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 79 year-old Japanese man was admitted because of brownish urine and Raynaud phenomenon. Laboratory data showed mild anemia with reticulocytosis, positive direct Coombs test against anti-C3, elevated level of lactate dehydrogenase, undetectable level of serum haptoglobin and low titer of cold agglutinin (1:256 at 4 degrees C), the immunoglobulin subclass of which was IgM. Cold agglutinin disease is usually associated with very high levels of cold agglutinins, the specificity of which is anti-I. This case had low titer cold agglutinin disease due to anti-HI cold agglutinin.
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PMID:[Low titer cold agglutinin disease due to anti-HI antibody and a review of this disease in Japan]. 754 Feb 24

We have administered Isobutyramide as a suspension over a period of 3 months, from a starting dose of 50 mg/kg/day up to 150 mg/kg/day, to four adult sickle cell (SS) anemia patients. The maximum dose was maintained for 3 weeks. The blood counts remained stable and the Hb F levels decreased slightly. The G gamma levels increased at the end of the trial, suggesting activation of the G gamma gene at the highest dose of Isobutyramide. Three patients showed a stable rate of hemolysis, while in one patient, an increase of lactate dehydrogenase occurred. None of the patients experienced pain crisis or organ-specific crisis, but all four complained about mild epigastric burning and a bitter taste. After the first month of treatment one patient complained about intolerable epigastric discomfort which was relieved by Omeprazole. Another patient complained about increasing dyspepsia in the 12th week leading to the termination of the trial. Oral Isobutyramide administration does not qualify as an effective treatment of SS patients.
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PMID:Isobutyramide therapy in patients with sickle cell anemia. 754 4

Recombinant human interleukin-6 (rhIL-6) is a pluripotent cytokine with proinflammatory, antitumor, and growth factor effects. Clinical investigations of rhIL-6 either alone as immunotherapy or as a colony-stimulating factor in conjunction with chemotherapy have shown a dose-dependent, rapid onset, and largely reversible decrease in venous hematocrit levels. In an effort to determine the mechanism for the rhIL-6-associated anemia, we measured red blood cell volume serially in patients receiving rhIL-6 at either 30 micrograms/kg/day as a 120-hour continuous intravenous infusion (renal cell carcinoma) or 100 micrograms/kg/d intravenously over 1 hour for 5 days (melanoma) as part of two separate phase II trials. Radioisotope dilution assays with 51Cr-labeled autologous red blood cells and hemolysis screens were performed on day 1 before the initiation of therapy and on day 5 shortly before the end of therapy. In the 6 patients studied, the mean decrease in hemoglobin concentration was 1.9 +/- 0.94 g/dL. The mean decrease in the hematocrit level was 6% +/- 2% and the mean increase in total blood volume was 731 +/- 337 mL. These changes were explained by a mean decrease in red blood mass of 106 +/- 109 mL and a mean increase in plasma volume of 743 +/- 289 mL. The decrease in red blood cell mass was largely explained by phlebotomy during the hospitalization, but was not statistically significant (paired t-test, P = .06). All other changes were statistically significant (P < .05). Simple regression analysis indicated that the decrease in hematocrit level and increase in plasma volume were related (y = -1.78 - .0066X; R = -.74). Measurements of lactate dehydrogenase, bilirubin, haptoglobin, and reticulocyte counts and serial stool hemoccults did not indicate hemolysis or blood loss. We conclude that the anemia caused by IL-6 is caused by an increase in plasma volume.
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PMID:Interleukin-6-associated anemia: determination of the underlying mechanism. 763 34

Twenty chronic hemodialysis patients with renal anemia (hematocrit < 25%) received recombinant human erythropoietin (40 IU/kg body weight 3 x weekly) intravenously after each dialysis. Prior to and at 4, 8 and 12 weeks after commencement of erythropoietin therapy, hematocrit together with hemostasis and microhemolysis parameters were determined. There were significant increases in hematocrit, platelet count and platelet retention, but a significant fall in the initial clearly prolonged bleeding time. Free plasma hemoglobin likewise increased. Conversely, lactate dehydrogenase, prothrombin time, fibrinogen, antithrombin III activity, protein C activity and protein S concentration were all unaltered. The positive effect on bleeding time and platelet retention is most probably caused by an increase in adenosine diphosphate due to the hematocrit-dependent rise in the blood shear stress via physiologic microhemolysis (raised free plasma hemoglobin).
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PMID:Influence of recombinant human erythropoietin on hematological and hemostatic parameters with special reference to microhemolysis. 777 78

