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Journal articles on the topic 'Acquired hemophilia'

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Published: 4 June 2021
Last updated: 13 February 2022

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1

Kimura, Kenji, Akira Kuriyama, Naoki Kuninaga, and Akira Sasaki. "Acquired Hemophilia." Internal Medicine 54, no. 7 (2015): 865. http://dx.doi.org/10.2169/internalmedicine.54.3862.

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2

Özsoylu, Şinasi. "Acquired Hemophilia." Turkish Journal of Hematology 31, no. 4 (December 5, 2014): 434. http://dx.doi.org/10.4274/tjh.2014.0252.

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3

Huisman, P. "Acquired hemophilia." Netherlands Journal of Medicine 56, no. 6 (June 2000): 229–31. http://dx.doi.org/10.1016/s0300-2977(00)00026-7.

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4

Litty, Cathy, and Ellinor I. B. Peerschke. "Acquired Hemophilia." Laboratory Medicine 22, no. 2 (February 1, 1991): 89–90. http://dx.doi.org/10.1093/labmed/22.2.89.

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5

Collins, Peter. "Acquired Hemophilia." Seminars in Hematology 43 (January 2006): S90. http://dx.doi.org/10.1053/j.seminhematol.2005.11.012.

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6

Lottenberg, Richard. "Acquired Hemophilia." Archives of Internal Medicine 147, no. 6 (June 1, 1987): 1077. http://dx.doi.org/10.1001/archinte.1987.00370060073014.

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7

Hollmig, S. Tyler, Adam G. Perry, and Joel Cook. "Acquired Hemophilia." Dermatologic Surgery 40, no. 9 (September 2014): 1056–58. http://dx.doi.org/10.1097/01.dss.0000452640.53468.ce.

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8

Boggio, Lisa N., and David Green. "ACQUIRED HEMOPHILIA." Reviews in Clinical and Experimental Hematology 5, no. 4 (December 2001): 389–404. http://dx.doi.org/10.1046/j.1468-0734.2001.00049.x.

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9

Tamai, Yoshiko, and Hideki Takami. "5. Acquired Hemophilia." Nihon Naika Gakkai Zasshi 103, no. 7 (2014): 1622–30. http://dx.doi.org/10.2169/naika.103.1622.

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10

Miyahira, Takeshi, Kazushi Kinjo, Kazumitsu Tamaki, and Yoshitaka Asakura. "Postpartum Acquired Hemophilia." Nihon Naika Gakkai Zasshi 96, no. 10 (2007): 2294–95. http://dx.doi.org/10.2169/naika.96.2294.

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11

Pandey, Yadav, Dinesh Atwal, Manojna Konda, Arya Roy, and Appalanaidu Sasapu. "Acquired hemophilia A." Baylor University Medical Center Proceedings 33, no. 1 (November 20, 2019): 71–74. http://dx.doi.org/10.1080/08998280.2019.1689024.

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12

Yang, Yanhui, Feng Xue, Hao Shi, Hongmei Wang, Lei Zhang, Linxiang Ji, and Renchi Yang. "Acquired Hemophilia A." Clinical and Applied Thrombosis/Hemostasis 21, no. 1 (May 14, 2013): 35–40. http://dx.doi.org/10.1177/1076029613488937.

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13

Maesako, Yoshitomo, Daiki Shimomura, and Hitoshi Ohno. "Acquired hemophilia A." Tenri Medical Bulletin 16, no. 2 (2013): 133–35. http://dx.doi.org/10.12936/tenrikiyo.16-015.

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14

Franchini, Massimo. "Acquired hemophilia A." Hematology 11, no. 2 (April 2006): 119–25. http://dx.doi.org/10.1080/10245330600574185.

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15

Kim, Jin Seok. "Acquired Hemophilia A." Clinical & Experimental Thrombosis and Hemostasis 5, no. 1 (May 10, 2019): 11–14. http://dx.doi.org/10.14345/ceth.19003.

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16

Webert, Kathryn. "Acquired Hemophilia A." Seminars in Thrombosis and Hemostasis 38, no. 07 (September 1, 2012): 735–41. http://dx.doi.org/10.1055/s-0032-1326779.

