Alteration in faecal bile acids, gut microbial composition and diversity after laparoscopic sleeve gastrectomy.

BACKGROUND: Laparoscopic sleeve gastrectomy (LSG) is a well established treatment for severe obesity and type 2 diabetes. Although the gut microbiota is linked to the efficacy of LSG, the underlying mechanisms remain elusive. The effect of LSG for morbid obesity on the gut microbiota and bile acids was assessed here. METHODS: Severely obese subjects who were candidates for LSG were included and followed until 6 months after surgery. The composition and abundance of the microbiota and bile acids in faeces were assessed by 16S ribosomal RNA sequencing, quantitative PCR and liquid chromatography-mass spectrometry. RESULTS: In total, 28 patients with a mean(s.d.) BMI of 44·2(6·6) kg/m2 were enrolled. These patients had achieved excess weight loss of 53·2(19·0) per cent and showed improvement in metabolic diseases by 6 months after LSG, accompanied by an alteration in the faecal microbial community. The increase in α-diversity and abundance of specific taxa, such as Rikenellaceae and Christensenellaceae, was strongly associated with reduced faecal bile acid levels. These changes had a significant positive association with excess weight loss and metabolic alterations. However, the total number of faecal bacteria was lower in patients before (mean(s.d.) 10·26(0·36) log10 cells per g faeces) and after (10·39(0·29) log10 cells per g faeces) operation than in healthy subjects (10·83(0·27) log10 cells per g faeces). CONCLUSION: LSG is associated with a reduction in faecal bile acids and greater abundance of specific bacterial taxa and α-diversity that may contribute to the metabolic changes.

ANTECEDENTES: La gastrectomía vertical laparoscópica (laparoscopic sleeve gastrectomy, LSG) es un tratamiento bien establecido para la obesidad grave y la diabetes tipo 2. Aunque la microbiota intestinal se ha vinculado con la eficacia de LSG, los mecanismos subyacentes siguen siendo poco conocidos. En este estudio se evaluó el efecto de LSG en la obesidad mórbida sobre la microbiota del intestino y de los ácidos biliares (bile acids, BA). MÉTODOS: Tras la aprobación del Comité ético y la obtención del consentimiento informado, los sujetos con obesidad grave que eran candidatos para LSG fueron incluidos en el estudio y seguidos durante 6 meses después de la operación. Se evaluaron la composición y abundancia de la microbiota y BA en las heces mediante secuenciación del gen 16S rRNA, PCR cuantitativa y cromatografía líquida-espectrometría de masas. RESULTADOS: En total, 28 pacientes con una mediana (rango) del IMC de 43,9 kg/m2 (35,0-61,9) fueron reclutados y a los 6 meses tras una LSG, consiguieron una pérdida del exceso de peso de 47,3% (20,7-95,1) y mejoría de las enfermedades metabólicas acompañada de una alteración en la comunidad microbiana fecal. El aumento en la diversidad α y abundancia de especies taxonómicas específicas como Rikenellaceae y Christensenellaceae, se asociaba fuertemente con niveles fecales reducidos de BA. Estos cambios se asociaban de manera positiva y significativa con la pérdida del exceso de peso y las alteraciones metabólicas. Sin embargo, el número total de bacterias fecales en los pacientes fue inferior al de los sujetos sanos (10,84 log10 células/g heces (9,46-11,35)) antes de la operación (10,26 log10 células/g heces (9,44-10,91)) y después de la misma (10,42 log10 células/g heces (9,57-10,96)). CONCLUSIÓN: LSG se asoció con menos BA fecal y mayor abundancia de especies bacterianas específicas y diversidad α lo que puede contribuir a los cambios metabólicos.

Effect of laparoscopic splenectomy on portal haemodynamics in patients with liver cirrhosis and portal hypertension.

