Group B Streptococcus, phospholipids and pulmonary hypertension

Curtis, Jerri; Kim, Geumsoo; Wehr, Nancy B.; Levine, Rodney L.

doi:10.1038/jp.2010.168

Cited by 3 publications

(3 citation statements)

References 34 publications

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“…Thus, early administration of penicillin after birth may help to reduce the severity of PPHN associated with GBS infection. However, penicillin treatment of Streptococci also induces an immediate secretion of phospholipids, which may contribute to developing PPHN ( 22 ). Furthermore, long-term usage of penicillin increases lipid synthesis.…”

Section: Discussionmentioning

confidence: 99%

A nomogram prediction model for early death in patients with persistent pulmonary hypertension of the newborn

Lin

Mi²,

Zhang³

et al. 2022

Front. Cardiovasc. Med.

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BackgroundPersistent pulmonary hypertension of the newborn (PPHN) is a major lethal disorder in neonates that leads to an extremely high mortality rate. Thus, the early identification of adverse outcomes in PPHN is critical for clinical practice. This research attempted to develop a nomogram prediction system for assessing the mortality of newborns with PPHN.MethodsTwo hundred and three newborns with PPHN diagnosed from January 2015 to March 2022 were involved in the study. The clinical features of these newborns and pregnancy details were compared between newborns in the survival and lethal groups. Univariable and multivariate analyses were established in sequence to demonstrate the essential risk factors. The nomogram prediction model was built.ResultsA total of 203 newborns were included in the analysis. 136 (67.0%) newborns represented the hospital survival group. Plasma pH value (OR = 0.606, p = 0.000, 95% CI 0.45715–0.80315), septicemia (OR = 3.544, p = 0.000, 95% CI 1.85160–6.78300), and abnormal pregnancy history (OR = 3.331, p = 0.008, 95% CI 1.37550–8.06680) were identified as independent risk factors for neonatal death in newborns associated with PPHN. Finally, the nomogram predictive model was established based on multivariate analysis results, indicating the efficacies of prediction and calibration.ConclusionThis study generated an applicable risk score formula using the plasma pH value, septicemia, and abnormal pregnancy history to recognize neonatal death in newborns with PPHN, presenting a sufficient predictive value and calibration.

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Section: Discussionmentioning

confidence: 99%

A nomogram prediction model for early death in patients with persistent pulmonary hypertension of the newborn

Lin

Mi²,

Zhang³

et al. 2022

Front. Cardiovasc. Med.

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“…Group B Streptococcus (GBS) infection continues to be the predominant cause of early onset sepsis. The Phosphatidylglycerol and cardiolipin are the dominant phospholipids of GBS that are associated with PPHN; and animal studies have shown that indomethacin can lower the PVR induced by these agents ( 20 ). There are case reports of ureaplasma infection causing PPHN with a high case fatality rate, and Phospholipase A and C as the incriminating agents ( 21 ).…”

Section: Risk Factorsmentioning

confidence: 99%

Pathophysiology, Management, and Outcome of Persistent Pulmonary Hypertension of the Newborn: A Clinical Review

Puthiyachirakkal¹,

Mhanna²

2013

Front. Pediatr.

131

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Persistent Pulmonary Hypertension of the Newborn (PPHN) results from the failure of relaxation of the pulmonary vasculature at birth, leading to shunting of non-oxygenated blood from the pulmonary to the systemic circulation. More often, full term and near-term infants are affected, however it is not uncommon to see PPHN in preterm infants who have respiratory distress syndrome. In some infants pulmonary vascular remodeling is present at birth, pointing toward the prenatal onset of the disease process. Regardless of the etiology, PPHN should be diagnosed and treated as soon as possible to avoid hypoxia related short term and long-term morbidities. The mainstay therapy is the treatment of the underlying condition along with several promising therapeutic modalities such as oxygen supplementation, mechanical ventilation, nitric oxide, phosphodiesterase inhibitors, prostaglandins analogs, endothelin receptor antagonists, and extracorporeal membrane oxygenation. The optimal approach to the management of PPHN remains controversial. After discharge from the NICU, infants with PPHN warrant long-term follow up since they are at risk for neurodevelopmental disabilities and chronic health conditions.

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“…In experimentally induced streptococcal infections it was observed that cycloxygenase inhibitors, such as indomethacin, can prevent pulmonary hypertension [ 34 ]. Recent studies have revealed that vasoconstriction can also be determined by some phospholipids (in particular, phosphatidyl-glycerol and cardiolipin) present in the bacterial wall of streptococcus B [ 35 ]. Studies on perinatal asphyxia have focused on leukotrienes [ 36 ] and, especially, on endothelin whose plasma concentrations were markedly higher than observed in normal controls [ 37 ].…”

Section: Introductionmentioning

confidence: 99%

Molecular physiopathogenetic mechanisms and development of new potential therapeutic strategies in persistent pulmonary hypertension of the newborn

Distefano

Sciacca

2015

Ital J Pediatr

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Persistent pulmonary hypertension of the newborn (PPHN) is a cyanogenic plurifactorial disorder characterized by failed postnatal drop of pulmonary vascular resistance and maintenance of right-to-left shunt across ductus arteriosus and foramen ovale typical of intrauterine life. The pathogenesis of PPHN is very complex and can result from functional (vasoconstriction) or structural (arteriolar remodeling, reduced pulmonary vessels density) anomalies of pulmonary circulation. Etiopathogenetic factors heterogeneity can strongly condition therapeutical results and prognosis of PPHN that is particularly severe in organic forms that are usually refractory to selective pulmonary vasodilator therapy with inhaled nitric oxide. This paper reports the more recent acquisitions on molecular physiopathogenetic mechanisms underlying functional and structural forms of PPHN and illustrates the bases for adoption of new potential treatment strategies for organic PPHN. These strategies aim to reverse pulmonary vascular remodeling in PPHN with arteriolar smooth muscle hypertrophy and stimulate pulmonary vascular and alveolar growth in PPHN associated with lung hypoplasia.In order to restore lung growth in this severe form of PPHN, attention is focused on the results of studies of mesenchymal stem cells and their therapeutical paracrine effects on bronchopulmonry dysplasia, a chronic neonatal lung disease characterized by arrested vascular and alveolar growth and development of pulmonary hypertension.

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Group B Streptococcus, phospholipids and pulmonary hypertension

Cited by 3 publications

References 34 publications

A nomogram prediction model for early death in patients with persistent pulmonary hypertension of the newborn

A nomogram prediction model for early death in patients with persistent pulmonary hypertension of the newborn

Pathophysiology, Management, and Outcome of Persistent Pulmonary Hypertension of the Newborn: A Clinical Review

Molecular physiopathogenetic mechanisms and development of new potential therapeutic strategies in persistent pulmonary hypertension of the newborn

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