Sclerotherapy of Symptomatic Nonparasitic Splenic Cysts: Excellent Long-Term Treatment Response'

Background Splenic cysts are rare and occur in 0.5 to 2% of the population. They are usually asymptomatic and do not require therapy. In case of symptomatic nonparasitic splenic cysts, potential therapy includes partial splenectomy or laparoscopic cyst de-roofing as well as ultrasound-guided sclerotherapy with 1% polidocanol or 10% sodium chloride (NaCl) as an interventional alternative. So far, single-session sclerotherapy of symptomatic nonparasitic cysts is recommended only if clear-transparent cyst fluid is aspirated. Materials and Methods We report a case series of 17 patients with symptomatic macroscopically turbid nonparasitic splenic cyst fluid who underwent ultrasound-guided fine needle sclerotherapy with either polidocanol ± 10% NaCl (n = 12) or 10% NaCl alone (n = 5) and a follow-up of a maximum of 12 years after first intervention. Clinical, sonographic, and laboratory chemistry data were recorded at baseline and during the follow-up. Results The mean follow-up time was 43.65 ± 40.18 months. At the end of the follow-up, a 79% reduction of cyst size was achieved. The maximum size reduction in the polidocanol group was 76 ± 18% and 84 ± 21% in the sodium chloride group (p >0.05). At the end of follow-up, 15 out of the 17 patients did not have any further symptoms. Despite the cystic fluid being turbid, it was hardly possible to detect a microbiological superinfection. Conclusion Sclerotherapy of splenic cysts leads to a significant size regression in all patients, independent of the sclerotherapy agent used with fewer systemic toxic side effects of polidocanol treatment. It was shown that in a tertiary care center with significant experience, sclerotherapy of splenic cysts is also safe and successful and can lead to a drastic regression of cyst size and symptoms. This shows that interventional therapy is a good alternative to surgical procedures.

Adamantinomatous Craniopharyngioma Cyst Fluid can Trigger Inflammatory Activation of Microglia to Damage the Hypothalamic Neurons by Inducing the Production of β-Amyloid

Introduction: The mechanism by which adamantinomatous craniopharyngioma (ACP) damages the hypothalamus is still unclear. Cyst fluid rich in lipids and inflammatory factors is a characteristic pathological manifestation of ACP and may play a very important role in hypothalamic injury caused by tumors. Objective: To construct a reliable animal model of ACP cyst fluid-induced hypothalamic injury and explore the specific mechanism of hypothalamic injury caused by cyst fluid. Methods: An animal model was establish by injecting human ACP cyst fluid into the bilateral hypothalamus of mice . ScRNA-seq was performed on the mice hypothalamus and on an ACP sample to obtain a complete gene expression profile for analysis. Data verification was performed through pathological means. Results: ACP cystic fluid caused growth retardation and an increased obesity index in mice, affected the expression of the Npy, Fgfr2, Rnpc3, Sst, and Pcsk1n genes that regulate growth and energy metabolism in hypothalamic neurons, and enhanced the cellular interaction of Agrp-Mc3r. ACP cystic fluid significantly caused inflammatory activation of hypothalamic microglia. The cellular interaction of CD74-APP is significantly strengthened between inflammatory-activated microglia and hypothalamic neurons. Beta-amyloid, a marker of neurodegenerative diseases, was deposited in the ACP tumor tissues and in the hypothalamus of mice injected with ACP cyst fluid. Conclusion: In this study, a novel animal model of ACP cystic fluid-hypothalamic injury was established. For the first time, it was found that ACP cystic fluid can trigger inflammatory activation of microglia to damage the hypothalamus, which may be related to the upregulation of the CD74-APP interaction and deposition of β-amyloid, implying that there may be a similar mechanism between ACP cystic fluid damage to the hypothalamus and neurodegenerative diseases.

