Ibrutinib platelet dysfunction induced intracranial hemorrhage management with activated factor VII and transfusion of platelets

2021 ◽  
Vol 5 (4) ◽  
pp. 71
Author(s):  
LuisRafael Moscote-Salazar ◽  
Tariq Janjua
2006 ◽  
Vol 63 (5) ◽  
pp. 310-317 ◽  
Author(s):  
Christopher E. White ◽  
Amber E. Schrank ◽  
Toney W. Baskin ◽  
John B. Holcomb

2021 ◽  
Vol 9 ◽  
Author(s):  
Yuan-Chun Lo ◽  
Ching-Tien Peng ◽  
Yin-Ting Chen

Introduction: Factor VII deficiency is a rare inherited autosomal recessive bleeding disorder with a global prevalence of 1/500,000. Most cases remain asymptomatic, and cases with severe clinical presentation are rarely reported.Case Presentation: A newborn male with no relevant maternal antenatal history, delivered via vacuum-assisted cesarean section, presented with a large cephalohematoma after delivery. Poor appetite, pale appearance, and bulging fontanelles were observed 2 days later, progressing to hypovolemic shock. Further imaging examination revealed a large intracranial hemorrhage. Serial laboratory examination revealed remarkable coagulopathy with prolonged prothrombin time and factor VII deficiency (<1%, severe type). The patient was genetically confirmed to have the FVII:c 681+1 G>T homozygous mutation. Brain hemorrhage was resolved with high-dose factor VII replacement therapy with recombinant activated factor VII. However, repeated hemothorax and intracranial hemorrhage were detected. Therefore, the patient was under regular factor VII supplementation with a rehabilitation program for cerebral palsy.Conclusions: A case of factor VII deficiency with large cephalohematoma and intracranial hemorrhage after birth is described herein, which was treated with high-dose replacement therapy. Variants of the FVII:c 681+1 G>T (IVS6+1G>T) homozygous genotype may present with a severe phenotype at the neonatal stage. We aim to share a unique neonatal presentation with a certain genotype and treatment experience with initial replacement therapy, followed by regular prophylactic dosage.


2021 ◽  
Vol 9 (10) ◽  
Author(s):  
Amir M. Ansari ◽  
Adam Khorasanchi ◽  
Armaghan Faghihimehr ◽  
Amir Toor

1994 ◽  
Vol 47 (1) ◽  
pp. 36-40 ◽  
Author(s):  
M. L. Schmidt ◽  
S. Gamerman ◽  
H. E. Smith ◽  
J. P. Scott ◽  
D. M. DiMichele

2010 ◽  
Vol 74 (6) ◽  
pp. 631-635 ◽  
Author(s):  
Nathan A. Pinner ◽  
April C. Hurdle ◽  
Carrie Oliphant ◽  
Anne Reaves ◽  
Bob Lobo ◽  
...  

1998 ◽  
Vol 80 (08) ◽  
pp. 233-238 ◽  
Author(s):  
K. A. Mitropoulos ◽  
M. N. Nanjee ◽  
D. J. Howarth ◽  
J. C. Martin ◽  
M. P. Esnouf ◽  
...  

SummaryAbetalipoproteinaemia is a rare disorder of apolipoprotein B metabolism associated with extremely low plasma concentrations of triglyce-ride. To discover whether the general positive association between factor VII and triglyceride levels extends to this condition, 5 patients were compared with 18 controls. All patients had a triglyceride below 100 μmol/l. Plasma unesterified fatty acid concentration was normal. Although factor IX activity was only slightly reduced (mean 88% standard) and factor IX antigen was normal, mean activated factor VII in patients was strikingly reduced to 34% of that in controls, a level similar to that found in haemophilia B. The patients’ mean factor VII activity and factor VII antigen were also significantly reduced to 54% and 63% of those in controls, respectively. Mean factor XI activity and tissue factor pathway inhibitor activity were reduced in patients to 70% and 75% of control values respectively, while factor XII, factor XI antigen, factor X, prothrombin and protein C were normal.


1994 ◽  
Vol 72 (04) ◽  
pp. 649-650 ◽  
Author(s):  
Anthony R Hubbard ◽  
Trevor W Barrowcliffe

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