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Pathophysiology of Preeclampsia: The Role of Adiposity and Serum Adipokines
DOI: http://dx.doi.org/10.5772/.104752
These biomarkers can be used in combination with maternal characteristics for the
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early prediction of PE. This will help health care providers to institute measures such
as diet control, medication, and exercises tailored for pregnant women with these risk
factors so as to reduce the incidence of preeclampsia.
Acknowledgements
i. Prof. Francis Agyemang Yeboah, Department of Molecular Medicine, School
Medical Sciences, Kwame Nkrumah University of Science and Technology,
Kumasi, Ghana. Telephone: +233 24 5005500. Email: drfay1801@gmail.com.
ii. Prof. Robert Amadu Ngala, Department of Molecular Medicine, School Medical
Sciences, Kwame Nkrumah University of Science and Technology, Kumasi,
Ghana. Telephone: +233 207722162. Email: rngala2000@yahoo.com.
iii. Mr. Salifu Nanga, School of Basic and Biomedical Sciences, University of Health and
Allied Sciences, Ho, Ghana. Telephone: +233 243667951. Email: snanga@uhas.edu.
Conflict of interest
The authors declare no conflict of interest.
Abbreviations
BMI body mass index
PE preeclampsia
ADP adiponectin
LP leptin
RTN resistin
VF visfatin
TG triglycerides
TC total cholesterol
HDL high-density lipoprotein cholesterol
LDL low-density lipoprotein cholesterol
VLDL very low-density lipoprotein cholesterol
Novel Pathogenesis and Treatments for Cardiovascular Disease
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Pathophysiology of Preeclampsia: The Role of Adiposity and Serum Adipokines
DOI: http://dx.doi.org/10.5772/.104752
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Chapter 12
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Cardiovascular Health in Kawasaki
Disease
MitsuruSeki
Abstract
Ka
wasaki disease (KD) is a self-limiting vasculitis of unknown etiology primarily
affecting young children. The most important aspect in the treatment of KD is the
prevention of coronary artery lesions (CALs) because myocardial ischemia or
infarction due to coronary artery stenosis or occlusion may be lethal. In addition,
patients with a history of KD have systemic vasculitis, which indicates vascular
endothelial damage. Therefore, patients with CAL are at a high risk of atherosclerosis. While some reports have shown an increase in vascular stiffness, others have
not, and the presence of atherosclerotic lesions in patients with KD is controversial.
Appropriate acute-phase treatment to prevent CAL and systemic vasculitis and subsequent regular follow-ups are important. This chapter deals with the cardiovascular
health of patients with a history of KD.
Keywords: vasculitis, aortic stiffness, atherosclerosis, vascular health, Kawasaki
disease
. Introduction
Kawasaki disease (KD) was first reported as acute febrile mucocutaneous lymph
node syndrome by Tomisaku Kawasaki in . KD is a self-limited vasculitis affecting
children mainly under years of age, the etiology is still unknown [, ]. KD is one
of the most common acquired cardiac disorders in children, causing coronary artery
dilatation or aneurysms. Coronary artery lesion (CAL) develop in approximately
of KD patients who do not receive appropriate treatment []. As KD is a systemic
vasculitis, vessel walls other than coronary arteries are affected. KD patients with
cardiovascular complications should be closely monitored for cardiovascular events
throughout their lives. Furthermore, even in the absence of obvious complications,
patients with a history of KD are likely to experience underlying vascular endothelial
damage. This chapter deals with long-term cardiovascular health in this population.
. Epidemiology
KD is a systemic vasculitis that mainly affects children younger than years of
age. Currently, more than countries in Asia, the Middle East, the Americas, Africa,
and Europe have reported KD cases []. The incidence of KD is high in Japan, Korea,
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and Taiwan, but low in North America and European countries. These incidences
reported in different regions of the world can be affected by the survey/surveillance
methods used, clinical diagnostic and treatment practices, physician awareness of
KD, and data sources used to estimate incidence [].
According to a nationwide epidemiological survey of KD in Japan, more than
, patients were reported annually until , which was before Coronavirus
disease (COVID-) pandemic []. The annual number of patients with KD in
Japan was , in ; however, it decreased to , in . The incidence rate
(per , children aged –years per year) was . (. in boys, and . in
girls) in , and . (. in boys, and . in girls) in . Although infectious factors or foreign antigens can trigger KD, the cause of this syndrome remains
unclear. Several children diagnosed with COVID- have developed multisystem
inflammatory syndrome in children (MIS-C), which shows KD-like symptoms [,].
On the other hand, the decline in the incidence of KD remains small, despite the
extreme reduction in common pediatric infectious diseases during the COVID-
pandemic period in Japan, KD may be triggered by unidentified respiratory pathogens
that can be acquired both within and outside the household [].
Genetic factors appear to be involved in KD pathogenesis, as suggested by the highest incidence among Asians and Pacific Islanders, and in boys versus girls. In a genomewide linkage study, several functional polymorphisms such as inositol ,,-trisphosphate
-kinase C (ITPKC) and caspase- (CASP) have been identified as common susceptibility genes for KD. Siblings of children with KD have an increased risk of developing the
disease []. Sibling pairs with KD within a short time interval may be due to environmental triggers, including infectious antigens. Both genetic and environmental factors
are thought to interact with each other during the onset of KD; therefore, a detailed
study of these contributing factors may help elucidate the pathogenesis of KD.
. Histopathology of vasculitis
The histopathological characteristics of KD are as follows: () major muscular
arteries branching from the aorta, including the coronary arteries, are predominantly
injured; () the damaged arteries are extra-arterial, not arteries within organs; ()
acute vasculitis occurs synchronously throughout the body; and () vasculitis is a
proliferative inflammation consisting of an abnormal accumulation of monocytes/
macrophages.
KD is characterized by inflammation of the coronary artery in the acute phase,
which usually lasts for approximately weeks. The earliest histological changes in
coronary arteritis are seen on sixth to eighth day of illness, starting with the infiltration of inflammatory cells in the tunica adventitia and tunica intima. Inflammatory
cells infiltrate the tunica media, leading to inflammation of all layers of the vessel wall
by the tenth day of illness. Subsequently, the artery begins to dilate owing to significant damage to the internal elastic lamina or tunica media. Inflammatory cell infiltration continues for approximately weeks and then gradually fades. If the vessel wall
undergoes a certain degree of damage, even after vasculitis subsides, inflammatory
scarring of the coronary artery remains for a long time. In particular, in patients with
coronary aneurysms, various findings, such as stenotic lesions or extensive calcification of the aneurysm wall, are observed [].
In addition to the coronary arteries, other systemic blood vessels are injured by
vasculitis []. Whole-body examination for KD to evaluate systemic vasculitis shows
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