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17

Reeves, Brandi N., and Nigel S. Key. "Acquired hemophilia in malignancy." Thrombosis Research 129 (April 2012): S66—S68. http://dx.doi.org/10.1016/s0049-3848(12)70019-1.

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18

Nilsson, Inga Marie, and Stefan Lamme. "On Acquired Hemophilia A." Acta Medica Scandinavica 208, no. 1-6 (April 24, 2009): 5–12. http://dx.doi.org/10.1111/j.0954-6820.1980.tb01142.x.

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19

Kitchens, Craig S. "Dealing with acquired hemophilia." Blood 103, no. 12 (June 15, 2004): 4375. http://dx.doi.org/10.1182/blood-2004-04-1356.

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20

Tiede, Andreas, Roswith Eisert, Andreas Czwalinna, Wolfgang Miesbach, Inge Scharrer, Arnold Ganser, and Mario von Depka. "Acquired Hemophilia Caused by Non-Hemophilic Factor VIII Gene Variants." Blood 104, no. 11 (November 16, 2004): 3083. http://dx.doi.org/10.1182/blood.v104.11.3083.3083.

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Abstract The development of inhibitory antibodies against coagulation factor VIII (FVIII) in patients without congenital hemophilia A is a rare disorder known as acquired hemophilia. The etiology of the disease remains obscure. In approximately half of the patients, acquired hemophilia is associated with autoimmune disease, malignancy, multiple transfusions or the postpartum period. The remaining patients present without concomitant disorders. We hypothesized that anti-FVIII inhibitor formation might result from allo-immunization against antigenetically different FVIII variants in some patients with acquired hemophilia. The FVIII gene sequence was analyzed in 18 patients with acquired hemophilia and in two kindred of female patients with postpartal inhibitors. A hemizygous missense mutation (E2004K) was found in a male patient who developed an inhibitor after receiving multiple blood transfusions. This mutation has not been reported in the HAMSTeRS database and was not found in 50 male and 50 female healthy blood donors. It does not cause inherited hemophilia A as demonstrated by the patient’s unremarkable bleeding history before the onset of acquired hemophilia and a FVIII activity of >100 % after eradication of the inhibitor. Peptides containing E2004 or K2004 scored among the top 1 % of A3 domain-derived peptides presented on the patient’s major histocompatibility complex (MHC) class II allele, HLA-DRB1*0101. A further single amino acid substitution (D1241E) was found in four male patients and three female patients. This substitution resides in the FVIII B domain and represents a previously unknown polymorphism as it was also found in eight out of 50 male and in 17 out of 50 female controls. Comparing the allelic frequency of FVIII gene variants in patients and controls, these were equally frequent in female patients (3/18 or 17 %) and controls (18/100 or 18 %, P=0.74), but significantly more frequent in male patients (5/9 or 56 %) compared to male controls (8/50 or 16 %, P<0.01). Peptides containing D1241 or E1241 scored among the top 2 % of B domain-derived peptides presented on some MHC class II alleles (HLA-DRB1*0701 and *1501), but were unlikely to be presented on other alleles (*0101, *0301, *0401, *1101). In summary, we report allo-immunization against antigenetically relevant FVIII variants presented in a suitable MHC class II background as a novel potential mechanism of inhibitor development. Thus, exposure to ‘foreign’ FVIII variants during pregnancy or transfusion may elicit an immune response that eventually cross-reacts with ‘self’ FVIII in some patients resulting in acquired hemophilia. Similar inhibitory immune reactions may also cause loss of efficacy in patients receiving other therapeutic proteins, e.g. erythropoietin, or multiple transfusions.
21

Barg, Assaf A., Tami Livnat, and Gili Kenet. "An extra X does not prevent acquired hemophilia – Pregnancy-associated acquired hemophilia A." Thrombosis Research 151 (March 2017): S82—S85. http://dx.doi.org/10.1016/s0049-3848(17)30074-9.

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22

Madurantakam, Parthasarathy, Gary Bowlin, and Keith A. Moskowitz. "Woundstat™ Topical Hemostat Reverses Clotting Diatheses in Models of Acquired and Congenital Hemophilia." Blood 112, no. 11 (November 16, 2008): 2267. http://dx.doi.org/10.1182/blood.v112.11.2267.2267.

