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Fetal hydrocephalus and neonatal stroke as the first presentation of protein C deficiency.

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Severe protein C-deficiency is a rare heritable thrombophilia of the newborn. Infants with biallelic PROC mutations present purpura fulminans and intracranial thromboembolism, while the prenatal onset of mutated heterozygotes remains unclear. We herewith present the first case of fetal

Ischemic stroke due to protein C deficiency.

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Plasma protein C exerts anticoagulatory effects by inactivating factors V and VIII. Hereditary protein C deficiency is transmitted as an autosomal dominant disorder. Homozygous individuals usually develop purpura fulminans as newborns; heterozygous protein C-deficient individuals are at increased

Use of protein-C concentrate, heparin, and haemodiafiltration in meningococcus-induced purpura fulminans.

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BACKGROUND Inflammatory and coagulation processes are both affected in meningococcaemia. Severe acquired protein-C deficiency in meningococcaemia is usually associated with substantial mortality: in survivors, skin grafts, amputation, and end-organ failure are not uncommon. Protein C is a natural

Rupert Waterhouse and Carl Friderichsen: adrenal apoplexy.

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The Waterhouse-Friderichsen (WFS) syndrome, also known as purpura fulminans, is described as acute hemorrhagic necrosis of the adrenal glands and is most often caused by meningococcal infection. This clinical entity is more frequently seen in the pediatric than the adult population and is associated

Protein C anticoagulant and cytoprotective pathways.

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Plasma protein C is a serine protease zymogen that is transformed into the active, trypsin-like protease, activated protein C (APC), which can exert multiple activities. For its anticoagulant action, APC causes inactivation of the procoagulant cofactors, factors Va and VIIIa, by limited proteolysis,

Clinical and laboratory characteristics of children with venous thromboembolism and protein C-deficiency: an observational Israeli-German cohort study.

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Venous thromboembolism [TE] is a multifactorial disease and protein C deficiency [PCD] constitutes a major risk factor. In the present study the prevalence of PCD and the clinical presentation at TE onset, including neonatal purpura fulminans, in a cohort of children are reported. In 367 unselected

Testing for heritable thrombophilia in children at Starship Children's Hospital: an audit of requests between 2004 and 2009.

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OBJECTIVE The aim of this study was to review patterns of requests for heritable thrombophilia and to audit these findings against an international standard. METHODS Review of requests for antithrombin, protein C, protein S, activated protein C resistance, Factor V Leiden and prothrombin G20210A

Heartfelt sepsis: microvascular injury due to genomic storm.

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Sepsis is one of the ten leading causes of death in developed and developing countries. In the United States, sepsis mortality approaches that of acute myocardial infarction and exceeds deaths from stroke. Neonates and the elderly are the most vulner-able patients, with these groups suffering from

A unique fatal case of Waterhouse-Friderichsen syndrome caused by Proteus mirabilis in an immunocompetent subject: Case report and literature analysis.

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The Waterhouse-Friderichsen syndrome (WFS), also known as purpura fulminans, is a potentially lethal condition described as acute hemorrhagic necrosis of the adrenal glands. It is often caused by infection. Classically, Neisseriae meningitidis represents the main microorganism related

Thrombotic complications of BMT: association with protein C deficiency.

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A decrease in levels of circulating anticoagulant protein C has been shown to occur following autologous BMT, and this deficiency may contribute to a hypercoagulable state placing patients at risk for thromboembolic events. We report four patients who suffered a variety of thrombotic complications

Thrombosis in newborn infants.

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The incidence of thrombosis is higher among newborn infants than in any other stage of pediatric development. This fact is the consequence of labile characteristics of the neonatal hemostatic system, in addition to exposure to multiple risk factors and the wide use of vascular catheters. Venous

Importance of hemostatic gene polymorphisms for susceptibility to and outcome of severe sepsis.

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Individuals vary considerably in their susceptibility to infection and in their ability to recover from apparently similar infectious processes. These differences can be partially explained by polymorphisms of the genes encoding proteins involved in mediating and controlling the innate immune

Varicella and thrombotic complications associated with transient protein C and protein S deficiencies in children.

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We report six cases of protein S deficiency secondary to varicella. Five cases were complicated by thrombotic and vascular events, namely purpura fulminans and necrotic vasculitis, deep vein thrombosis and stroke. Two cases were associated with protein C deficiency and one case revealed a

The clinical presentation and genotype of protein C deficiency with double mutations of the protein C gene.

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BACKGROUND Severe protein C (PC) deficiency is a rare heritable thrombophilia leading to thromboembolic events during the neonatal period. It remains unclear how individuals with complete PC gene (PROC) defects develop or escape neonatal stroke or purpura fulminans (PF). METHODS We studied the onset

Incidences, risk factors and outcomes of neonatal thromboembolism.

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BACKGROUND The incidences of thromboembolism (TE) in neonates were reported to be around 0.51 per 10,000 live births per year for overall TE and 24 per 10,000 NICU admissions per year. As the incidences of TE in children and adults are lower in Asian populations, the incidences, risk factors, and

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