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Biomedical subjects

A J Erslev

Publications and source records attributed to A J Erslev.

At least 73 records · Page 4Linked to original sources
PubMed1979

Erythropoietin levels in uremic nephric and anephric patients.

Erythropoietin titers were measured in anemic nephric and anephric patients undergoing chronic hemodialysis by utilizing a plasma concentration technique. In eight out of 11 anephric patients studied, decreased but detectable levels of erythropoietin were found, suggesting that extrarenal erythropoietin plays a role in the regulation of red cell production in anephric patients. In 14 nephric uremic patients, erythropoietin production was found to be more variable, with one group of eight patients having erythropoietin levels in the range for normal nonanemic individuals (3.9 to 15 mU/ml), and a second group of six patients with erythropoietin higher than normal (greater than 15 mU/ml). Both groups were found to be equally anemic, indicating that in the second group the bone marrow is less responsive to erythropoietin. The severity of secondary hyperparathyroidism was found to be higher in this second group, suggesting a role of PTH in the bone marrow unresponsiveness. A good correlation between biological and immunological erythropoietin activities was found in the plasma from normal subjects and uremic nephric and anephric patients.

Animals↗
PubMed1978

Erythropoietin concentration in amphotericin B-induced anemia.

Amphotericin B was given to six patients with systemic fungal infections. A dose averaging 1.78 g, administered from 42 to 144 days, was associated with a fall in hematocrit to a mean value of 25.8%. Despite this degree of anemia, no elevation of erythropoietin concentrations in urine or serum could be detected. Thus, amphotericin appears to cause anemia by inhibiting erythropoietin production rather than by suppressing bone marrow activity directly.

Adult↗
PubMed1978

Thrombocytopenia in polycythemic mice.

Significant and sustained thrombocytopenia in mice maintained in a polycythemic state with weekly injections of washed packed RBCs prompted the examination of the relationship between the observed thrombocytopenia and the polycythemic state. Platelet production was determined by measurement of 75SeM incorporation into platelets. Platelet survival was studied with 51Cr-labeled platelets. Platelet sequestration was assessed by measuring the trapped platelet 51Cr-bound radioactivity in the spleens of these animals. Blood volume was calculated by measuring the dilution of injected 59Fe-tagged RBCs. These studies failed to reveal decreased platelet production, a shortening of the platelet survival, or significant splenic pooling as factors contributing to the observed thrombocytopenia. The blood volumes in the polycythemic group of animals were 8.9% +/- 0.15 (1 S.D.) body weight vs. 6.4% +/- 0.69 in the normals (p less than 0.001). Contrary to what has been reported for hypoxia-induced polycythemia, our results indicate that transfusion-induced polycythemia does not cause thrombocytopenia by decreasing platelet production. We suggest instead that the observed thrombocytopenia is mainly due to dilution of the circulating platelet mass by the expanded blood volume.

Animals↗
PubMed1976

Aplastic anaemia with 'hot pockets'.

4 patients with chronic severe aplastic anaemia and with persistent foci of intense haematopoietic activity, so-called 'Hot Pockets', in their bone marrow were studied. In all patients the remainder of the bone marrow was morphologically and erythrokinetically hypoplastic. The cellular morphology in these 'Hot Pockets' displayed megaloblastic features and definite maturation abnormalities in erythroblasts, but no consistent changes in the myeloid or megakaryocytic series. The presence of persistent 'Hot Pockets' presents a conceptual challenge since these pockets contain multipotential stem cells capable of differentiation and self-renewal, but obviously incapable of repopulation of the bone marrow. In view of additional evidence for dyserythropoiesis in aplastic anaemia such as changes in erythroblast morphology and the production of macrocytes, fetal haemoglobin and complement sensitive cells, it seems likely that the bone marrow of aplastic anaemia patients is totally dyserythropoietic rather than hypoactive and that bone marrow transplantation in many cases may be both justified and necessary.

Adult↗
PubMed1975

Renal biogenesis of erythropoietin.

The widespread and ever expanding use of dialysis in the maintenance of patients with chronic renal disease has added an urgency to the study of the biogenesis of erythropoietin. It seems almost certain that erythropoietin could ameliorate, if not eliminate, the anemia of uremia, but unfortunately, erythropoietin is still not available in therapeutic quantities. Initially, erythropietin was though to be produced by the kidneys" but then the attention became directed at the liver. It was proposed that erythropoietin was produced there as an inactive precursor and that the kidney only acted as an oxygen sensor and as a producer of an erythropoietin-activating enzyme. Recent studies summarized here show that an isolated perfused kidney in the absence of any extrarenal substrate or precursor can synthesize erythropoietin. Consequently, it appears almost certain that the kidney is the endocrine organ of origin of erythropoietin. Further studies suggest that erythropoietin formation involves a phase of oxygen sensing and programming and a phase of synthesis. These phases probably occur in the same cell, and the renal cortex appears to be the most likely location for such cells. The current inability to extract erythropoietin from kidney homogenates is discussed but, unfortunately, not adequately explained.

Animals↗
PubMed1974

Fibrinogen Philadelphia. A hereditary hypodysfibrinogenemia characterized by fibrinogen hypercatabolism.

A new, autosomally inherited abnormal fibrinogen associated with hypofibrinogenemia has been described in several members of a family. Plasma fibrinogen measured either as thrombin-clottable protein or by immunodiffusion revealed a fibrinogen level ranging between 60 and 90 mg/100 ml. The thrombin time of plasma or purified fibrinogen was prolonged and only partially corrected by the addition of calcium. Purified fibrinogen prolonged the thrombin time of normal plasma. Fibrinopeptide release by thrombin was normal in rate and amount, but fibrin monomer aggregation was grossly disturbed, especially in a high ionic strength medium. We have designated this fibrinogen "fibrinogen Philadelphia." Acrylamide gel electrophoresis of mixtures of [121I]normal and [125I]abnormal fibrinogens revealed a slight increase in the anodal mobility of fibrinogen Philadelphia. Similarly, DEAE-cellulose chromatography showed slightly stronger binding of fibrinogen Philadelphia than normal. To elucidate the mechanism responsible for the low plasma fibrinogen concentration, simultaneous metabolic studies of autologous (patient) and homologous (normal) fibrinogen, labeled with 125I and 121I, respectively, were performed in two affected subjects. Autologous fibrinogen half-life was short and the fractional catabolic rate was markedly increased in both family members. In contrast, homologous fibrinogen half-life and fractional catabolic rate were normal. These metabolic studies demonstrate that rapid degradation of fibrinogen Philadelphia is largely responsible for the depressed levels of a plasma fibrinogen. This represents the first example of a mutant plasma protein in which the molecular defect is associated with an altered catabolism.

Adolescent↗