Modified del Nido cardioplegia is associated with low incidence of low main strong ion difference and hyperchloremia in pediatric patients after cardiac surgery.

PURPOSE: The aims of this study were (1) to determine the associations of cardioplegic solutions with postoperative main strong ion difference (mSID), which is the difference between sodium ion concentration and chloride ion concentration ([Cl-]) and (2) to determine the associations of cardioplegic solutions with markers of organ dysfunction. METHODS: In this retrospective cohort study, patients aged <5 years who underwent cardiac surgery in a tertiary teaching hospital were included. Patients were classified on the basis of the type of cardioplegic solution: modified del Nido cardioplegia (mDNC) and conventional cardioplegia (CC). The effects of mDNC on postoperative mSID and markers of organ functions were examined using propensity-matched analysis. RESULTS: A total of 500 cases were included. mDNC solution was used in 163 patients (32.6%). After propensity score matching, patients in the mDNC group (n = 152) had significantly higher minimum mSID [28 (26, 30) mEq/L vs. 27 (25, 29) mEq/L, p = 0.02] and lower maximum [Cl-] [112 (109, 114) mEq/L vs. 113 (111, 117) mEq/L, p < 0.001] than patients in the CC group (n = 304). The incidences of low mSID and hyperchloremia in the mDNC group were significantly lower than those in the CC group (63.8 vs. 75.7%, p = 0.01 and 63.2 vs. 79.3%, p < 0.001, respectively). There was no significant difference in the incidence of postoperative acute kidney injury and B-type natriuretic peptide level between the two groups. CONCLUSION: The use of modified del Nido cardioplegia may reduce the incidence of abnormal mSID and hyperchloremia compared with the use of a chloride-rich cardioplegic solution.

Adult-onset Still's disease-like manifestation accompanied by the cancer recurrence after long-term resting state.

A 72-year-old woman presented 9 months ago with skin rash on her bilateral forearms, which was followed by intermittent high fever, and stiffness and swelling of her bilateral fingers. She was diagnosed with seronegative rheumatoid arthritis (RA). She had a past history of breast cancer and had undergone breast preservation surgery 13 years previously. During admission in our hospital, she developed high fever and leukocytosis with a relapsing skin rash, sore throat, polyarthralgia and increased levels of serum ALT/AST and ferritin, all of which fulfilled Yamaguchi's criteria for adult-onset Still's disease (AOSD). While we tried to exclude other diseases that may show AOSD-like manifestations, pancytopenia rapidly developed and bone marrow biopsy strongly suggested the diagnosis of macrophage activating syndrome (MAS). Accordingly, steroid pulse therapy was begun, followed by oral glucocorticoid therapy. Thereafter, all of her symptoms improved, but systemic rash, inflammatory signs and pancytopenia gradually progressed. The results of bone marrow pathology, which returned 2 weeks after the beginning of treatment, revealed hemophagocytosis with CK7-positive/CK20-negative atypical cells that suggested recurrence of breast cancer in the bone marrow, thus all of her AOSD-like symptoms were considered to be paraneoplastic manifestations of late-onset metastatic breast cancer. She was treated successfully with chemotherapy. When we see the patients showing AOSD-like symptoms with a history of malignancy, we should consider the possibility of paraneoplastic syndrome due to cancer recurrence.

Utility of three-dimensional transthoracic echocardiography in diagnosis of intermediate atrioventricular septal defect: report of an adult case.

We present the case of a 54-year-old male with an intermediate atrioventricular septal defect (AVSD). He was referred to our institute for treatment of shortness of breath. Two-dimensional transthoracic echocardiography demonstrated an ostium primum defect of the atrial septum, a common atrioventricular valve with mild regurgitations, and an interventricular communication, which are the features of complete AVSD. However, three-dimensional transthoracic echocardiography (3D-TTE) could clearly visualize the tricuspid pouch (i.e., persistence of the tissue in the endocardial cushion), a feature of partial AVSD. 3D-TTE appears to be a useful modality for diagnosis of intermediate AVSD.