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Abstract Globally over 200,000 persons are afflicted with hemophilia. Topical treatments for perioperative intervention of hemophiliac bleeding are currently limited to fibrin glues, which have been used successfully to carry out dental extractions, orthopedic and non-orthopedic surgeries, and for circumcisions. Drawbacks of fibrin glues include risk of blood borne pathogen contamination and immunologic cross-reaction to factors II and V. Although topical hemostatic agents are available for treating traumatic bleeding in the field by military and EMS first responders, their effectiveness for treating bleeding in hemophilia, platelet disorders, surgery; and for other hemostatic defects observed in cirrhosis and other liver diseases and during anticoagulation therapy overdose, have not been studied. A new granular smectite hemostatic agent (WoundStat™ [WS]) has demonstrated 100% efficacy in producing hemostasis during high pressure traumatic arterial bleeding (Ward et al., J Trauma, 63:276–284, 2007; Carraway et al., Resuscitation, 78:230–235, 2008) and has been cleared for external use in cases of moderate to severe bleeds. Here, we evaluated the effectiveness of WS in models of acquired and congenital hemophilia using a modified whole blood recalcified clotting time assay on the Actalyke Mini II activated clotting time (ACT) analyzer and empty G-ACT tubes devoid of contact phase activating reagents. Whole citrated blood recalcified to 10 mM with CaCl2 yielded clot times (CT) of 220 s, 210 s, and 230 s, respectively, for three normal donors. Acquired hemophilia A and B bloods were prepared by incubating normal citrated blood from an individual subject with function-blocking affinity purified polyclonal antibodies to factors VIII and IX, respectively. At near saturation, antibody to FIX (150 μg/ml) increased clotting times from 213 ±3 s to 405±11 s, while antibodies to FVIII (50 μg/ml) increased CT from 229 ± 6 s to 436 ± 17 s. Matched antibody controls to prothrombin fragment 1+2 (200 μg/ml) did not prolong baseline clot time (242 ± 5 s). Addition of WS at 1 mg/ml, shortened the prolonged clotting times of the acquired hemophilia bloods from 436 ± 17 sec to 223 ±2 sec (p< 10−4) and from 405 ±11 s to 204 ± 5 s (p< 10−4) for the hemophilia A and B bloods, respectively. Notably no differences were observed between CT of normal blood relative to acquired hemophilia bloods treated with WS (p < 0.3). Corresponding normal control blood clotting times were shortened by 1 mg/ml WS to 92 ± 8 s. To simulate classic hemophilia, plasma derived from hemophilia A and B bloods containing < 1% normal clotting activity or autologous plasma were mixed with fresh total washed blood cells from a type O subject at 40% Hematocrit. Recalcified CT for the autologous, hemophilia A and hemophilia B bloods were 251 ±5, 596 ± 36 and 370 ± 36 s, respectively. The addition of 3 mg/ml WS normalized CT of the congenital hemophilia A (183 ± 2 s) and B (245 ± 2) bloods and was procoagulant of autologous control blood (92 ± 7 s). In contrast to WS, CELOX chitosan hemostatic granules (1–3 mg/ml) did not accelerate clotting of acquired (444 ± 43 s) or congenital (508 ± 23 s) hemophilia A; acquired (474 ± 62 s) or congenital (643± 20 s) hemophilia B or normal autologous bloods (345 ± 32 s). These results suggest that WS may be a viable, cost effective, and safe treatment for hemophiliac bleeds during traumatic injury prior to emergent care or surgical intervention. Further animal and laboratory studies are required before WS can be shown to be effective during moderate to severe bleeding in hemophilia and other coagulopathies such as VWD or patients administered anticoagulant therapy.
23

Barlamov, Pavel Nikolaevich, E. R. Vasilieva, M. E. Golubeva, V. G. Zelobov, O. S. Starikova, and A. A. Shutylev. "Acquired inhibitory form of hemophilia." Clinical Medicine (Russian Journal) 96, no. 4 (September 26, 2018): 361–64. http://dx.doi.org/10.18821/0023-2149-2018-96-4-361-364.

