scholarly journals Central neuraxial blockade in chronic immune thrombocytopenic purpura: Platelet count or function and the concept of rebalanced hemostasis

2016 ◽  
Vol 17 (2) ◽  
pp. 48
Author(s):  
Tasneem Dhansura ◽  
Nabila Shaikh ◽  
Tarana Shaikh ◽  
Mohtasib Madaoo
1993 ◽  
Vol 21 (03n04) ◽  
pp. 251-255 ◽  
Author(s):  
K. Yamaguchi ◽  
H. Kido ◽  
T. Kawakatsu ◽  
T. Fukuroi ◽  
M. Suzuki ◽  
...  

We studied the effect of Kami-kihi-to (Jia-Wei-Gui-Pi-Tang) on the production of autoantibodies in ten patients with chronic immune thrombocytopenic purpura. After administration of Kami-kihi-to, platelet count was increased in seven of the ten patients ( p <0.05). Using Western blotting, we demonstrated the disappearance of autoantibody reaction with antigen in one patient. However, platelet-associated IgG was decreased in eight of ten patients ( p <0.05). Kami-kihi-to appears to promote the suppression of autoantibodies in patients with chronic immune thrombocytopenic purpura. No side effects were observed in any patient. Thus, Kami-kihi-to may be a useful and safe drug in the management of chronic immune thrombocytopenic purpura.


Blood ◽  
1993 ◽  
Vol 81 (11) ◽  
pp. 2872-2877 ◽  
Author(s):  
K Fujisawa ◽  
P Tani ◽  
L Piro ◽  
R McMillan

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.


Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 4660-4660 ◽  
Author(s):  
Katherine E. Hampilos ◽  
Joshua Corn ◽  
Wendy Hodsdon ◽  
Elise N. Anderes ◽  
Ryan P. Roop ◽  
...  

Abstract Background: The leaves of Carica papaya have been used to treat thrombocytopenia in the critical phase of Dengue fever in areas where the virus is endemic. This case series describes the use of C. papaya leaf liquid extract (CPLE) as an adjunctive therapy for four patients receiving standard-of-care treatment for chronic immune thrombocytopenic purpura (ITP). Case 1: A 67 yo M diagnosed with ITP in 1999 presented on 8/17/2013 with bruising and a platelet count of 5 x 103/ml. No response was seen to prednisone 125 mg QD. He subsequently received a course of IV Ig and IV methylprednisolone sodium succinate, but platelet count remained under 5 x 103/ml on 9/13/13. He was prescribed CPLE 3,000 mg QD on 9/30/13. Platelets increased to 148 x 103/ml by 10/8/13 and remained elevated above 250 x 103/ml for five months. Case 2: A 21 yo F diagnosed with ITP in 2011 underwent splenectomy on 11/7/13. Despite this intervention, platelet count decreased to 95 x 103/ml on 4/22/14. She was prescribed CPLE 3,000 mg QD as a monotherapy and by 5/8/14, platelet count increased to 156 x 103/ml. CPLE was discontinued and platelet count remained in normal range at 146 x 103/ml on 5/15/14. Case 3: A 56 yo M diagnosed with ITP in 2011 was referred for splenectomy on 9/19/12 after his platelet count dropped below 40 x 103/ml despite corticosteroid therapy. Prior to surgery, on 9/30/12, he initiated CPLE 3,000 mg QD in addition to prednisone 10 mg QD. On 11/7/12, pre-surgical labs revealed a platelet count of 115 x 103/ml and splenectomy was cancelled due to adequate platelet count. Platelets remained elevated over threshold for surgery for over four months. Case 4: A 60 yo F diagnosed with ITP in 1992 was referred for splenectomy and refused the procedure on 6/5/13. The patient's platelet count was 86 x 103/ml while on prednisone 10 mg QD and she was prescribed CPLE 3,000 mg QD. Her platelet count increased to 109 x 103/ml on 5/12/13 but subsequently dropped to 98 x 103/ml on 5/20/13. CPLE was discontinued at this time due to lack of beneficial action on platelet count. Conclusion: CPLE may prove beneficial in the management of refractory ITP for patients interested in alternative therapy before progressing to second-line treatments. Based on the association observed in these cases, a larger clinical trial is warranted to evaluate CPLE as an adjunctive therapy in chronic ITP. Disclosures No relevant conflicts of interest to declare.


Blood ◽  
1993 ◽  
Vol 81 (11) ◽  
pp. 2872-2877 ◽  
Author(s):  
K Fujisawa ◽  
P Tani ◽  
L Piro ◽  
R McMillan

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.


Blood ◽  
2001 ◽  
Vol 97 (7) ◽  
pp. 2171-2172 ◽  
Author(s):  
Robert McMillan ◽  
Jennifer Lopez-Dee ◽  
Joseph C. Loftus

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.


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