Acquired haemophilia in a patient treated with interferon‐α for hepatitis C infection

Hepatitis C and history of FVIII inhibitor development in a long‐term cohort of Brazilian patients with haemophilia A

“…We believe that in individuals who are already forced to maintain a constant state of tolerogenic response due to repeated exposure to exogenous FVIII, another persistent exposition to a non-self antigen (HCV) would facilitate the break of this tolerogenic mechanism, resulting in immune reactions towards administered FVIII. Indeed, HCV inducing development of FVIII inhibitors leading to acquired haemophilia A has been reported 8,9. In contrast, HIV was associated with significantly fewer inhibitor development in patients with haemophilia A, probably due to immunosuppression caused by the virus, unlike what occurs in HCV infection 10.…”

Activated prothrombin complex concentrate to treat bleeding events in acquired hemophilia A: BAHAS study

“…The association of AHA with interferon used to treat hepatitis C has been widely reported. [17][18][19][20] Many of AHA patients had at least one risk factor for thrombosis. Not surprisingly, according to Spanish registry data, close to 30% of AHA patients were under anticoagulant or antiplatelet treatment before AHA diagnosis.…”

“…The hallmarks of our cohort are comparable to those of other series, with a notable prevalence of subjects >60‐year‐old, and underlying conditions classically associated with AHA, especially autoimmune diseases. The association of AHA with interferon used to treat hepatitis C has been widely reported 17–20 . Many of AHA patients had at least one risk factor for thrombosis.…”

“…treatment than those of Grade ≤2 (n = 5) (74.000[6.500-189.063] UF vs. 47.000[19.500-144.250] UF, 19 vs. 8[3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] doses, and 14[6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] days vs. 5[1][2][3][4][5][6][7][8][9][10][11] days).When considering all the bleeding events overall, aPCC stopped bleeding and eradicated pain in 48 of 51 (96.0%) and 42 of 45 (93.3%) cases, respectively (there were 6 bleeding not related to pain, epistaxis, and rectorrhagia). Hemoglobin was partially recovered at 23 days after the start of aPCC therapy: 11.3 (9.9-12.5) g/dl vs. 10.3 (8.3-11.1) g/dl at AHA diagnosis (n = 16).…”

Development of anti‐factor XIII antibodies in a patient with hereditary factor XIII deficiency receiving therapy for chronic hepatitis C

“…This strongly suggests that the immune response to FXIII was induced by exposure to IFN and/or ribavarin. Although there is no previous report of a FXIII inhibitor developing in a FXIII-deficient patient receiving treatment for chronic active hepatitis, there are reports of FVIII inhibitors developing after such therapy in patients with or without hereditary haemophilia A [6][7][8][9][10]. We suspect that the capacity of IFN to modulate immune responses contributed to development of one or more antibodies that facilitated rapid clearance and/or neutralized infused FXIII.…”