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The article presents a brief review of the literature on the current understanding of the etiology, pathogenesis, clinic, diagnosis and treatment of the acquired form of hemophilia, as well as the clinical case of this pathology with successful treatment.
24

Banerjee, A. K., J. Llewelyn, K. Harrison, and A. Dyson. "Acquired Hemophilia and Diabetes Mellitus." Diabetes Care 11, no. 4 (April 1, 1988): 366–67. http://dx.doi.org/10.2337/diacare.11.4.366b.

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25

COLLINS, P. W. "Treatment of acquired hemophilia A." Journal of Thrombosis and Haemostasis 5, no. 5 (May 2007): 893–900. http://dx.doi.org/10.1111/j.1538-7836.2007.02433.x.

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26

Flisiński, Mariusz, Jerzy Windyga, Ewa Stefańska, Sławomir Huszcza, Rafał Donderski, and Jacek Manitius. "Acquired hemophilia: a case report." Polish Archives of Internal Medicine 118, no. 4 (April 1, 2008): 228–33. http://dx.doi.org/10.20452/pamw.368.

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27

Baudo, Francesco, and Francesco de Cataldo. "The problem of acquired hemophilia." Blood 125, no. 7 (February 12, 2015): 1052–53. http://dx.doi.org/10.1182/blood-2014-12-618959.

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28

G., Theodossiades, Tsevrenis V., Nomikou E., Dadiotis L., and Kontopoulou-Griva I. "Surgery-associated acquired hemophilia A." Annals of Hematology 80, no. 11 (November 1, 2001): 691–93. http://dx.doi.org/10.1007/s002770100367.

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29

Sotak, Štefan, and Miriam Mitníková. "Acquired hemophilia A: case report." Vnitřní lékařství 64, no. 4 (April 1, 2018): 427–31. http://dx.doi.org/10.36290/vnl.2018.060.

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30

Knoebl, Paul, Francesco Baudo, Peter W. Collins, Angela Huth-Kuehne, Herve Levesque, Pascual Marco, Laszlo Nemes, Fabio Pellegrini, and Lilian Tengborn. "Management of Bleeding In Acquired Hemophilia: Results of the European Acquired Hemophilia Registry (EACH2)." Blood 116, no. 21 (November 19, 2010): 716. http://dx.doi.org/10.1182/blood.v116.21.716.716.

