, a mixed flora of Gram positive and negative bacteria of various shapes invaded epithelial as well as connective tissue cells and came in contact with the alveolar crestal bone. Resorption of the alveolar crestal bone scored according to the Keyes and Gold method (1955) was significantly more important in the cyclosporine and the cyclophosphamide group when compared to the controls (p less than 0.05). No statistical difference in bone resorption was noted between the cyclosporine and the cyclophosphamide groups. It can be concluded that the PMN layer constitutes the first line of defense opposed to bacterial invasion of the periodontal tissues.
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PMID:Bacterial invasion of periodontal tissues after experimental immunosuppression in rats. 179 Nov 64

Eight patients with Hyper-IgM syndrome were subjected to clinical and immunological evaluation. There were seven males and one female. All the patients had recurrent pyogenic infections; one had lymphoid hyperplasia with centrally necrotic granulomas, and one had gingivitis with neutropenia. Isohemagglutinin titers were either high or normal in all the patients and five had group 0 blood. The percentage of IgM-bearing cells were normal in five patients. The percentage of T cells were normal in all the patients, helper T cells were decreased in two patients, and suppressor T cells were increased in four patients. These results suggest that at least in some patients, the imbalances of T cell subsets may play a role in the pathogenesis of the disease rather than it being attributed to an intrinsic B cell defect.
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PMID:Clinical and immunological aspects of hyper-IgM syndrome. 228 14

Six patients with cyclic neutropenia were treated with recombinant human granulocyte colony-stimulating factor (G-CSF) for 3 to 15 months. All had a history of recurrent aphthous stomatitis, pharyngitis, lymphadenopathy, fever, and numerous infections during periods of neutropenia. Serial blood-cell counts, findings on bone marrow examination, and signs and symptoms were evaluated before and during the daily administration of G-CSF (3 to 10 micrograms per kilogram of body weight per day), either intravenously or subcutaneously. The kinetics of labeled autologous blood neutrophils and the migration of neutrophils to skin chambers were also measured. Recombinant human G-CSF increased the mean (+/- SEM) neutrophil counts from 717 +/- 171 per microliter to 9814 +/- 2198 per microliter (P = 0.009). In five of the six patients, the cycling of blood-cell counts continued, but the length of the period decreased from 21 to 14 days. The number of days of severe neutropenia was reduced (P = 0.002). Neutrophil turnover increased almost four-fold (P = 0.005), whereas neutrophil migration to a skin chamber was normal. G-CSF therapy reduced the frequency of oropharyngeal inflammation, fever, and infections in these patients. During the first 40 months of treatment, no typical mouth ulcers or bacterial infections occurred; recurrent gingivitis improved. We conclude that G-CSF is effective for the treatment of cyclic neutropenia in humans.
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PMID:Treatment of cyclic neutropenia with granulocyte colony-stimulating factor. 246 56

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

Persistent neutropenia (0-0.6 X 10(9) neutrophils/l) was documented during a 10-month period in a 4-year-old spayed female domestic shorthair cat that was presented for anorexia and depression. Salient abnormalities detected on physical examination were fever (40.3 degrees C), dehydration, and gingivitis. The cat was neutropenic (0.5 X 10(9) neutrophils/l) and enzyme-linked immunosorbent assay (ELISA) test for feline leukemia virus was negative. A bone marrow aspirate showed decreased numbers of mature granulocytic cells. In vitro bone marrow cultures for colony-forming units-granulocyte/macrophage (CFU-GM) were performed comparing bone marrow from the patient with that of a normal cat. The patient had fewer CFU-GM than the control. The number of CFU-GM increased when bone marrow mononuclear cells were cultured in the presence of 10(-5) and 10(-6) mol/l of hydrocortisone, but the cat did not respond to oral prednisolone therapy. The pathogenesis of the neutropenia in this cat remains obscure, but resembles the chronic idiopathic neutropenia syndrome of man.
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PMID:Chronic idiopathic neutropenia in a cat. 322 55


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