BACKGROUND: The effect of splenomegaly in patients with liver cirrhosis and portal hypertension is not fully understood. This study was designed to determine the effect of laparoscopic splenectomy on portal haemodynamics in these patients. METHODS: Patients with liver cirrhosis and portal hypertension who underwent laparoscopic splenectomy in Kyushu University Hospital from January 2006 to March 2009 were evaluated retrospectively. Correlations between splenic size and portal haemodynamics, and changes in portal haemodynamics and in levels of the vasoactive agents endothelin (ET) 1 and nitric oxide metabolites (NOx) before and 7-10 days after laparoscopic splenectomy were analysed. RESULTS: Portal venous (PV) blood flow, PV cross-sectional area and PV congestion index correlated significantly with splenic size (P < 0·050). All three were significantly reduced following splenectomy in 59 patients. The hepatic venous pressure gradient, measured in 18 patients, decreased by 25 per cent after splenectomy (P < 0·001). Portal vascular resistance was also reduced, by 21 per cent (P = 0·009). The peripheral blood concentration of ET-1 decreased from 2·95 to 2·11 pg/ml (P < 0·001), and that of NOx tended to decrease (from 29·2 to 25·0 pg/ml; P = 0·068). In hepatic venous blood, the level of ET-1 decreased from 2·37 to 1·83 pg/ml (P = 0·006), whereas NOx concentration tended to increase (from 24·5 to 30·9 pg/ml; P = 0·067). CONCLUSION: In patients with liver cirrhosis and portal hypertension, splenectomy reduced portal venous pressure. A decrease in splanchnic blood flow, by eliminating splenic blood flow, and reduction in intrahepatic vascular resistance, by normalizing hepatic concentrations of ET-1 and NOx, may both have contributed.

Characteristics of splenic CD8+ T cell exhaustion in patients with hepatitis C.

There is increasing interest in the role of T cell exhaustion and it is well known that the natural history of chronic hepatitis C virus infection (HCV) is modulated by CD8(+) T cell immunobiology. There are many pathways that alter the presence of exhaustive T cells and, in particular, they are functionally impaired by inhibitory receptors, such as programmed death-1 (PD-1) and T cell immunoglobulin and mucin domain-containing protein 3 (Tim-3). We obtained spleen, liver and peripheral blood (before and after splenectomy) lymphoid cells from 25 patients with HCV-related cirrhosis undergoing liver transplantation for end-stage disease or splenectomy for portal hypertension. In all samples we performed an extensive phenotypic study of exhaustion markers [PD-1, Tim-3, interferon (IFN)-γ) and their ligands (PD-L1, PD-L2, galectin-9] in CD8(+) T cell subpopulations (both total and HCV-specific) and in antigen-presenting cells (APC; monocytes and dendritic cells). In the spleen, total and HCV-specific CD8(+) T cells demonstrated enhanced markers of exhaustion, predominantly in the effector memory subpopulation. Similarly, splenic APC over-expressed inhibitory receptor ligands when compared to peripheral blood. Finally, when peripheral blood CD8(+) T cells were compared before and after splenectomy, markers of exhaustion were reduced in splenic CD8(+) T cells and APC. Our data in HCV-related cirrhosis suggest that CD8(+) T cells in the spleen manifest a significantly higher exhaustion compared to peripheral blood and may thus contribute to the failure to control HCV. Counteracting this process may contribute to inducing an effective immune response to HCV.

Modulation of CD4⁺ T cell responses following splenectomy in hepatitis C virus-related liver cirrhosis.

Dysfunction of T cells is a common feature in chronic persistent viral infections, including hepatitis C virus (HCV), and although hepatic and peripheral T cells have been studied extensively in chronic HCV hepatitis, the role of splenic T cell responses in such patients is poorly defined. This is an important issue, as thrombocytopenia is a complication of HCV-related liver cirrhosis (LC), due to splenic platelet sequestration and bone marrow suppression; splenectomy has been proposed to treat such patients. Herein, we studied peripheral blood mononuclear cells (PBMC) and splenic lymphoid subpopulations from a total of 22 patients, including 15 with HCV-related LC with marked thrombocytopenia treated with splenectomy, and seven controls. CD4(+) T cells from peripheral blood and spleen were isolated and phenotype and function evaluated. Splenic CD4(+) T cells in patients with LC expressed molecules associated with inhibitory signalling, including increased frequency of negative markers such as cytotoxic T lymphocyte associated antigen-4 (CTLA-4) and programmed death 1 (PD-1) and decreased production of cytokines. Patients with LC manifest higher levels of splenic CD4(+) regulatory T cells and PD-L1- and PD-L2-expressing cells than controls. Blocking of PD-1/PD-1 ligand interaction reconstituted proliferative and cytokine responses of splenic mononuclear cells (SMC) from patients with LC. Splenectomy was followed by an increase in the ratio of interferon (IFN)-γ to interleukin (IL)-10 and a reduction of PD-1-expressing CD4(+) T cells in peripheral blood. Our data suggest that peripheral tolerance is promoted by the spleen in LC via the up-regulated expression of PD-1 ligands.

