• Vol. 31 No. 3, 276–280
  • 15 May 2002

Pregnancy in Women with Idiopathic Thrombocytopaenic Purpura

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ABSTRACT

Introduction: Idiopathic thrombocytopaenic purpura (ITP) is a common haematological disorder in young women. The management of ITP in pregnancy is controversial, particularly with regards to the mode of delivery. To date, there is no systematic study of the outcome of these pregnancies in Singapore.

Aim: To study the outcomes of pregnancies in Asian women with a proven diagnosis of ITP.

Materials and Methods: Retrospective study of 27 pregnancies in 18 women managed at the Singapore General Hospital from 1 January 1994 to 30 June 2001.

Results: The mean age of the women was 30 years (range, 20 to 41 years) and the mean parity was 1 (range, 0 to 3). Thrombocytopaenia (platelet count <150 x 109/L) occurred in 18 pregnancies (67%). There were 3 first trimester missed abortions (11%), 1 termination of pregnancy (4%), 1 stillbirth (4%) and 22 livebirths (81%) in this series. The mode of delivery was spontaneous vaginal in 14 women (64%), vacuum extraction in 2 women (9%), elective caesarean section in 5 women (23%) and emergency caesarean section in 1 woman (4%). All liveborn neonates were delivered in good condition at term. Neonatal thrombocytopaenia occurred in 4 neonates (18%). Two neonates had cord platelet counts of less than 50 x 109/L and 1 required therapy with corticosteroids and intravenous immune globulins. No bleeding complications occurred in any of the neonates.

Conclusion: Our experience supports the increasingly prevalent practice of managing pregnancies in women with ITP with a conservative approach to investigations and treatment. Caesarean sections should be performed for obstetric indications only, given the rarity of bleeding complications in the offspring of these women and the lack of evidence to support its role in the prevention of neonatal intracranial haemorrhage.


Idiopathic thrombocytopaenic purpura (ITP) is the most common autoimmune haematological disorder in pregnancy. The pathophysiology of the disease is peripheral destruction of platelets mediated by antiplatelet antibodies.

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