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At least 199 records · Page 11Linked to original sources
PubMed1988

Benign familial leukopenia and neutropenia in different ethnic groups.

Benign hereditary leukopenia-neutropenia has been reported in several ethnic groups, including Yemenite Jews, Blacks of South African extraction, West Indians and Arab Jordanians. The subjects with BFL were shown not to have an increased incidence of infections, and their response to infection did not differ from subjects having normal white blood cell counts. This study entails the report of two additional unrelated ethnic groups with familial neutropenia - Black Beduin and Falashah Jews. The familial nature of the phenomenon was confirmed. The suggested mechanism of this type of neutropenia is a defect in release of mature WBC from the bone marrow to the peripheral circulation. All ethnic groups thus far reported have tanned or dark skin. The significance of this common feature has still to be elucidated.

Adolescent↗
PubMed2005

Reversible leukoencephalopathy syndrome associated to leukopenia in a chronic hemodialysis patient.

Reversible leukoencephalopathy syndrome (RLS) is a rare brain disorder, characterized by diffuse attenuation of cerebral white matter, which has been most commonly observed in transplant patients receiving calcineurin inhibitors or in patients with severe hypertension. We report an episode of RLS in a 22-year-old male patient on chronic hemodialysis with well-controlled moderate hypertension who presented with de novo headache and generalized seizures. Cranial magnetic resonance image (MRI) revealed multiple areas of increased signal intensity in the white matter on T2-weighed images which resolved spontaneously at subsequent MRIs. White blood cell count showed leucopenia with normal CD4 count at flow cytometry. A viral etiology could not be demonstrated. Reversible leukoencephaolopathy syndrome symptoms remitted within 72 h but leukopenia persisted over 10 months. The patient received a kidney transplant 15 months after RLS onset and has received cyclosporine since the second post-transplant day. No recurrence of RLS symptoms has been observed. The etiology of the MRI changes in the present case seemed not to be either vasogenic or cytotoxic.

Adult↗
PubMed2000

Bioavailability of aciclovir after oral administration of aciclovir and its prodrug valaciclovir to patients with leukopenia after chemotherapy.

The median bioavailabilities of aciclovir after administration of aciclovir and its prodrug valaciclovir were 21.5 and 70.1%, respectively, in 12 patients with malignant hematological diseases with leukopenia after chemotherapy. The interindividual variations of the bioavailability were 48.5 and 21.0% after administration of aciclovir and valaciclovir, respectively. Neither the bioavailability nor the interindividual variation of area under the concentration-time curve of oral aciclovir or valaciclovir differed from that reported in healthy volunteers.

Acyclovir↗
PubMed1971

Comparison between the polymyxins and gentamicin in preventing endotoxin-induced intravascular coagulation and leukopenia.

Three antimicrobial agents were evaluated as to their ability to neutralize the toxic effects of endotoxin in rabbits. These consisted of two cyclic polypeptides, polymyxin B sulfate and colymycin M (sodium colistimethate), and an aminoglycoside, gentamicin sulfate. Polymyxin B regularly prevented endotoxin-induced leukopenia, thrombocytopenia, and disseminated intravascular coagulation. Colymycin M had similar activity but was not as effective as polymyxin B. Gentamicin demonstrated no neutralizing ability in this study.

Animals↗
PubMedDate not supplied

Systemic lupus erythematosus - associated acute severe thrombocytopenia and leukopenia first presented in pregnancy.

We report a rare case of acute severe thrombocytopenia and leukopenia, which first presented at 37 weeks' gestation. Based on clinical as well as on laboratory findings the diagnosis of systemic lupus erythematosus was made. The patient was successfully managed with an emergency transfusion of 6 units of platelets and intravenous immunoglobulin infusion followed by methylprednisolone administration. A caesarean section was performed at 39 weeks. The neonate was not thrombocytopenic at birth, nor at the age of 1 month.

Adrenal Cortex Hormones↗
PubMed1988

T-cell acute lymphoblastic leukemia with severe leukopenia: evidence for suppression of myeloid progenitor cells by leukemic blasts.

A patient with T-cell acute lymphoblastic leukemia presented with leukopenia due to neutropenia, no circulating blasts and normal hemoglobin level. Marrow leukemic T lymphoblasts inhibited in vitro normal CFU-GM colony growth and released an activity that stimulated normal BFU-E growth. This patient demonstrates that immature T cells may modify hematopoietic stem cell growth both in vitro and in vivo.

Adult↗
PubMed1981

Effect of physical effort on the white blood cells in benign familial leukopenia.

