Publication: Acquired hypoprothrombinemia inducing bleeding in a girl with transient antiphospholipid antibody: Case report
Issued Date
2012-02-01
Resource Type
ISSN
01252208
Other identifier(s)
2-s2.0-84858031806
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Journal of the Medical Association of Thailand. Vol.95, No.2 (2012), 282-287
Suggested Citation
Usanarat Anurathapan, Werasak Sasanakul, Nongnuch Sirachainan, Chanchai Kasemkosolsri, Suphaneewan Jaovisidha, Ampaiwan Chuansumrit Acquired hypoprothrombinemia inducing bleeding in a girl with transient antiphospholipid antibody: Case report. Journal of the Medical Association of Thailand. Vol.95, No.2 (2012), 282-287. Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/14968
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Acquired hypoprothrombinemia inducing bleeding in a girl with transient antiphospholipid antibody: Case report
Other Contributor(s)
Abstract
Background: Congenital or acquired prothrombin deficiency is a rare condition. Case Report: A 2-year-7-month old Thai girl presented with ecchymosis, bleeding at both thighs and right ear lobe after a self-limited viral infection. Results: The investigations revealed prolonged APTT and PT, prothrombin level 6% and positive anticardiolipin antibody 26.2 IU/mL. The 1:1 mixture of her plasma and normal plasma could not normalize her APTT and PT. The inhibitor to prothrombin determined by Bethesda method was 0.62 BU. She was responsive to 20 ml/kg of FFP transfusion, followed by 10 ml/kg at an interval of 12 h for three days and daily 500 units of prothrombin complex concentrate administration for three days. At two-week follow-up, she had no bleeding symptom, coagulation tests were normal, prothrombin level was normalized at 94%, no inhibitor to prothrombin was detected, and anticardiolipin antibody became negative. The additional DNA analysis of her prothrombin gene revealed nine different polymorphisms for which seven had been found in patients with congenital prothrombin deficiency and two were novel (4096T→C, 4097T→C). These single nucleotide polymorphisms are not the disease-causing mutations. In addition, neither known mutations inducing congenital prothrombin deficiency were identified. Conclusion: The acquired hypoprothrombinemia was concluded as the cause of bleeding in this reported patient. It might be caused by the transient low titer of antiphospholipid antibody, which was responsive to replacement therapy of FFP and prothrombin complex concentrate.