Induction of high-affinity interleukin 1 receptor on human peripheral blood lymphocytes by glucocorticoid hormones.

The in vitro effect of glucocorticoids (GCs) on IL-1-R expression of human PBMCs was investigated. Both physiological and pharmacological concentration ranges of GC increased the specific binding of 125I-labeled human rIL-1 alpha to PBMCs. This enhancement was specific for GC, since other steroid hormones, such as progesterone, 17 beta-estradiol, and testosterone failed to elevate the binding of 125I-IL-1 alpha to PBMCs. The effect was time dependent with maximal effect occurring 6 h after treatment and dose dependent with half-maximal effect elicited by 100 nM prednisolone. Scatchard plot analysis indicated that 125I-IL-1 alpha binding increased from approximately 100 IL-1-R per cell to 2 X 10(3) receptors per cell without a major change in affinity (Kd = 2.6 X 10(-10) M). The subpopulation of PBMCs induced by GC to express higher levels of IL-1-R consisted predominantly of B lymphocytes, but not T lymphocytes, large granular lymphocytes, or monocytes. GCs also induced the expression of IL-1-R on some other cell types, including normal human dermal fibroblasts and the human large granular lymphocyte cell line YT. Since cycloheximide and actinomycin D inhibited the induction of IL-1-R by GC, synthesis of both new RNA and protein seems to be required for IL-1-R induction. This study presents the first evidence of upregulation of the receptors for IL-1 by GC, and may account for the reported enhancement of in vitro and in vivo humoral immune responses by GCs.

Risk factors for portal venous thrombosis after splenectomy in patients with cirrhosis and portal hypertension.

BACKGROUND: Portal venous thrombosis (PVT) is a potentially fatal complication following splenectomy. Its mechanisms and risk factors are poorly understood, especially in patients with cirrhosis and portal hypertension. This study investigated risk factors for PVT following splenectomy in such patients. METHODS: All consecutive patients with cirrhosis who underwent splenectomy in Kyushu University Hospital between 1998 and 2004 were included in this retrospective study. They were divided into two groups based on the presence or absence of postoperative PVT. Preoperative and operative factors were compared, and the relationships between formation of PVT and its independent variables were analysed. In some cases, portal venous flow was measured before and after splenectomy using duplex Doppler ultrasonography. RESULTS: PVT developed after surgery in 17 (24 per cent) of 70 patients studied. Multivariable analysis showed that increased splenic vein diameter and low white cell count were significant independent risk factors for PVT. Portal venous flow after splenectomy was greatly reduced in the PVT group, but not in patients without PVT. CONCLUSION: Large splenic vein diameter and low white cell count are independent risk factors for PVT after splenectomy in patients with cirrhosis and portal hypertension.

A foodborne outbreak of a group A streptococcal infection in a Japanese university hospital.

We describe an outbreak of foodborne tonsillopharyngitis caused by group A streptococcus (GAS), a rarely reported event that occurred during a campus orientation meeting in Japan. Of 461 students and staff members who had eaten boxed lunches during a meeting at Kitasato University, 298 developed sore throat and/or fever, and 285 underwent medical examination. Amoxicillin was prescribed when throat culture specimens yielded GAS. The attack rate was 64.6%. T-25 GAS was isolated from 150 examined persons. Of 65 patients who received amoxicillin for 3 days, GAS was eradicated before the first follow-up throat culture in 46 (70.8%) cases. Susceptibility was demonstrated to penicillins, cephalosporins, and macrolides in 86 GAS isolates obtained more than once from a given patient. GAS strains isolated at various time points were indistinguishable by pulsed-field gel electrophoresis (PFGE), and prtF1 was present. GAS strains were often difficult to eradicate because of a short initial treatment period, patient compliance problems, and the presence of prtF1.

Interleukin 1 stimulates its own receptor expression on human fibroblasts through the endogenous production of prostaglandin(s).

The regulation of interleukin 1 receptor (IL 1R) expression on human dermal fibroblasts was investigated. On exposure to IL 1 for 3 h at 37 degrees C, the capacity of fibroblasts to bind 125I-labeled human recombinant IL 1 alpha (125I-IL 1 alpha) was reduced by 75%. The IL 1 binding capability of the fibroblasts was restored to control levels by 16 h after removal of unbound IL 1, and then increased to about twofold over that of control cells by 48 h. This later enhancement of IL 1 receptor expression after IL 1 treatment was abolished by indomethacin. Addition of exogenous (PGE1 and PGE2, also analogues of AMP, or forskolin increased the specific binding of 125I-IL 1 alpha to fibroblasts. Scatchard analysis indicated that PGE2 increased the number of IL 1R from approximately 1.6 X 10(3) to 5.4 X 10(3) per cell without change in the binding affinity. These data suggest that the later IL 1-induced up-regulation of IL 1R is mediated by IL 1 stimulation of endogenous prostaglandin production. The combination of PGE2 and prednisolone increased the number of IL 1R on fibroblasts in an additive manner.

