PubMed Health⌕ Search

PubMed · 7137120

Trapped plasma in the microhematocrit.

Abstract

The amount of trapped plasma in the microhematocrit red blood cell column of samples from 25 normal individuals and 102 patients was investigated. The mean value for the normal individuals was 1.53%, and the mean values for the samples from the patient groups ranged from 1.41% to 1.82%. These groups included patients with sickle cell disease, iron deficiency, and hereditary spherocytosis. There was an inverse correlation between trapped plasma and the MCH in the samples from patients with iron-deficiency (MCH less than or equal to 25.0 pg). These findings have relevance to the determination of the PCV and derived red blood cell indices.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

T C Pearson, D L Guthrie. 1982. Trapped plasma in the microhematocrit.. https://doi.org/10.1093/ajcp%2F78.5.770

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

[Erythropoietin is a novel therapeutic option in the treatment of anemia caused by small cell lung cancer].

Anemia is very common among patients with malignant tumors, due to the disease and chemotherapy. Anemia decreases the patient's quality of life. Erythropoietin therapy is accessible in Hungary for the treatment of chemotherapy-induced anemia in patients suffering from small cell lung cancer. In our case report we present the case of a 62-year-old female small cell lung cancer patient with severe anemia, treated by erythropoietin-beta. The erythropoietin treatment provided the possibility of effective chemo- and radiotherapy. The patient's quality of life greatly improved due to the lack of the symptoms of anemia. The adequate use of erythropoietin is of great help to the physician in the management of small cell lung cancer patients, by improving the quality of life.

Anemia, Hypochromic↗

Increased plasma transferrin, altered body iron distribution, and microcytic hypochromic anemia in ferrochelatase-deficient mice.

Patients with deficiency in ferrochelatase (FECH), the last enzyme of the heme biosynthetic pathway, experience a painful type of skin photosensitivity called erythropoietic protoporphyria (EPP), which is caused by the excessive production of protoporphyrin IX (PPIX) by erythrocytes. Controversial results have been reported regarding hematologic status and iron status of patients with EPP. We thoroughly explored these parameters in Fechm1Pas mutant mice of 3 different genetic backgrounds. FECH deficiency induced microcytic hypochromic anemia without ringed sideroblasts, little or no hemolysis, and no erythroid hyperplasia. Serum iron, ferritin, hepcidin mRNA, and Dcytb levels were normal. The homozygous Fechm1Pas mutant involved no tissue iron deficiency but showed a clear-cut redistribution of iron stores from peripheral tissues to the spleen, with a concomitant 2- to 3-fold increase in transferrin expression at the mRNA and the protein levels. Erythrocyte PPIX levels strongly correlated with serum transferrin levels. At all stages of differentiation in our study, transferrin receptor expression in bone marrow erythroid cells in Fech(m1Pas) was normal in mutant mice but not in patients with iron-deficiency anemia. Based on these observations, we suggest that oral iron therapy is not the therapy of choice for patients with EPP and that the PPIX-liver transferrin pathway plays a role in the orchestration of iron distribution between peripheral iron stores, the spleen, and the bone marrow.

Anemia, Hypochromic↗