Erythrocytic Hypoplasia Research Articles

Differential pathogenicity of two feline leukemia virus subgroup A molecular clones, pFRA and pF6A.

F6A, a molecular clone of subgroup A feline leukemia virus (FeLV) is considered to be highly infectious but weakly pathogenic. In recent studies with a closely related subgroup A molecular clone, FRA, we demonstrated high pathogenicity and a strong propensity to undergo recombination with endogenous FeLV (enFeLV), leading to a high frequency of transition from subgroup A to A/B. The present study was undertaken to identify mechanisms of FeLV pathogenesis that might become evident by comparing the two closely related molecular clones. F6A was shown to have an infectivity similar to that of FRA when delivered as a provirus. Virus load and antibody responses were also similar, although F6A-infected cats consistently carried higher virus loads than FRA-infected cats. However, F6A-infected cats were slower to undergo de novo recombination with enFeLV and showed slower progression to disease than FRA-infected cats. Tumors collected from nine pF6A- or pFRA-inoculated cats expressed lymphocyte markers for T cells (seven tumors) and B cells (one tumor), and non-T/B cells (one tumor). One cat with an A-to-A/C conversion developed erythrocyte hypoplasia. Genomic mapping of recombinants from pF6A- and pFRA-inoculated cats revealed similar crossover sites, suggesting that the genomic makeup of the recombinants did not contribute to increased progression to neoplastic disease. From these studies, the mechanism most likely to account for the pathologic differences between F6A and FRA is the lower propensity for F6A to undergo de novo recombination with enFeLV in vivo. A lower recombination rate is predicted to slow the transition from subgroup A to A/B and slow the progression to disease.

Serum erythropoietin level: Relationships to blood hemoglobin concentration and erythrocytic activity of the bone marrow

The question as to whether the serum concentration of erythropoietin is relatively high for the degree of anemia in patients with erythrocytic hypoplasia has regained interest, since recombinant human-like erythropoietin has become available as a drug for replacement therapy. We have compared the concentration of serum immunoreactive erythropoietin in nonrenal anemic patients with erythrocytic hypoplasia (22 cases) or active erythropoiesis (82 cases). In both groups a negative correlation was determined between the blood hemoglobin concentration and the logarithm of the erythropoietin concentration. However, the two regression lines were not identical, and the serum erythropoietin concentration was significantly higher for the degree of anemia in the patients with erythrocytic hypoplasia. Additional measurements in four patients suffering from acute leukemia with marrow failure showed that the erythropoietin concentration decreased towards the values observed in anemic patients with active erythropoiesis when the erythron recovered in the early phase of complete remission. These data support the idea that, independent of the O2 offer, the proliferating erythrocytic progenitors by negative feedback lower the blood level of erythropoietin.

Bone Marrow Findings in Acquired Immunodeficiency Syndrome (AIDS)

Bone marrow aspirates and biopsies from 35 AIDS/AIDS-related complex patients, consisting primarily of intravenous drug abusers, were studied. The most common findings included hypercellularity (86%), plasmacytosis (63%), reticular fibrosis (50%), and lymphocytosis (37%) occasionally admixed with histiocytes. Granulocytic hyperplasia was present in 27 patients (77%). Erythrocytic hypoplasia was observed in 15 patients (43%). Megaloblastic changes of intermediate form were seen in two cases and serous fat atrophy was noted in another three patients. One M. tuberculosis granuloma, a foreign body granuloma and two granulomas of undetermined etiology were seen, each in separate patients. A previously unreported focal vascular proliferation was seen in one case. The majority of cases showed increased stainable iron. Some of our findings are at variance with previous reports. This may reflect differences in patient population, geographic distribution, risk factors and epidemiologic mode in our cases.

Bone marrow transplantation with major ABO blood group incompatibility using erythrocyte depletion of marrow prior to infusion

Twenty-five patients with major ABO blood group incompatibility between donor and recipient underwent allogeneic bone marrow transplantation using erythrocyte depletion of the bone marrow infusate prior to administration. Over 95% of the original erythrocyte content of the marrows was removed, while retaining 75% of the mononuclear cell content and 57% of the granulocyte-monocyte colony-forming units. Recipients, well hydrated and premedicated with corticosteroids, diphenhydramine, and mannitol, tolerated infusions well. The frequency of engraftment, rate of recovery of peripheral blood leukocytes, granulocytes, and platelets, and the incidence of graft-versus-host disease was similar to that observed following ABO blood group compatible bone marrow transplantation. Erythroid development following ABO blood group incompatible transplantation was significantly impaired until hemagglutinins fell to 1:4 or lower, at which time recovery of erythrocytes was detected in the peripheral blood. The erythrocyte hypoplasia associated with incompatible hemagglutinins was temporary. Erythrocyte purging is a safe and effective technique to perform bone marrow transplantation across major ABO blood group incompatibilities.