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Abstract Abstract 716 Objective. Acquired hemophilia (AH) is a hemorrhagic syndrome, caused by autoantibodies inhibiting coagulation FVIII. The optimal hemostatic therapy is not clear. This analysis aimed to describe the first-line management of bleeding in AH within Europe. Methods. Data from the EACH2 registry, a multicentre, international, web-based registry, were used to analyze the use of recombinant activated factor VII (rFVIIa), activated prothrombin complex concentrates (APCC), FVIII concentrates, and DDAVP as first line hemostatic therapy. There was no predefined treatment protocol, each center was free to follow local clinical practice. Response rate is the number of bleeds resolved as judged by each investigator. Data on demographics, pregnancy and immunosuppression will be presented in other abstracts. Data are given as medians and interquartile ranges (IQR) or odds ratios (OR) and 95% confidence intervals (CI). Results. Data of 501 patients (pts) (235 male, 266 female, median age 74 years (range 14–104)) were prospectively collected between 2003 and 2009 in 90 centers of 11 European countries. In 474 pts at least one bleeding episode is reported; 159 pts had 2 episodes (the second bleeding episode a median 26 (13/67) days after the first), 51 pts had 3 episodes, 16 pts. more than 3 bleedings. Of the 474 initial bleeding episodes, 70.3% were reported as severe (criteria prospectively defined), 50.2% had deep musculoskeletal or retroperitoneal bleeding, 53.2% skin hematomas, 31.6% mucosal bleeding, and only 4.9% hemarthroses. In 77.4% the bleedings occurred spontaneous, 8.4% after trauma, 8.2% after surgery. Median FVIII activity at the time of bleeding was 0.02 U/mL (0.01/0.05 U/mL), the inhibitor titer 19 BU/mL (5.5/64 BU/mL). There was no significant association between FVIII activity or inhibitor titer and severity of bleeding. Hemostatic therapy was given in 70.5% of the bleedings. First line therapy is presented in the table: Desmopressin was given in 6%, antifibrinolytic drugs in 18%, and high dose immunoglobulin infusions in 11.1%; immunoadsorption was performed in 5.4%, plasmapheresis in 0.6%. Overall bleeding resolved in 76.4%, in median after 4 days (IQR 2–10 days). Second line therapy with an alternative substance was applied in 23.6% (in 17.4% because bleeding did not resolve). The use of bypassing agents (rFVIIa or APCC) resulted in a significant higher rate of bleeding control (91.2 %) than the use of FVIII or desmopressin (71.0 %) (p<0.001), there was no difference between rFVIIa (90.9 %) and APCC (94.3 %). To minimize bias, propensity score matched data analysis (1) based on age, gender, FVIII level, inhibitor titre, hemoglobin level, site, severity and cause of bleeding was carried out. It confirmed that first line treatment with a bypassing agent resulting in a better control of bleeding compared to FVIII or desmopressin (OR 0.25, 95% CI 0.12–0.53; p=0.004). There was no difference in efficacy between rFVIIa and APCC (OR 1.0, 95%CI 0.24–4.18). No other patient- or disease-related parameters affected response rate. Deaths due to bleeding occurred in 3% of the patients, only few serious adverse events were recorded: 1.4% myocardial infarction, 0.2% stroke, 1.0% venous thromboembolic events. There was no significant association of death or severe adverse events with a specific hemostatic therapy. Conclusion. Bypassing agents are the preferred first line hemostatic therapy in AH (70.1% of the episodes) and have a significantly better efficacy than FVIII or DDAVP; rFVIIa was the agent preferred by most clinicians (~50%), rFVIIa and APCC were equally efficacious. Treatment with bypassing agents was safe and highly effective in controlling bleeding in AH. 1. D'Agostino RB Jr: Propensity score methods for bias reduction in the comparison of a treatment to a non-randomized control group. Stat Med 1998; 17:2265–2281. Disclosures: Knoebl: Novo Nordisk: Consultancy, Membership on an entity's Board of Directors or advisory committees, NovoNordisk fund the EACH2 registry, Research Funding; Baxter Healthcare: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding. Baudo:NovoNordisk: Consultancy, Honoraria, NovoNordisk fund the EACH2 registry, Speakers Bureau; Bayer Healthcare: Honoraria, Speakers Bureau. Collins:NovoNordisk: Consultancy, Honoraria, The EACH2 registry was funded by Novonordisk; Baxter Healthcare: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau. Huth-Kuehne:NovoNordisk: Consultancy, Membership on an entity's Board of Directors or advisory committees, NovoNordisk fund the EACH2 registry; Baxter Healthcare: Consultancy, Membership on an entity's Board of Directors or advisory committees. Levesque:NovoNordisk: NovoNordisk fund the EACH2 registry. Marco:Novo Nordisk: Novonordisk fund the EACH2 registry. Nemes:Novo Nordisk: Novonordisk fund the EACH2 registry. Pellegrini:Novonordisk: Consultancy, Honoraria, Speakers Bureau, The EACH2 registry is funded by Novonordisk. Tengborn:Novo Nordisk: Novonordisk fund the EACH2 registry.
31

Sihombing, Rasco Sandy, Henry Ratno Diono Silalahi, Hamzah Shatri, Lugyanti Sukrisman, Ikhwan Rinaldi, Findy Prasetyawati, Endy Novianto, and Em Yunir. "Diagnosis dan Tata Laksana Acquired Hemophilia A (AHA) dengan Pemfigoid Bulosa." Jurnal Penyakit Dalam Indonesia 3, no. 4 (January 27, 2017): 218. http://dx.doi.org/10.7454/jpdi.v3i4.56.

