scholarly journals Acquired Factor VIII Inhibitor in a Non-Hemophilic Patient with Chronic Hepatitis C Viral Infection.

1999 ◽  
Vol 38 (3) ◽  
pp. 283-286 ◽  
Author(s):  
Kazuro SUGISHITA ◽  
Hiroyuki NAGASE ◽  
Toshiyuki TAKAHASHI ◽  
Katsu TAKENAKA ◽  
Yasushi SHIRATORI ◽  
...  
2000 ◽  
Vol 84 (10) ◽  
pp. 733-734 ◽  
Author(s):  
Franz Rommel ◽  
Josef Eberle ◽  
Helmut Schiffl ◽  
Michael Spannagl ◽  
Wolfgang Schramm ◽  
...  

1967 ◽  
Vol 18 (03/04) ◽  
pp. 354-363
Author(s):  
C. F Abildgaard ◽  
J Vanderheiden ◽  
A Lindley ◽  
F Rickles

SummaryThe plasma of a hemophilic patient with acquired factor VIII inhibitory activity was found to be time and temperature dependent, resistant to heat and stable on storage at -20°. Studies revealed cross-reactivitiy with 11 different mammalian plasmas but no cross-reaction was found with chicken plasma. The inhibitory activity of the plasma studied was neutralized by fresh normal plasma and normal serum but not by aged normal plasma or hemophilic plasma (20 patients). Comparison of the present findings with other reports suggest a difference in cross-reactivity of acquired inhibitors and inhibitory activity induced by immunization of animals.


2018 ◽  
Vol 6 (23) ◽  
pp. 17-21
Author(s):  
Abdussalam Shredi ◽  
Benjamin W. Elberson ◽  
Saif El Nawaa ◽  
Amr Ismail

Acquired inhibitors of coagulation are antibodies that either inhibit the activity or increase the clearance of a clotting factor. A hemorrhagic diathesis is a common clinical manifestation in affected patients. Acquired factor VIII inhibitor – or acquired hemophilia A – is a rare disorder and presents similarly to hemophilia A, though patients are less likely to develop hemarthroses. This inhibition is most commonly due to autoantibodies against coagulation factor VIII. These autoantibodies often occur in pregnancy, autoimmune disorders, solid tumors, and lymphoproliferative syndromes. Several drugs, including penicillins, phenytoin, and sulfa drugs, have also been associated with antibodies to factor VIII. Chronic infection with the hepatitis C virus (HCV), in addition to various degrees of liver inflammation and fibrosis, can have extrahepatic manifestations, especially autoimmune disorders. The most common hematological complications of HCV infection are thrombocytopenia, cryoglobulinemia, and anti-cardiolipin antibodies. A few cases of factor VIII inhibitors occurring in HCV patients have been reported, with a higher incidence after prolonged treatment with interferon-α. Here, we present a case of a patient with chronic untreated HCV infection developing acquired factor VIII deficiency.


Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4064-4064 ◽  
Author(s):  
Mercedes Maruscak ◽  
Barry Cohan ◽  
Linda Aghakhanian ◽  
Kalust Ucar

Abstract Rituximab is a monoclonal antibody directed against the CD20 antigen found on both malignant and normal B lymphocytes. It was given FDA approval in 1997 for relapsed or refractory, low grade or follicular, CD20+ non-Hodgkin’s lymphoma. We report the use of selective B-cell depletion with Rituximab on a fifty-nine year old male with acquired Factor VIII inhibitor who failed to respond to convential therapy. The patient presented with compartment syndrome of the left calf due to spontaneous severe hematoma, and was subsequently hospitalized. The patient was found to have a PTT of 86, Factor VIII <3%, and Factor VIII inhibitor 108 b.u. The patient had completed forty-eight weeks of interferon and ribavirin for Hepatitis C one month prior to admission. The PTT was normal nineteen months prior when liver biopsies were obtained. The patient was subsequently diagnosed with acquired Factor VIII deficiency, thought to be secondary to either the Hepatitis C infection or the interferon therapy. He improved with Factor VIII concentrate therapy, but did not spontaneously recover from the inhibitor. He had minimal response to IVIG. Rituxin was subsequently started (intravenously at 375mg/m2) once a week for eight consecutive weeks, and repeated every six months. After four cycles, a consistent response was documented by increased Factor VIII activity (as high as 62%), and decreased Factor VIII inhibitor (stable at <0.5%). The treatment was well tolerated, and no infusion related side effects were observed. The patient did well with no bleeding on maintenance therapy for approximately twenty-one months. Unfortunately, two weeks after completion of the fourth cycle the patient suffered a ruptured AAA, and upon surgical intervention became unresponsive and a right cerebral infarct was identified. The patient’s family subsequently discontinued life support and the patient died. This experience suggests that further investigation of Rituximab therapy in this defined population might benefit similar patients.


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