Bone Marrow Transplantation With Major ABO Blood Group Incompatibility Using Erythrocyte Depletion of Marrow Prior to Infusion

Twenty-five patients with major ABO blood group incompatibility between donor and recipient underwent allogeneic bone marrow transplantation using erythrocyte depletion of the bone marrow infusate prior to administration. Over 95% of the original erythrocyte content of the marrows was removed, while retaining 75% of the mononuclear cell content and 57% of the granulocyte-monocyte colony-forming units. Recipients, well hydrated and premedicated with corticosteroids, diphenhydramine, and mannitol, tolerated infusions well. The frequency of engraftment, rate of recovery of peripheral blood leukocytes, granulocytes, and platelets, and the incidence of graft-versus-host disease was similar to that observed following ABO blood group compatible bone marrow transplantation. Erythroid development following ABO blood group incompatible transplantation was significantly impaired until hemagglutinins fell to 1:4 or lower, at which time recovery of erythrocytes was detected in the peripheral blood. The erythrocyte hypoplasia associated with incompatible hemagglutinins was temporary. Erythrocyte purging is a safe and effective technique to perform bone marrow transplantation across major ABO blood group incompatibilities.

Thymoma

In 54 patients with thymoma, the factors having the greatest bearing on prognosis were presence or absence of gross tumor invasion or an associated clinical syndrome of myasthenia gravis, anemia due to erythrocytic hypoplasia or hypogammaglobulinemia. Of 17 patients with invasive tumors, 14 were either dead of tumor or living with disease, while 34 of 37 patients with encapsulated tumors were either living or dead of other causes without evidence of neoplasm. A clinical syndrome associated with thymoma was present in 15 patients. Thymectomy appeared to have little if any effect on the syndrome; in three instances the syndrome appeared after removal of the thymoma. Analysis of the histological findings, including type of epithelium, degree of lymphocytic infiltration and presence of other patterns such as rosettes, perivascular spaces and germinal centers, showed that there was no consistent relationship between the microscopic appearance of thymomas and their clinical behavior. Knowledge of the striking variations in histopathologic features is necessary in differential diagnosis.

Annotation: pure red cell aplasia.

Pure red cell aplasia (PRCA) was first described by Kaznelson (1922) as an anemia due to an almost complete cessation of erythropoiesis, but without leukopenia or thrombocytopenia. This condition usually can be clearly distinguished from aplastic anemia in which low blood white cell and platelet concentrations accompany the anemia (Van Der Weyden and Firkin, 1972). In PRCA the bone marrow has an isolated absence of erythroblasts with normal granulocytopoiesis and megakaryocytopoiesis (DiGiacomo et al., 1966; Jacobs et al., 1959), whereas in aplastic anemia all three hematopoietic lineages are markedly reduced (Van Der Weyden and Firkin, 1972). In children PRCA has been called “chronic (congenital) hypoplastic anemia,” the Diamond-Blackfan anemia, or erythrogenesis imperfecta (Diamond and Blackfan, 1938; Gasser, 1957; Tsai and Levin, 1957). In adults it has been termed isolated aplastic anemia, aplastic crisis, erythroblastopenia, erythrophthisis, chronic erythrocytic hypoplasia, red cell aplastic anemia, or red cell agenesis (Gasser, 1957; Tsai and Levin, 1957). Although these cases could represent a variety of pathogenetic mechanisms they all have in common an isolated absence of marrow erythroblasts and are now considered together as cases of PRCA.

Chronic Erythrocytic Hypoplasia Following Pernicious Anemia

Abstract A case of chronic erythrocytic hypoplasia of the bone marrow following Addisonian pernicious anemia, treated for 30 years, is reported. Treatment with different erythropoietic agents was completely unsuccessful. The possibility of a causal relationship is suggested.

Chronic erythrocytic hypoplasia in adults: Review of literature and report of a case

Chronic erythrocytic hypoplasia in adults: Review of literature and report of a case

The treatment of refractory anemia with cobalt.