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Acquired hemophilia A merupakan kondisi dimana faktor koagulasi VIII menjadi tidak aktif akibat pembentukan autoantibodi. Kondisi ini dikaitkan dengan kehamilan, keganasan, dan penyakit auitoimun dengan kelainan kulit. Pada kasus ini, seorang wanita berusia 66 tahun, datang dengan keluhan perdarahan paska tindakan yang disertai dengan lesi kulit. Pasien didiagnosis dengan acquired hemophilia A dengan ditemukannya inhibitor faktor VIII terkait dengan pemfigoid bulosa.Kata Kunci: Acquired hemophilia A, diagnosis, pemfigoid bulosa, tata laksana Diagnosis and Treatment of Acquired Hemophilia A (AHA) with Bullous PemphigoidAcquired hemophilia A is a condition in which coagulation factor VIII become inactive due to autoantibody formation. This condition is related to pregnancy, malignancy, and autoimmune disease with skin disorder. In this case report, a 66 years woman with a post procedural bleeding with skin disorder. Later on, patient diagnosed with acquired hemophilia A with a factor VIII inhibitors related to bullous pemphigoid. Keywords : Acquired hemophilia A, bullous pemphigoid, diagnosis, treatment
32

Shen, Mark, Shan Wang, Julia Sessa, Adel Hanna, Alexander Axelrad, and Fahd Ali. "Acquired Hemophilia A: A Case Report." Journal of Pharmacy Practice 33, no. 4 (February 6, 2019): 562–66. http://dx.doi.org/10.1177/0897190019826474.

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Hemophilia A, also known as factor VIII deficiency, is a rare disorder caused by an insufficient level of factor VIII, an essential clotting protein. Hemophilia A can be inherited or acquired. Inherited hemophilia A is caused by a mutation to the factor VIII gene on the X chromosome, which is commonly passed down from parents to children. However, in about one-third of cases, the cause is a spontaneous mutation in that gene. Acquired hemophilia A is due to an autoantibody to factor VIII, which is termed an inhibitor. This rare disorder can cause life-threatening bleeding complications. Management relies on a rapid and accurate diagnosis, control of bleeding episodes, and eradication of the inhibitor by immunosuppression therapy. Most treatment strategies are centered around anecdotal reports or small case series. This case report summarizes the successful treatment of a patient with acquired hemophilia A and major bleeding following a surgical procedure, with the use of desmopressin, recombinant factor VIIa, repeated doses of recombinant factor VIII, rituximab, and prednisone.
33

Barlamov, P. N., E. R. Vasilyeva, M. E. Golubeva, V. G. Zhelobov, A. A. Shutylev, and T. Yu Kravtsova. "Clinical case of an acquired hemophilia." Clinician 13, no. 3-4 (January 30, 2020): 74–77. http://dx.doi.org/10.17650/1818-8338-2019-13-3-4-74-77.

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The aim of the work is to describe the clinical case of formation, diagnosis and treatment of the acquired form of blood clotting factor VIII deficiency – of acquired hemophilia A.Material and methods. Patient R., 71 years, from April 2018, was found an acute hemorrhagic syndrome in the hematomic type of large hematomas manifested submandibular region, neck, chest, right breast, pubic and inguinal regions on the right, the anterior-medial surface of the left femur, anterior surface of left tibia. Standard laboratory tests, computed tomography of soft tissues of the neck, lungs, abdomen; coagulogram; blood clotting factors; inhibitor of factor VIII were evaluated in dynamics during the patient’s stay in the hospital; platelet aggregation function.Results. Typical gematomny type of bleeding, prolongation of coagulation indicators, the presence of the inhibitor factor VIII (7,0 BAA), the decrease in factor VIII (2 %) allowed diagnosis of acquired hemophilia A. Anti-inhibitory coagulant complex, fresh frozen plasma was successfully used for treatment. The patient is under observation in the regional Hematology center. The hematomas were not renewed.Conclusion. Our clinical observation demonstrates the features of the course, the algorithm of diagnosis and management of patients with of acquired hemophilia A.
34

Windyga, Jerzy, Beata Baran, Edyta Odnoczko, Anna Buczma, Krzysztof Drews, Piotr Laudanski, Bronislawa Pietrzak, and Piotr Sieroszewski. "Treatment guidelines for acquired hemophilia A." Ginekologia Polska 90, no. 6 (June 28, 2019): 353–64. http://dx.doi.org/10.5603/gp.2019.0063.

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35

Green, David. "Oral Immunosuppressive Therapy for Acquired Hemophilia." Annals of Internal Medicine 128, no. 4 (February 15, 1998): 325. http://dx.doi.org/10.7326/0003-4819-128-4-199802150-00034.