The components of the peripheral white blood cells (WBC) were determined before and after 10 min of submaximal ergometric work in two groups of subjects: 34 healthy Yemenite Jews with benign familial leukopenia (BFL) and 34 healthy Yemenite Jews without BFL. The mean +/- SEM of the increase in the peripheral WBC following the effort in the control group was 2,606 +/- 1,272 cells/mm3, due to the relative rise in the neutrophils, eosinophils, monocytes and lymphocytes. The identical ergometric work, performed by BFL subjects, brought about significantly lower increase (700 +/- 865 cells/mm3) in the peripheral WBC, the majority of which were lymphocytes. It seems that subjects with this form of BFL lack granulocytes in the marginal pool.

Adolescent↗
PubMed1984

Aminoglutethimide-induced leukopenia: a case report and review of the literature.

A 67-year-old patient with breast carcinoma on treatment with aminoglutethimide (AG) developed profound leukopenia and sepsis. WBC count recovered within 1 week and the drug was renewed without further complications. The hematological toxicity of AG is reviewed. Detailed descriptions of this side effect of AG are usually lacking in most published series. It appears though that blood dyscrasia due to AG occurs rarely and is promptly reversible upon discontinuation of the drug, but renewal of its administration is not always possible.

Aged↗
PubMed1977

Hemodialysis leukopenia. Pulmonary vascular leukostasis resulting from complement activation by dialyzer cellophane membranes.

Acute leukopenia occurs in all patients during the first hour of hemodialysis with cellophanemembrane equipment. This transient cytopenia specifically involves granulocytes and monocytes, cells which share plasma membrane reactivity towards activated complement components. The present studies document that complement is activated during exposure of plasma to dialyzer cellophane, and that upon reinfusion of this plasma into the venous circulation, granulocyte and monocyte entrapment in the pulmonary vasculature is induced. During early dialysis, conversion of both C3 and factor B can be demonstrated in plasma as it leaves the dialyzer. Moreover, simple incubation of human plasma with dialyzer cellophane causes conversion of C3 and factor B, accompanied by depletion of total hemolytic complement and C3 but sparing of hemolytic C1. Reinfusion of autologous, cellophane-incubated plasma into rabbits produces selective granulocytopenia and monocytopenia identical to that seen in dialyzed patients. Lungs from such animals reveal striking pulmonary vessel engorgement with granulocytes. The activated complement component(s) responsible for leukostasis has an approximate molecular weight of 7,000-20,000 daltons. Since it is generated in C2-deficient plasma and is associated with factor B conversion, it is suggested that activation of complement by dialysis is predominantly through the altermative pathway.

Adult↗
PubMed1984

A case report of leukopenia associated with phenelzine.

Leukopenia, a rare but serious side effect of many psychotropic agents including monoamine oxidase inhibitors (MAOIs), has not been reported in the literature in association with phenelzine. The authors report such a case and suggest a toxic etiology independent of MAOI activity.

Adult↗
PubMed2005

Outcomes of febrile children presumed to be immunocompetent who present with leukopenia or neutropenia to an ambulatory setting.

UNLABELLED: To determine significant medical outcomes in febrile children presenting to an ambulatory setting with neutropenia and/or leukopenia. METHODS: Retrospective medical record review conducted on febrile patients who had a blood culture drawn, with white blood cell counts less than 5,000/mm3 and/or an absolute neutrophil count less than 1000/mm3. Ninety-one patients were identified; 5 with positive blood culture results, 13 with significant non-oncologic disease, and 3 patients with leukemia who had involvement of 2 or more cell lines. CONCLUSIONS: In the majority of patients, clinical judgment, physical findings, and review of all cell lines of the complete blood cell count identified those with significant disease.

Ambulatory Care↗
PubMed1980

Lithium carbonate in the treatment of drug-induced leukopenia in patients with solid tumors.

The authors report on the first part of an ongoing controlled trial (52 cases) on the evaluation of the effectiveness of Li2CO3 treatment of drug-induced leukopenia in patients with solid tumors. The results indicate that treatment with 750 mg/day per os of Li2CO3 for 7 days is capable of raising the leukocyte count to a highly significant extent, without serious side effects. The leukocytosis is due to an increase in neutrophil granulocytes.

Administration, Oral↗
PubMed1981

Treatment of neuroleptic-induced leukopenia with lithium carbonate.

Based on the finding that lithium carbonate administration can stimulate leukocyte production, six patients were treated with neuroleptic and other drug-induced granulocytopenia with lithium carbonate. The average total leukocyte count of 2500/mm3 increased to 4566/mm3. Similarly the average neutrophil count of 1028/mm3 increased to 2893/mm3 after lithium therapy. In all six patients, neutrophils decreased upon discontinuation of lithium. On the other hand, total WBC count of 4566/mm3 decreased to 2650/mm3, and the total neutrophil count of 2893/mm3 decreased to 966/mm3 after four weeks without lithium. The results suggest that lithium carbonate is effective in the treatment of drug-induced leukopenia.

