Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 47-year-old female was admitted in October 1988 because of anemia and lymphoblastic cells in peripheral blood. A bone marrow aspirate was hypercellular with 93.9% lymphoblasts negative for peroxidase staining. The case was diagnosed as ALL (L2), and treated with JALSG ALL-87 regimen. She developed spiky fever and endotoxin shock due to bacteremia caused by pseudomonas aeruginosa, then was treated with several antibiotics. With the recovery of leukocytes, the chest X-ray showed an infiltrative shadow and a cavity forming lung abscess resembling aspergilloma in her left lung. The cavity improved of transbronchial infusion following amphotericin B (AMPH-B). Although she achieved complete remission, she felt severe lumbago accompanied by a marked erosion of the vertebral body with disc space narrowing on her X-ray. Then she underwent surgery to remove a disc abscess, and 1 colony of the aspergillus species was cultured from the specimen. She was treated with intravenous AMPH-B, and post remission therapies were performed under the injection of anti-fungal agents. No remarkable symptoms of complications were recognized during the chemotherapy. AMPH-B is useful and safe for the management of aspergillus discitis.
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PMID:[Aspergillus lumbar discitis in a patient with acute lymphoblastic leukemia following induction therapy]. 778 23

A patient is presented who had acute basophilic leukaemia with intense erythroblastic reaction. The patient, a 66 year-old man, complained of general malaise, increased abdominal perimeter and melena. Leucocytosis, as well as severe anaemia and thrombocytopenia, were found in his peripheral blood. Basophils were present in all maturation stages, along with 7% blast-cells showing basophilic stippling, and there were 210 erythroblasts per 100 white cells. Erythropoietic hyperplasia (75%) was found in the bone-marrow aspirate, without dyserythropoietic signs; the PAS-stain reaction was negative. Of the non-erythroid cells, 63% were basophils and 34% blast-cells, some of them showing basophilic stippling plus metachromasia for tholuidin-blue, positivity for omegaexonuclease and negativity for peroxidase stains. The diagnosis of acute basophilic leukaemia was confirmed upon demonstration of basophilic stippling in the ultrastructural study of the blast-cells. The patient developed acute liver failure and renal insufficiency which led him to death. The basis of the diagnosis of acute basophilic leukaemia is discussed, as well as the differential diagnosis with other conditions presenting with basophilia and the probably reactive erythroblastic increase appearing in this case.
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PMID:[Acute basophilic leukemia with an intense erythroblastic reaction]. 814 May 1

Detection systems for chicken anemia virus (CAV) antigen in paraffin sections were evaluated. Mouse monoclonal antibodies to CAV used in conjunction with an avidin-biotin-peroxidase-complex detection system gave best results. Immunoreactivity of CAV was markedly affected by fixation. Fixation in neutral buffered formalin for 6 hours gave best results. Use of decalcifying fluid containing formic acid eliminated immunoreactivity of CAV, whereas use of an EDTA solution did not. In a sequential study, CAV antigen and lesions were first detected in bone marrow, thymus, and spleen at days 3-4 postinoculation (PI). Subsequently, antigen and/or cells containing nuclear inclusions were found in many tissues, but usually within lymphoid tissue therein. Thymus, spleen, bone marrow, proventriculus, and ascending duodenum contained most antigen. No antigen was detected after 26 days PI. The results indicated that CAV replicates in thymic lymphoblasts, intra- and extra-sinusoidal hemocytoblasts, and reticular cells, with consequent lymphocytic depletion of the thymic cortex and hypoplasia of the bone marrow, and that CAV antigen is widely distributed in the body.
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PMID:A sequential histopathologic and immunocytochemical study of chicken anemia virus infection at one day of age. 836 98

