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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Moderately increased blood levels of endogenous erythropoietin (Epo) usually induce complete restoration of renal anemia after successful kidney transplantation. With good graft function erythropoiesis is maintained by normal Epo serum levels. Persistent anemia can be related to iron deficiency, low excretory graft function, and high dosage of immunosuppressive agents leading to marrow suppression or nephrotoxicity. Acute early rejection is associated with a fall in serum Epo and abrogation of reticulocytosis. About 15% of recipients fail to exhibit the normal feedback regulation and develop a mostly transient posttransplant erythrocytosis. Both an increased sensitivity of erythrocytic progenitors to Epo and inappropriate Epo secretion by the native kidneys may account for this overshooting reaction.
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PMID:Erythropoiesis and erythropoietin levels in renal transplant recipients. 202 70

Erythroid colony growth in the presence and absence of erythropoietin was compared in 23 patients with primary proliferative polycythaemia (PPP), nine with idiopathic erythrocytosis, 10 with secondary polycythaemia, 15 with pseudopolycythaemia and in 76 normal subjects. Erythroid colonies growing without erythropoietin stimulation (endogenous erythroid colonies) from peripheral blood (BFU-E) were found in 20 of 22 patients with PPP and in two of seven with idiopathic erythrocytosis. None was found in secondary polycythaemia, pseudopolycythaemia, or in normal subjects. Small numbers of endogenous colony forming units-erythroid (CFU-E) (though not BFU-E) were cultured from the bone marrow of three of 24 normal subjects, suggesting that peripheral blood cultures provide a more specific indicator of clonal erythropoiesis. Peripheral blood endogenous erythroid colony growth is an effective and convenient means of distinguishing patients with clonal erythrocytosis and may be of particular value when iron deficiency obscures the diagnosis of PPP on conventional criteria.
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PMID:Erythroid colony growth from peripheral blood and bone marrow in polycythaemia. 226 65

Hematologic management of adults with cyanotic congenital heart disease has received little recent attention. The lack of practical therapeutic guidelines prompted us to consolidate our observations on 124 cyanotic adults for general physicians, cardiologists, and hematologists who care for these patients. Specific attention focused on regulation of erythrocyte mass and concepts of compensated and decompensated erythrocytosis, symptoms of deficient tissue oxygen transport, hyperviscosity and iron deficiency, the potential relation between elevated hematocrit levels and brain injury, hemostasis, urate metabolism, and renal function. Cerebral infarction was not seen in any patient. Phlebotomy is best reserved for treatment of symptomatic hyperviscosity. Iron therapy is indicated for symptomatic iron deficient erythropoiesis. Abnormal hemostatic mechanisms are the rule. Antithrombotic medications have little or no role in treatment. Hyperuricemia is the result of abnormal renal uric acid excretion not urate overproduction, and serves as a marker of abnormal renal function. Drugs that promote urate excretion are the preferred maintenance treatment in symptomatic hyperuricemic patients.
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PMID:Adults with cyanotic congenital heart disease: hematologic management. 304 12

The haematological indices of Peninsular Arabs (United Arab Emirate Nationals, Yemeni and Omani) have been examined. The most outstanding feature, seen in 40-50% of all subjects, was one of hypochromia, microcytosis associated with erythrocytosis. In approximately 5% the hypochromia was severe (MCH 19-22 pg) and 20% of these were found to have beta thalassaemia trait. In 10% of subjects the hypochromia was moderate (MCH 23-24 pg) and beta thalassaemia was confirmed in only 10%. The remaining 25% had a mild hypochromia (MCH 25-27 pg) and no beta thalassaemia was detected. The cause of the hypochromia in subjects with a normal Hb A2 (30% of the total population) is probably alpha thalassaemia, firstly because in those patients with an MCH of 19-24 pg the other haematological parameters are statistically the same as those with proven beta thalassaemia and, secondly, in those with an MCH of 25-27 pg iron deficiency is not common (6% of the population). The degree and pattern of the distribution of hypochromia of the three major ethnic groups of the Peninsular Arabs could be explained either by different alpha and beta thalassaemia genes being operative or by different degrees of inbreeding of the same genes.
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PMID:Thalassaemia genes in Peninsular Arabs. 383 31

The red blood cell distribution width (RDW) has been proposed as an additional variable that would improve the initial classification of anemia. Microcytic anemias with an elevated RDW (greater heterogeneity) were used to distinguish iron deficiency from heterozygous thalassemia, which was said to have a normal RDW (more homogeneous). The authors attempted to classify their population of microcytic cases using the RDW as a major variable, but found only limited utility. While most of the iron-deficient cases had an increased RDW, almost one-half of the thalassemia cases also were classified as microcytic heterogeneous (increased RDW). The authors also found that target cells, erythrocytosis, and the ratios alone or in combination with the RDW were not specific in separating heterozygous thalassemia from iron deficiency. They conclude that a sequential evaluation (to include iron and hemoglobin studies) of cases of microcytosis is still needed.
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PMID:Limitations of red blood cell distribution width (RDW) in evaluation of microcytosis. 395 99

