Part of the book: Medical Complications of Type 2 Diabetes
Part of the book: Type 2 Diabetes
Preeclampsia (PE) is the leading cause of preterm birth by medical indication when associated with premature detachment of placenta normoinserta, and Intrauterine growth restriction (IUGR) is associated with high perinatal morbidity and mortality and long-term sequelae. The main problem of PE is threefold: the diagnostic difficulty, the complicated interrelationship of the pathophysiological processes, and the vulnerability of the maternal-fetal binomial to the therapeutic interventions. The approach for management with PE is preventing its late occurrence in pregnancy. The key to preventing PE is knowledge of the factors that trigger the pathophysiological processes that culminate in the presentation of PE. Understanding the developmental characteristics of the placenta in pregnancy at high risk for PE is essential for understanding the pathophysiology and developing strategies for prevention. When deciding that the population of study is a group of pregnant women, the first ethical criteria that need to be reviewed are those aimed at the protection of the fetus. There are no specific guidelines on how to assess fetal well-being during pregnancy routinely in the clinic, and this deficiency is shifted to clinical research with pregnant women.
Part of the book: Clinical Trials in Vulnerable Populations
Preeclampsia (PE) is a disorder that occurs during pregnancy, it has an estimated worldwide prevalence of 5–8%, being one of the leading causes of maternal and perinatal morbidity and mortality. Currently, different diagnostic criteria exist, however, due to its complexity; the clinical presentation that makes up this syndrome could make its presence unclear. The pathophysiology of PE has been recently postulated and divided into three processes: inadequate uterine remodeling, placental dysfunction and maternal endothelial dysfunction. Despite the advances in the treatment of PE, the outcome of the medical interventions has failed to decrease the morbidity and mortality of this disease. The main reason might be the multifactorial origin of pathogenic processes that lead to the development of PE. That is why treatment is focused on the prevention of PE in patients that might present the risk before developing it late in pregnancy. The knowledge of the pathophysiological factors that trigger the processes that culminate in the presentation of PE, is key for prevention of this disease. However, the origin of these processes is poorly understood. It may be attributed to the ethical considerations that come with the study of these population of patients compared with the study of non-pregnant women.
Part of the book: Obstetrics
Endothelial cell dysfunction has lately become one of the principal subjects being incorporated into the assessment of cardiovascular risk because of the relevance that has been shown in several clinical studies. Comprehending and incorporating basic physiological knowledge, about endothelium molecular biology and vascular tonicity, is key to understanding the relevance of this topic. The approach of endothelial dysfunction physiopathology is overly complex and widely studied, but it can be enrolled into both consumption of bioavailable NO and deficit production of NO. In the last decades, scientific equipment has been developed from the necessity of creating non-invasive tools to measure arterial stiffness, being FMD one of the first and most used ones. Once the endothelial cell dysfunction was identified, several drugs and bioactive substances were evaluated because of their potential to decrease the level of arterial stiffness and improve life quality, such as polyphenols, phosphodiesterase five inhibitors, and new incoming therapies.
Part of the book: Endothelial Dysfunction
Nowadays, we are seeing radically interesting and promising changes in the treatment of patients with type-2 diabetes mellitus (T2 D), which favorably modify the prognosis related to fundamentally neuro-nephro and cardiorenal outcomes. Since no more than two decades ago, the pharmacological armamentarium for the treatment of people with T2D has basically consisted of the use of biguanides, sulfonylureas, insulin sensitizers, and insulins. A great amount of information has been accumulated through the results of new molecules such as sodium/glucose co-transporter type-2 inhibitors (SGLT2i), based on robust data arising from the experience of numerous studies, both clinical and experimental, as well as the glucagon-like peptide 1 receptor agonists (GLP-1ra), that has clearly shown multisystem benefits that improve the function of target organs and delay the onset of complications that ultimately impact the quality of life and the neuro-nephro-cardiovascular outcomes. In this review chapter, we not only highlight the different strategies for glucose control through SGLT2i, GLP-1ra or insulin, including even some fixed combinations, but also some information on different studies with GIP/GLP1 biagonist tirzepatide and on GIP/GLP1/Glucagon triagonist retatrutide primarily focused on weight loss, even though today, they are neither FDA approved nor a part of routine treatment.
Part of the book: Type 2 Diabetes in 2024