Second-trimester ovarian pregnancy mimicking intrauterine pregnancy and causing hemorrhagic shock in surgery: a case report and review of the literature.
Authors: Xiang Y, Zhou Q, Wu H, Huang W, Wei L, Li X, Wu W, Ou Y, Shen L, Huang S, Li Z
Journal: BMC pregnancy and childbirth
mental health
psychology
open access
Abstract
Type 2 diabetes mellitus (T2DM), the most prevalent form of diabetes, is a significant global health concern, affecting over 90% of diabetes patients worldwide []. T2DM is not only characterized by insulin resistance and hyperglycemia but also by its profound impact on cognitive function. T2DM has been identified as a significant risk factor for cognitive impairment, with diabetic patients facing a notably elevated risk of mild cognitive impairment, ranging from 1.5 to 2.5 times higher than that of non-diabetic individuals [, ]. The cognitive decline associated with T2DM manifests in various domains, including memory, learning, orientation, judgment, and understanding, leading to a diminished capacity for daily living activities, social interactions, and work capabilities. In severe cases, this cognitive impairment may necessitate professional care, thereby imposing substantial economic burdens on both families and society []. Consequently, identifying novel biomarkers for early diagnosis and intervention in cognitive impairment among T2DM patients is of paramount importance for improving their quality of life. The complement system, a critical component of the innate immune system, has been implicated in the pathogenesis of both T2DM and cognitive impairment. The activation of complement pathways is observed in a variety of diseases, including cognitive impairment and T2DM []. The classical pathway, which involves proteins such as C1q, C3, and C4, has been linked to neuroinflammation and synapse loss in Alzheimer’s disease (AD) [, ]. Furthermore, the levels of complement proteins have been correlated with the incidence of T2DM, suggesting that complement-mediated inflammation may contribute to the pathophysiology of T2DM []. In addition to the complement system, the broader context of immune system activation and inflammation is increasingly recognized as a common denominator in cognitive impairment. Cerebrospinal fluid (CSF) biomarkers indicative of immune activation have been demonstrated to predict the progression of cognitive impairment over time []. Immunoglobulins, particularly immunoglobulin A (IgA) and immunoglobulin G (IgG), are also intricately involved in the pathogenesis and progression of T2DM and its associated complications, including cognitive dysfunction. These immunoglobulins contribute to the inflammatory milieu, influence insulin resistance and metabolic dysregulation, and may even exert protective effects against certain complications [, ].