Aged↗
PubMed1989

Methazolamide-associated temporary leukopenia and thrombocytopenia.

A three-week course of methazolamide therapy for chronic open-angle glaucoma resulted in marked leukopenia and thrombocytopenia. Prompt discontinuation of therapy resulted in complete recovery of white blood cell and platelet counts within five days. The recommendations for patients receiving carbonic anhydrase inhibitors for blood count control at six-month intervals are discussed.

Aged↗
PubMed2004

Responsiveness to G-CSF before leukopenia predicts defense to infection in high-dose chemotherapy recipients.

An active assessment of the host capacity to prevent infection during myelosuppression should be beneficial in patients receiving high-dose chemotherapy. A single dose of granulocyte colony-stimulating factor (G-CSF) (5 microg/kg) was given to 57 patients with multiple myeloma early after the completion of 85 high-dose chemotherapy (melphalan 200 mg/m2) courses. This provoked a highly variable white blood cell (WBC) peak after 12 to 14 hours. The median WBC count was 21,000/microL (range, 6400-60,600/microL) after a first high-dose therapy (n = 50) and 13,500/microL (range, 4700-24,800/microL) after a second high-dose therapy (n = 35). The responsiveness to single G-CSF was associated with the risk of infection during subsequent cytopenia (P =.003). This association was significant after adjustment for neutropenia duration. Notably, the result of testing G-CSF responsiveness was opportunely available before the onset of leukopenia, and G-CSF responsiveness was more informative than neutropenia duration regarding the risk of infection. Furthermore, there was an association between the responsiveness to G-CSF and stem cell engraftment (P <.005), which remained significant after adjustment for the number of transplanted CD34+ cells. Our results show for the first time that G-CSF potentially could be used for an early in vivo assessment of defense to infection in recipients of high-dose chemotherapy.

Adult↗
PubMed1988

A study on the mechanism of anemia and leukopenia in liver cirrhosis.

To elucidate the mechanism of anemia and leukopenia in the patients with liver cirrhosis, we investigated hematopoietic progenitor cell contents in their bone marrow, and the effects of their sera and blood mononuclear cells on hematopoietic progenitors from normal subjects. While there was no significant difference in the number of marrow CFU-E and BFU-E between the patients with liver cirrhosis and normal subjects, the number of marrow CFU-C was significantly reduced in liver cirrhosis patients. Patients' sera suppressed in vitro colony formation of normal CFU-E, BFU-E, and CFU-C, and the degree of suppression was well correlated with severity of anemia or granulocytopenia. In vitro colony formation of normal hematopoietic progenitor cells was not affected by blood mononuclear cells from liver cirrhosis patients. These results indicate that the appearance of humoral inhibitor(s) of hematopoietic progenitors plays a role in the development of anemia and granulocytopenia in liver cirrhosis.

Adult↗
PubMed1994

Effect of leukopenia on experimental post-traumatic retinal detachment.

Macrophages are invariably present in the intraocular membranes of patients with traumatic proliferative vitreoretinopathy (PVR). There are two sources from which these macrophages could be recruited: adjacent tissues and the systemic circulation. In the study described herein, the role of circulating white blood cells and monocytes in experimental, traumatic PVR was studied. The circulating white blood cells of 20 rabbits were depleted by intravenous injection of strontium-89. Posterior perforating eye injury with subsequent intravitreal injection of autologous whole blood or autologous activated macrophages was then performed on these leukopenic animals. The experiments demonstrated that severe bone marrow depression reduced significantly the incidence of retinal detachments in eyes receiving whole blood, and reduced the severity of retinal detachments in eyes injected with activated macrophages. An association between the degree of leukopenia, monocytopenia, and protection from retinal detachment was demonstrated. These results support the hypothesis that macrophage infiltration is an important component of intraocular cellular proliferation, but does not exclude the role of other types of white blood cells in the pathogenesis of PVR.

Animals↗
PubMedDate not supplied

Captopril-induced granulocyte aggregation. A possible complement mediated mechanism of peripheral leukopenia.

Captopril, competitive inhibitor of angiotensin converting enzyme, is clinically employed for its antihypertensive activity and drug-dependent granulocytopenia or agranulocytosis have been seldom observed during treatment. In previous unpublished studies an activating effect of the drug on the complement alternate pathway has been demonstrated. In this paper we demonstrate that captopril-treated serum is able to "in vitro" induce granulocyte activation and aggregation. Granulocyte aggregation was shown by the turbidimetric method and cellular activation was confirmed by the release of the granule associated enzyme lysozyme and beta-glucuronidase. On this basis complement-mediated leukoaggregation and leukosequestration in vivo could be proposed as the effector mechanism of peripheral leukopenia.

Captopril↗