scholarly journals Erythroid progenitors in adult chronic pure red cell aplasia: relationship of in vitro erythroid colonies to therapeutic response

Blood ◽  
1984 ◽  
Vol 64 (1) ◽  
pp. 71-77 ◽  
Author(s):  
C Lacombe ◽  
N Casadevall ◽  
O Muller ◽  
B Varet
Keyword(s):  
Myeloproliferative Disorders ◽  
Pure Red Cell Aplasia ◽  
Type I ◽  
Red Cell ◽  
Type Ii ◽  
Erythroid Progenitors ◽  
Chronic Myeloproliferative Disorders ◽  
Type Iii ◽  
Red Cell Aplasia

Twenty-two cases of idiopathic chronic pure red cell aplasia (PRCA) in adults have been studied to evaluate their erythroid progenitors in vitro using the plasma clot technique. Three types of culture growth patterns were observed and classified as follows. Type I: showing a normal number of autologous CFU-E; type II: CFU-E and BFU-E were detectable but constantly decreased; type III: CFU-E and BFU-E were undetectable. The results were reproducible when patients were studied on two or more occasions. A strong correlation was found between the in vitro growth of autologous erythroid colonies and the results of immunomodulating therapy in 18 evaluable patients. A constant response to immunomodulating treatment was observed in type I patients. A constant failure of treatment was observed in type III patients, whereas results of therapy were unpredictable in type II patients. Two patients with chronic PRCA associated with thymoma and three with chronic myeloproliferative disorders were also studied. Patients with PRCA and thymoma behaved in vitro like type I patients. Patients with chronic myeloproliferative disorders exhibited very low numbers or no CFU-E or BFU-E (type II or III). These data support the hypothesis that at least two mechanisms are responsible for PRCA--one immunologically mediated and the other resulting from a stem cell defect. Moreover, they suggest that the study of erythroid progenitors in vitro might be useful in predicting the immunosuppressive therapy effect in adult chronic PRCA.

scholarly journals Erythroid progenitors in adult chronic pure red cell aplasia: relationship of in vitro erythroid colonies to therapeutic response

Blood ◽  
1984 ◽  
Vol 64 (1) ◽  
pp. 71-77 ◽  
Author(s):  
C Lacombe ◽  
N Casadevall ◽  
O Muller ◽  
B Varet
Keyword(s):  
Myeloproliferative Disorders ◽  
Pure Red Cell Aplasia ◽  
Type I ◽  
Red Cell ◽  
Type Ii ◽  
Erythroid Progenitors ◽  
Chronic Myeloproliferative Disorders ◽  
Type Iii ◽  
Red Cell Aplasia

Abstract Twenty-two cases of idiopathic chronic pure red cell aplasia (PRCA) in adults have been studied to evaluate their erythroid progenitors in vitro using the plasma clot technique. Three types of culture growth patterns were observed and classified as follows. Type I: showing a normal number of autologous CFU-E; type II: CFU-E and BFU-E were detectable but constantly decreased; type III: CFU-E and BFU-E were undetectable. The results were reproducible when patients were studied on two or more occasions. A strong correlation was found between the in vitro growth of autologous erythroid colonies and the results of immunomodulating therapy in 18 evaluable patients. A constant response to immunomodulating treatment was observed in type I patients. A constant failure of treatment was observed in type III patients, whereas results of therapy were unpredictable in type II patients. Two patients with chronic PRCA associated with thymoma and three with chronic myeloproliferative disorders were also studied. Patients with PRCA and thymoma behaved in vitro like type I patients. Patients with chronic myeloproliferative disorders exhibited very low numbers or no CFU-E or BFU-E (type II or III). These data support the hypothesis that at least two mechanisms are responsible for PRCA--one immunologically mediated and the other resulting from a stem cell defect. Moreover, they suggest that the study of erythroid progenitors in vitro might be useful in predicting the immunosuppressive therapy effect in adult chronic PRCA.

scholarly journals Diphenylhydantoin-induced pure red cell aplasia

Blood ◽  
1985 ◽  
Vol 65 (4) ◽  
pp. 789-794 ◽  
Author(s):  
EN Dessypris ◽  
S Redline ◽  
JW Harris ◽  
SB Krantz
Keyword(s):  
Colony Formation ◽  
Cytotoxic Effect ◽  
Autologous Blood ◽  
Pure Red Cell Aplasia ◽  
Red Cell ◽  
Erythroid Progenitors ◽  
Red Cell Aplasia ◽  
Serum Igg ◽  
Allogeneic Marrow

Abstract The pathogenesis of diphenylhydantoin-induced pure red cell aplasia was investigated in the case of a 32-year-old man who developed pure red cell aplasia while he was under treatment with diphenylhydantoin. The patient's serum IgG purified from serum drawn at the time of diagnosis suppressed normal allogeneic marrow colony-forming (CFU-E) and burst- forming (BFU-E) and autologous blood BFU-E growth in vitro only in the presence of diphenylhydantoin. This IgG-diphenylhydantoin complex had no effect on CFU-GM growth in vitro. Normal IgG or patient's IgG purified from serum drawn after the remission of red cell aplasia had no effect on erythroid colony formation in vitro in the presence of diphenylhydantoin. The IgG-diphenylhydantoin complex exerted no direct cytotoxic effect on normal marrow erythroblasts, CFU-E, and BFU-E, nor did it interfere with the action of erythropoietin on marrow erythroblasts. These studies suggest that diphenylhydantoin-induced red cell aplasia is immunologically mediated through an IgG inhibitor, which requires the presence of the drug to suppress erythroid colony formation in vitro. This inhibitor seems to exert its effect on erythroid progenitors at or beyond the stage of differentiation of CFU- E, but not on erythroblasts.

