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Am J Perinatol 2016; 33(11): 1099-1103
DOI: 10.1055/s-0036-1586102
Original Article
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Portal Vein Thrombosis in a Preterm Newborn with Mutation of the MTHFR and PAI-1 Genes and Sepsis by Candida parapsilosis

On behalf of the Study Group of Neonatal Infectious Diseases Affiliated to the Italian Society of Neonatology.
Mario Giuffrè
1   Neonatology and Neonatal Intensive Care Unit, Department of Sciences for Health Promotion and Mother and Child Care, Palermo University, Palermo, Italy
,
Clelia Lo Verso
1   Neonatology and Neonatal Intensive Care Unit, Department of Sciences for Health Promotion and Mother and Child Care, Palermo University, Palermo, Italy
,
Gregorio Serra
1   Neonatology and Neonatal Intensive Care Unit, Department of Sciences for Health Promotion and Mother and Child Care, Palermo University, Palermo, Italy
,
Giovanni Moceri
1   Neonatology and Neonatal Intensive Care Unit, Department of Sciences for Health Promotion and Mother and Child Care, Palermo University, Palermo, Italy
,
Marcello Cimador
1   Neonatology and Neonatal Intensive Care Unit, Department of Sciences for Health Promotion and Mother and Child Care, Palermo University, Palermo, Italy
,
Giovanni Corsello
1   Neonatology and Neonatal Intensive Care Unit, Department of Sciences for Health Promotion and Mother and Child Care, Palermo University, Palermo, Italy
› Author Affiliations
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Publication History

Publication Date:
07 September 2016 (online)

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Abstract

Objective This report discusses the role of both congenital and acquired risk factors in the pathogenesis of portal vein thrombosis (PVT).

Study Design We describe the clinical management and treatment of PVT in a preterm newborn with a homozygous mutation of the methylenetetrahydrofolate reductase (MTHFR) and plasminogen activator inhibitor-1 (PAI-1) genes and sepsis by Candida parapsilosis.

Results Although literature data suggest a minor role of genetic factors in thrombophilia in the case of only one mutation, we hypothesize that combined thrombophilic genetic defects may have a cumulative effect and significantly increase the thrombotic risk.

Conclusion It could be appropriate to include more detailed analyses of procoagulant and fibrinolytic factors in the diagnostic workup of neonatal thrombosis, also through the investigation of genetic polymorphisms. The anticoagulant therapy and the removal of concurrent risk factors remain basic steps for the adequate management and prevention of complications.

Keywords

portal thrombosis - umbilical catheter - fungal infection - anticoagulation therapy - thrombophilia - gene polymorphism