This book is an authentic microscopic observation of mesenteric adipose tissue and lymph nodes of a woman with severe preeclampsia/eclampsia by an experienced pathologist of 50 years.
The pathogenesis of preeclampsia (PE)/eclampsia(E) or pregnancy-induced hyperten- sion (PIH) and pregnancy associated metabolic disorders are still not clearly elucidated in current molecular biological era, because there has been no link to the tissue changes.
Current clinicians and molecular biologists do not examine or acknowledge the link to any observed tissue changes. There is an increase of incidence of PE/E in USA due to overweight and obesity (Ananth et al 2013). There is also an increase of lifetime risk of cardiovascular disease for women with a history of PE/E. The serum cytokines especially leptin, TNF-alpha and IL-6 are increased in PE/E. The source of hypertriglyceridemia and atherogenic lipid profile in pregnancy and PE/E is not clearly explained. If you perform a web search for images of adipose tissue inflammation, you will find that they do not show actual tissue changes. The images in this book will demonstrate real tissue changes: vasoconstriction, decreased capillary density (rarefaction), macrophages and fibrin-platelet thrombi in the vascular lumens of adipose tissue. The reported articles of Inflammation of adipose tissue and endothelial dysfunction in PubMed do not clearly show a link between placental tissue to maternal tissue. The changes of the target end-organs uterus, cervix and ovary are already published by the author (Updated histopathology of preeclampsia/eclampsia in uterus, cervix and ovary, Amazon, 2011) and are a good example of tissue affected by production of hypoxic lipolysis, adipose tissue inflammation and hypertension. Inflammation of adipose tissue especially in the mesenteric adipose tissue
is called as a cytokine factory of the body (Gerner et al. 2013) and inflammation draining and extending to the regional lymph nodes is called as a metabolic lymphadenopathy or metabolic lymphadenitis (as differentiated from suppurative and granulomatous lymphadenitis). All immuno-histopathologal pictures are illustrated in this book, and the histopathological changes of the other target end-organs affected by production of adipose tissue inflammation will be demonstrated in publication in this series. The adipose tissue in a female body (as an organ with triglyceride storage and endocrine function) takes up 30% or more of body weight, and is a longterm,
persistent supplier of pro-inflammatory cytokines, and blood lipid from inflammatory adipose tissue. All these seem to follow the old “focal infection theory” of untreated endodontal disease (Pallasch and Wahl 2000) in its ability to affect the health of a human for their whole life.
The pathogenesis of preeclampsia (PE)/eclampsia(E) or pregnancy-induced hyperten- sion (PIH) and pregnancy associated metabolic disorders are still not clearly elucidated in current molecular biological era, because there has been no link to the tissue changes.
Current clinicians and molecular biologists do not examine or acknowledge the link to any observed tissue changes. There is an increase of incidence of PE/E in USA due to overweight and obesity (Ananth et al 2013). There is also an increase of lifetime risk of cardiovascular disease for women with a history of PE/E. The serum cytokines especially leptin, TNF-alpha and IL-6 are increased in PE/E. The source of hypertriglyceridemia and atherogenic lipid profile in pregnancy and PE/E is not clearly explained. If you perform a web search for images of adipose tissue inflammation, you will find that they do not show actual tissue changes. The images in this book will demonstrate real tissue changes: vasoconstriction, decreased capillary density (rarefaction), macrophages and fibrin-platelet thrombi in the vascular lumens of adipose tissue. The reported articles of Inflammation of adipose tissue and endothelial dysfunction in PubMed do not clearly show a link between placental tissue to maternal tissue. The changes of the target end-organs uterus, cervix and ovary are already published by the author (Updated histopathology of preeclampsia/eclampsia in uterus, cervix and ovary, Amazon, 2011) and are a good example of tissue affected by production of hypoxic lipolysis, adipose tissue inflammation and hypertension. Inflammation of adipose tissue especially in the mesenteric adipose tissue
is called as a cytokine factory of the body (Gerner et al. 2013) and inflammation draining and extending to the regional lymph nodes is called as a metabolic lymphadenopathy or metabolic lymphadenitis (as differentiated from suppurative and granulomatous lymphadenitis). All immuno-histopathologal pictures are illustrated in this book, and the histopathological changes of the other target end-organs affected by production of adipose tissue inflammation will be demonstrated in publication in this series. The adipose tissue in a female body (as an organ with triglyceride storage and endocrine function) takes up 30% or more of body weight, and is a longterm,
persistent supplier of pro-inflammatory cytokines, and blood lipid from inflammatory adipose tissue. All these seem to follow the old “focal infection theory” of untreated endodontal disease (Pallasch and Wahl 2000) in its ability to affect the health of a human for their whole life.
