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)

The hematologic toxicity of doxorubicin, 30 mg/m2 body surface area (BSA) every 21 days to a cumulative dose of 300 mg/m2, was evaluated in six cats. Complete blood and platelet counts were performed daily during the first treatment cycle. They were monitored before treatment for all remaining cycles, and at the average neutrophil nadir (day 8) starting with cycle 4. Significant poikilocytosis developed after the first treatment and remained throughout the study, although anemia did not occur. No other red blood cell abnormalities were seen. Platelet counts remained within the reference range throughout the first treatment cycle, but mild thrombocytopenia (88,000-288,000/uL) was found in 11.3% of subsequent complete blood counts (CBCs). Thrombocytosis was seen in 30.9% of CBCs. Neutropenia did not occur during the first treatment cycle although neutrophil counts did decrease, with the nadir occurring between days 8 and 11. All neutrophil counts returned to pretreatment values by day 14. Neutropenia was documented after 14 of 46 (30.4%) doxorubicin treatments, and was associated with fever in 5 cats (10.9%). All fevers responded to oral antibiotic therapy. Neutropenia that lasted more than 14 days developed in two cats, necessitating dosage reduction to 25 mg/m2 BSA. At the dose used in this study, doxorubicin administration was associated with acceptable hematologic toxicosis in most cats.
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PMID:Hematologic toxicosis associated with doxorubicin administration in cats. 143 1

Five cats were treated with an azathioprine suspension (2.2 mg/kg of body weight on alternate days) and 2 cats were given vehicle (controls) for 9 weeks. Complete blood and platelet counts and serum biochemistry variables were monitored weekly. Bone marrow aspirates were evaluated every 3 weeks, and core bone marrow biopsy was performed at the end of the study. Profound neutropenia (less than 600 cells/microliters) was observed in all treated cats, and 1 cat developed pancytopenia. Treatment was discontinued if the WBC count was less than 3,000 cells/microliters. Four weeks after discontinuation of azathioprine, 1 treated cat again was given azathioprine at a lower dosage (1.1 mg of azathioprine/kg on alternate days) and neutropenia recurred within 2 weeks. During treatment, 3 cats developed thrombocytosis, and 2 developed thrombocytopenia. In 4 of 5 cats, neutropenia and thrombocytopenia resolved when azathioprine was discontinued. Bone marrow cytologic examination during treatment revealed reduction of the neutrophil line, with relative increase in monocytes. Core bone marrow biopsy at the completion of the study revealed hypocellular marrow with marked decrease in the myeloid series in cats given azathioprine. One of the cats that was treated with azathioprine had a hypercellular marrow with increased numbers of mature granulocytes and precursors; however, azathioprine had been discontinued 3 weeks prior to biopsy. Alterations in serum biochemical variables were not associated with azathioprine. Two cats that were treated with azathioprine developed respiratory tract infections, and 1 of them was euthanatized during the study.
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PMID:Systemic toxicosis associated with azathioprine administration in domestic cats. 149 96

Localized plasma cell type Castleman's disease (CD) is an unusual pathologic entity. It is frequently associated with clinical and laboratory characteristics and rarely occurs in children. Total surgical excision results in cure in all aspects. To make early diagnosis of mesenteric CD is not easy, especially for children. An 11-year-old Taiwanese boy was recently evaluated for anemia and delayed growth. His clinical findings included a syndrome of severe hypochromic microcytic anemia, neutropenia, thrombocytosis, hypoferremia, hypergammaglobulinemia, and growth failure. Radiological examinations (abdominal ultrasound, small intestinal series, and computerized tomography) identified hepatosplenomegaly, nephromegaly, and huge masses in the middle abdomen with precaval, celiac, and paraaortic lymph nodal enlargement. However, detailed physical examination failed to detect a mass. At laparotomy a double-fist-sized confluent mass was found arising from the mesenteric root. Most masses were discrete and were excised individually. The pathologic diagnosis was plasma-cell type angiofollicular lymph node hyperplasia (Castleman's disease). Seven weeks after surgery, he had an episode of acute hepatitis B. Postoperatively, he exhibited a dramatic growth spurt; the hemoglobin, red blood cell indices, serum iron, and immunoglobulins returned to normal in 2 months. Neutropenia, which has not been previously related to mesenteric CD, was an unexpected finding in our case; however, it resolved spontaneously 3 months after the surgery, suggesting its causal relationship with the tumor.
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PMID:New observations in a child with angiofollicular lymph node hyperplasia (Castleman's disease) originated from the mesenteric root. 151 Jan 96

