title: Liver dysfunction in triplet pregnancies: relation to antenatal changes in antithrombin activity and platelet count.
abstract: OBJECTIVE
  The aim of this study was to determine whether antenatal decline in antithrombin (AT) activity occurs frequently and precedes the development of perinatal liver dysfunction in women with triplet pregnancies.
  
  
  METHODS
  A retrospective observational study was conducted on all women who gave birth to triplets at gestational week ≥ 22 at a single centre during a study period from January 2001 to March 2013. The following eight blood parameters were monitored weekly during the last 5 weeks of pregnancy and postpartum: AT activity, platelet count, fibrinogen, D-dimer, aspartate aminotransferase (AST), lactate dehydrogenase (LDH), uric acid and creatinine. Pregnancy-induced AT deficiency (PIATD) and gestational thrombocytopenia were defined as antenatal AT activity < 70% of normal level and antenatal platelet count < 150 × 10(9) /L, respectively. Liver dysfunction was defined as AST >  40 IU/L. LDH elevation was defined as LDH >  450 IU/L.
  
  
  RESULTS
  Sixteen women were eligible for this study. All variables except LDH exhibited significant changes antenatally: AT activity, platelet count and fibrinogen decreased, while D-dimer, AST, urate and creatinine increased. LDH increased significantly postpartum. PIATD, gestational thrombocytopenia, perinatal liver dysfunction, and LDH elevation occurred in eight, seven, six, and eight women, respectively. Liver dysfunction was preceded by PIATD alone in three, by both PIATD and gestational thrombocytopenia in one and by gestational thrombocytopenia alone in none of the subjects. After delivery, laboratory abnormalities similar to HELLP syndrome were seen in three women exclusively in the presence of PIATD.
  
  
  CONCLUSIONS
  Reduced AT activity was likely to precede perinatal liver dysfunction in women with triplets.
authors.affiliation: Department of Obstetrics, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido, Japan.
authors.forename: Ryutaro
authors.initials: R
authors.lastname: Nishida
authors.forename: Mamoru
authors.initials: M
authors.lastname: Morikawa
authors.forename: Takahiro
authors.initials: T
authors.lastname: Yamada
authors.forename: Rina
authors.initials: R
authors.lastname: Akaishi
authors.forename: Takashi
authors.initials: T
authors.lastname: Yamada
authors.forename: Hisanori
authors.initials: H
authors.lastname: Minakami
mesh_terms: D000328:Adult; D000991:Antithrombins / Q000097:blood; D003937:Diagnosis, Differential; D015536:Down-Regulation; D005260:Female; D017359:HELLP Syndrome / Q000097:blood / Q000175:diagnosis / Q000453:epidemiology / Q000503:physiopathology; D006801:Humans; D046110:Hypertension, Pregnancy-Induced / Q000097:blood / Q000175:diagnosis / Q000453:epidemiology / Q000503:physiopathology; D007564:Japan / Q000453:epidemiology; D008099:Liver / Q000503:physiopathology*; D065626:Non-alcoholic Fatty Liver Disease / Q000209:etiology*; D010976:Platelet Count; D049590:Postpartum Period; D011247:Pregnancy; D011250:Pregnancy Complications, Hematologic / Q000097:blood / Q000175:diagnosis / Q000453:epidemiology / Q000503:physiopathology*; D011263:Pregnancy Trimester, Third; D059286:Pregnancy, Triplet / Q000097:blood; D015995:Prevalence; D012189:Retrospective Studies; D012307:Risk Factors; D013921:Thrombocytopenia / Q000209:etiology*; D019851:Thrombophilia / Q000097:blood / Q000175:diagnosis / Q000453:epidemiology / Q000503:physiopathology*
chemical_list: D000991:Antithrombins
keywords: HELLP syndrome; acute fatty liver of pregnancy; antithrombin activity; blood vessel permeability; liver dysfunction; thrombocytopenia