The aim of this study was to evaluate the possible prognostic relevance of thymidine kinase serum levels (s-TK), an indirect marker of proliferative activity, in myelodysplastic syndromes (MDS). S-TK levels were monitored by means of a radioenzyme assay in 90 patients affected by MDS (22 refractory anaemia, RA; 17 RA with ring sideroblasts, RARS; 21 RA with blast excess, RAEB; 15 RAEB in transformation, RAEB-T; 15 chronic myelomonocytic leukaemia, CMMoL). Mean s-TK levels (U/microliter) measured at diagnosis were 11.9 +/- 12.6 for RA, 11.4 +/- 13.6 for RARS, 19.9 +/- 28.4 for RAEB, 39.6 +/- 34.3 for RAEB-T and 77.7 +/- 69.7 for CMMoL (normal values < 5 U/microliter). With the only exception of a weak relationship with lactate dehydrogenase, no correlation was found between initial s-TK values and other clinical or laboratory parameters, such as age, haemoglobin, white blood cell or platelet count, percentage of bone marrow blasts. MDS patients with s-TK > 38 U/microliters, a cut-off level selected by means of ROC statistical analysis, showed a significantly shorter survival than those with s-TK < 38 U/microliter (8.2 v 37.4 months, respectively; P < 0.0001). In particular, transformation in acute myeloid leukaemia (AML) occurred in 17/21 (81%) of patients with s-TK > 38 U/microliters and 9/69 (13%) of those with lower levels at diagnosis (P < 0.0001), independently of FAB subtype. High s-TK levels were also useful to predict evolution in AML during the course of the disease in patients with normal initial values. Multivariate analysis confirmed the independent prognostic value of s-TK on both overall survival and risk of acute transformation. We conclude that s-TK may be an important prognostic factor in MDS, strongly correlated with development of AML.
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PMID:Prognostic relevance of serum thymidine kinase in primary myelodysplastic syndromes: relationship to development of acute myeloid leukaemia. 778 74

Development of pathology varies widely between different strains of mice after intracerebral inoculation with the so-called 'docile' isolate of Lymphocytic Choriomeningitis (LCM) virus. The C3HeB/FeJ and B10. Br/SgSnJ mouse strains have been of special interest because they display autoimmune haemolytic anaemia with varying degrees of apparent immunological involvement. In this report, we examined the role of CD4+ T helper cells in this autoimmune response by treating mice with the CD4-specific GK1.5 monoclonal antibody. We also determined if polyclonal activation of B lymphocytes, induced either by LCM virus or by lactate dehydrogenase-elevating virus, another well known B cell activator, correlated with the development of anaemia in these mice. Our results strengthened the central role of the immune system in the anaemia in C3H mice by showing that depletion of CD4+ cells largely, if not completely, abrogated this anti-erythrocyte autoimmune reaction. As reported by others, we found that the anaemia was more mild in B10.BR mice than in C3H mice. However, we could not confirm the difference in the degree of B lymphocyte polyclonal activation between these mice. Furthermore, lactate dehydrogenase-elevating virus had no apparent effect on erythrocytes, even though this virus also induced a sharp increase in plasma IgG levels.
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PMID:Involvement of CD4+ cells in lymphocytic choriomeningitis virus-induced autoimmune anaemia and hypergammaglobulinaemia. 784 Aug 52

The crucial first step in management of multiple myeloma is to be certain regarding the diagnosis. Multiple myeloma must be distinguished from monoclonal gammopathy of undetermined significance (MGUS) and smoldering multiple myeloma. Therapy should be administered to patients with advanced and active myeloma involving anemia, osteolysis or renal failure. Chemotherapy with a single agent (melphalan) is the preferred initial treatment for overt, symptomatic multiple myeloma. Cytostatic drug combinations produce a higher response rate, but survival and remission during are the same compared with melphalan/prednisone therapy. However, in patients with renal failure and/or poor prognostic factors (advanced stage, elevated beta 2-microglobulin, high bone marrow plasma cell labeling index, high levels of C-reactive protein and lactate dehydrogenase and/or nodular pattern of bone marrow infiltration), combined treatment with adriamycin, vincristine and prednisone should be administered to prevent nephrotoxicity and attain a rapid paraprotein decrease. Alpha interferon treatment as maintenance seems to prolong the duration of the plateau state after response to chemotherapy, but apparently does not prolong survival. Allogeneic bone marrow transplantation involves significant early mortality (50%); the risk of graft versus host disease, infections and renal failure is a problem, and relapse is common. High dose chemotherapy followed by autologous bone marrow transplantation or peripheral blood stem cell reinfusion may prolong survival and free time to progression, but, to date, there are no indications of cure. This therapeutic procedure, therefore, should be considered for randomized trials for young patients with poor prognostic factors.
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PMID:[Diagnosis and therapy of multiple myeloma: current aspects]. 789 48

