Carcinoid heart disease (CHD) is a serious cardiac manifestation of carcinoid syndrome (CS), characterized by progressive fibrotic degeneration of cardiac valves and right-sided heart failure. We report the case of a 72-year-old man with a history of metastatic small-intestinal neuroendocrine tumor and CS diagnosed four years earlier, who presented with worsening dyspnea and peripheral edema. Transthoracic echocardiography revealed characteristic findings of advanced CHD, including severely thickened, retracted, and immobile tricuspid and pulmonary valve leaflets, resulting in severe tricuspid and pulmonary regurgitation. Additional findings included right ventricular dilatation, severe biatrial enlargement, moderate mitral regurgitation, a small pericardial effusion, and a 7-cm ascending aortic aneurysm. The diagnosis was established based on the characteristic echocardiographic appearance and elevated N-terminal pro-B-type natriuretic peptide levels. Notably, no routine cardiological surveillance had been performed following the diagnosis of CS. The patient was managed conservatively with intravenous diuretic therapy and optimization of heart failure treatment. Following multidisciplinary evaluation, surgical intervention was not pursued because of the patient's advanced disease stage, clinical instability, and concomitant ascending aortic aneurysm, which collectively rendered him a prohibitive surgical candidate. His clinical course was subsequently complicated by acute kidney injury with progressive renal dysfunction and anuria, and he ultimately died during hospitalization. This case highlights the importance of regular cardiovascular follow-up in patients with CS, as delayed recognition of cardiac involvement may lead to advanced and potentially irreversible valvular disease. Early detection remains crucial for timely intervention and may improve clinical outcomes.

Middle aortic syndrome is a rare cause of renovascular hypertension in infants. We report a 21-month-old boy weighing 11 kg who presented with severe systemic hypertension (205/117 mmHg) and left ventricular (LV) dysfunction due to diffuse hypoplasia of the thoracoabdominal aorta. Echocardiography and computed tomography angiography showed two coarctation segments involving the superior mesenteric and renal arteries without inflammatory signs. After medical stabilization, acute pulmonary edema and cardiogenic shock developed. A hybrid transabdominal approach with sequential covered-stent implantation achieved favorable recovery, with normalization of blood pressure and improvement in LV function.

This case report describes the successful management of a dichorionic-diamniotic twin pregnancy in a 35-year-old woman with end-stage renal disease (ESRD) on hemodialysis. The patient had established kidney failure secondary to presumed hypertensive nephrosclerosis, complicated by a previous pregnancy with preeclampsia, and was maintained on home hemodialysis (five hours per session on alternate days) since 2022. Upon confirmation of twin pregnancy, her dialysis regimen was immediately intensified from alternate-day sessions to daily treatments totaling 35 hours/week, with parameters including five-hour duration, blood flow rate of 250 mL/min, and ultrafiltration of 1.2-1.5 kg/session. During the second trimester, maternal weight was carefully monitored alongside fetal growth, with an expected increase of 0.5-1 kg weekly. At 27 weeks' gestation, significant fetal growth discordance prompted further dialysis intensification to six times weekly with increased blood and dialysate flow rates. The pregnancy was complicated by intrahepatic cholestasis and therapy-resistant hypertension. At 31 weeks, the patient developed acute pulmonary edema with severe preeclampsia features despite optimal volume management, requiring emergent cesarean delivery of two live infants. This case demonstrates that intensive dialysis protocols are essential for achieving favorable outcomes in twin pregnancies complicated by ESRD. Success depends on three critical components: early recognition of maternal and fetal complications, intensive fetal surveillance throughout pregnancy, and precise control of dialysis parameters with frequent adjustments based on clinical status and fetal development.

Elevated lactate levels in lung tissue are a distinct hallmark of acute lung injury (ALI), but the biological functions of glycolytic reprogramming and lactate-derived protein modification in damaged alveolar epithelial cells remain poorly elucidated. In the present study, we validated markedly increased lactate abundance in peripheral samples and lung tissues of multiple ARDS patients and multiple ALI mouse models. Administration of glycolysis inhibitor 2-DG to deplete endogenous lactate effectively mitigated lung injury and alveolar epithelial barrier dysfunction, whereas exogenous lactate supplementation significantly worsened these pathological manifestations. Genetic silencing of pulmonary LDHA via intratracheal injection of AAV9-shLdha successfully reproduced the protective phenotypes conferred by 2-DG treatment. Mechanistically, accumulated lactate facilitated Tip60-dependent lactylation modification of YY1 at lysine 183. Biochemical assays confirmed that YY1 K183 lactylation inhibited the expression of PGC-1α at transcriptional level, further causing mitochondrial homeostasis disorder and destruction of alveolar epithelial barrier. In vivo rescue experiments using lactylation-deficient YY1-K183R mutant verified the essential pathogenic role of this site-specific lactylation in LPS-triggered ALI progression. Additionally, we established two feasible translational therapeutic strategies, including K183-targeted cell-penetrating peptide and glycyrrhizin screened from compound libraries. Both candidates efficiently suppressed YY1 K183 lactylation, restored PGC-1α expression and mitochondrial function, and relieved pulmonary edema, inflammatory infiltration and cell apoptosis. In summary, lactate-driven YY1 K183 lactylation disrupts PGC-1α-mediated mitochondrial quality control and epithelial barrier stability. Intervening this lactate-YY1 lactylation axis provides a reliable and promising therapeutic direction for clinical treatment of ALI and ARDS.