In an attempt to stimulate endogenous erythrocyte production and thereby provide an alternative to erythrocyte transfusions, we administered recombinant human erythropoietin (rHuEpo) in doses of 75 to 300 units/kg/wk to seven infants with the anemia of prematurity. Treatment was started between 21 and 33 days of life, maintained for 4 weeks, and was well tolerated. All the patients had low baseline serum erythropoietin levels. After rHuEpo therapy, the number of reticulocytes increased from a mean baseline count of 75 x 10(9)/L to 95, 141, and 165 x 10(9)/L on days 7, 10, and 14 of therapy, respectively. Correction or stabilization of the anemia was observed in six of seven patients, whose estimated total erythrocyte volume increased by 49% during therapy (vs a predicted increment of 18% in the absence of rHuEpo). In one patient, however, the hematocrit declined during the treatment, and in three of the responders a secondary fall in hematocrit was noted either during therapy or after its discontinuation. Serum iron and ferritin levels rapidly decreased after the initiation of rHuEpo therapy, and in most patients transient early thrombocytosis and late neutropenia were observed. These data suggest that rHuEpo may correct or stabilize the anemia of prematurity. Its effects, however, may be limited by a variety of factors, among which iron availability probably plays an important role. Controlled studies will be needed to confirm these preliminary observations.
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PMID:Effects of recombinant human erythropoietin in infants with the anemia of prematurity: a pilot study. 169 80

Canine cyclic hematopoiesis (CH) is an autosomal recessive disease of gray collie dogs that is characterized by 14-day cycles of neutropenia, monocytosis, thrombocytosis, and reticulocytosis. Platelets from CH dogs have decreased dense-granule serotonin pools and decreased aggregation responses to collagen, platelet-activating factor (PAF), and thrombin. Recombinant granulocyte colony-stimulating factor (rG-CSF) was administered (5 micrograms/kg, b.i.d.) to four CH and six normal dogs to determine if G-CSF therapy corrected qualitative platelet defects in CH dogs. Neutrophil counts increase to greater than 25,000 cells/microliters within 24 h after starting treatment in all dogs. Treatment with G-CSF blocked neutropenic episodes in the CH dogs. Platelet aggregation, and serotonin content and secretion were significantly (p less than 0.05) decreased in the CH dogs both before and during recombinant human (rh) G-CSF treatment compared to normal dogs. Neutrophil myeloperoxidase, a primary granule enzyme, was significantly (p less than 0.05) decreased in CH dogs and was not corrected by rhG-CSF treatment. Administration of rG-CSF to CH dogs eliminated cell cycles but apparently did not correct cellular defects in CH dogs. Identification of primary biochemical defects in cells from CH dogs may be crucial to investigating the biochemical basis for cyclic hematopoiesis.
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PMID:Effects of recombinant granulocyte colony-stimulating factor treatment on hematopoietic cycles and cellular defects associated with canine cyclic hematopoiesis. 169 76

The paraneoplastic syndrome (PNS) is an association of symptoms and signs not directly related to the site or local manifestations of a malignant tumor or its metastases. Hematologic abnormalities as PNS include erythrocytosis, anemia, neutrophilia, neutropenia, eosinophilia, thrombocytosis, thrombocytopenia, venous thromboembolism and disseminated intravascular coagulation (DIC). These abnormalities are, by and large, due to the production of biologically active growth factors, hormones or as yet unidentified "humors" by the tumor. As our understanding of growth factors controlling hematopoiesis has increased in recent years, the biologic basis of hematologic PNS are better understood. For instance, tumor-associated neutrophilia is now known to be caused by the production of G-CSF by the tumor. The mechanism by which tumor causes thromboembolism have also been extensively investigated. Cancer cells induce platelet aggregation both in vitro and in vivo. Platelet aggregating material has been isolated and partially characterized from tumor cells. The involvement of platelet glycoprotein II b/IIIa in the tumor-platelet interaction has also been shown. Malignant cells contain a unique procoagulant, cancer procoagulant A, that directly activates factor X. Together with tissue factor, this procoagulant appears to have been contribute to a high incidence of thromboembolism in cancer patients. Better understanding of hematologic PNS is important for clinical care of the patients with cancer.
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PMID:[Paraneoplastic syndrome hematologic abnormalities]. 200 36

A rare case of erythroblastopenia associated with essential thrombocythemia (ET) is described. The patient had markedly elevated platelet count (5200 x 10(9)/1) and significant platelet dysfunction leading to extensive soft tissue and gastrointestinal hemorrhage. There was paucity of erythroid precursors in the bone marrow - a feature hitherto undescribed in ET. The thrombocytosis responded to well busulphan therapy but patient succumbed to fulminant infection consequent upon drug induced neutropenia.
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PMID:Pure red cell aplasia associated with essential thrombocythemia (a case report). 212 31