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36

Shaffer, Linda G. "Oral Immunosuppressive Therapy for Acquired Hemophilia." Annals of Internal Medicine 128, no. 4 (February 15, 1998): 325. http://dx.doi.org/10.7326/0003-4819-128-4-199802150-00035.

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37

RATNOFF, OSCAR D. "Hemophilia and the Acquired Immunodeficiency Syndrome." Annals of Internal Medicine 102, no. 3 (March 1, 1985): 412. http://dx.doi.org/10.7326/0003-4819-102-3-412_2.

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38

Kantor, Rami, Haim Mayan, Lena Puritz, Zvi Farfel, and David Varon. "Acquired Hemophilia Masked by Warfarin Therapy." American Journal of the Medical Sciences 319, no. 3 (March 2000): 197–201. http://dx.doi.org/10.1016/s0002-9629(15)40722-0.

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39

Park, Narae, Jin Seok Jang, and Jae Hwang Cha. "Acquired Hemophilia A with Gastrointestinal Bleeding." Clinical Endoscopy 53, no. 1 (January 30, 2020): 90–93. http://dx.doi.org/10.5946/ce.2019.036.

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40

Chen, Ching-Yin, Ya-Hui Chen, Ji-Chen Ho, and Chieh-Shan Wu. "Bullous pemphigoid associated with acquired hemophilia." Dermatologica Sinica 28, no. 4 (December 2010): 173–76. http://dx.doi.org/10.1016/s1027-8117(10)60038-9.

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41

Uggla, Bertil, Olle Linder, and Sam Schulman. "Acquired hemophilia masked by warfarin therapy." Blood Coagulation & Fibrinolysis 14, no. 8 (December 2003): 769–72. http://dx.doi.org/10.1097/00001721-200312000-00014.

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42

Mady, Ahmed F., Basim R. Huwait, Muhammad Asim Rana, Omar E. Ramadan, Abulrahman Al-Harthy, and Abdul Kareem M. Al-Momen. "Acquired Hemophilia Network;non Hematologist Perspectives." Blood 124, no. 21 (December 6, 2014): 5978. http://dx.doi.org/10.1182/blood.v124.21.5978.5978.

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Abstract:
Abstract Background: Acquired hemophilia (AH) is an autoimmune disease caused by an autoantibody to factor VIII (FVIII). Morbidity and mortality are high due to the age of the patients, underlying diseases, the toxic effects of immunosuppression, bleeding and is in part attributable to sequential delays in diagnosis and appropriate treatment. Objective: AH usually presents to clinicians without prior experience of the disease, therefore diagnosis is frequently delayed and bleeds under treated. Therefore improving the awareness among health care professionals to whom AH patients are likely to present is our main objective. Also, we believe that, optimal management of AH requires active participation of non-hematologist physicians, pharmacists and laboratory staff with hematologists. Method: For this objective, in May 2013, we carried out a survey among non-hematologist health care professionals including clinicians, clinical pharmacists and laboratory staff in 10 tertiary medical care Arabian Gulf centres to assess the degree of awareness regarding AH diagnosis and management and to address the difficulties they could face during management of such cases. To our surprise very informative data was collected. In December 2013, the second stage of our work we have established a network of health care workers among all gulf countries to continue our mission. This network has been named Acquired Hemophilia Network (AHN). Board members were designated representing 6 gulf countries including haematologists, pathologists and other healthcare specialists involved in the treatment and management of patients with acquired haemophilia. A case report form (CRF) was prepared and posted on AHN website to collect and document the cases of acquired hemophilia. Results of survey Total responders of our survey were 1104 ,953 of them were physicians, 57 laboratory staff physicians and 94 pharmacists. out of all physicians responded, 42% were not aware about AH, 45% would not consider mixing test for isolated prolonged aPTT and 47% of them would start bypassing agents in bleeding AH, but only 26% would use inhibitor eradication immediately upon confirmation. Almost half of the clinicians showed the haematologist‘s response in more than 24 hrs. The majority of clinicians, lab and pharmacists agreed that the lack of awareness about the disorder and its complications is the most important obstacle in achieving the optimal management of AH. Despite shortage of haematologists in the Arab Gulf countries, 46 of them don’t believe that non-hematologists should be empowered to start bypassing agents and inhibitor eradications in such a fatal disorders even after increasing awareness among them. Expected outcomes of AHN We expect Increasing awareness among non-hematology physicians for AH knowledge, Gathering information on past and present cases of Acquired Hemophilia for case series publication and Drawing expert-opinion and guidelines for recognition, diagnosis and management of acquired hemophilia & publish Gulf AH diagnosis and management consensus. Disclosures No relevant conflicts of interest to declare.
43

