23-year old man with a long history of abdominal pain, nausea and vomiting: Case report of a splenic cyst.

INTRODUCTION: Splenic cysts are rare. They are usually incidentally diagnosed and there is no harmonised treatment pathway. We report a case of a large splenic epidermoid type cyst without history of previous abdominal trauma. PRESENTATION OF CASE: A 23-year old male patient presented with symptoms of upper abdominal pain, nausea and vomiting. Except for a tenderness in the upper and lower left quadrant of the abdomen, the initial examination showed no extraordinary findings. A contrast enhanced computed tomography revealed a large singular splenic cyst displacing neighbouring structures. Echinococcus serology was tested negative. A laparoscopic fenestration of the superficially located splenic cyst was performed. Perioperative course was free of complications. Histopathological analysis of the excisate showed a squamous lining indicating the cyst as epidermoid type. DISCUSSION: Non-parasitic cyst types include traumatic, neoplastic, degenerative and congenital cysts. Due to its considerable size, our patients splenic cyst was diagnosed after occurring symptoms lead to further examination (CT scan). Laparoscopic fenestration of the cyst was chosen as the optimal surgical approach because of the superficial location of the cyst and to preserve residual splenic parenchyma. In the present case, recurrence of the splenic cyst appeared, which left the patient with a total splenectomy as the final treatment choice. CONCLUSION: Due to the unspecific symptoms, the diagnosis of a splenic cyst can be prolonged. Choosing the adequate surgical technique to avoid complications is crucial. By deepening the understanding of the condition and surgical approaches, we can improve diagnostic and therapeutic management for affected patients.

Stimulatory MAIT cell antigens reach the circulation and are efficiently metabolised and presented by human liver cells.

OBJECTIVE: Mucosal-associated invariant T (MAIT) cells are the most abundant T cells in human liver. They respond to bacterial metabolites presented by major histocompatibility complex-like molecule MR1. MAIT cells exert regulatory and antimicrobial functions and are implicated in liver fibrogenesis. It is not well understood which liver cells function as antigen (Ag)-presenting cells for MAIT cells, and under which conditions stimulatory Ags reach the circulation. DESIGN: We used different types of primary human liver cells in Ag-presentation assays to blood-derived and liver-derived MAIT cells. We assessed MAIT cell stimulatory potential of serum from healthy subjects and patients with portal hypertension undergoing transjugular intrahepatic portosystemic shunt stent, and patients with inflammatory bowel disease (IBD). RESULTS: MAIT cells were dispersed throughout healthy human liver and all tested liver cell types stimulated MAIT cells, hepatocytes being most efficient. MAIT cell activation by liver cells occurred in response to bacterial lysate and pure Ag, and was prevented by non-activating MR1 ligands. Serum derived from peripheral and portal blood, and from patients with IBD stimulated MAIT cells in MR1-dependent manner. CONCLUSION: Our findings reveal previously unrecognised roles of liver cells in Ag metabolism and activation of MAIT cells, repression of which creates an opportunity to design antifibrotic therapies. The presence of MAIT cell stimulatory Ags in serum rationalises the observed activated MAIT cell phenotype in liver. Increased serum levels of gut-derived MAIT cell stimulatory ligands in patients with impaired intestinal barrier function indicate that intrahepatic Ag-presentation may represent an important step in the development of liver disease.

Correction to: Prophylactic Intraperitoneal Onlay Mesh Following Midline Laparotomy-Long-Term Results of a Randomized Controlled Trial.

In the original version of the article, Philippe M. Glauser's, Philippe Brosi's, Benjamin Speich's, Samuel A. Käser's, Andres Heigl's, and Christoph A. Maurer's first and last names were interchanged. The names are correct as reflected here. The original article has been corrected.

Prophylactic Intraperitoneal Onlay Mesh Following Midline Laparotomy-Long-Term Results of a Randomized Controlled Trial.

