Rheumatology Advance Access originally published online on February 27, 2008
Rheumatology 2008 47(4):554-555; doi:10.1093/rheumatology/ken043
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Elevation of alkaline phosphatase in a pregnant patient with antiphospholipid syndrome: HELLP syndrome or not?
1Université Pierre et Marie Curie-Paris 6, Assistance Publique-Hôpitaux de Paris, Hôpital Pitié-Salpêtrière, Centre de Référence National pour le Lupus Systémique et le Syndrome des Antiphospholipides, Service de Médecine Interne and 2Assistance Publique-Hôpitaux de Paris, Hôpital Pitié-Salpêtrière, Service de Gynécologie Obstétrique, Paris, France
Correspondence to: N. Costedoat-Chalumeau, AP-HP, Service de Médecine Interne, Centre de Référence National pour le Lupus Systémique et le Syndrome des Antiphospholipides, Centre Hospitalier Universitaire Pitié-Salpêtrière, 47-83 Boulevard de l’Hôpital, 75651 Paris Cedex 13, France. E-mail: nathalie.costedoat{at}psl.aphp.fr
SIR, Pregnant patients with APS may develop HELLP syndrome (haemolysis; elevated liver enzymes; low platelet count) that can manifest first by elevation of ALP level. However, other causes of ALP elevation must be discussed and include elevation of ALP of placental origin. We report for the first time an APS pregnant patient presenting with ALP increased over 15-fold of placental origin.
A 40-yr-old patient with an APS was followed for her fifth pregnancy. Past obstetrical history included a normal pregnancy followed by two foetal deaths at 18 weeks of gestation (WG) and a spontaneous abortion at 8 WG. Repeated searches for aCL antibodies were positive. ANA were negative. Her clinical history was otherwise unremarkable. A diagnosis of primary obstetrical APS was made according to the usual criteria [1].
She was treated with aspirin and low molecular weight heparin (enoxaparin 0.4 ml twice a day). At 19 WG, serum ALP level was 200 U/l (normal values: 40–120). She had neither hypertension nor oedema. Results of other liver function tests, blood cell counts and urine tests were normal. Liver ultrasonographic examination was normal. During follow-up, as the patient remained symptom free, ALP increased and reached 1722 U/l at 36 WG without other biochemical abnormality. Obstetrical ultrasonographic examination and Doppler blood flow remained normal.
At that time, given the absence of any clinical or biochemical abnormalities suggestive of HELLP syndrome, an isolated placental ALP elevation was suspected. Serum ALP electrophoresis showed normal ALP level of liver (57 U/l) and bone (146 U/l) origin, whereas placental isozyme 1 ALP was 1054 U/l and placental isozyme 2 ALP was 465 U/l.
She delivered a healthy newborn of 2560 g at 37 WG. The placenta was normal and weighed 435 g. Serum ALP level was 216 U/l at 4 weeks post-partum and normal at 5 weeks post-partum (Fig. 1).
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ALP is an enzyme produced by liver, bones, kidneys, small intestine and placenta. In a pregnant patient, elevation of ALP may be related to HELLP syndrome, intrahepatic cholestasis, malignancy and liver or bone diseases. However, a placental origin of ALP must also be discussed.
ALP is physiologically produced by placenta at the brush border membranes of the syncytiotrophoblast [2]. It appears in maternal serum between the 15th and the 26th WG [3] and increases during the third trimester [4]. Usually, ALP production or diffusion in maternal serum is not major and total serum ALP level remains normal. Some cases of unusual elevation of placental ALP have been described [2, 5–7]. The mechanism of serum placental ALP increase is not well understood. A genetic abnormality has been suspected in one case [6] and a link with a risk of pre-term delivery has been discussed [7].
Our case is the first described in a patient with APS and we did not observe any other cases among more than 200 pregnant patients with APS followed in our centre. In this setting, ALP electrophoresis can be useful to distinguish placental from hepatic or bone isozymes.
Disclosure statement: The authors have declared no conflicts of interest.
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