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Preeclampsia is a severe pregnancy complication with high potential for adverse effects on maternal and fetal health during the perinatal period. It is also associated with an increased risk of maternal cardiovascular disease later in life. Development of preeclampsia can be decreased by prescribing low-dose aspirin to high-risk women. At present, maternal and pregnancy factors are used to assess the risk of preeclampsia. One additional factor that could add to the assessment of risk is a family history of hypertension, cardiovascular disease, or diabetes, especially for nulliparous women who do not have a pregnancy history to inform treatment decisions. Therefore, we conducted a systematic review to assess the association between family history of the aforementioned conditions and preeclampsia. Four databases including MEDLINE, EMBASE, the Cochrane Library, and CINAHL/pre-CINAHL were searched for observational studies that examined a family history of hypertension, cardiovascular disease, or diabetes in women with preeclampsia and in a control population. Studies were evaluated for quality using the Newcastle-Ottawa Scale. A total of 84 relevant studies were identified. A meta-analysis was not conducted due to suspected heterogeneity in the included studies. Most studies reported a positive association between a family history of hypertension or cardiovascular disease and the development of preeclampsia. The majority of studies examining family history of diabetes reported non-significant associations. Overall, family history of hypertension or cardiovascular disease is associated with a higher risk for developing preeclampsia and should be considered when assessing women in the first trimester for low-dose aspirin., (Copyright © 2020. Published by Elsevier Inc.)

This article reviews the evidence and nutrition practice recommendations from the American Dietetic Association's nutrition practice guidelines for type 1 and type 2 diabetes in adults. The research literature was reviewed to answer nutrition practice questions and resulted in 29 recommendations. Here, we present the recommendations and provide a comprehensive and systematic review of the evidence associated with their development. Major nutrition therapy factors reviewed are carbohydrate (intake, sucrose, non-nutritive sweeteners, glycemic index, and fiber), protein intake, cardiovascular disease, and weight management. Contributing factors to nutrition therapy reviewed are physical activity and glucose monitoring. Based on individualized nutrition therapy client/patient goals and lifestyle changes the client/patient is willing and able to make, registered dietitians can select appropriate interventions based on key recommendations that include consistency in day-to-day carbohydrate intake, adjusting insulin doses to match carbohydrate intake, substitution of sucrose-containing foods, usual protein intake, cardioprotective nutrition interventions, weight management strategies, regular physical activity, and use of self-monitored blood glucose data. The evidence is strong that medical nutrition therapy provided by registered dietitians is an effective and essential therapy in the management of diabetes., (Copyright © 2010 American Dietetic Association. Published by Elsevier Inc. All rights reserved.)

Objective: To (a) explore the contribution of infant, environmental, and historical factors to the number of days from initiation to achievement of full nipple feeding (transition time) for premature infants with a history of lung disease; (b) examine differences in the contribution of infant and environmental factors to transition time made by historical era, either earlier (in the 1980s) or later (in the 1990s); and (c) compare, within eras, the contribution to transition time of infant and environmental factors for infants with each lung diagnosis, respiratory distress syndrome (RDS) without bronchopulmonary dysplasia (BPD) or BPD., Design: Data were collected at two midwestern hospitals from the records of premature infants with a diagnosis of either RDS without BPD or BPD. The influence on transition time of infant, environmental and historical factors was assessed with the Cox proportional hazards model. This analytic model, a form of regression analysis, also was used to explore how era influenced the contribution to transition time of infant and environmental factors. Finally, the contribution to transition time of infant and environmental factors was examined within diagnostic group for each era., Sample: The hospital records audited were for infants who were 32 weeks gestational age or less with weight appropriate for gestational age. The number in each diagnostic group for each era was (a) BPD--Early, n = 35; (b) RDS--Early, n = 21; (c) BPD--Late, n = 21; and (d) RDS--Late, n = 15)., Results: All three types of factors (infant, environmental, and historical) contributed significantly (p < .05) to shortening or lengthening transition time. A diagnosis of BPD lengthened transition time only in the early era. Across both eras, the number of days on tube feedings significantly lengthened transition time, and the older the infant in postconceptional age (PCA) at initiation of nipple feeding, the shorter the transition time., Conclusion: The contribution of infant, environmental, and historical factors to transition time confirmed the basic structure of the theoretical model of transition time for premature infants with a history of lung disease. The influence of era on the contributions to transition time of infant and environmental factors suggests that care policy and practice have shortened the transition time. Although the current findings support the basic structure of the theoretical model for infants with either RDS or BPD, the marginally significant (p < .10) shortening effect of PCA on transition time for infants with BPD in both eras suggests that advancement to full nipple feeding may be limited by neurodevelopmental capacities, including respiratory control. How these capacities can be supported for advancement to full nipple feeding is a challenge for nursing practice and research.

