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Spontaneous portosystemic shunt (SPSS) refers to collateral vessels that communicate between the portal vein system and systemic circulation. SPSS mainly includes esophageal varices, gastric varices, left gastric vein, recanalized paraumbilical vein, abdominal wall varices, and spontaneous splenorenal shunt. SPSS contributes to the development of hepatic encephalopathy caused by portal vein inflow bypassing and carries a higher risk of death in liver cirrhosis. Abdominal contrast-enhanced computed tomography is a major imaging approach to establish a diagnosis of SPSS and evaluate its location and feature. This review primarily describes the main contrast-enhanced CT features of SPSS in liver cirrhosis.

Background Morphologic changes in the gallbladder and gallstones are common in cirrhotic patients, but their associations with outcomes of cirrhotic patients are unclear. Methods We retrospectively enrolled 206 cirrhotic patients and measured their gallbladder length and width, gallbladder wall thickness, presence of gallstones, and gallstones’ length and width in axial contrast-enhanced computed tomography (CT) images. X-tile software was utilized to calculate the optimal cutoff values of these parameters for evaluating survival and hepatic decompensation events in the cirrhosis group. Their associations with survival were explored by Cox regression analyses and Kaplan–Meier curve analyses. Their associations with hepatic decompensation events were evaluated by competing risk analyses and Nelson-Aalen cumulative risk curve analyses where death was a competing event. Results Cirrhotic patients with gallbladder length < 72 mm had a significantly higher cumulative survival rate than those with a length of ≥ 72 mm (P = 0.049 by log-rank test), but gallbladder width, gallbladder wall thickness, presence of gallstones, and gallstones’ length and width were not significantly associated with survival (P = 0.10, P = 0.14, P = 0.97, P = 0.73, and P = 0.73 by log-rank tests, respectively). Cirrhotic patients with gallbladder wall thickness < 3.4 mm had a significantly lower cumulative rate of hepatic decompensation events than those with a wall thickness of ≥ 3.4 mm (P = 0.02 by Gray’s test), but gallbladder length and width, presence of gallstones, and gallstones’ length and width were not significantly associated with hepatic decompensation events (P = 0.15, P = 0.15, P = 0.54, P = 0.76, and P = 0.54 by Gray’s tests, respectively). Conclusion Changes in gallbladder length and gallbladder wall thickness, rather than gallstone parameters, may be in parallel with the long-term outcomes of cirrhotic patients.

Gastric antral vascular ectasia (GAVE) is an uncommon clinical entity leading to recurrent gastrointestinal bleeding. There is no consensus regarding treatment of GAVE. Endoscopic therapy is the preferred treatment option, but has a fairly high recurrence rate. Surgical resection can completely resolve GAVE, but is invasive with a relatively high risk of postoperative complications. Recently, the role of pharmacotherapy for GAVE has been recognized. However, the evidence is limited to scattered case reports or small case series. This review comprehensively summarizes the efficacy and side effects of drugs commonly used for the treatment of GAVE, including octreotide, cyproheptadine, cyclophosphamide, prednisolone, estrogen-progesterone, thalidomide, bevacizumab, and tranexamic acid.

Acute portomesenteric vein thrombosis is potentially lethal. In the present paper, a cirrhotic patient with a previous history of esophageal variceal bleeding presented with acute occlusive portomesenteric vein thrombosis, but achieved complete recanalization by low-molecular-weight heparin followed by rivaroxaban. Notably, no bleeding episode occurred during anticoagulation therapy. This case supported early initiation of anticoagulation in such patients.

Portal venous system thrombosis (PVST), a common complication of liver cirrhosis, is closely associated with thrombophilia. To explore the association of homocysteine (Hcy), anticardiolipin antibody (aCL), and anti-β2 glycoprotein I antibody (aβ2GPI), which are possible thrombophilic factors, with PVST in liver cirrhosis. Overall, 654 non-malignant patients (219 with and 435 without liver cirrhosis) admitted between January 2016 and June 2020 were retrospectively evaluated. Presence of PVST, degree of main portal vein (MPV) thrombosis, and clinically significant PVST were identified. Hcy level, hyperhomocysteinemia (HHcy), aCL positivity, and aβ2GPI positivity were compared according to the presence of liver cirrhosis and PVST. Positive aβ2GPI was significantly more frequent in patients with liver cirrhosis than those without, but Hcy level and proportions of HHcy and positive aCL were not significantly different between them. PVST could be evaluated in 136 cirrhotic patients. Hcy level [10.57 μmol/L (2.71-56.82) versus 9.97 μmol/L (2.05-53.44); P = 0.796] and proportions of HHcy [4/44 (9.1%) versus 13/81 (16.0%); P = 0.413] and positive aCL [1/23 (4.3%) versus 10/52 (19.2%); P = 0.185] and aβ2GPI [9/23 (39.1%) versus 21/52 (40.4%); P = 0.919] were not significantly different between cirrhotic patients with and without PVST. There was still no significant association of Hcy level, HHcy, aCL, or aβ2GPI with PVST based on Child-Pugh classification, MPV thrombosis >50%, and clinically significant PVST. Hcy, aCL, and aβ2GPI may not be associated with PVST in liver cirrhosis, suggesting that routine screening for Hcy, aCL, and aβ2GPI should be unnecessary in such patients.

