The Results of Danazol Therapy in Patients with Chronic Immune Thrombocytopenic Purpura Who Failed with Corticosteroid Therapy

2007 ◽  
Vol 42 (4) ◽  
pp. 353
Author(s):  
Jae Beom Lee ◽  
Yeung-Chul Mun ◽  
Hea Sung Park ◽  
Moon Young Choi ◽  
Hye Jung Chang ◽  
...  
Keyword(s):  
Corticosteroid Therapy ◽  
Immune Thrombocytopenic Purpura ◽  
Thrombocytopenic Purpura ◽  
Chronic Immune Thrombocytopenic Purpura ◽  
Danazol Therapy

Danazol Therapy in Refractory Chronic Immune Thrombocytopenic Purpura

1987 ◽  
Vol 77 (1) ◽  
pp. 45-47 ◽  
Author(s):  
M.G. Mazzucconi ◽  
M. Francesconi ◽  
E. Falcione ◽  
A. Ferrari ◽  
G.M. Gandolfo ◽  
...  
Keyword(s):  
Immune Thrombocytopenic Purpura ◽  
Thrombocytopenic Purpura ◽  
Chronic Immune Thrombocytopenic Purpura ◽  
Danazol Therapy

scholarly journals The effect of therapy on platelet-associated autoantibody in chronic immune thrombocytopenic purpura

Blood ◽  
1993 ◽  
Vol 81 (11) ◽  
pp. 2872-2877 ◽  
Author(s):  
K Fujisawa ◽  
P Tani ◽  
L Piro ◽  
R McMillan
Keyword(s):  
Platelet Count ◽  
Immune Thrombocytopenic Purpura ◽  
Autoimmune Disorder ◽  
Major Effect ◽  
Autoantibody Production ◽  
Thrombocytopenic Purpura ◽  
Chronic Immune Thrombocytopenic Purpura ◽  
Effect Of Therapy ◽  
Danazol Therapy ◽  
Therapy Treatment

Abstract Chronic immune thrombocytopenic purpura (ITP) is an autoimmune disorder due to autoantibody-induced destruction of platelets. Several forms of therapy have been used, including corticosteroids, splenectomy, danazol, and a variety of immunosuppressants. We studied the mechanism of action of some of these treatments by evaluating patients' platelet- associated autoantibodies (PAAb) and platelet count before and serially following therapy. Treatment with corticosteroids, splenectomy, cyclophosphamide, and combination chemotherapy resulted in a progressive decrease in PAAb associated with an improvement in the platelet count, and appeared to act by primarily affecting autoantibody production. Conversely, PAAb levels either remained stable or increased during vincristine or danazol therapy despite improvement in the platelet count, suggesting that the major effect of these agents was decreased platelet removal by the reticuloendothelial (RE) system.

scholarly journals The effect of therapy on platelet-associated autoantibody in chronic immune thrombocytopenic purpura

Blood ◽  
1993 ◽  
Vol 81 (11) ◽  
pp. 2872-2877 ◽  
Author(s):  
K Fujisawa ◽  
P Tani ◽  
L Piro ◽  
R McMillan
Keyword(s):  
Platelet Count ◽  
Immune Thrombocytopenic Purpura ◽  
Autoimmune Disorder ◽  
Major Effect ◽  
Autoantibody Production ◽  
Thrombocytopenic Purpura ◽  
Chronic Immune Thrombocytopenic Purpura ◽  
Effect Of Therapy ◽  
Danazol Therapy ◽  
Therapy Treatment

Chronic immune thrombocytopenic purpura (ITP) is an autoimmune disorder due to autoantibody-induced destruction of platelets. Several forms of therapy have been used, including corticosteroids, splenectomy, danazol, and a variety of immunosuppressants. We studied the mechanism of action of some of these treatments by evaluating patients' platelet- associated autoantibodies (PAAb) and platelet count before and serially following therapy. Treatment with corticosteroids, splenectomy, cyclophosphamide, and combination chemotherapy resulted in a progressive decrease in PAAb associated with an improvement in the platelet count, and appeared to act by primarily affecting autoantibody production. Conversely, PAAb levels either remained stable or increased during vincristine or danazol therapy despite improvement in the platelet count, suggesting that the major effect of these agents was decreased platelet removal by the reticuloendothelial (RE) system.

