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.

The Expression of Prolactin Receptors in Benign Breast Tumors Is Not Associated with Serum Prolactin Level

The role of prolactin (PRL) and its receptors in the initiation and development of benign breast tumors (BBT) has not been sufficiently studied. An imbalance in the system of hormone homeostasis is crucial in the development of BBT. In particular, an association between elevated prolactin levels and the development of BBT has been reported. Our study showed no significant differences between PRL receptor (PRL-R) expression in BBT tissue under normal and elevated serum PRL levels. There was also no significant correlation between age, PRL-R expression in BBT tissue, intact tissue, and PRL level in the serum. There was a strong significant correlation (p < 0.01; r = 0.92) between PRL-R expression in BBT samples and intact breast tissue, which did not depend on the serum PRL level. There was also no significant difference in the expression of the proliferative marker Ki-67 in BBT tissues from women with normal and elevated levels of serum PRL (p > 0.05). No signs of PRL and its receptors were detected in the BBT cystic fluid women with elevated serum PRL levels. In summary, our prospective study showed that the expression of PRL-R in the tissue of BBT and physiological breast tissue does not depend on the level of serum PRL.

Humoral Predictors of Malignancy in IPMN: A Review of the Literature

Pancreatic cystic lesions are increasingly detected in cross-sectional imaging. Intraductal papillary mucinous neoplasm (IPMN) is a mucin-producing subtype of the pancreatic cyst lesions arising from the pancreatic duct system. IPMN is a potential precursor of pancreatic cancer. The transformation of IPMN in pancreatic cancer is progressive and requires the occurrence of low-grade dysplasia, high-grade dysplasia, and ultimately invasive cancer. Jaundice, enhancing mural nodule >5 mm, main pancreatic duct diameter >10 mm, and positive cytology for high-grade dysplasia are considered high-risk stigmata of malignancy. While increased levels of carbohydrate antigen 19-9 (CA 19-9) (>37 U/mL), main pancreatic duct diameter 5–9.9 mm, cyst diameter >40 mm, enhancing mural nodules <5 mm, IPMN-induced acute pancreatitis, new onset of diabetes, cyst grow-rate >5 mm/year are considered worrisome features of malignancy. However, cross-sectional imaging is often inadequate in the prediction of high-grade dysplasia and invasive cancer. Several studies evaluated the role of humoral and intra-cystic biomarkers in the prediction of malignancy in IPMN. Carcinoembryonic antigen (CEA), CA 19-9, intra-cystic CEA, intra-cystic glucose, and cystic fluid cytology are widely used in clinical practice to distinguish between mucinous and non-mucinous cysts and to predict the presence of invasive cancer. Other biomarkers such as cystic fluid DNA sequencing, microRNA (mi-RNA), circulating microvesicles, and liquid biopsy are the new options for the mini-invasive diagnosis of degenerated IPMN. The aim of this study is to review the literature to assess the role of humoral and intracystic biomarkers in the prediction of advanced IPMN with high-grade dysplasia or invasive carcinoma.

PATH-06. DNA METHYLATION PATTERNS AND IMMUNE MICROENVIRONMENT IN CYSTICGBM

As a rare subtype of glioblastomas (GBM), genetic features in cystic GBM (cGBM) are still largely unknown. We have previously identified a series of active T cell subsets and positive cytokines/chemocytokines in the cystic fluid of cGBMs, including IFN-gamma, IL-2, IL-6, IL-8, TNF-alpha, and MIP-1alpha/beta. This study aimed to evaluate the prognosis of cGBM through DNA methylation patterns and immune microenvironment transcriptional signatures. IvyGAP, EGA and fresh samples from a prospective Chinese cohort were collected to investigate genomic signatures, immune microenvironment and survival outcomes in patients with cGBMs. Gd T1-weighted, T2-weighted, T2-Flair, DWI or ADC images were used to classify cGBM. 143 cases with MGMT/IDH record were used to compare survival time and genomic analysis. Among the three cohorts, Kaplan-Meier analysis showed cystic features have benefit to overall survival (OS). Moreover, cyst feature is the forth factor (HR=0.65, [95% CI 0.42, 1.01]) of survival after IDH, MGMT and Stupp therapeutic regimen. Interestingly, in IDH-wild/MGMT-unmethyled subtype, cGBM patients have longer OS vs noncystic GBM (noncGBM) patients (HR = 0.57, [95% CI 0.33, 0.99]). Compared to noncGBM, cGBM patients have hypomethylation state both in whole gene region and cpG islands. Ivygap database showed between cystic and noncystic group, in sub-structures such as CT (cellular tumor region), CTpan (pseudopalisading cells around necrosis) and CTpnz (perinecrotic zone) there are differential gene expressions and different enrichment pathways. GSEA analysis showed within cGBM group, many gene sets associated with immune function activation such as TRL1/2/3/7 and IFN pathways. These results suggest that cysts of GBM may be associated with hypomethylation status an activated immune microenvironment which is associated with longer survival and may define a unique subgroup of GBM with intrinsically different biology and prognosis.

Recent advances in understanding ion transport mechanisms in polycystic kidney disease

This review focuses on the most recent advances in the understanding of the electrolyte transport-related mechanisms important for the development of severe inherited renal disorders, autosomal dominant (AD) and recessive (AR) forms of polycystic kidney disease (PKD). We provide here a basic overview of the origins and clinical aspects of ARPKD and ADPKD and discuss the implications of electrolyte transport in cystogenesis. Special attention is devoted to intracellular calcium handling by the cystic cells, with a focus on polycystins and fibrocystin, as well as other calcium level regulators, such as transient receptor potential vanilloid type 4 (TRPV4) channels, ciliary machinery, and purinergic receptor remodeling. Sodium transport is reviewed with a focus on the epithelial sodium channel (ENaC), and the role of chloride-dependent fluid secretion in cystic fluid accumulation is discussed. In addition, we highlight the emerging promising concepts in the field, such as potassium transport, and suggest some new avenues for research related to electrolyte handling.

