Adobe Gastroenterology

Abstract Background Dyspepsia, characterized by symptoms in the gastroduodenal region, poses diagnostic challenges despite Rome IV criteria. Aim This study aimed to investigate the prevalence of two underreported symptoms, Empty Stomach Sensation and Bothersome Hunger Sensation, in dyspeptic patients, and their association with the disorder of gut-brain interaction. Methods A cross-sectional study surveyed 1,211 individuals in northwest Mexico, assessing dyspeptic symptoms with pictograms and a 7-point Likert scale. Logistic regression analyzed associations between dyspepsia, Empty Stomach Sensation, and Bothersome Hunger Sensation. Results Dyspepsia prevalence was 39.1%, being overlap syndrome the most common (42.7%) phenotypic presentation. Empty Stomach Sensation prevalence in dyspeptic patients was 43.8% versus 12.6% in non-dyspeptics (p < 0.001). Bothersome Hunger Sensation prevalence in dyspeptics was 25.4% compared to 5.6% in non-dyspeptics (p < 0.001). Both symptoms were associated with epigastric pain syndrome, postprandial distress syndrome, overlap syndrome, anxiety disorders and other gastroduodenal symptoms. Conclusions Empty Stomach Sensation and Bothersome Hunger Sensation, though prevalent in dyspeptic patients, are often overlooked. Strengths of this study include its large sample size and comprehensive assessment of symptoms. Limitations include the lack of diagnostic endoscopy and long-term follow-up. Future research should explore the underlying mechanisms of these symptoms and their implications for clinical management.

Background: Metastasis from hepatocellular carcinoma to spleen is unusual and only 5 cases were reported in the literature. Case Report: Here, we encountered a patient with recurrent hepatocellular carcinoma with isolated splenic metastasis. Conclusion: This is one of the rare cases of isolated solitary splenic metastasis from hepatocellular carcinoma.

Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with a poor prognosis. Patients with inoperative PDAC require effective chemotherapy and pain control to increase their quality of life. We investigated whether duloxetine, a serotonin-noradrenaline reuptake inhibitor, improves quality of life in a KPPC (LSL-Kras;Trp53;Pdx1-cre) mouse model of PDAC. Six-week-old KPPC mice were orally administered 4 mg/kg/d duloxetine (n = 12); 4 mg/kg/d duloxetine with 0.15 mg/kg/d atipamezole, a synthetic α2 adrenergic receptor antagonist (n = 9); or vehicle water (n = 11). Body weight and food intake were measured daily, and cancer pain was evaluated by the hunching score and mouse grimace scale. At the endpoint, the tumor status, angiogenesis, and immunoinflammatory condition were analyzed. The pain level using the hunching and mouse grimace scale scores improved by duloxetine in KPPC mice (P < 0.01), whereas the scores that had been reduced by duloxetine were elevated by administration of atipamezole. Kaplan-Meier analysis demonstrated that duloxetine-treated mice had significantly prolonged survival (P < 0.05) with delayed appetite loss, cachexia, and body weight loss. Duloxetine inhibited the proliferation of PDAC cells and cancer-associated fibroblasts in vivo with a shift into an antitumor immunoinflammatory condition and the corresponding plasma cytokine levels. The migrative/invasive potentials of PDAC were inhibited by duloxetine in vitro. Meanwhile, atipamezole did not inhibit the antitumor effects of duloxetine in vitro and in vivo. Therefore, our results indicate that duloxetine mainly improves cancer-associated pain by enhancement of the noradrenergic pathway rather than the serotonergic pathway, whereas duloxetine modulates antitumor effects on PDAC without involvement of the noradrenergic pathway.

The aim of this study was to evaluate the diagnostic and prognostic impact of systemic inflammatory markers for IPMN with high-grade dysplasia (HGD)/invasive carcinoma. Neutrophil-to-lymphocyte ratio (NLR), derived NLR, platelet-to-lymphocyte ratio, and C-reactive protein-to-albumin ratio were compared across the different histological grades of 205 IPMN cases. We also tested the diagnostic performance for IPMN with HGD/invasive carcinoma. The median (interquartile range) preoperative NLR was higher in IPMN with HGD/invasive carcinoma (2.03 [1.48-2.93]) than IPMN with low-grade dysplasia (1.74 [1.42-2.24], P = 0.0137). The C-reactive protein-to-albumin ratio and derived NLR values were also significant higher in cases with HGD/invasive carcinoma. A combination assay of NLR, carcinoembryonic antigen, and carbohydrate antigen 19-9 revealed a 58.8% sensitivity and 76.8% specificity. Among the cases with worrisome features, the high NLR values increased the positive predictive value (68.8%) compared with low values (31.8%). In IPMN cases with the associated invasive carcinoma, high NLR values showed association with the deeper vertical invasion and shorter survival periods. Preoperative NLR, combined with tumor markers and image findings, can be a useful predictive marker for the presence of HGD/invasive carcinoma in IPMNs. Preoperative NLR also predicts the long-term outcomes in IPMN cases with invasive carcinoma.

