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)

Hematologic abnormalities associated with penicillin compounds are uncommon, and neutropenia associated with ampicillin is reported even less frequently. Neutropenia developed in three pediatric patients after high-dose (150-400 mg/kg) ampicillin therapy over a period of 3 to 12 days. In all cases, the white blood cell and neutrophil counts returned towards normal within 4 to 11 days after discontinuation of the antibiotic. Bone marrow examination revealed a maturation arrest in one and slight shift to the left in the maturation of granulocytic cells in another. Other marrow components were normal. Red blood cells, reticulocytes, platelets, and hemoglobin did not show any abnormal alteration in any of the patients. Physicians administering ampicillin, particularly in high doses, should be alert to the possible development of neutropenia; however, all reported neutropenias have been reversible.
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PMID:Reversible neutropenia associated with ampicillin therapy in pediatric patients. 728 2

Investigations were carried out with 10 clinically normal calves, aged 1 to 6 months, through transfusion of 2-4 cm3/kg incompatible isogenic blood against which the recipients had immune isoerythrocyte antibodies of 1:2 to 1:32 titers. All animals, were studied for hemoglobin content, total erythrocyte and leukocyte count, leukocyte formula, and erythrocyte sedimentation rate (ESR) prior to the transfusion of blood and at the 1st, 4th and 24th hour and on the 4th and 7th day. An abrupt drop of hemoglobin was established at the 1st and 4th hour following hemotransfusion, while the erythrocytes dropped at the 4th hour. Within the remaining periods of time these two indices fluctuated around the normal value. Low or high ESR/1 and 2 hours showed no connection with the changes in the erythrocyte count. Lasting leukopenia was established along with transient eosinopenia, well exposed neutropenia, lymphocytosis, and monocytosis.
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PMID:[Morphological blood changes in calves with secondary immune blood transfusion shock caused by the recipients' immune erythrocyte isoantibodies]. 731 43

Shwachman's syndrome is a rare congenital disorder associated with neutropenia and exocrine pancreatic insufficiency. We describe the development of acute myeloid leukemia in a 38-year-old patient with Shwachman's syndrome following three years of pancytopenia. After chemotherapy the leukemic clone was eradicated, however, the patient's bone-marrow hypoplasia persisted beyond 180 days with neutropenia that responded to administration of granulocyte colony-stimulating factor. Despite the patient's low erythropoietin levels, administration of erythropoietin did not improve his hemoglobin. We review previously reported cases of leukemia complicating Shwachman's syndrome with emphasis on the persistent risk of complications in patients with congenital bone-marrow failure syndromes.
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PMID:Acute leukemia complicating bone marrow hypoplasia in an adult with Shwachman's syndrome. 751 52

Mycobacterium avium intracellulare (MAI) infection is a serious opportunistic infection that occurs in children with human immunodeficiency virus (HIV) infection. In MAI the hematologic system is profoundly affected. In the present study the hematologic manifestations of MAI in 37 HIV-infected infants and children were reviewed. Anemia was the predominant feature in all patients, with severe anemia (hemoglobin < 6 g/dL) occurring in 7 of 34 (21%) patients. This was followed by leukopenia (79%), monocytosis (82%), thrombocytopenia (59%), leukoerythroblastic reaction (68%), and neutropenia (41%). Serum tumor necrosis factor (TNF)-alpha was markedly elevated in all patients with MAI with an X +/- SE of 702 +/- 182 pg/mL. There was an association between elevated TNF-alpha and anemia in these patients.
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PMID:Elevated tumor necrosis factor-alpha in association with severe anemia in human immunodeficiency virus infection and Mycobacterium avium intracellulare infection. 764 Jan 75