Essential involvement of interleukin-8 (IL-8) in acute inflammation.

Neutrophil infiltration into inflammatory sites is one of the hallmarks of acute inflammation. Locally produced chemotactic factors are presumed to mediate the sequence of events leading to the infiltration at inflammatory sites. Interleukin-8 (IL-8), a novel leukocyte chemotactic activating cytokine (chemokine), is produced by various types of cells upon stimulation with inflammatory stimuli and exerts a variety of functions on leukocytes, particularly, neutrophils in vitro. However, no definitive evidence has been presented on its role in recruiting and activating neutrophils in the lesions of various types of inflammatory reactions. We administered a highly specific neutralizing antibody against IL-8 in several types of acute inflammatory reactions, including lipopolysaccharide (LPS)-induced dermatitis, LPS/IL-1-induced arthritis, lung reperfusion injury, and acute immune complex-type glomerulonephritis. Anti-IL-8 treatment prevented neutrophil-dependent tissue damage as well as neutrophil infiltration in these conditions. These results suggest that IL-8 plays a causative role in acute inflammation by recruiting and activating neutrophils.

Rapid induction of neutrophil apoptosis by sulfasalazine: implications of reactive oxygen species in the apoptotic process.

Accumulating evidence indicates that neutrophils are crucially involved in the pathogenesis of inflammatory bowel diseases and rheumatoid arthritis. We therefore investigated the effect of sulfasalazine (SSZ), which is widely used in the treatment of these diseases, on neutrophil apoptosis in vitro. The apoptosis of neutrophils was determined by morphology, a DNA histogram of propidium iodide-stained nuclei, and DNA fragmentation. SSZ rapidly accelerated the rate of spontaneous neutrophil apoptosis within clinically relevant concentrations. This effect is unique to neutrophils because other types of leukocytes and a number of leukocyte cell lines are resistant to SSZ. Neutrophil apoptosis caused by SSZ was abrogated by a tyrosine kinase inhibitor, a protein kinase A inhibitor, and antioxidants. The subsequent results provided pharmacological evidence that the phosphorylation of tyrosine kinase and protein kinase A and generation of reactive oxygen species are involved in SSZ-mediated neutrophil apoptosis. These data suggest that SSZ-induced neutrophil apoptosis may account, in part, for the clinical benefits of SSZ on inflammatory bowel diseases and rheumatoid arthritis.

Induction of neutrophil death resembling neither apoptosis nor necrosis by ONO-AE-248, a selective agonist for PGE2 receptor subtype 3.

An increase of intracellular cAMP mediated by prostaglandin E2 (PGE2) has been shown to delay spontaneous apoptosis of neutrophils. It has been demonstrated that a selective agonist for PGE2 receptor subtype 3 (the EP3 receptor) is capable of decreasing cAMP and stimulating phosphoinositide turnover in various types of cells. We investigated the effect of a selective EP3 receptor agonist, ONO-AE-248, on neutrophil viability. ONO-AE-248 rapidly caused a unique form of neutrophil death. The agonist primarily induced morphological changes of the nucleus, including fusion of the lobules, decreased compactness of the chromatin, and blebbing and rupture of the nuclear membrane. This was followed by an increase of plasma membrane permeability and cell lysis. During these processes, neither apoptotic changes such as nuclear condensation, DNA fragmentation, and expression of phospholipid phosphatidylserine on the plasma membrane nor necrotic changes such as chromatin clumping and organelle destruction were apparent in the treated neutrophils. The fatal effect of the agonist night be specific for neutrophils because it failed to promote the rapid death of other types of cells. Although activation of neutrophils by ONO-AE-248 was not evident, experiments using metabolic inhibitors demonstrated that the agonist caused neutrophil death via the activation of protein kinase C in the presence of intracellular ATP. These findings indicated that EP3 receptor-mediated signals might promote a novel form of neutrophil death, which differs from typical apoptosis or necrosis.

Attenuation of monosodium urate crystal-induced arthritis in rabbits by a neutralizing antibody against interleukin-8.

