Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Pre-eclampsia is associated with Helicobacter pylori seropositivity in Italy Antonio Ponzetto a , Simona Cardaropoli b , Ettore Piccoli b , Alessandro Rolfo b , Luisa Gennero a , Darja Kanduc c and Tullia Todros b Objectives Pre-eclampsia (PE) is characterized by an excess of inflammation and endothelial dysfunction. Helicobacter pylori (H. pylori) causes chronic inflammatory changes and endothelial damage. We investigated the prevalence of seropositivity for IgG against H. pylori and cytotoxin-associated antigen A (CagA) in PE patients and the presence of H. pylori DNA in their placentas. Methods We tested 47 pregnant women with PE and 47 with uneventful pregnancies for serum antibodies against H. pylori (enzyme immunoassays) and CagA protein (immunoblot assays). In 20 of them (10 normal and 10 PE) we assessed the presence, in the placenta, of H. pylori DNA by means of nested polymerase chain reaction (PCR). The odds ratios (OR) and 95% confidence intervals (CI), adjusted for parity, were calculated using logistic regression analysis to assess the risk of PE associated with H. pylori infection. Results Helicobacter pylori seropositivity frequency was higher in mothers with PE (51.1%) compared to women with uneventful pregnancy (31.9%) (OR, 2.668; 95% CI, 1.084– 6.566; P U 0.033). The difference was even greater for CagA seropositivity (80.9 and 14.9%, respectively) (OR, 26.035; 95% CI, 8.193–82.729; P < 0.001). All placentas were negative for H. pylori DNA. Conclusions Helicobacter pylori, and especially strains carrying the CagA gene, may contribute to the inflammatory mechanisms involved in the pathogenesis of PE. J Hypertens 24:2445–2449 Q 2006 Lippincott Williams & Wilkins. Journal of Hypertension 2006, 24:2445–2449 Keywords: CagA protein, Helicobacter pylori, pre-eclampsia a Department of Internal Medicine, b Department of Obstetrics and Gynecology, University of Turin and c Department of Biochemistry and Molecular Biology, University of Bari, Italy Correspondence and requests for reprints to Simona Cardaropoli, Department of Obstetrics and Gynecology, University of Turin, via Ventimiglia 3, 10126 Torino, Italy Tel: +39 011 3134436; fax: +39 011 3134450; e-mail: simona.cardaropoli@unito.it Sponsorship: A.P. was supported by grants from the Ministry of University, University of Turin, Regione Piemonte and the Stola Auto group. S.C. was supported by grants from Compagnia di San Paolo, Turin, Italy. Received 2 March 2006 Revised 22 June 2006 Accepted 28 July 2006 See editorial commentary on page 2353 Introduction Pre-eclampsia (PE) is a hypertensive and coagulative disorder affecting 2–7% of all pregnancies and remains one of the major causes of maternal and fetal mortality and morbidity. Maternal mortality attributable to PE has been reduced in developed countries; however, perinatal mortality, perinatal and long-term morbidity, and neuro- logical sequelae resulting from fetal growth restriction and/or preterm delivery are still unresolved [1]. More- over, it has been shown that PE mothers are at increased risk for ischaemic heart disease and death from cardio- vascular causes later in life [2,3]. The disappointing therapeutic results for child well- being reflect the fact that the aetiology and pathogenesis of PE are largely unknown. The most likely hypothesis is that a generalized endothelial dysfunction is the first step in the development of PE [4]. It has been proposed that in PE, the normal inflammatory response of pregnancy, involving intravascular leucocytes and the clotting sys- tem, is exaggerated [5]. There is mounting evidence that certain infectious agents can induce endothelial inflammation and injury; the bacterium Helicobacter pylori (H. pylori) is one of these agents [6]. Helicobacter pylori is the aetiological cause of the large majority of peptic ulcer diseases, gastric cancer, and gastric MALT lymphoma [7]. Moreover, it has been demonstrated that this pathogen enhances platelet acti- vation and therefore thrombus formation [6,8]. The par- tial or complete vascular obstruction in H. pylori-infected individuals may lead to acute myocardial infarction [9] or ischaemic stroke [10]. It has been demonstrated that some H. pylori strains express genes (VacA, CagA, IceA, etc.) conferring specific biological properties – proinflam- matory, cytotoxic, vacuolating – which could enhance the in vivo pathogenicity of H. pylori. The strains carrying the cytotoxin-associated antigen A (CagA) gene are among the most virulent and associated with increased inflam- mation [11]. Original article 2445 Part of this work was presented in abstract form at the First SGI International Summit ‘Preterm Birth’ (10–12 November 2005, Siena, Italy). 0263-6352 ß 2006 Lippincott Williams & Wilkins