A 45-year-old female with a long history of HLA-B27-positive ankylosing spondylitis and ulcerative colitis developed cyclic neutropenia. She was hospitalized for high fever during each of three consecutive episodes of absolute neutropenia. On the third hospitalization, granulocyte-colony-stimulating factor (G-CSF), 5 micrograms/kg/day, was given by subcutaneous injection and resulted in an increase of absolute neutrophil count from 0 to 2.2 x 10(9)/liter and an associated decrease of platelet count and hemoglobin as well as severe bone and joint pain predominantly in the middle and lower back and purulent diarrhea. The back pain necessitated discontinuation of the drug. Oral cyclosporine therapy was begun, and although the neutrophil count continued to oscillate, both the peaks and the nadirs were higher than previously, and symptoms of neutropenia subsided. We conclude that cyclosporine can be an effective treatment for cyclic neutropenia associated with autoimmunity since G-CSF may cause exacerbations of autoimmune disorders.
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PMID:Adult-onset cyclic neutropenia responsive to cyclosporine therapy in a patient with ankylosing spondylitis. 768 78

The effect of rhIL-3 was investigated in 32 patients with newly diagnosed non-Hodgkin lymphoma in a phase I/II trial. All patients received 6 cycles of standard CHOP chemotherapy, and each patient was his own control where rhIL-3 was given as a daily s.c. injection for 14 days (day 2-15) in cycle 2 and 4, while cycle 1 and 3 were control cycles. Five dose levels were examined (0.5 - 1 - 5 - 7.5 - 10 micrograms/kg). Compared to the other more lineage-specific hemopoietic growth factors G- and GM-CSF, the effect of rhIL-3 on the hemopoiesis was less dramatic and more delayed, i.e. the most apparent effect was observed in the 2 weeks of treatment. Thus, the neutrophil counts from days 15 to 22 following CHOP were significantly raised and the duration of neutropenia was shorter (significantly only at 10 micrograms/kg), while the nadir values were unaffected. Platelet recovery from days 12-22 was significantly increased and nadir values occurred earlier compared to control cycles, but were only increased in some subsets. Other cell populations affected moderately in the recovery period were eosinophils and monocytes. Reticulocytes increased, but no effect on hemoglobin or RBC transfusion requirement was noted. Only moderate adverse reactions occurred such as fever, chills, flushing of the face and flu-like symptoms. There was no evidence of stimulation of tumor growth. Most significant, the rhIL-3 treatment at all but the lowest dose levels led to an improved tolerance to chemotherapy, as indicated by a decline in number of delayed cycles. A conclusion concerning the role of rhIL-3 as post-chemotherapy adjuvant should await studies using rhIL-3 in combination with more lineage-restricted hemopoietic growth factors.
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PMID:Effects of interleukin-3 following chemotherapy of non-Hodgkin's lymphoma. A prospective, controlled phase I/II study. 769

Human parvovirus B19 has been associated with several diseases. Aplastic crisis in patients with chronic hemolytic anemia, erythema infectiosum, hydrops fetalis and arthritis are among the common diseases caused by this virus infection. In the period between July, 1991, and March, 1992, 48 patients with aplastic crises were hospitalized at Saudi Aramco-Dhahran Health Center, Dhahran, Saudi Arabia. Forty-six patients had homozygous sickle cell disease, one had hemoglobin H disease and one had hereditary elliptocytosis. Evidence of recent human parvovirus infection was present in 91% of the cases. Leukopenia was present in 21%, neutropenia in 27% and thrombocytopenia in 42%. This differs from previous reports in which red blood cell aplasia causing anemia was the only hematologic finding reported in most patients. There were no cases of erythema infectiosum in either the patients or the community during the epidemic and the reason for this phenomenon is not obvious. The almost limited occurrence of aplastic crisis in patients with sickle cell disease in a population with a high incidence of other types of chronic hemolytic anemias is of interest.
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PMID:An epidemic of aplastic crisis caused by human parvovirus B19. 771 86

