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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin A deficiency produces anemia and altered iron status. In this study with rats we tested two hypotheses regarding vitamin A deficiency: (1) that it impairs erythropoiesis, leading to an increased red cell turnover, and (2) that it inhibits the glycosylation of transferrin. Erythropoietic activity was assessed indirectly by determining the myeloid:erythroid ratio in bone marrow smears, the number of erythroid colonies in the red pulp of spleen, the blood reticulocyte index, and zinc protoporphyrin and plasma transferrin receptor concentrations. Transferrin glycosylation was assessed by measuring the sialic acid content of transferrin. The effects of vitamin A deficiency were compared with those of iron deficiency. Iron deficiency produced anemia and low iron levels in organs. Vitamin A deficiency produced low levels of plasma and hepatic retinol, and it induced decreased plasma total iron-binding capacity and raised iron levels in tibia and spleen. Short- but not long-term iron deficiency reduced the number of erythroid colonies in spleen; vitamin A deficiency had no influence. Neither iron nor vitamin A deficiency influenced the myeloid:erythroid ratio in bone marrow smears and the blood reticulocyte production. Plasma transferrin receptor and erythrocyte zinc protoporphyrin concentrations were not affected by vitamin A deficiency but increased with iron deficiency. Vitamin A deficiency did not stimulate erythrocyte breakdown, as indicated by unaltered plasma lactate dehydrogenase activity and reduced plasma total bilirubin levels. Both vitamin A and iron deficiencies raised the proportion of multiple sialylated transferrins in plasma. Thus, we have not found evidence that vitamin A deficiency affects erythropoiesis and erythrocyte turnover. The iron accumulation in spleen and bone marrow may be related to reduced iron transport due to inhibition of transferrin synthesis rather than inhibition of transferrin sialylation.
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PMID:Indicators of erythrocyte formation and degradation in rats with either vitamin A or iron deficiency. 1082 45

Strong enhancement of the pathogenicity of an antierythrocyte monoclonal antibody was observed after infection of mice with lactate dehydrogenase-elevating virus. While injection of the antierythrocyte antibody alone induced only moderate anemia, concomitant infection with this virus, which is harmless in most normal mice, led to a dramatic drop in the hematocrit and to death of infected animals. In vitro and in vivo analyses showed a dramatic increase in the ability of macrophages from infected mice to phagocytose antibody-coated erythrocytes. These results indicate that viruses can trigger the onset of autoimmune disease by enhancing the pathogenicity of autoantibodies. They may explain how unrelated viruses could be implicated in the etiology of autoantibody-mediated autoimmune diseases.
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PMID:Exacerbation of autoantibody-mediated hemolytic anemia by viral infection. 1084 87

In this study we described four cases of bilateral ectropion in pigeons that were investigated in Greece. Anemia, leukocytosis, and increased levels of enzymes lactate dehydrogenase, aspartate aminotransferase, creatine phosphokinase, and total serum proteins were found. Chlamydial elementary bodies were observed by modified Ziehl-Neelsen stain in direct smears of conjunctiva, liver, and spleen as well as in yolk sac samples after egg inoculation with eyelid material. Histologically, significant hyperplasia of the conjunctival epithelium was observed. Using immunohistochemical methods, chlamydial antigen was revealed in eyelid, liver, and spleen paraffin sections. This study suggests that Chlamydia spp. was the causative agent that induced ectropion.
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PMID:Chlamydia-induced bilateral ectropion of the inferior eyelids in pigeons. 1087 18

The authors submit the case-history of a 29-year-old man, followed up on account of liver steatosis with a toxic-nutritional etiology who developed, after previous increased physical exertion and alcohol abuse, fever associated with major muscular weakness. Gradually he developed an amental delirious state which was evaluated as suspect delirium tremens. Fever of 40-41 degrees C continued, the patient developed muscular rigidity, tremor and hypotension. After intubation during which succinylcholine was administered, the patient's condition deteriorated further with a rise of temperature and muscular rigidity. The patient developed acute renal failure with anuria and the necessity of repeated haemodialyses and severe acidosis of the mixed type on account of which he was intubated and switched to artificial ventilation. According to the case-history clinical and laboratory picture of the disease (extremely high creatine kinase activity, hyperkalaemia, acidosis, hepatorenal failure) malignant hyperthermia was suspected. After a single intravenous injection of sodium dantrolene, 2.5 mg/kg, the temperature dropped and within 24 hours the patient was afebrile. Gradually the acidosis improved, the blood pressure became stabilized and artificial ventilation was no longer used. The patient was discharged after 34 days in hospital in a state of cardiopulmonary compensation with mild polyuria but without signs of retention of nitrogenous substances with sideropenic anaemia and marginal creatine kinase and lactate dehydrogenase values. Within one month after discharge the laboratory values reached normal levels and only slight muscular weakness and greater fatiguability persisted.
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PMID:[An attack of malignant hyperthermia caused by a combination of the effects of succinylcholine, increased physical exertion and alcohol abuse]. 1095 47