Spontaneous closure of degenerative lamellar macular hole with epiretinal membrane proliferation

Background To describe the spontaneous closure of a degenerative lamellar macular hole with epiretinal proliferation (LHEP) as documented with tracked spectral domain optical coherence tomography (SD-OCT). Case presentation A 54-years-old diabetic female patient presented with progressive vision loss in the left eye. SD-OCT illustrated LHEP associated with cystic fluid in the outer nuclear layer. Sequentially tracked SD-OCT showed progressive closure of the degenerative lamellar macular hole and resolution of the CME over almost 4 years, in the absence of any surgical intervention. Discussion/conclusion LHEP may represent a specialized form of degenerative epiretinal membrane associated with Muller cell activation. Spontaneous degenerative LMH closure may rarely occur with these lesion types, in the absence of surgical intervention, possibly due to Muller cell proliferation preceded by PVD.

Laparoscopic Deroofing and Excision of a Large Left Renal Cyst Mimicking Chest Infection: Case Report

Background: The routine use of abdominal ultrasonography and computed tomography scan has increased the detection of asymptomatic renal cysts. Laparoscopy is usually suitable for treating large symptomatic renal cysts. Objective: To report a case of laparoscopic treatment of a man with large left renal cyst mimicking chest infection. Case presentation: A 75-year-old man, known hypertensive who had empirical treatment for chest infection without resolution of symptoms of cough and chest pain. He was on treatment for storage and voiding lower urinary tract symptoms with 10mg alfuzocin. Abdominal ultrasound and computed tomography scan confirmed a large left renal cortical cyst that measured 380mls. He subsequently had transperitoneal laparoscopic deroofing and excision of the renal cyst with operation finding of 300mls of straw coloured fluid excluding spillage. The immediate postoperative period was uneventful, and he was discharged home in a stable condition on the second day. The aspirate yielded no growth while the cytology report of cystic fluid was acute-on-chronic inflammation. Histology was reported as chronic pyelonephritis with cystic degeneration. Conclusion: Large renal cyst should be considered as differential diagnosis of unresolved chest infection and is safely treated by laparoscopic deroofing and excision.

Gastrointestinal Intramural Pancreatic Pseudocysts in a Dog: A Case Report and Human Literature Review

ABSTRACT A 9.5 yr old Yorkshire terrier presented with chronic intermittent vomiting and lethargy of 1.5 yr duration that progressed to generalized weakness. Insulin:glucose ratio was consistent with an insulinoma. Triple-phase computed tomography revealed a mid-body pancreatic nodule. The mid-body pancreatic nodule was enucleated; histopathology was consistent with an insulinoma. Two weeks after the operation, the dog presented for anorexia and diarrhea. Abdominal ultrasound revealed a thick-walled cystic lesion along the dorsal stomach wall. An intramural gastric pseudocyst was diagnosed via exploratory laparotomy and intraoperative gastroscopy. Comparison of amylase and lipase levels of the cystic fluid with that of concurrent blood serum samples confirmed the lesion was of pancreatic pseudocyst origin. The gastric pseudocyst was omentalized. Two weeks after the operation, the dog re-presented for anorexia, regurgitation, and diarrhea. An intramural duodenal pseudocyst was identified and treated with a duodenal resection and anastomosis. The dog has remained asymptomatic and recurrence free based on serial abdominal ultrasounds 22 mo following insulinoma removal. To our knowledge, this phenomenon of pancreatic pseudocysts forming in organs other than the pancreas has not been reported in dogs. This case report and comprehensive human literature review purpose is to raise awareness of this disease process in dogs.

Evaluation of pancreatic cyst prostaglandin E2 as a Marker for Differentiation between Mucinous and Non Mucinous Cysts and Prediction of Dysplasia in Mucinous Pancreatic Cysts

Background There are different types of pancreatic cysts.They can be classified by different ways. Each of them has different plan of management. that is why their differentiation became mandatory before setting their treatment plans. Aim of the study To Evaluate PGE2 as a marker of differentiation of mucin containing pancreatic cysts and prediction of dysplasia in these cyst. A Secondary aim is differentiation of mucin from non mucin containing pancreatic cystic lesions Patients and Methods 40 patients were recruited from the Department of Internal Medicine and the Outpatient Clinic of Cairo University hospital in the period between December 2018 and August 2019. A case control study design was adopted where the patients were grouped as follow : Group 1 - composed of 20 patients with pancreatic mucinous cystic lesions defined by EUS guided samples, Histopathology and Radiological findings. Group 2: - composed of 20 patients with pancreatic non mucinous cystic lesions defined by EUS guided samples, Histopathology and Radiological findings. Results In our study, there was a significant differences in PGE2 level between true and inflammatory pancreatic cysts (p = 0.001) .However, there is insignificant differences between mucinous, non mucinous (p = 0.406). There was insignificant differences between different grades of IPMN dysplasia (p = 0.615) Conclusion Prostaglandin E2 is pancreatic cystic fluid marker which can be used for differentiation between true pancreatic cysts from inflammatory pancreatic cysts which have different plans of management. Prostaglandin E2 is not good marker to be used for differentiation between different grades of IPMN dysplasia.