Septic shock is a critical clinical condition with a high mortality rate. A better understanding of the underlying mechanisms is important to develop effective therapies. Basic and clinical studies suggest that activation of complements in the common cascade, for example, complement component 3 (C3) and C5, is involved in the development of septic shock. The involvement of three upstream complement pathways in septic shock is more complicated. Both the classical and alternative pathways appear to be activated in septic shock, but the alternative pathway may be activated earlier than the classical pathway. Activation of these two pathways is essential to clear endotoxin. Recent investigations have shed light on the role of lectin complement pathway in septic shock. Published reports suggest a protective role of mannose-binding lectin (MBL) against sepsis. Our preliminary study of MBL-associated serine protease-2 (MASP-2) in septic shock patients indicated that acute decrease of MASP-2 in the early phase of septic shock might correlate with in-hospital mortality. It is unknown whether excessive activation of these three upstream complement pathways may contribute to the detrimental effects in septic shock. This paper also discusses additional complement-related pathogenic mechanisms and intervention strategies for septic shock.

Importance: Preeclampsia is a devastating disease of pregnancy associated with increased risk of fetal and maternal complications. African American pregnant women have a high prevalence of preeclampsia, but there is a need of systemic analyses of this high-risk group regarding complications, etiology, and biomarkers. Objective: The aim of this study was to provide a synopsis of current research of preeclampsia specifically related to African American women. Evidence Acquisition: A comprehensive search was performed in the bibliographic database PubMed with keywords “preeclampsia” and “African American.” Results: African American women with preeclampsia were at an increased risk of preterm birth, which resulted in low-birth-weight infants. Intrauterine fetal death among African American preeclamptic patients occurs at twice the rate as in other races. On the maternal side, African American mothers with preeclampsia have more severe hypertension, antepartum hemorrhage, and increased mortality. Those who survive preeclampsia have a high risk of postpartum cardiometabolic disease. Preexisting conditions (eg, systemic lupus erythematosus) and genetic mutations (eg, sickle cell disease in the mother, FVL or APOL1 mutations in the fetus) may contribute to the higher prevalence and worse outcomes in African American women. Many blood factors, for example, the ratio of proteins sFlt/PlGF, hormones, and inflammatory factors, have been studied as potential biomarkers for preeclampsia, but their specificity needs further investigation. Conclusions: Further studies of preeclampsia among African American women addressing underlying risk factors and etiologies, coupled with identification of preeclampsia-specific biomarkers allowing early detection and intervention, will significantly improve the clinical management of this devastating disease. Target Audience: Obstetricians and gynecologists, family physicians. Learning Objectives: After completing this activity, the learner should be better able to describe the difference in prevalence of fetal and maternal complications among African American women with preeclampsia versus women of other races; explain updated genetic studies of preeclampsia specifically related to African American women; and analyze current research of biomarkers for prediction of status and progress of preeclampsia.

Recent studies showed that innate autoimmunity is an early mechanism for ischemia–reperfusion (I/R) injury. Results from different animal models showed that reperfusion of ischemic tissues elicits an acute inflammatory response involving a complement system, which is activated by autoreactive natural IgM. Moreover, ischemia-specific self-targets were identified. In contrast to the unsuccessful attempts in the past to treat I/R injury, targeting natural IgM-mediated innate autoimmunity may open a new avenue for early intervention.