PIVKA-II showed superior sensitivity and specificity for HCC compared with the other three markers. GP73 may be useful for detecting cirrhosis as a risk factor for HCC. Fuc-HPX showed inferior sensitivity and specificity compared to the other markers.

There are several types of abnormalities in the integrated physiology of pulmonary circulation in congenital heart disease. The main pathology of Eisenmenger syndrome involves a change in pulmonary resistance and is the most commonly observed pathophysiology in pulmonary hypertension. Other diseases also present with the main pathophysiological characteristic of reduced pulmonary compliance, such as tetralogy of Fallot and multiple peripheral pulmonary stenosis. In addition, the cavo-pulmonary connection has the unique feature of both pulmonary circulation and regulation. According to the differences in the pathophysiological features of pulmonary circulation, therapeutic approaches may considerably differ between diseases and conditions. Physiology-based clinical insights with regard to pulmonary circulation in congenital heart disease will be discussed in this chapter.

Objective: Terminating pregnancy appropriately before intrauterine infection has progressed may have an improved prognosis for preterm infants. We evaluate how the combination of histological chorioamnionitis (hCAM) and clinical chorioamnionitis (cCAM) affects the short-term prognosis of infants. Study Design: This retrospective multicenter cohort study based on the Neonatal Research Network of Japan included extremely preterm infants born weighing <1500 g between 2008 and 2018. Demographic characteristics, morbidity, and mortality were compared between the cCAM(−)hCAM(+) and cCAM(+)hCAM(+) groups. Results: We included 16,304 infants. The progression to cCAM in infants with hCAM was correlated with the increase in home oxygen therapy (HOT) (adjusted odds ratio [aOR], 1.27; 95% confidence interval [CI], 1.11–1.44) and persistent pulmonary hypertension of the newborn (PPHN) (1.20, 1.04–1.38). Furthermore, increased progression of the hCAM stage in infants with cCAM correlated with an increase in bronchopulmonary dysplasia (BPD) (1.05, 1.01–1.11), HOT (1.10, 1.02–1.18), and PPHN (1.09, 1.01–1.18). However, it had a negative impact on hemodynamically significant patent ductus arteriosus (hsPDA) (0.87, 0.83–0.92) and death before discharge from the neonatal intensive care unit (NICU) (0.88, 0.81–0.96). Conclusion: Progression to cCAM in infants with hCAM positively correlated with HOT and PPHN. Progression of hCAM staging in infants with cCAM further increases the prevalence of BPD and the need for HOT and PPHN while reducing the prevalence of hsPDA and death before discharge from the NICU. The effects of the progressive hCAM stage in infants with cCAM vary from positive to negative by disease.

Splanchnic circulation constitutes a major portion of the vasculature capacitance and plays an important role in maintaining blood perfusion. Because patients with asplenia syndrome lack this vascular bed as a blood reservoir, they may have a unique blood volume and distribution, which may be related to their vulnerability to the haemodynamic changes often observed in clinical practice. During cardiac catheterisation, the mean circulatory filling pressure was calculated with the Valsalva manoeuvre in 19 patients with Fontan circulation, including 5 patients with asplenia syndrome. We also measured the cardiac output index and circulatory blood volume by using a dye dilution technique. The blood volume and the mean circulatory filling pressure and the venous capacitance in patients with asplenia syndrome were similar to those in the remaining patients with Fontan circulation (85 ± 14 versus 77 ± 18 ml/kg, p = 0.43, 31 ± 8 versus 27 ± 5 mmHg, p = 0.19, 2.8 ± 0.6 versus 2.9 ± 0.9 ml/kg/mmHg, p = 0.86). Unexpectedly, our data indicated that patients with asplenia syndrome, who lack splanchnic capacitance circulation, have blood volume and venous capacitance comparable to those in patients with splanchnic circulation. These data suggest that (1) there is a blood reservoir other than the spleen even in patients with asplenia; (2) considering the large blood pool of the spleen, the presence of a symmetrical liver may represent the possible organ functioning as a blood reservoir in asplenia syndrome; and (3) if this is indeed the case, there may be a higher risk of hepatic congestion in patients with Fontan circulation with asplenia syndrome than in those without.