Bioinformatic Analysis and Integration of Transcriptome and Proteome Results Identify Key Coding and Noncoding Genes Predicting Malignancy in Intraductal Papillary Mucinous Neoplasms of the Pancreas

Background. Intraductal papillary mucinous neoplasms (IPMNs) are precursor lesions of pancreatic ductal adenocarcinoma (PDAC). IPMNs are generally associated with high risk of developing malignancy and therefore need to be diagnosed and assessed accurately, once detected. Existing diagnostic methods are inadequate, and identification of efficient biomarker capable of detecting high-risk IPMNs is necessitated. Moreover, the mechanism of development of malignancy in IPMNs is also elusive. Methods. Gene expression meta-analysis conducted using 12 low-risk IPMN and 23 high-risk IPMN tissue samples. We have also listed all the altered miRNAs and long noncoding RNAs (lncRNAs), identified their target genes, and performed pathway analysis. We further enlisted cyst fluid proteins detected to be altered in high-risk or malignant IPMNs and compared them with fraction of differentially expressed genes secreted into cyst fluid. Results. Our meta-analysis identified 270 upregulated and 161 downregulated genes characteristically altered in high-risk IPMNs. We further identified 61 miRNAs and 14 lncRNAs and their target genes and key pathways contributing towards understanding of the gene regulation during the progression of the disease. Most importantly, we have detected 12 genes altered significantly both in cystic lesions and cyst fluid. Conclusion. Our study reports, for the first time, a meta-analysis identifying key changes in gene expression between low-risk and high-risk IPMNs and also explains the regulatory aspect through construction of a miRNA-lncRNA-mRNA interaction network. The 12-gene-signature could function as potential biomarker in cyst fluid for detection of IPMN with a high risk of developing malignancy.

Co-analysis of pancreatic cyst fluid carcinoembryonic antigen and glucose with novel cut-off levels better distinguishes between mucinous and non-mucinous neoplastic pancreatic cystic lesions

Background Pancreatic cyst fluid analysis plays an important role in distinguishing between mucinous and non-mucinous cyst lesions. We aimed to compare the diagnostic performances of cyst fluid carcinoembryonic antigen (CEA), CA 19-9, and glucose in differentiating mucinous from non-mucinous neoplastic pancreatic cystic lesions (PCLs) and determine the best cut-off levels. Methods Patients’ data were evaluated retrospectively. 102 patients’ PCLs were grouped as non-neoplastic ( n = 25), non-mucinous neoplastic ( n = 20), mucinous neoplastic ( n = 47) and pancreatic adenocarcinomas with cystic degeneration ( n = 10); and CEA, CA 19-9, and glucose levels were compared. Receiver-operating characteristic analysis was performed, and the ideal cut-off values were determined. Results Cyst fluid CEA and CA 19-9, levels were significantly higher ( P < 0.001, P < 0.001, respectively) and glucose levels were significantly lower ( P = 0.001) in mucinous than in non-mucinous neoplastic PCLs. Area under curve with 95% confidence interval of CEA, glucose and CEA and glucose test combination was 0.939 (95% CI = 0.885–0.993, P = 0.001), 0.809 (95% CI = 0.695–0.924, P < 0.001) and 0.937 (95% CI = 0.879–0.995), respectively. CEA cut-offs to rule-in and rule-out mucinous neoplastic were 135.1 ng/mL (sensitivity = 62%, specificity = 94.7%) and 6.12 ng/mL (sensitivity = 94.1%, specificity = 80.4%), respectively. Glucose cut-off of 2.8 mmol/L was chosen both to rule-in and rule-out mucinous neoplastic PCLs (sensitivity = 78%, specificity = 80%). Co-analysis of CEA and glucose to distinguish mucinous from non-mucinous neoplastic PCLs had sensitivity = 87.8%, specificity = 93.3%, and diagnostic accuracy = 89.3%. Conclusions We concluded that co-analysis of cyst fluid CEA (cut-off = 135.1 ng/mL) and glucose (cut-off = 2.8 mmol/L) at novel cut-offs had the best testing performance to rule-in mucinous neoplastic PCLs. To rule-out mucinous PCLs co-analysis of CEA (cut-off = 6.12 ng/mL) and glucose (cut-off = 2.8 mmol/L) added value to prediction.