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Prevalence of Anti‐human and Anti‐bovine Thrombin Antibodies in Healthy Individuals and Patients with End Stage Renal Disease
Author(s) -
Fareed Jawed,
Hoppensteadt Debra,
Cunanan Josephine,
Maddineni Jyothi,
Walenga Jeanine M,
Bick Rodger
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1124-c
Subject(s) - thrombin , antibody , medicine , end stage renal disease , coagulation , immunology , disease , gastroenterology , platelet
Topical use of bovine thrombin has been suggested to result in the generation of antibodies whose clinical importance is unclear. In a recent clinical trial, 20% of patients treated with bovine (B) thrombin developed anti‐(B) antibodies while less than 2% of human (H) thrombin‐treated patients developed anti‐(H) thrombin antibodies. To test the hypothesis that anti‐(B) thrombin antibodies pre‐exist in human blood, purified (B) (King Pharma, Bristol, TN) and (H) thrombins were used as capture probes to test samples from 200 healthy individuals and 240 end stage renal disease (ESRD) patients. Anti‐(H) antibodies occurred 4% of normals and 7% of ESRD patients while anti‐(B) thrombin antibodies occurred in 12% of normals and 19% of ESRD patients. Both normals and ESRD patients were free of thrombin treatment. These results show that the prevalence of anti‐(B) thrombin antibodies as captured by ELISA is higher than anti‐(H) thrombin antibodies. This may be due to widespread exposure to (B) products or non‐specific interactions. Such findings underscore the importance of analyzing all patients in a clinical trial for anti(H)‐ and anti‐(B) thrombin antibodies. Non‐specific antibodies to (B) protein may pre‐exist in healthy normals or patients which may cross‐react to bovine proteins such as the coagulation factors and collagens. The antigenicity of recombinant (H) thrombin needs to be evaluated as its precursors are activated by venoms which may result in molecularly variant forms of thrombin.