Although full blood counts (FBC) are among the most commonly performed laboratory tests, the contribution of routine FBCs to the diagnosis of new problems is controversial. This study represents a unique linkage of a consultant haematology team, reviewing all abnormal blood counts, to an organization providing ambulatory health care to 350,000 patients. The objective was to establish the underlying clinical disorders responsible for all abnormal FBCs during a 2-month period, and to estimate the impact of the haematology team on the diagnostic work-up and management of newly identified problems. 572 (2.55%) of the 22,454 FBCs were abnormal. Of these, 357 showed microcytosis, caused by iron deficiency (58%), thalassaemia minor (35%), inflammation (6%) or chronic renal failure (1%). The most common causes of normocytic anaemia (25 patients) were disseminated malignancy and acute blood loss; of macrocytosis (27 patients), chronic liver disease and cancer; of erythrocytosis (16 patients), chronic hypoxia; of thrombocytopaenia (48 patients), chronic liver disease and ITP; of thrombocytosis (47 patients), iron deficiency and inflammation; of leukopaenia or pancytopaenia (20 patients), cirrhosis and disseminated malignancy; and of leukocytosis (26 patients), chronic leukaemias in the elderly and infection in children. Major new haematological abnormalities were encountered in 0.24% of all blood counts, representing about one new diagnosis per day. Routine blood counts do contribute to the health care of a population. Screening for haematological disease through a central clinical laboratory covering a large high-risk ambulatory population offers a cost-effective way of searching for serious clinical problems, alerting the primary physicians of their existence, and offering advice in continued evaluation and problem management.
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PMID:The haematologist as watchdog of community health by full blood count. 779 88

The authors describe an 18 year old athlete, a carrier of Hasharon haemoglobinopathy, pathology which had been checked in some ascendants too. Such a haemoglobinopathy, which has at first been verified in Ashkenazy Hebrew people and is nowadays rather common in North East Italy, shows clinical and laboratory features which are slightly or not at all mentioned in the literature. The leading reference point in the disease's development is the connection between splenomegaly and repetitive low erythrocytosis with serum iron deficiency and increase of the reticulocyte number. The same laboratory data had been observed in his father and in his paternal grandmother; both of them proved to te heterozygous carriers of Hasharon haemoglobinopathy. In all cases we caught the diagnostic validation by the means of isoelectrophoresis involving haemoglobin lysate in polyacrylamide gel. The authors think that the Hasharon shape they verified may be a variant of the classic phenotype: the splenomegaly and erythrocytosis may signify a brisk and primitive erythropoiesis with increasing reticulocytes, which might compensate for the anomalous synthesis of the alpha chains. Serum iron deficiency may signify an increase of the iron consumption. Moreover, the authors do not exclude the possibility of further associational abnormalities.
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PMID:[Hasharon hemoglobinopathy in a family]. 780 84

Patients with HIV infection frequently develop clinically significant anemia, either as a manifestation of the HIV or as a result of therapy with medications such as zidovudine. Therapy with recombinant human erythropoietin can increase hemoglobin levels in these patients, decreasing transfusion requirements and improving some aspects of the quality of life. Once erythropoietin therapy is started, it is important to monitor patients carefully for the development of iron deficiency and erythrocytosis.
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PMID:The clinical application of recombinant erythropoietin in the HIV-infected patient. 785 17

A case of posttransplant erythrocytosis in a 51-year-old diabetic man is described. This problem, which can occur in 5 to 15% of renal transplant patients, can result from a contracted plasma volume (diuretics, pressure natriuresis, or glycosuria) or from a true elevation in red blood cell mass. Once the diagnosis of true erythrocytosis is made by a radiolabeled red blood cell mass study, secondary causes such as hypoxia, liver disease, polycythemia rubra vera, renal artery stenosis, and cystic kidney disease should be excluded. Posttransplant erythrocytosis has only been observed in renal transplant recipients and appears to be more frequent with cyclosporine compared with azathioprine therapy. An inappropriately high level of erythropoietin has been described in some, but not all patients, suggesting stimulation of erythropoietin production as the mechanism. Posttransplant erythrocytosis can be associated with an increased incidence of thrombotic events. The presence of this potential complication has prompted intervention to maintain the hematocrit below 50 to 55%. Measures such as discontinuation of diuretics as well as better control of blood pressure and plasma glucose should be used to facilitate the correction of extracellular volume contraction. Phlebotomy has been the most accepted intervention to intermittently lower the hematocrit when needed, but this can lead to iron deficiency. Newer therapeutic modalities are now being used to treat the problem medically. Theophylline, which reduces adenosine-mediated erythropoietin synthesis, is effective but may be associated with side effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Posttransplant erythrocytosis: case report and review of newer treatment modalities. 831 81

A group of 67 children with cyanotic congenital heart disease (CCHD) were studied, and 35 were given iron treatment according to a regimen that gives iron to patients with a hematocrit (Hct) below 60%. The patients were categorized as iron-deficient and iron-sufficient according to their transferrin saturation and ferritin values. The pretreatment hemoglobin (Hb) and Hct values of the groups were similar. The mean Hct was nearly three times as much as the mean Hb in the iron-sufficient group and more than three times as much as the Hb in the iron-deficient group. Excessive erythrocytosis in the iron-deficient group was impressive. Mean corpuscular volume (MCV) values were below 72.7 fl in all of the iron-deficient patients. After treatment the Hb, Hct, transferrin saturation, and ferritin increased significantly in both groups, with the increments greater in the iron-deficient group. Increments in the erythrocyte (RBC) count were significant in the iron-sufficient group but insignificant in the iron-deficient one. Increments of MCV in the iron-deficient group were significant but insignificant in the iron-sufficient group. Our study demonstrated that prediction of Hb, RBC count, and MCV, measurements of which are easy and inexpensive and require little blood, can suffice for the diagnosis of iron deficiency in patients with CCHD without altering systemic perfusion.
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PMID:Parameters of iron deficiency in children with cyanotic congenital heart disease. 866 27


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