OBJECTIVES: Incisional hernia, a serious complication after laparotomy, is associated with high morbidity and costs. This trial examines the value of prophylactic intraperitoneal onlay mesh to reduce the risk of incisional hernia after a median follow-up time of 5.3 years. METHODS: We conducted a parallel group, open-label, single center, randomized controlled trial (NCT01003067). After midline incision, the participants were either allocated to abdominal wall closure according to Everett with a PDS-loop running suture reinforced by an intraperitoneal composite mesh strip (Group A) or the same procedure without the additional mesh strip (Group B). RESULTS: A total of 276 patients were randomized (Group A = 131; Group B = 136). Follow-up data after a median of 5.3 years after surgery were available from 183 patients (Group A = 95; Group B = 88). Incisional hernia was diagnosed in 25/95 (26%) patients in Group A and in 46/88 (52%) patients in Group B (risk ratio 0.52; 95% CI 0.36-0.77; p < 0.001). Eighteen patients with asymptomatic incisional hernia went for watchful waiting instead of hernia repair and remained free of symptoms after of a median follow-up of 5.1 years. Between the second- and fifth-year follow-up period, no complication associated with the mesh could be detected. CONCLUSION: The use of a composite mesh in intraperitoneal onlay position significantly reduces the risk of incisional hernia during a 5-year follow-up period. TRIAL REGISTRATION NUMBER: Ref. NCT01003067 (clinicaltrials.gov).

Differential effects of 17beta-estradiol on function and expression of estrogen receptor alpha, estrogen receptor beta, and GPR30 in arteries and veins of patients with atherosclerosis.

Venous complications have been implicated in the adverse effects of hormone replacement therapy. This study investigated acute effects of the natural estrogen, 17beta-estradiol, on function, estrogen receptors/GPR30 expression, and kinase activation in vascular rings and cultured smooth muscle cells from arteries and veins of patients with coronary artery disease. Changes in vascular tone of internal mammary arteries and saphenous veins exposed to the steroid were recorded. 17Beta-estradiol caused concentration-dependent, endothelium-independent relaxation in arteries (P<0.05 versus solvent control) but not in veins (P not significant). 17Beta-estradiol enhanced contractions to endothelin-1 in veins but not in arteries. The novel membrane estrogen receptor GPR30 was detected in both vessels. Moreover, gene expression of estrogen receptor beta was 10-fold higher than that of estrogen receptor alpha or GPR30 (P<0.05). Expression of all 3 of the receptors was reduced after exposure to 17beta-estradiol in arteries but not in veins (P<0.05). Basal phosphorylation levels of extracellular signal-regulated kinase were higher in venous than in arterial smooth muscle cells and were increased by 17beta-estradiol in arterial cells only. In summary, this is the first study to report that, in human arteries but not in veins, 17beta-estradiol acutely affects vascular tone, estrogen receptor expression, including GPR30, and extracellular signal-regulated kinase phosphorylation. These data indicate that effects of natural estrogens in humans differ between arterial and venous vascular beds, which may contribute to the vascular risks associated with menopause or hormone therapy.

Acute effects of 17 beta-oestradiol on functional activity of endothelin-converting enzymes in human arteries and veins.

In this study, we investigated the short-term effect of 17 beta-oestradiol on functional enzyme activity (FEA) of endothelin-converting enzymes in vitro using human internal mammary arteries (n=7-8) and human saphenous veins (n=16-17) obtained from patients undergoing coronary artery bypass graft surgery. Vascular rings were preincubated with either solvent control (0.2% ethanol) or 17 beta-oestradiol (1 microM) for 30 min and concentration-response curves to big ET-1 (0.1-100 nM) or ET-1 (0.1-100 nM) were performed. FEA for each concentration was calculated as the percentage activity [(contraction to big ET-1/contraction to ET-1)x100] normalized to KCl (100 mM). In control experiments, at low concentrations FEA was lower in internal mammary arteries than in saphenous veins (P<0.05). While FEA was suppressed in saphenous veins by 10 nM (4+/-1 versus 22+/-5%, P<0.01) and 30 nM (26+/-4 versus 48+/-7%, P<0.05) 17 beta-oestradiol, FEA was markedly enhanced in internal mammary arteries by 10 nM (33+/-12 versus 1+/-1%, P<0.001) and 30 nM (44+/-12 versus 8+/-3%, P<0.01) 17 beta-oestradiol. FEA was not affected by 100 nM 17 beta-oestradiol. These results demonstrate for the first time that short-term exposure to 17 beta-oestradiol affects FEA in vitro. Human internal mammary arteries have lower FEA than the saphenous veins, but FEA is differentially affected by acute exposure to 17 beta-oestradiol in human arteries and veins. Whether changes in FEA play a role in the vascular effects of 17 beta-oestradiol in vivo remains to be determined.