Case Reports1 February 1956THE TREATMENT OF REFRACTORY ANEMIA WITH COBALTE. D. THOMASE. D. THOMASSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-44-2-412 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptSince Waltner and Waltner1 first discovered that cobalt produces polycythemia in animals, physicians have attempted to employ this element in the therapy of anemia. One group of anemias that has attracted particular attention is that of the refractory anemias. Most investigators have found cobalt to have no therapeutic value in this type of anemia. Berk, Burchenal and Castle2 treated five patients with refractory anemia and hypercellular marrow with 300 mg. of cobaltous chloride daily with no reticulocyte response or rise in blood values. Weissbecker3 found cobalt to be of no value in six cases of aplastic anemia.However, a few...Bibliography1. WaltnerWaltner KK: Kobalt und Blut, Klin. Wchnschr. 8: 313, 1929. CrossrefGoogle Scholar2. BerkBurchenalCastle LJHWB: Erythropoietic effect of cobalt in patients with or without anemia, New England J. Med. 240: 754-760, 1949. CrossrefMedlineGoogle Scholar3. Weissbecker L: Kobalttherapie der Anamien, Proceedings of the Third International Congress of the International Society of Hematology, Cambridge, England, 1950, 1951, Grune & Stratton, New York, pp. 68-70. Google Scholar4. SeamanKoler AJRD: Acquired erythrocytic hypoplasia: a recovery during cobalt therapy, Acta haemat. 9: 153, 1953. CrossrefMedlineGoogle Scholar5. Seaman AJ: Cobalt and cortisone therapy of chronic erythrocytic hypoplasia, Am. J. Med. 13: 99, 1952. CrossrefGoogle Scholar6. RohnBond RJWH: Observations of some hematological effects of cobalt-iron mixtures, Journal Lancet 73: 317, 1953. Google Scholar7. ThomasHersheyAbbateLoofbourow EDFBAMJR: Chromatographic determination of nucleotides in the suspending medium from irradiated yeast, J. Biol. Chem. 196: 575, 1952. CrossrefMedlineGoogle Scholar8. BomfordRhoads RRCP: Refractory anaemia, clinical and pathological aspects, Quart. J. Med. 10: 175, 1941. Google Scholar9. Osgood EE: Drug induced hypoplastic anemias and related syndromes, Ann. Int. Med. 39: 1173, 1953. LinkGoogle Scholar10. Hunter FT: Chronic exposure to benzene (benzol). II. The clinical effects, J. Indust. Hyg. and Toxicol. 21: 331, 1939. Google Scholar11. KleinbergGordonCharipper WASHA: Effect of cobalt on erythropoiesis in anemic rabbits, Proc. Soc. Exper. Biol. and Med. 42: 119, 1939. CrossrefGoogle Scholar12. RoelsenOhlsen EAS: Achrestic anemia, Acta med. Scandinav. 150: 17, 1954. CrossrefMedlineGoogle Scholar13. LoebMooreDubach VCVR: The physiologic evaluation and management of chronic bone marrow failure, Am. J. Med. 15: 499, 1953. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Boston, Massachusetts*Received for publication December 18, 1954.From the Department of Medicine, Harvard Medical School, the Medical Clinic, Peter Bent Brigham Hospital, Boston.†Cobaltous chloride was supplied through the courtesy of the Smith, Kline & French Laboratories.‡Present address: Mary Imogene Bassett Hospital, Cooperstown, N. Y. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byDerivation of a chronic oral reference dose for cobaltStimulation of Hemopoiesis in Aplastic Anemia by Hormones and Other AgentsDie Panmyelopathie und andere Formen der PancytopenieThe Effect of Some Erythropoietic Agents on the ‘Tissue’ Tension of OxygenThe treatment of refractory anemia or bone marrow failure 1 February 1956Volume 44, Issue 2Page: 412-419KeywordsAnemiaAplastic anemiaBloodBone marrowChloridesCirrhosisFolic acidHospital medicinePolycythemiaReticulocytes Issue Published: 1 February 1956 PDF downloadLoading ...

Drug induced hypoplastic anemias and related syndromes.

Excerpt The object of this paper is to give a concise review of current concepts of the diagnosis and therapy of hypoplastic anemias and the closely related conditions known as erythrocytic hypopla...

Hypoplastic anemias and related syndromes caused by drug idiosyncrasy.

Hypoplastic anemia is essentially the simultaneous occurrence of erythrocytic, granulocytic, and thrombocytic hypoplasia. These conditions may occur separately or in any combination. An absolute decrease in the lymphocytic series of cells is often associated, although they are relatively less affected as a rule. Agents that produce one of these syndromes will often produce two or more of these syndromes simultaneously in different persons or in larger doses. DIAGNOSIS Pure erythrocytic hypoplasia is characterized by normocytic anemia with a decrease in reticulocytes in the blood to few or none and a great decrease in the number of nucleated erythrocytes in the aspirated marrow. Granulocytic hypoplasia is characterized by a decrease in the absolute number of cells of the granulocytic series in the peripheral blood and also a great decrease in the number of these cells in the aspirated bone marrow. When the total number of neutrophils in the blood falls below

Acquired erythrocytic hypoplasia: a recovery during cobalt therapy; report of two cases with review of the literature.

Acquired erythrocytic hypoplasia: a recovery during cobalt therapy; report of two cases with review of the literature.

Cobalt and cortisone therapy of chronic erythrocytic hypoplasia

Cobalt and cortisone therapy of chronic erythrocytic hypoplasia