Accumulating evidence implicates interleukin-8 (IL-8) as an essential mediator in neutrophil-mediated acute inflammation. Neutrophils have also been shown to have a crucial role in the pathogenesis of acute gouty arthritis. Thus, we investigate the pathophysiological role of IL-8 in an experimental model of acute gout, monosodium urate (MSU) crystal-induced arthritis in rabbits. The injection of MSU crystals into knee joints caused a marked swelling of joints. Concomitantly, the infiltration ofleukocytes, mostly neutrophils, was observed in synovial membrane and synovial fluids. The injection of MSU crystals also induced an elevation in synovial fluid IL-8 levels preceding neutrophil infiltration into synovial fluids, without an accompanying increase in plasma IL-8 levels. Immunoreactive IL-8 protein was detected in synovial lining cells at 12-24 h after the injection. IL-8 protein was also observed in infiltrated leukocytes in synovium as early as 3-24 h after the injection. Finally, the intraarticular injection of a neutralizing anti-IL-8 antibody significantly attenuated the crystal-induced joint swelling that occurred at 12 h, and neutrophil infiltration into arthritic joints at 12 and 24 h after the induction. These results provide evidence on the pathogenic roles of locally produced IL-8 in MSU crystal-induced gouty arthritis.

Comparison of recombinant human thrombomodulin and gabexate mesylate for treatment of disseminated intravascular coagulation (DIC) with sepsis following emergent gastrointestinal surgery: a retrospective study.

PURPOSE: Recombinant thrombomodulin (rTM) has been available in Japan since 2008, but there is concern about its association with postoperative hemorrhage. The efficacy and safety of rTM were examined in patients with disseminated intravascular coagulation (DIC) caused by a septic condition after gastrointestinal surgery. METHODS: Forty-two patients were emergently admitted to the intensive care unit after emergent gastrointestinal surgery in Kyushu University Hospital from May 2008 to April 2013. Of these patients, 22 had DIC (defined as an acute DIC score ≥ 4). All but three patients received treatment with gabexate mesylate (GM) (n = 9) or rTM (n = 10). The causes of sepsis were peritonitis with colorectal perforation, anastomotic leakage, and intestinal necrosis. Acute DIC score, sepsis-related organ failure assessment score, platelet count, and a variety of biochemical parameters were compared between rTM and GM recipients after treatment administration. RESULTS: There were no significant differences between the groups for any parameter except C-reactive protein levels. The CRP level tended to be lower in the rTM group than in the GM group. Acute DIC score in the rTM group resolved significantly earlier than that in the GM group. No patient stopped the administration of rTM because of postoperative bleeding. CONCLUSION: rTM may be an effective therapeutic drug for the treatment of septic patients with DIC following emergent gastrointestinal surgery.

Development of a multi-field fundus photographing system using a non-mydriatic camera for diabetic retinopathy.

A new fundus photographing system was developed for diabetic subjects with or without simple diabetic retinopathy using a non-mydriatic fundus camera. Eight internal fixation targets were incorporated in a non-mydriatic fundus camera (TRC-NW5S; TOPCON, Tokyo, Japan), interfaced with a 3CCD color camera. Nine 45 degrees fundus photographs were taken in 22 healthy volunteers and 16 diabetic subjects, and stored as digital images. Fundus images were reconstituted as collages on the monitor and printed out. The combined angle reached 94 degrees in collage, and the average times required for photographing with and without mydriasis were 3 min 26 s and 4 min 36 s, respectively. The concordance of fundus images between the first and second photographs of healthy volunteers with and without mydriasis was 95.4% (n = 22). The quality of the photographs, graded on a five-point scale (5, full) by three doctors, was 4.3 +/- 0.6 in the volunteers without mydriasis, 4.7 +/- 0.4 in the diabetics without mydriasis, and 4.8 +/- 0.3 in the volunteers with mydriasis. In retinas with diabetic retinopathy, the system was able to depict microaneurysms, hemorrhages, hard exudates and soft exudates. This new system was satisfactory for the screening and follow-up of diabetic retinopathy.

Surface quality of intraocular lenses.

We observed circular furrow-like patterns on the implanted intraocular lens surface in postoperative follow-up examination by specular microscopy. The patterns may have been deep lathe-cut marks or compression-related marks on the optics. Specular microscopy, polarized light microscopy, and scanning electron microscopy detected a similar circular mark on the optic surface of a control intraocular lens of the same model. A reconsideration of surface quality is indicated.