Mytopher, K., J. Dudebout, R. Card, and B. Gilliland. "Acquired hemophilia A presenting post partum." Canadian Medical Association Journal 177, no. 4 (August 14, 2007): 339–40. http://dx.doi.org/10.1503/cmaj.070414.

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44

Gill, Joan Cox. "Acquired hemophilia A: is more better?" Blood 109, no. 5 (March 1, 2007): 1793–94. http://dx.doi.org/10.1182/blood-2006-12-061960.

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45

Vinayek, Namita, Goetz H. Kloecker, and Beth C. Riley. "Acquired Hemophilia After a Spider Bite." Blood 120, no. 21 (November 16, 2012): 4637. http://dx.doi.org/10.1182/blood.v120.21.4637.4637.

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Abstract Abstract 4637 A 59 year old white female with no history of bleeding diathesis presented with swelling of her left forearm two days after a brown recluse spider bite. Hematology was consulted for uncontrolled bleeding from the fasciotomy site after compartment syndrome. The hand surgeons did not see any vascular abnormality at the site of surgery. Due to ongoing bleeding for days from the surgical site, she required 8 PRBCs, 6 FFPs and 6 apheresis platelets units. PT, PTT, and platelet count were normal, ristocetin cofactor was 339% and vWF antigen 306% and vW Factor VIII binding capacity was normal. Her platelet functional assay was normal. Factor levels of II, V, VII, XI, X, XI and lupus anticoagulant were all with in normal range. A Bethesda assay however showed a low titer of antibody against factor VIII (1.25 BU). Factor VIII was low at 6% and remained low at 16% with no significant response to recombinant factor VIII.The bleeding however responded well to recombinant factor VIIa. She was maintained on high dose steroids for few months and tapered. She eventually had a skin graft to the site of injury and is now followed in our hemophilia clinic with no further bleeding complications. To our knowledge only one case of spider bite resulting in factor VIII inhibitor has been documented in the literature. We hypothesize that direct antigenic stimulation by spider venom can transiently develop factor VIII inhibitor in individuals. Disclosures: No relevant conflicts of interest to declare.
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Brunetta, Denise Menezes, Fabiana Aguiar Carneiro-Silva, João Batista Marinho Vasconcelos, Rosângela de Albuquerque Ribeiro, Denissa Ferreira Gomes Mesquita, Gustavo Rego Coelho, Fernando Barroso-Duarte, and José Huygens Parente Garcia. "Hemophilia B acquired through liver transplantation." Liver Transplantation 22, no. 2 (January 27, 2016): 254–56. http://dx.doi.org/10.1002/lt.24364.

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47

Franchini, Massimo, Giorgio Gandini, Tiziana Di Paolantonio, and Guglielmo Mariani. "Acquired hemophilia A: A concise review." American Journal of Hematology 80, no. 1 (2005): 55–63. http://dx.doi.org/10.1002/ajh.20390.

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48

Hashizume, Hideo, Takatsune Umayahara, and Maki Hata. "Acquired hemophilia eclipsed by psoriatic arthralgia." Journal of Dermatology 40, no. 12 (December 2013): 1070–71. http://dx.doi.org/10.1111/1346-8138.12324.

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49

Mahipal, Amit, and S. Bilgrami. "Acquired hemophilia in chronic lymphocytic leukemia." Leukemia & Lymphoma 48, no. 5 (January 2007): 1026–28. http://dx.doi.org/10.1080/10428190701203962.

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50

Kantor, Rami, Haim Mayan, Lena Puritz, David Varon, and Zvi Farfel. "Acquired Hemophilia Masked by Warfarin Therapy." American Journal of the Medical Sciences 319, no. 3 (March 2000): 197–201. http://dx.doi.org/10.1097/00000441-200003000-00013.

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