Background: Meningococcal sepsis remains an important cause of morbidity and mortality. We hypothesised that children with severe meningococcaemia might benefit from inhibition of the inflammatory processes thought responsible for fulminant disease. rBPI21 is a recombinant, N-terminal fragment of human bactericidal/permeability-increasing protein, which kills meningococci and binds to and clears bacterial endotoxin, these being the primary inducers of the systemic inflammation. The aim of this study was to determine the safety and kinetics of rBPI21 in children with severe meningococcaemia and to make a preliminary assessment of clinical outcome., Methods: In this open-label, dose-escalation, phase I/II trial in severe meningococcaemia (Glasgow meningococcal prognostic septicaemia score [GMSPS] > or = 8), 26 patients aged 1-18 years, who had received their first dose of antibiotics no more than 8 hours earlier were given rBPI21 by infusion at total doses of 1.0, 2.0, and 4.0 mg/kg., Findings: The patients had significantly raised plasma concentrations of bacterial endotoxin and cytokines. Peak and steady state BPI concentrations were comparable with pharmacokinetic data in healthy adults. All complications were compatible with the expected pattern for severe meningococcal sepsis. Only one patient died. This outcome was found to compare favourably with a predicted mortality of > or = 30% by GMSPS, > or = 15% by plasma endotoxin values, > or = 28% by plasma interleukin-6 concentrations, 29-49% by severity of coagulopathy, and 20% (11/54) by comparison with recent historical patients consecutively treated in participating centres before this study., Interpretation: This, the first clinical trial or rBPI21, shows that rBPI21 can be safely administered to children with severe meningococcaemia and that the pharmacokinetics are consistent with patterns seen in healthy adults. Predicted mortality, on the basis of GMSPS, laboratory indices of inflammation and coagulopathy, and historical controls, was for between four and eight deaths. These findings have prompted a phase III randomised trial.

A recombinant endotoxin-neutralizing protein, rBPI23, was shown to partially prevent endotoxin-induced activation of the fibrinolytic and coagulation systems in experimental endotoxemia in humans. In a placebo-controlled, blinded crossover study, eight volunteers were challenged twice with an intravenous bolus injection of endotoxin (40 EU/kg of body weight) and concurrently received either rBPI23 (1 mg/kg) or placebo (human serum albumin, 0.2 mg/kg). rBPI23 treatment significantly lowered the endotoxin-induced fibrinolytic response, ie, reduced the release of tissue-type plasminogen activator, urokinase-type plasminogen activator, plasminogen activator inhibitor antigen, and complex formation of plasmin alpha 2-antiplasmin (P = .0078 for each). Plasminogen activator inhibitor activity was also reduced, but not significantly according to the Hochberg method (P = .0304). The endotoxin-induced activation of the procoagulant state as reflected by increase in F1 + 2 fragments and TAT complexes was blunted by rBPI23 infusion (P = .0391 [not significant according to the Hochberg method] and .0078, respectively). These results indicate that rBPI23 is capable of reducing both the activation of the fibrinolytic and the coagulation systems after low-dose endotoxin infusion in humans.