There is no report in which three episodes of delayed hemolytic transfusion reaction (DHTR) occurred from multiple antibodies to red cells (RBCs) in the course of treatment of a patient. This paper describes episodes of anemia and hyperbilirubinemia in concert with the development of three alloantibodies in a multiple transfused patient. The patient was a 71-year-old male suffering from valvular heart disease and hemophilia B with a history of transfusions. Although he received compatible RBCs from 14 donors as judged by a crossmatch test using the albumin-antiglobulin method, three episodes of DHTR occurred after surgery. The first hemolytic episode on day 7 after surgery was due to anti-Di(a) because of clinical and laboratory evidence which included jaundice, sudden increases in total bilirubin (T-Bil) and lactate dehydrogenase (LD) levels, and a decrease (2.2 g/dl) in hemoglobin (Hb) level. The second hemolytic episode on day 16 resulted from newly producted anti-Jk(b). The patient experienced fever, fatigue, nausea and anorexia, and laboratory data showed a second increase in T-Bil, a second decrease (3 g/dl) in Hb, and moderate elevations of blood urea nitrogen (BUN) and creatinine (CRE) levels. The third hemolytic episode on day 39 was due to anti-E. The patient complained of fever and fatigue and had a third unexplained drop (1.5 g/dl) in Hb despite no bleeding. This is the first reported case in which three episodes of DHTR occurred from different red cell antibodies.
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PMID:Three episodes of delayed hemolytic transfusion reactions due to multiple red cell antibodies, anti-Di, anti-Jk and anti-E. 1103 71

Haemolysis is the major cause of anaemia in acute Plasmodium falciparum malaria, destroying both parasitized and non-parasitized erythrocytes. Oxidative stress on erythrocytes is considered an important mechanism of haemolysis. Since non-parasitized erythrocytes are also destroyed, the extracellular environment of the erythrocyte may be a contributor to the oxidative stress. To examine the influence of extracellular factors on oxidative stress and haemolysis, baseline values of erythrocyte thio-barbituric acid-reactive substance (ETBAR) and haemolytic indices such as plasma haemoglobin and lactate dehydrogenase (LDH) were estimated in 19 children in Orissa (India) with acute P. falciparum malaria (haemoglobin level < or = 70 g/L). The indices were measured after incubating cross-matched isogroup adult control erythrocytes with patient's plasma, and patient's erythrocytes with adult control plasma both in presence of and in absence of t-butyl hydroperoxide (t-BHP). The procedure was repeated in the blood of 19 age- and sex-matched non-malarial children. Baseline plasma LDH, haemoglobin and ETBAR concentrations were significantly greater in malaria patients than non-malarial children (P < 0.001 for all). Post-incubation values of ETBAR and plasma haemoglobin were significantly higher (P < 0.05) when adult control erythrocytes were incubated with patient plasma, and plasma haemoglobin was significantly higher (P < 0.05) in incubates of patient erythrocytes with adult control plasma, than their respective pre-incubation values when incubated in absence of t-BHP. These differences were not noticed in the incubates of non-malarial children with healthy adult control samples. When incubated in presence of t-BHP all the post-incubation values in the patients were significantly higher than their respective pre-incubation values and post-incubation values without t-BHP (P < 0.001). In non-malarial control samples, only ETBAR concentration was higher than their respective pre-incubation and post-incubation values without t-BHP (P < 0.01). All the values for post-incubation samples with t-BHP were significantly higher in patients than controls (P < 0.001). In post-incubation samples of control erythrocytes and patient plasma in presence of t-BHP, ETBAR correlated inversely with pre-incubation haptoglobin values (P < 0.001). Thus, plasma of acute malaria patients appears to contain pro-oxidants, which may contribute to extracellular oxidative stress on both parasitized and non-parasitized erythrocytes.
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PMID:Presence of pro-oxidants in plasma of patients suffering from falciparum malaria. 1119 57

To characterize the toxicity of phosphorothioate antisense oligodeoxynucleotides ([S]ODNs) in vivo, the mice received intravenously 26-mer bcr-abl antisense oligodeoxynucleotides (1 mg/mice/day) for 9 consecutive days. The organs and tissues were removed on the indicated days (+1, +7, +30) after the treatment. Our investigation revealed middle elevation of aminotransferases activity, lactate dehydrogenase level, total protein level and globulin level, decrease of glucose, albumin and blood urea nitrogen level in the peripheral blood. The mild anaemia and thrombocytopenia were observed too. The most significant treatment-related findings in the antisense treated mice were splenomegaly, reactive hepatitis and atrocytosis of kidney. These findings together with previous results demonstrate little and temporary toxicity effects mainly in organs known from cumulating of [S]ODNs.
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PMID:[Adverse effects of parenteral administration of antisense oligonucleotides]. 1186 87