Extensive bilateral renal metastases of non-small cell lung carcinoma caused acute kidney injury resulting in end-stage renal disease.

Non-small cell lung carcinoma unusually causes clinically relevant metastases in the kidney while they are usually found only in autopsy. Acute kidney injury (AKI) due to direct metastatic invasion of a solid tumor is also very rare whereas it usually happens with hematologic malignancy, including lymphoma. We report a case with these two rarities. A 54-year-old man who had a 6.7 × 6.0 cm-sized tumor in the left upper lobe of the lung in computed tomography was diagnosed as squamous cell lung carcinoma with bronchoscopy with biopsy. His renal function was normal and no proteinuria or hematuria was recognized. He underwent left upper lobectomy and the pathologic examination revealed pT4N1M0 stage IIIA disease. Four months after the surgery, a single brain metastasis in the right frontal lobe found in brain magnetic resonance imaging was treated with Gamma Knife radiosurgery. He presented with macroscopic hematuria and AKI (the serum creatinine level was 1.35 mg/dL) nine months after surgery. The cause was enormous bilateral renal metastases, maximally 8 cm-sized lesions with poor enhancement, which were found in enlarged bilateral kidneys in enhanced CT. Intrapulmonary metastatic lesions were also newly detected. Chemotherapy with pembrolizumab, an antibody against anti-programmed cell death protein 1, had little effect and his renal function continued to decline rapidly, resulting in end-stage renal disease and maintenance hemodialysis. Chemotherapy with carboplatin and paclitaxel was additionally performed. However, two months after hemodialysis induction, the patient died with pneumonia and acute respiratory distress syndrome.

TNFalpha gene silencing reduced lipopolysaccharide-promoted proliferation of endometriotic stromal cells.

PROBLEM: We previously reported that lipopolysaccharide (LPS)-promoted endometriotic stromal cell (ESC) proliferation by inducing TNFalpha production. The aim of this study was to investigate the efficacy of TNFalpha gene silencing on LPS-treated ESCs. METHOD OF STUDY: Endometriotic stromal cells (ESCs) and endometrial stromal cells (ESCs) (EMSCs) were obtained from ovarian chocolate cysts and uterine myoma, respectively. Using PCR array, LPS-induced gene expression profiling after transfection of TNFalpha siRNA into ESCs was performed. Down-regulated genes by TNFalpha silencing were examined using real-time RT-PCR. Effect of TNFalpha silencing was examined using ELISA and BrdU incorporation, respectively. RESULTS: In PCR array, TNFalpha silencing in ESCs repressed LPS-induced expression of cIAP2 and IL-8, NFkappaB pathway responsive genes. After adding LPS, the levels of cIAP2 and IL-8 expression in ESCs were higher compared with those in EMSCs. TNFalpha silencing attenuated the LPS-induced ESC proliferation. CONCLUSION: Tumor necrosis factor alpha may be involved in cell proliferation of endometriotic tissues.

TAK1 activation for cytokine synthesis and proliferation of endometriotic cells.

Endometriosis causes pelvic pain and infertility in women of reproductive age. We explored TNFalpha-induced specific signaling pathways and gene expressions in endometriotic stromal cells (ESCs). Based on the data of the pathway specific cDNA array, we analyzed the role of TAK1, which is believed to work as a common mediator for NF-kappaB and MAPK pathways. Using the NF-kappaB pathway array, we found that TNFalpha upregulated ICAM-3, IL-6, IL-8, TAK1, JNK2, RelA, and TLR4 expressions. TNFalpha augmented the phosphorylation of TAK1. By transfection of TAK1 siRNA, TNFalpha-induced phosphorylation of IkappaBalpha, JNK1/2, and p38MAPK, as well as IL-6 or IL-8 expression, were repressed. TAK1 silencing in TNFalpha-pretreated ESCs caused a decrease in the proportion of cells in S-phase, and reduced TNFalpha-promoted BrdU incorporation. We provide the first evidence that TNFalpha and its downstream TAK1, which are key mediators for NF-kappaB and MAPK pathways, may be involved in the pathogenesis of endometriosis.