Quinine-induced immune thrombocytopenia with hemolytic uremic syndrome (HUS) is a recently defined clinical entity. In this paper we have attempted to characterize the natural history and laboratory abnormalities typical of quinine-induced immune thrombocytopenia associated with hemolytic uremic syndrome in nine patients experiencing ten episodes of the disease. In addition, review of other reported cases of probable quinine-induced HUS is presented. The disease was characterized by the onset of chills, diapheresis, nausea and vomiting, abdominal pain, decreased urine output, and petechiae following quinine exposure. All patients experience significant anemia, severe thrombocytopenia, increased lactate dehydrogenase, elevated serum creatinine, and oliguria. Quinine-dependent platelet-reactive antibodies were identified in eight of nine using flow cytometry. Unexpectedly, drug-dependent antibodies reactive with red cells and granulocytes were identified in four and eight patients, respectively. All patients were treated with plasma exchange (range 1-12 procedures), and seven required hemodialysis. All survive without residual abnormality. Our experience with nine patients with quinine-induced HUS and the nine additional cases reported by others and reviewed in this paper establishes this condition as a distinct clinical entity. Adult patients presenting with HUS should routinely be asked about exposure to quinine in the form of medication or beverages. The mechanism by which quinine-dependent antibodies produce renal failure is uncertain, but preliminary studies (described elsewhere) suggest that drug-induced antibodies reactive with endothelial cells and possibly margination of granulocytes in renal glomeruli may be responsible for this complication. The prognosis in quinine-induced HUS is better than in other forms of adult HUS.
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PMID:Quinine-induced immune thrombocytopenia with hemolytic uremic syndrome: clinical and serological findings in nine patients and review of literature. 797

Natural or deliberate activation of the immune system of pathogen-free mice markedly affected their response to an autoimmune-inducing stimulus. Specifically, mice immunized with rat red blood cells were found to make antibodies reactive with both rat and mouse erythrocytes. Animals housed for an extended period in a conventional environment developed an autoimmune response twice as fast as those kept in isolators. In an attempt to emulate this effect, mice kept in a sterile environment were infected with a potent polyclonal activator of B lymphocytes, lactate dehydrogenase-elevating virus, at the same time as they were inoculated with rat erythrocytes. Whereas uninfected animals developed a progressively increasing autoantibody titer, infected mice quickly attained high anti-erythrocyte autoantibody titers that remained rather constant. Contrary to circulating autoantibodies, bound anti-erythrocyte antibodies decreased with time. Virus infection enhanced all the IgG subclass responses, with the exception of IgG1, to both rat and mouse erythrocytes. None of the modifications of the autoimmune responses resulted in anemia.
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PMID:Influence of viral infection on anti-erythrocyte autoantibody response after immunization of mice with rat red blood cells. 802 15

This is a case report on an infant with de novo terminal deletions on the long arm of chromosome 14 and on the short arm of chromosome 20 [46, XX, del(14)(q32)del(20)(p11)]. Examination revealed that the infant had a peculiar face, a cleft and high palate, abnormal dentition, butterfly-like vertebral defects, finger anomalies, a simian line on the left hand, talipes equinovarus, deep plantar furrows, abnormally high values of alkali phosphatase and lactate dehydrogenase, mild anemia and psychomotor retardation. Comparing the present case with previously reported cases of a single deletion on chromosome 14q or chromosome 20p, the infant showed some symptomatic and dysmorphic features of both deletions.
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PMID:A case of a female infant with simultaneous occurrence of de novo terminal deletions on chromosome 14q and 20p. 831 27


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