Peripheral T-cell proliferative disease/lymphoma is a group of diseases which exhibits heterogeneity in clinical manifestations, pathological findings and outcomes. They are highly associated with the Epstein-Barr virus (EBV) infection. It is likely that EBV plays an important role in the tumorigenesis. From January 1997 through April 2000, we identified 100 patients. One hundred healthy age- and sex- matched controls were selected. Serologic tests for the EBV infection and the study of EBV genomes in circulating non-T cells (CD3- cells), T cells (CD3+ cells), and T-cell subsets (CD4+ and CD8+ cells) were performed. The main features were prolonged fever, weight loss, hepatosplenomegaly, lymphadenopathy, multiorgan involvement, anemia, and high serum alkaline phosphatase and lactate dehydrogenase. Fifty-one patients had an aggressive course and died; median survival was 21 months. Chemotherapy was not effective in improving survival. Anti-viral capsid antigen-IgG and anti-early antigen-IgG were significantly elevated, whereas there was no significant difference in anti-EBV nuclear antigen. EBV internal repeat-1 region (IR-1) in the peripheral blood CD3+ cells was detected in 65% of the patients but in none of the controls. For the CD3- cells, EBV IR-1 was detected in 88% of the patients and 50% of the controls. Among twenty-five patients whose CD3+ cells were positive for EBV IR-1, 6 (24%) showed EBV IR-1 in only CD4+ cells, 6 (24%) in only CD8+ cells, and 13 (52%) in both CD4+ and CD8+ cells. The 30-bp deletion variant of the EBV latent membrane protein-1 gene was significantly higher in the patients than in the controls. These data support the chronic infective process. The EBV which is dormant in non-T cells may infect T cells and contribute to the pathogenesis of disease in a select group of patients.
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PMID:Epstein-Barr virus-associated peripheral T-cell and NK-cell proliferative disease/lymphoma: clinicopathologic, serologic, and molecular analysis. 1199 79

Renal cell cancer is resistant to most forms of therapy. Cytokine therapy with either interleukin-2 or interferon-alpha yields the best results, with response rates from 10% to 20%. Therapy is not without toxicity, which means that the majority of patients treated with cytokines suffer toxicity without any therapeutic benefit. Recent endeavors have tried to find new ways to identify responders to cytokine therapy. Prognostic factors, such as good performance status, lack of anemia, normal calcium, normal lactate dehydrogenase, and prior nephrectomy, correlate with an increased likelihood of responding to cytokine therapy. Recent studies have examined whether altered subpopulations of lymphocytes, the presence of eosinophils, or altered levels of cytokines can predict response to cytokine therapy. Although prior nephrectomy does correlate with improved survival while the patient is receiving cytokine therapy, it is unclear if this is due to a significant alteration in the tumor's response to cytokine or some unrelated benefit from surgery. Further studies are needed to confirm the current immune parameters and disease characteristics that suggest a better response to cytokine therapy.
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PMID:Prognostic factors for biologic therapy in kidney cancer. 1208 17

A rare case of thrombotic microangiopathy in a patient with hemophagocytic syndrome is reported. An 18-year-old girl was admitted following prolonged fever, watery diarrhea, abdominal discomfort, and a 2-week history of rhinorrhea, cough, and painful cervical lymph nodes. Anemia, thrombocytopenia, jaundice, hepatomegaly, and mild azotemia developed within 2 weeks of admission. The diagnosis of a reactive hemophagocytic syndrome, probably secondary to infection, was made based on the findings of bone marrow examination. Extensive investigation failed to identify a causative agent. The disease initially responded rapidly to intravenous steroids and high-dose immunoglobulin therapy but relapsed soon after tapering of the steroids. Although her condition improved again on resumption of treatment with high-dose steroids, nephrotic range proteinuria and microscopic hematuria developed after the steroids were tapered. Fragmented erythrocytes were seen in peripheral blood with elevated serum lactate dehydrogenase and decreased serum haptoglobin concentrations. The results of subsequent renal pathology examination were also compatible with thrombotic microangiopathy. The disease course finally stabilized after a course of pulse methylprednisolone therapy. Immune hyperactivity, particularly hypercytokinemia and monocyte hyperactivity, could have accounted for the development of thrombotic microangiopathy in this case. Only strong immunosuppressive therapy can control such disease activity.
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PMID:Thrombotic microangiopathy in hemophagocytic syndrome: a case report. 1210 56


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