We report the case of a 48-year-old, leukodermic female diagnosed with ulcerative proctitis for 4 years and latent tuberculosis. She was allergic to salicylates and had a minor allergic reaction to infliximab (rash, vertigo, and headache). Thereafter, she started azathioprine (2.5 mg/kg/day). She maintained intravenous infliximab, together with prophylaxis with clemastine and hydrocortisone, due to the steroid-dependent proctitis. The therapy was continued every 8 weeks with anti-tumor necrosis factor for about 3 years. The analytical evaluation when she was diagnosed with ulcerative proctitis (February 2011) showed negative antinuclear antibodies (ANA), double-stranded-DNA antibodies (anti-dsDNA), antineutrophil cytoplasmic antibodies and anti-Saccharomyces cerevisiae antibodies, and a positive outer membrane protein antibody. About 2 years and 6 months after starting infliximab (November 2013), the patient complained of inflammatory symmetrical polyarthralgia (knee, shoulder, elbow, and wrist) without synovitis, which started every week before the administration of infliximab. Resolution of symptoms was observed after each infliximab infusion. In July 2014, the autoantibody re-evaluation showed positive ANA with a homogeneous pattern with a titer of 1:640, weak positive anti-dsDNA (30.2), and positive anti-histone with C3 decreased (80.3). She was then diagnosed with lupus induced by infliximab and initiated hydroxychloroquine 400 mg. Infliximab was suspended. On re-evaluation, the erythrocyte sedimentation rate was 25 mm/h (1st hour), C-reactive protein 0.5 mg/dL (previously erythrocyte sedimentation rate 15 mm/h and C-reactive protein 1.2 mg/dL), and endoscopically, the mucosa was scarred, with some atrophy and scarce mucus in the lower rectum. About 10 months after discontinuation of infliximab, repeated autoantibodies proved all negative, keeping only low C3 (87). The patient also reported complete resolution of the arthralgia.

Objective: To present the mesalamine-induced acute exacerbation of symptoms and inflammatory markers in children with Crohn's disease (CD). Clinical Presentation and Intervention: Three children who presented with CD had acute exacerbation of colitis symptoms or elevated inflammatory markers when mesalamine was added to treatment while tapering/ceasing steroid treatment. While on steroid treatment, the patients maintained clinical and laboratory remission, but with the initiation of mesalamine treatment, they had abdominal pain and bloody mucoid diarrhoea and/or elevation of white blood cell count, C-reactive protein level and erythrocyte sedimentation rate. Bacterial pathogens were excluded from the urine, throat and blood cultures, parasites with stool examination, viral pathogens with serology. Within 3-7 days after the mesalamine treatment had been stopped, the patients showed improvement of colitis symptoms and normalisation of white blood cell count, C-reactive protein level and erythrocyte sedimentation rate. Conclusion: In this study mesalamine mimicked CD relapse in children with CD while tapering or after stopping steroid treatment. Awareness of this side effect of mesalamine could prevent a misdiagnosis of steroid dependency.

Background: Motility disorders of the biliary tree [biliary dyskinesia, including both gallbladder dysfunction (GBD), and sphincter of Oddi dysfunction] are difficult to diagnose and to treat. Summary: There is controversy in the literature in particular regarding the criteria that should be used to select patients for cholecystectomy (CCY) in cases of suspected GBD. The current review covers the history, diagnosis, and treatment of GBD. Key Messages: Only >85% of patients with suspected GBD have relief following CCY, a much lower rate than the nearly 100% success rate following CCY for gallstone disease. Unfortunately, the literature is lacking, and there are no universally agreed-upon criteria for selecting which patients to refer for operation, although cholecystokinin (CCK)-enhanced hepatobiliary iminodiacetic acid scan is often used, with emphasis on an abnormally low gallbladder ejection fraction or pain reproduction at CCK administration. There is a clear need for large, well-designed, more definitive, prospective studies to better identify the indications for and efficacy of CCY in cases of GBD. i 2014 S. Karger AG, Basel

The role of radiologists in the management of portal hypertension (PHT) had been confined to its diagnosis and treatment planning. However, with the advancements in the field of interventional radiology various minimally invasive techniques have been evolved for the management of portal hypertension and its complications such as recanalisation techniques, shunt creation and variceal bleeding control. Thus, with these technical advances, there is shift in the role of radiologist from diagnosis to management of portal hypertension. In this review, we discuss the nuances of various radiological interventions available for the treatment of portal hypertension.