Cutaneous vasculitis in a patient with dermatomyositis without muscle involvement.

A 74-year-old female patient with cutaneous ulcerations and typical dermatomyositis (DM) skin rash had no muscle disease for a 1-year and 5 months period. Histological examination of the skin ulceration indicated vascular occlusion without cellular infiltration. Cutaneous ulceration is a very rare manifestation of adult-onset DM patients without inflammatory myopathy.

Acute effects of nasal continuous positive airway pressure on 24-hour blood pressure and catecholamines in patients with obstructive sleep apnea.

To assess the acute effects of nasal continuous positive airway pressure (CPAP) on the 24-hour blood pressure and the secretion of catecholamines in urine and plasma, we investigated the changes in the 24-hour blood pressure and urinary and plasma concentrations of epinephrine (E) and norepinephrine (NE) in 26 men with obstructive sleep apnea (OSA) with and without nasal CPAP. Nasal CPAP resulted in significant decreases in the daytime diastolic pressure (from 86 +/-16 mmHg to 83+/-12 mmHg), the nighttime diastolic pressure (from 81+/-12 mmHg to 77+/-9 mmHg) and the nighttime systolic pressures (from 125+/-15 mmHg to 120+/-10 mmHg). There was no significant difference between patients with and without CPAP in the daytime or nighttime urinary E level, but patients who received CPAP showed a significant decrease in daytime urinary NE level (from 156+/-112 microg/14h to 119+/-101 microg/14h) and nighttime urinary NE level (from 143+/-91 microg/10h to 112+/-65 microg/10h). The morning plasma level of NE also decreased (from 371+/-181 pg/ml to 273 +/-148 pg/ml) in patients who received nasal CPAP (p<0.02), but the plasma level of E remained unchanged. There were no correlations between PSG parameters and the reductions in blood pressure and the catecholamine levels induced by nasal CPAP. These findings suggest that OSA contributes, at least in part, to the development of systemic hypertension by increasing sympathetic nervous activity.

Hyperbilirubinemia induced by endoscopic variceal ligation for esophageal varices in a patient with primary biliary cirrhosis: a case report.

We describe the case of a 51-year-old woman with primary biliary cirrhosis who developed hyperbilirubinemia with transient liver dysfunction after undergoing endoscopic variceral ligation to control hemorrhaging from esophageal varices. After undergoing a variceal ligation, the serum total bilirubin increased from 4.0 mg/dL to 9.5 mg/dL, and the degree of liver failure worsened. She finally had to undergo a liver transplant. We discuss the mechanism of hyperbilirubinemia after endoscopic variceal ligation.

Laparoscopic splenectomy: the latest modern technique.

BACKGROUND/AIMS: Recent advances in technical instruments have resulted in increased safety and simplicity in laparoscopic surgery. The purpose of this article is to introduce our latest operative techniques for laparoscopic splenectomy. METHODOLOGY: The patient is placed in the right semidecubitus position and the gastrosplenic ligament including the short gastric vessels was performed by using an ultrasonically activated scalpel. The splenic artery and vein were resected at the splenic hilum with an autosuture device. The electromechanical morcellator was used to remove the spleen. RESULTS: The laparoscopic splenectomy was successfully performed in all 74 patients from 1992-1997. There was no deaths related to the operation. Conversion to open surgery with a small incision of 5 cm was required in one patient with advanced liver cirrhosis and portal hypertension and 45 patients with portal hypertension. CONCLUSIONS: A laparoscopic splenectomy is considered to be a safe and feasable modality for the treatment for hematologic disorders of both the spleen and other benign tumors.

Portal-systemic encephalopathy due to a congenital extrahepatic portosystemic shunt: three cases and literature review.

Extrahepatic portal-systemic encephalopathy due to congenital extrahepatic portosystemic shunt has so far been rarely reported in the literature. We herein report 3 such cases without liver cirrhosis or portal hypertension which were presented with the chief complaint being disturbance of consciousness and abnormal behavior. In all cases the brain computed tomography scan revealed no pathological findings, while electroencephalogram showed a diffuse slow activity with triphasic waves. The laboratory data revealed a high serum ammonia level. Percutaneous transhepatic portography demonstrated portosystemic shunts. After these shunts were surgically occluded, the serum ammonia level reached a normal range and encephalopathy disappeared. A liver biopsy also revealed neither fibrosis nor cirrhosis in any of the cases. The 23 previously reported cases are also discussed.