The authors report a de novo AML (M2) patient associated with 5q- as the sole karyotypic abnormality. A 76-year-old woman was referred to our hospital because of anemia and leukocytosis. On examination a neck lymph node was enlarged, but neither the liver nor the spleen could be palpated. The hemoglobin level was 7.1g/dl, the mean corpuscular volume 102fl and the white-cell count was 256.1 x 10(3)/microliters with 87% blast cells. The platelet count was 10.9 x 10(4)/microliters. The bone marrow was hypercellular with 79.8% blast cells and showed dysmegakaryocytopoietic features (hypolobulation, multiple separated nuclei and micromegakaryocytes). Blast cells gave a positive reaction for peroxidase and alpha NB esterase which was not blocked by NaF. The diagnosis of AML (M2) was made but she died before chemotherapy. Autopsy revealed general hemorrhagic tendency and leukemic cell infiltration. Chromosome analysis of the bone marrow showed 46,XX,del(5) (q13q31). Electron micrographs revealed increase of micromegakaryocytes as small as myelocytes and aggregation of demarcation membranes in some megakaryocytes. This may suggest that some molecular changes, instead of karyotypic evolution, contributed to a leukemic transition from the 5q- syndrome to AML with 5q- as the sole abnormality.
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PMID:[Proliferation of micromegakaryocytes in acute myelocytic leukemia associated with 5 q- as the sole karyotypic abnormality]. 851 Mar 36

We report a patient with acute myeloid leukemia (AML) presenting with generalized lymphadenopathy, clinically stimulating aggressive non-Hodgkin's lymphoma. This patient presented with anemia and bulky lymphadenopathy in the oropharyngeal (Waldeyer's ring), submandibular, supraclavicular and inguinal nodal regions. Lymph node biopsy was initially suggestive of a T-cell lymphoblastic lymphoma, based on morphologic features together with positive immunohistochemical staining for CD7 and CD43 (Leu 22). Definitive diagnosis of AML was established when a more detailed immunophenotypic analysis showed expression of the myeloid markers CD13 and CD33, and by the demonstration of rare Auer rods and positive peroxidase staining in bone marrow blast cells. Although this is a rare presentation, AML must always be considered in the clinical and pathologic differential diagnosis of aggressive non-Hodgkin's lymphoma.
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PMID:Acute myelogenous leukemia presenting with bulky lymphadenopathy. Case report and literature review. 863 42

The molecular defect of the hereditary disease Fanconi anemia (FA) remains unknown. The two theoretical possibilities are (1) an impaired DNA crosslink-repair system or (2) a disturbed oxygen metabolism either by overproduction of reactive oxygen intermediates (ROI) or by diminished detoxification of ROI. In order to gain further insight into the molecular mechanism of this disease, we have determined the repair capacity of FA cells challenged by crosslinking agents and have analyzed diverse biological systems that are involved in oxygen metabolism. We have tested normal and FA cells for oxygen consumption and for the activity of the antioxidant phospholipid-hydroperoxide-glutathione-peroxidase (PHGPx). FA cells show a reduced oxygen consumption and an increased PHGPx activity. Since spontaneous and induced chromosomal instability is a main cellular feature of FA, we have analyzed the redox state of cells and the effect of cytochrome P-450 (Cyt P-450) inhibitors and inducers on chromosomal breaks and micronuclei production. Our results indicate that Cyt P-450 enzymes, especially Cyt P-450 1A2, play a crucial role in radical metabolism in FA cells. Furthermore, we have determined NF-kappa B activity in untransformed cells and in SV40-transformed cells by gel shift experiments. NF-kappa B is a multiunit transcription factor that is known to be induced by ROI and that activates the expression of various genes involved in cellular responses to stress. NF-kappa B is constitutively induced in SV40-transformed FA cells probably as a consequence of an increased ROI level. Our results suggest that enzymatic defects in oxygen metabolism mediate the FA phenotype via impaired reactivity with ROI. Cyt P-450 1A2 appears to be a good candidate for the defective enzyme, even though no differences have been measured in the activity of this enzyme in FA and control fibroblasts in pilot experiments.
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PMID:The role of oxygen metabolism for the pathological phenotype of Fanconi anemia. 918 62