Infection of naive North American horses with 10(4) cell culture infectious doses (CCID50) of virulence variants of African horsesickness virus (AHSV), designated AHSV/4SP, AHSV/9PI, and AHSV/4PI, reproduced three classical forms of African horsesickness: acute (pulmonary), subacute (cardiac), and febrile, respectively. Distinct clinicopathologic and hemostatic abnormalities were associated with each form of disease. Hemostatic abnormalities included increased concentration of fibrin degradation products and prolongation of prothrombin, activated partial thromboplastin, and thrombin clotting times. Hemostatic findings indicated activation of the coagulation and fibrinolytic systems with clotting factor consumption in acute and subacute cases of African horsesickness. Hematologic abnormalities in acute and subacute cases of African horsesickness included leukopenia, decreased platelet counts, elevated hematocrit, and increased erythrocyte counts and hemoglobin concentration. Leukopenia was characterized by lymphopenia, neutropenia, and a left shift. Increased levels of serum creatine kinase, lactate dehydrogenase, aspartate aminotransferase, and alkaline phosphatase, hypocalcemia, hypoalbuminemia, hypoproteinemia, and elevated creatinine, phosphorus, and total bilirubin levels were present in some but not all horses. Metabolic acidosis, indicated by decreased total bicarbonate and increased lactate and anion gap, was present in horses with the acute form of disease. Mild thrombocytopenia and leukopenia were occasionally associated with the febrile form of disease. These results suggest a role for intravascular coagulation in the pathogenesis of African horsesickness.
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PMID:Clinical pathology and hemostatic abnormalities in experimental African horsesickness. 777 Oct 50

Thirty seven hairy cell leukemia (HCL) patients, 35 males and 2 females with a median age of 53 years, were treated with a single course of 2-Chlorodeoxyadenosine (2-CdA) at a dose of 0.1 mg/kg daily for 7 days by continuous infusion. Twenty nine (78%) achieved a complete remission (CR) and 8 (22%) a partial remission (PR); four of the latter progressed after 6, 12, 18 and 24 months. All have been retreated with 2-CdA and 2 achieved a CR, 1 a PR and the last one is not yet evaluable. The overall median duration of response was 18 months, ranging from 4 to 30 months from the end of therapy. Circulating hairy cells and spleen enlargement, when present, disappeared within 2 weeks after completing treatment. A significant neutropenia was observed in almost all patients mainly in those who had less than 1,000/microliters neutrophils when treatment was started, together with a significant lymphocytopenia which lasted for more than 12 months. The hemoglobin and platelet levels were marginally affected. Fever was observed in 14 patients; in 8 of them it was short-lived (< or = 48 hours) and apparently not infection-related, while in the remaining 6 it was attributed to infection. Clinical tolerance was very good and none of the patients complained of nausea, vomiting or hair loss. In conclusion, our study confirms the efficacy of 2-CdA in HCL, including patients who progressed after treatment with 2-CdA.
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PMID:Retreatment with 2-CdA of progressed HCL patients. 782 47

Anemia and neutropenia caused by copper deficiency is a well-known consequence of long term total parenteral nutrition in the literature. We present 6 bed-ridden elderly patients who developed anemia and neutropenia after receiving enteral nutrition for a long time (mean: 3.3 years) In all 6 patients, serum copper and ceruloplasmin level were very low, and the mean of their hematological data were as follows: WBC 2,200/microliters, neutrophil 554/microliters, hemoglobin 8.1 g/dl, platelet 260 x 10(3)/microliters, respectively. The bone marrow examination showed cytoplasmic vacuolization of both myeloid and erythroid precursors, and maturation arrest of granulopoiesis. Then, copper sulfate was administrated by enteral tube to 6 patients, and the improvement of anemia and neutropenia was observed within a month. A 82-year-old woman who received enteral nutrition for 3.5 years with sever anemia (Hb 3.7 g/dl) and neutropenia (neutrophil 350/microliters), showed a marked improvement in hematological data (Hb 8.0 g/dl, neutrophil 4, 092/microliters, respectively) after two months by administering the copper supplementation. The exact cause of the anemia and neutropenia in copper deficiency is unclear, but it is suggested that the decreased activity of enzyme containing copper may be related. Hematological abnormalities due to copper deficiency should be cared during long term enteral nutrition with long termed bed-ridden elderly patients.
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PMID:[Anemia and neutropenia in elderly patients caused by copper deficiency for long-term enteral nutrition]. 782 95


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