scholarly journals Diphenylhydantoin-induced pure red cell aplasia

Blood ◽  
1985 ◽  
Vol 65 (4) ◽  
pp. 789-794 ◽  
Author(s):  
EN Dessypris ◽  
S Redline ◽  
JW Harris ◽  
SB Krantz
Keyword(s):  
Colony Formation ◽  
Cytotoxic Effect ◽  
Autologous Blood ◽  
Pure Red Cell Aplasia ◽  
Red Cell ◽  
Erythroid Progenitors ◽  
Red Cell Aplasia ◽  
Serum Igg ◽  
Allogeneic Marrow

The pathogenesis of diphenylhydantoin-induced pure red cell aplasia was investigated in the case of a 32-year-old man who developed pure red cell aplasia while he was under treatment with diphenylhydantoin. The patient's serum IgG purified from serum drawn at the time of diagnosis suppressed normal allogeneic marrow colony-forming (CFU-E) and burst- forming (BFU-E) and autologous blood BFU-E growth in vitro only in the presence of diphenylhydantoin. This IgG-diphenylhydantoin complex had no effect on CFU-GM growth in vitro. Normal IgG or patient's IgG purified from serum drawn after the remission of red cell aplasia had no effect on erythroid colony formation in vitro in the presence of diphenylhydantoin. The IgG-diphenylhydantoin complex exerted no direct cytotoxic effect on normal marrow erythroblasts, CFU-E, and BFU-E, nor did it interfere with the action of erythropoietin on marrow erythroblasts. These studies suggest that diphenylhydantoin-induced red cell aplasia is immunologically mediated through an IgG inhibitor, which requires the presence of the drug to suppress erythroid colony formation in vitro. This inhibitor seems to exert its effect on erythroid progenitors at or beyond the stage of differentiation of CFU- E, but not on erythroblasts.

scholarly journals Transepithelial Migration of Toxoplasma gondii Is Linked to Parasite Motility and Virulence

2002 ◽  
Vol 195 (12) ◽  
pp. 1625-1633 ◽  
Author(s):  
Antonio Barragan ◽  
L. David Sibley
Keyword(s):  
Toxoplasma Gondii ◽  
Ex Vivo ◽  
Type I ◽  
Type Ii ◽  
Long Distance ◽  
Type Iii ◽  
Migratory Capacity ◽  
Virulent Type ◽  
Parasite Motility

After oral ingestion, Toxoplasma gondii crosses the intestinal epithelium, disseminates into the deep tissues, and traverses biological barriers such as the placenta and the blood-brain barrier to reach sites where it causes severe pathology. To examine the cellular basis of these processes, migration of T. gondii was studied in vitro using polarized host cell monolayers and extracellular matrix. Transmigration required active parasite motility and the highly virulent type I strains consistently exhibited a superior migratory capacity than the nonvirulent type II and type III strains. Type I strain parasites also demonstrated a greater capacity for transmigration across mouse intestine ex vivo, and directly penetrated into the lamina propria and vascular endothelium. A subpopulation of virulent type I parasites exhibited a long distance migration (LDM) phenotype in vitro, that was not expressed by nonvirulent type II and type III strains. Cloning of parasites expressing the LDM phenotype resulted in substantial increase of migratory capacity in vitro and in vivo. The potential to up-regulate migratory capacity in T. gondii likely plays an important role in establishing new infections and in dissemination upon reactivation of chronic infections.

Response of Pure Red Cell Aplasia to Cyclophosphamide After Failure of Mycofenolate Mofetil in a Patient With Polyglandular Syndrome Type I

2013 ◽  
Vol 35 (8) ◽  
pp. e338-e340 ◽  
Author(s):  
Elizaveta M. Orlova ◽  
Maria A. Kareva ◽  
Maria A. Melikyan ◽  
Elena Boyakova ◽  
Valentina A. Peterkova ◽  
...  
Keyword(s):  
Pure Red Cell Aplasia ◽  
Type I ◽  
Syndrome Type ◽  
Red Cell ◽  
Red Cell Aplasia

Three Types of Hereditary Antiterombin III Deficiency

1979 ◽  
Author(s):  
I. Nagy ◽  
H. Losonczy
Keyword(s):  
Antithrombin Iii ◽  
Clinical Signs ◽  
Type I ◽  
Type Ii ◽  
Type Iii ◽  
Basic Activity ◽  
At Iii ◽  
And Function

The authors detected in the last seven years 15 patients with hereditary antithrombin III/AT III/ abnormality. All of them had typical clinical signs of recurrent arterious and venous thromboembolie. The abnormality inherited as an autosomal trait. Three types of the abnormality could be observed. In Type I both quantity and function of AT III were extremely decreased. In type II AT III is normal in quantity but abnormal in function. In Type III AT III is quantitatively normal and also its function seems normal as far as its basic activity is concerned /activity measured in absence of heparin/, but its abnormality becomes manifest in the presence of heparin in vitro/and also in vivo/. 5 of the patients belonged to Type I, 4 to Type II and 6 to Type III. In 60 examined family members of the 15 patients an abnormal AT III could be observed in 44, clinical signs in 23.The examination of AT III activity in the presence of a given amount of heparin ia of great importance in recognition of the different types of antithrombin III abnormalities.

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