ABSTRACT
Background and Objectives: Preterm birth, one of the leading causes of neonatal mortality, occurs in between 5 and 18% of births. Premature birth can be induced by a variety of triggers, including infection or inflammation. Serum amyloid A, a family of apolipoproteins, increases significantly and rapidly at the onset of inflammation. This study aims to systematically review the results of studies in the literature that have examined the correlation between SAA and PTB/PROM. Materials and Methods: To examine the correlation between serum amyloid A levels in women who gave birth prematurely, a systematic analysis was performed according to PRISMA guidelines. Studies were retrieved by searching the electronic databases PubMed and Google Scholar. The primary outcome measure was the standardized mean difference in serum amyloid A level comparing the preterm birth or premature rupture of membranes groups and the term birth group. Results: Based on the inclusion criteria, a total of 5 manuscripts adequately addressed the desired outcome and were thus included in the analysis. All included studies showed a statistically significant difference in serum SAA levels between the preterm birth or preterm rupture of membranes groups and the term birth group. The pooled effect, according to the random effects model, is SMD = 2.70. However, the effect is not significant (p = 0.097). In addition, the analysis reveals an increased heterogeneity with an I2 = 96%. Further, the analysis of the influence on heterogeneity found a study that has a significant influence on heterogeneity. However, even after outline exclusion, heterogeneity remained high I2 = 90.7%. Conclusions: There is an association between increased levels of SAA and preterm birth/PROM, but studies have shown great heterogeneity.
Subject(s)
Pregnancy Complications , Premature Birth , Pregnancy , Infant, Newborn , Female , Humans , Serum Amyloid A Protein , Inflammation , Patient Reported Outcome MeasuresABSTRACT
Sepsis-induced myocardial dysfunction (SIMD) is one of the major predictors of morbidity and mortality of sepsis. A high percentage of patients with SIMD develop a status similar to cardiogenic shock. A high level of bacterial lipopolysaccharide (LPS) associated with an overexpression of CD14 acts as the trigger for the release of a broad spectrum of cytokines. Our study aimed to understand the correlation between septic cardiomyopathy and CD14 immunohistochemical expression. The study included 29 patients who died of septic shock. Increased values of membranous CD14 and soluble CD14 in the heart tissue were correlated with adverse patient evolution. A high cellular expression of CD14 was noted in the study group vs. the control group (p = 0.0013). Therefore, a close positive association between the amount of LPS related to sCD14 and the cellular expression of mCD14 is probable. By extrapolation, we suggest that a large amount of sCD14 detected in the cardiac tissue will activate the mCD14-TRL4-LBP-LPS complex, which in turn will induce an inadequate immune response, resulting in heart damage proportional to the amount of LPS. CD14 could represent a valuable marker for septic cardiomyopathy; thus, apoptosis of cardiomyocytes could be foreseen by its high value.