Background Portal venous system thrombosis (PVST) will progress in some cases, indicating worse outcome and the necessity of antithrombotic treatment, but will spontaneously improve in others. It is crucial to understand the natural history of PVST in liver cirrhosis. However, the knowledge regarding how to predict the evolution of PVST in cirrhotic patients is very scant. Methods Sixty-nine cirrhotic patients without malignancy, who had undergone repeated contrast-enhanced computed tomography or MRI to evaluate the severity of PVST at the first and last admissions, were included. Logistic regression analysis was performed to identify the risk factors for the evolution of PVST in liver cirrhosis. Odds ratios (ORs) were calculated. Results Among 42 patients without PVST at the first admission, 10 (23.8%) developed PVST at the last admission. Serum albumin level (OR = 0.873), prothrombin time (OR = 1.619), activated partial thromboplastin time (OR = 1.169), Child-Pugh score (OR = 1.560) and model for end-stage liver disease (MELD) score (OR = 1.292) at the last admission were significant risk factors associated with the development of PVST. Among 27 patients with PVST at the first admission, 11 (40.7%), 4 (14.8%) and 12 (44.4%) had improvement, stabilization and progression of PVST at the last admission, respectively. ΔMELD score (OR = 0.714) was the only significant risk factor associated with the improvement of PVST; additionally, serum albumin level at the first admission (OR = 1.236) was the only significant risk factor associated with the progression of PVST. Conclusion Aggravation and amelioration of liver dysfunction may predict the development and improvement of PVST in liver cirrhosis, respectively.

We read with great interest the study by Semmler et al., which demonstrated that spontaneous bleeding episodes occurred in 28.6% of patients with advanced chronic liver disease and vascular live disease after direct oral anticoagulants (DOACs), and that Child-Pugh class B/C patients experienced more spontaneous bleeding episodes than Child-Pugh class A patients (36.9% versus 15.9%)(1). Notably, the authors emphasized the significance of collecting more data regarding safety of DOACs in such patients(1). Herein, we would like to further discuss this issue by reporting a Budd-Chiari syndrome (BCS) patient who developed gingival bleeding immediately after rivaroxaban.

Rationale Henoch-Schonlein purpura (HSP) is a small-vessel vasculitis that has been extensively studied in children, but little is known about its natural history in adults. There is no consensus regarding the treatment of glucocorticosteroids use for HSP. The efficacy of glucocorticoid for preventing from severe complications or relapse is also controversial in HSP. Patient concerns A 21-year-old male was admitted to the hospital due to abdominal pain for more than 20 days, hematochezia for more than 10 days, and rash for 2 days. Diagnoses The diagnosis of HSP is based on the European League against Rheumatism and the Paediatric Rheumatology European Society in 2006. Interventions The patient received glucocorticosteroids treatment for 17 days at the time of first hospitalization. Outcomes The abdominal pain and hematochezia completely disappeared on the 6th day after the use of glucocorticosteroids, and purpura completely disappeared on the 8th day. Lessons Our patient has a good response to glucocorticoid. Glucocorticosteroids may be effective for the treatment of HSP.

Repetitive nerve stimulation (RNS) is a valuable diagnostic method for myasthenia gravis (MG). However, its association with clinical severity was scarcely studied. We reviewed medical records and retrospectively enrolled 121 generalized MG patients. Sensitivity of different muscles to RNS and clinical scoring systems was evaluated. RNS testing revealed facial muscles have the highest positive rate, followed by proximal muscles and distal muscles, with the palpebral portion of the orbicularis oculi muscle most sensitive. Amplitude decrement of compound muscle action potential (CMAP) in the palpebral portion of the orbicularis oculi muscle is related to quantitative myasthenia gravis (QMG) scores, MG-specific manual muscle testing (MMT) scores and myasthenia gravis-related activities of daily living (MG-ADL) scores. We suggest that RNS testing of the palpebral portion of the orbicularis oculi muscle is a potential assessment indicator in patients with generalized MG.

Introduction: In the tumor micro-environment, extracellular ATP is sequentially hydrolyzed to adenosine by the ecto-nucleotidases CD39 (ATP→AMP) and CD73 (AMP→adenosine). Adenosine, through activation of the A2a receptor (A2aR), is a potent inhibitor of T-cell activation, resulting in an immunosuppressed phenotype. Thus, inhibition of A2aR has recently generated great interest in immuno-oncology. We present the characterization of a novel, selective, and highly potent small molecule antagonist of A2aR which is slated to enter the clinic in 2017. Methods: The cellular potency of A2aR antagonists was assessed as a function of decreased cAMP levels in CHO cells stably over-expressing hA2aR, a Gs coupled receptor, following stimulation with the agonist NECA. Experiments were conducted in the presence and absence of human serum. Selectivity against the Gi-coupled receptor A1R was assessed similarly as a function of cAMP elevation in CHO cells stably expressing hA1R, following pretreatment with forskolin and stimulation with NECA. The ability of AB928 to reverse adenosine-mediated immune suppression (25 μM) of human or mouse CD8+ T-cells was determined using standard CD3/CD28 activation conditions. CD25 expression and cytokine release were measured by flow cytometry and ELISA, respectively. The pharmacokinetic characteristics of AB928 were assessed in rodent and non-rodent species to facilitate calculation of a projected human dose. Results: AB928 represents a novel series of potent and selective compounds designed to inhibit adenosine-mediated A2aR activation. This molecule is different from most known A2aR antagonists in that it does not cross the blood brain barrier. AB928 inhibited NECA-mediated A2aR activation with a potency of Conclusions: AB928 is a potent, selective and peripherally restricted antagonist of the A2aR receptor which is slated to enter clinical development in 2017. Citation Format: Matt J. Walters, Joanne B. Tan, Annette Becker, Fangfang Yi, Tim Park, Manmohan R. Leleti, Brandon Rosen, Ehesan Sharif, Laurent Debien, Steve Young, Wan Hsin Lim, Stefan Garrido-Shaqfeh, Juan C. Jaen, Jay P. Powers. Characterization of the potent and selective A2aR antagonist AB928 for the treatment of cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4572. doi:10.1158/1538-7445.AM2017-4572