Autoantibodies to αIIbβ3 in patients with chronic immune thrombocytopenic purpura bind primarily to epitopes on αIIb

Blood ◽  
2001 ◽  
Vol 97 (7) ◽  
pp. 2171-2172 ◽  
Author(s):  
Robert McMillan ◽  
Jennifer Lopez-Dee ◽  
Joseph C. Loftus
Keyword(s):  
Immune Thrombocytopenic Purpura ◽  
Cho Cells ◽  
Chinese Hamster ◽  
Surface Proteins ◽  
Platelet Glycoprotein ◽  
Beta Chain ◽  
Platelet Destruction ◽  
Thrombocytopenic Purpura ◽  
Platelet Surface ◽  
Chronic Immune Thrombocytopenic Purpura

Abstract Chronic immune thrombocytopenic purpura (ITP) is an autoimmune disease caused by platelet destruction resulting from autoantibodies against platelet surface proteins, particularly platelet glycoprotein IIb/IIIa (αIIbβ3). To localize the auto-epitopes on platelet αIIbβ3, the binding of autoantibodies to Chinese hamster ovary (CHO) cells expressing either αIIbβ3 or αvβ3was studied. Thirteen of 14 ITP autoantibodies bound only to CHO cells expressing αIIbβ3. Because these 2 integrins have the same beta chain (β3), these results show that most epitopes in chronic ITP are dependent on the presence of glycoprotein αIIb.

Helicobacter pylori infection and chronic immune thrombocytopenic purpura: long-term results of bacterium eradication and association with bacterium virulence profiles

Blood ◽  
2007 ◽  
Vol 110 (12) ◽  
pp. 3833-3841 ◽  
Author(s):  
Giovanni Emilia ◽  
Mario Luppi ◽  
Patrizia Zucchini ◽  
Monica Morselli ◽  
Leonardo Potenza ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Chronic Gastritis ◽  
Immune Thrombocytopenic Purpura ◽  
Long Term Results ◽  
Platelet Response ◽  
Related Factors ◽  
Thrombocytopenic Purpura ◽  
Platelet Recovery ◽  
Chronic Immune Thrombocytopenic Purpura ◽  
H Pylori

AbstractEradication of Helicobacter pylori may lead to improvement of chronic immune thrombocytopenic purpura (ITP), although its efficacy over time is uncertain. We report the results of H pylori screening and eradication in 75 consecutive adult patients with ITP. We also used molecular methods to investigate lymphocyte clonality and H pylori genotypes in the gastric biopsies from 10 H pylori–positive patients with ITP and 19 H pylori–positive patients without ITP with chronic gastritis. Active H pylori infection was documented in 38 (51%) patients and successfully eradicated in 34 (89%) patients. After a median follow-up of 60 months, a persistent platelet response in 23 (68%) of patients with eradicated infection was observed; 1 relapse occurred. No differences in mucosal B- or T-cell clonalities were observed between patients with ITP and control participants. Of note, the frequency of the H pylori cagA gene (P = .02) and the frequency of concomitant H pylori cagA, vacAs1, and iceA genes (triple-positive strains; P = .015) resulted statistically higher in patients with ITP than in control participants. All asymptomatic H pylori–positive patients with ITP were suffering from chronic gastritis. Our data suggest a sustained platelet recovery in a proportion of patients with ITP by H pylori eradication alone. Overrepresentation of specific H pylori genotypes in ITP suggests a possible role for bacterium-related factors in the disease pathogenesis.

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