The efficacy and toxicity of oral azidothymidine has been studied in 145 patients with the acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (ARC). The median survival time of AIDS patients on azidothymidine was 4.5 times higher when compared to a historical AIDS group who had not received the drug. This result must be interpreted with caution because of changes in treatment of HIV infection and growing awareness of AIDS which may have led to earlier diagnosis in the group treated with azidothymidine. The mortality was significantly higher in those patients who received transfusions and was particularly high in those who were transfused before azidothymidine. There was a significant difference in the occurrence of opportunistic infections in the patients who received transfusions compared with those who did not. AIDS patients treated immediately after an episode of Pneumocystis carinii pneumonia survived significantly longer than those in whom treatment was delayed for three months or more, and longer than those who were treated with azidothymidine because of another opportunistic infection or Kaposi's sarcoma. The T4 cell median counts increased in patients treated with azidothymidine reaching a peak at the end of the fourth month of treatment in the ARC group and at the end of the first month in the AIDS group with a subsequent fall in both groups. Sixty per cent of patients were p24 viral antigen positive at the start of treatment and 19 per cent of these patients had a fall of more than 50 per cent in antigen level while 32 per cent became antigen negative following treatment with azidothymidine. The mortality in the patients where the antigen disappeared or in whom there was a major fall of more than 50 per cent in antigen level was significantly less than in those where there was no change in antigen level. Twenty-nine patients were treated with azidothymidine because of skin Kaposi's sarcoma and in 17 tumour regressed or was stable. Thirty-two per cent of patients treated with azidothymidine became anaemic. Neutropenia occurred in 3 per cent of patients. Platelets increased initially after treatment but subsequently fell to thrombocytopenic levels in eight patients. Nine of 12 patients with thrombocytopenia before azidothymidine was commenced responded with an increased platelet count.
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PMID:The efficacy and toxicity of azidothymidine (AZT) in the treatment of patients with AIDS and AIDS-related complex (ARC): an open uncontrolled treatment study. 251 92

We report a series of 39 cases of acquired idiopathic sideroblastic anemia accounting for 12 p. 100 of the 330 cases of myelodysplastic syndrome diagnosed in our department in six years. Patients' mean age was high (70.8 years). Anemia was present in 92 p. 100 of the cases and was of the macrocytic type in 87 p. 100 of the patients. Only two patients (5 p. 100) had neutropenia and two (5 p. 100) had thrombocytopenia. Thrombocytosis was observed in 17 cases (43 p. 100); it was usually moderate. The mean proportion of medullary ring-sideroblasts was 35 +/- 14 p. 100. A clonal abnormality was found in 4 of the 11 karyotype examinations performed. The course of the disease was marked by recurrences of anemia which required regular blood transfusions in 82 p. 100 of the cases. In at least 30 p. 100 of the patients followed up for more than 30 months, these transfusions were responsible for secondary haemochromatosis. Conversely, in only three patients (7.5 p. 100) the disease progressed to acute leukemia. On the other hand, 4 patients (10 p. 100) developed thrombocythemia (greater than 1,000 x 10(9)/1). Median actuarial survival rate was 48 months. There were only two factors of poor prognosis: age over 70 and anemia with less than 8 g/dl haemoglobin at the time of diagnosis. Transfusion haemochromatosis is the principal risk in acquired idiopathic sideroblastic anemia: this risk can be prevented by iron chelating agents in patients with frequent blood perfusions.
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PMID:[Acquired idiopathic sideroblastic anemia. Apropos of 39 cases]. 279 16

A pharmacokinetic and clinical study of ceftizoxime (CZX), a newly developed cephem antibiotic intended for parenteral use, was conducted in premature and newborn infants, and resulted in the following findings. 1. Pharmacokinetics (1) Average serum half-lives (T 1/2) following a one shot intravenous dose of 20 mg/kg of CZX to mature and premature newborn infants in age groups of 0-3, 4-7, 8-14, and 15-30 days were: 4.14, 3.01, 2.57, and 1.98 hours (for mature infants) and 5.26, 4.59, 3.71, and 2.64 hours (for premature infants), respectively, decreasing with ages in days of the infants. (2) Average T 1/2's after a one shot 10 mg/kg dose was similar to that after a 20 mg/kg dose. Serum concentrations of CZX were dose-dependent. (3) T 1/2 after 1-hour intravenous drip infusion revealed a same trend after one shot injection. (4) Urinary in the first approximately 6 hours recoveries following a 20 mg/kg one shot dose to mature and premature newborn infants were as follows: 35% (0-3 days old) and 45-55% (4 days old and older) in mature infants and 30% (0-3 days old) and 45% (4 days old and older) in premature infants. 2. Therapeutic effectiveness (1) The subjects examined were 112 newborn infants consisting of 83 with infections and 29 who received CZX for prophylaxis. The 83 infants had 86 cases of infections, which were classified as A, when the causative organisms were identified and as B, when the causative organisms were not identified. Rates of therapeutic effectiveness were 95.0% for group A and 95.7% for group B. Bacteriological effectiveness were studied on 41 strains isolated from group A, and were as high as 89.5% for Gram-positive organisms and 95.5% for Gram-negative organisms. The rate of successful prophylaxis for the 29 infants was 96.6%. (2) Side effects did not occur among the 120 newborn infants. Laboratory tests with abnormalities included leukopenia, neutropenia, eosinophilia, thrombocytosis and increased GOT or GPT. These pharmacodynamic and clinical findings have fully substantiated the satisfactory therapeutic usefulness of CZX in both the treatment and prevention of neonatal infections in the usual dose of 20 mg/kg, which is to be given b.i.d. for infants up to 3 days old; b.i.d. or t.i.d. for infants 4 to 7 days old, and t.i.d. or q.i.d. for infants 8 days old and older. The drug can be given in a daily dose as high as 120 mg/kg when infection is severe.
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PMID:[Pharmacokinetic and clinical studies on the use of ceftizoxime in premature and newborn infants. The Chemotherapy Research Group for Mother and Child]. 305 Jan 88


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