Human parvovirus B19, which infects and lyses erythroid precursors, can cause severe anemia in patients with immunodeficiency. The incidence of parvovirus infection in adult acquired immunodeficiency syndrome (AIDS) patients is unknown. Eighty-one archival formalin-fixed, paraffin-embedded (FFPE) bone marrow biopsies from 73 AIDS adults were immunostained with monoclonal R92F6 against B19 VP1 and VP2 capsid proteins using streptavidin peroxidase and streptavidin alkaline phosphatase techniques. In addition, the same tissues were hybridized in situ with a digoxigenin-labeled parvovirus B19 DNA probe. Five FFPE bone marrows, from 3 HIV-negative patients with positive immunoglobulin M (IgM) serology for parvovirus B19, and 1 parvovirus B19-infected fetal liver were positive controls. By immunoperoxidase, all tissues were negative with R92F6 except the fetal liver, which exhibited strong positivity predominantly in viral inclusions. With immunoalkaline phosphatase, all positive controls were immunoreactive with R92F6; however, the AIDS marrows were negative. With in situ hybridization (ISH), all positive controls and 7 of 81 (8.6%) of AIDS marrows were positive for B19 parvovirus DNA. We conclude that ISH is more sensitive than R92F6 immunohistochemistry in parvovirus B19 detection. A small but significant number of bone marrows from AIDS adults shows evidence of human parvovirus B19 infection.
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PMID:Human parvovirus B19 in bone marrows from adults with acquired immunodeficiency syndrome: a comparative study using in situ hybridization and immunohistochemistry. 922 41

The given report deals with investigation of the level of spontaneous lipid peroxidation (LPO) (as judged by the accumulation of MDA) and activity of antioxidative enzymes (GSH-peroxidase, GSH-reductase) in red blood cells of pregnant women (24-26 weeks) suffering from minor (blood Hb is 95 g/l) and medium (blood Hb is 85-90 g/l) anemias. We have found that as the anemia becomes deeper, the red blood cells of pregnant women demonstrate a linear increase in the level of spontaneous LPO, which rises by 54% during anemia of moderate severity (p < 0.02) as compared with control. At the same time, simultaneously with LPO, the activity of the above glutathione-containing enzymes increases as the anemia progresses, which, apparently, is of the compensatory nature, aimed at the maintenance of the reduced glutathione pool, the latter being an important component of the cell antioxidative system during LPO activation. The authors think the increased activity of the physiological antioxidative system and intensification of the LPO processes to be a natural adaptive process, since lipid hydroperoxides are the activators of synthesis of prostaglandins, which are required in delivery.
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PMID:[Intensity of lipid peroxidation processes and activity of antioxidant enzymes in erythrocytes during anemia in pregnancy]. 927 21

Computational analysis of the Fanconi anemia (FA) complementation group A protein suggests that it contains a peroxidase domain. FA proteins may be part of a general mechanism that protects cells from oxidative damage.
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PMID:The Fanconi anemia complementation group A protein contains a peroxidase domain. 960 46

Prior to 1972, the increased cardiovascular morbidity and mortality that diabetics endure had been attributed to vascular disease. In 1972, Rubler et al. proposed the existence of a diabetic cardiomyopathy based on their expereince with four adult diabetic patients who suffered from congestive heart failure (CHF) in the absence of discernable coronary artery disease, valvular or congenital heart disease, hypertension, or alcoholism. Alternative explanations for CHF, such as anemia and vascular and renal disease in these four patients, gave rise to criticisms, but a wave of subsequent studies in the 1970s and 1980s provided credence to this new disease entity. This review of the studies done since 1972 appears to support the concept of a diabetic cardiomyopathy independent of atherosclerotic cardiovascular disease. The exact mechanism is still questionable, and several mechanisms have been proposed including small and microvascular disease, autonomic dysfunction, metabolic derangements, and interstitial fibrosis. However, the weight of evidence leans toward the development of fibrosis, possibly caused by the accumulation of a peroxidase acid schiff (PAS)-positive glycoprotein, leading to myocardial hypertrophy and diastolic dysfunction.
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PMID:Diabetic cardiomyopathy. 985 79


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