Advances in Digestive Medicine最新文献

A 60-year-old previously healthy woman presented with a sudden onset of lower abdominal pain followed by watery diarrhea after hiking. A CT scan revealed portal venous gas (Figure 1A) and heterogeneous hypoattenuating wall thickening over the terminal ileum, without other lesions in the major vessels (Figure 1B). She left against medical advice but returned later with worsened abdominal pain and hematochezia. On examination, tachycardia (103 beats per minute), tachypnea (22 breaths per minute), and tenderness over the lower abdomen were recorded. Laboratory investigation revealed leukocytosis (1645/mL), azotemia (blood urea nitrogen is 29.3 mg/dL), lactic acidosis (2.75 mmol/L), and hyperglycemia (322 mg/dL). A colonoscopy revealed shallow ulcers with exudative discharge from 4 to 10 cm above the ileocecal valve (Figure 2). Biopsy showed ulcer debris, hyalinization of the lamina propria, smaller and decreased number of glands, which were compatible with ischemic change. Stool culture, tissue culture, and autoimmune profile were all negative. A diagnosis of ischemic ileitis was made, and the symptoms resolved under supportive care and empirical flomoxef. She was also diagnosed of type 2 diabetes mellitus and treatment was then started. Following colonoscopy 6 months later showed normal mucosa.

Ischemic bowel disease could be divided into colonic and mesenteric ischemia. Colonic ischemia is the most common form and has a more favorable outcome.¹ The possible etiology of this event could be dehydration due to hiking and a hyperglycemic state. The isolated ischemic change of the terminal ileum is unusual, since it is not in the traditional watershed zones.² Ileitis may result from a variety of disease such as Crohn's disease, infection, spondyloarthropathies, vasculitides, ischemia, neoplasms, medication-induced, and eosinophilic enteritis.³

We presented a case of ischemic ileitis, highlighting the importance of a comprehensive diagnostic approach and consideration of various etiologies.

The authors declare no conflicts of interest.

A 44-year-old woman with no known underlying diseases developed epigastric pain and abdominal fullness for 2 weeks. She denied prior proton pump inhibitor use and a family history of polypoid syndrome. Esophagogastroduodenoscopy revealed a 0.4-cm polyp with relatively intact mucosa on the esophago-cardiac junction (Figure 1A,B). The mucosal pattern of the stomach showed no atrophic change; the Campylobacter-like organism test showed negative, and the biopsy showed no Helicobacter pylori. Identified. The etiology was suspected to be a fundic gland polyp by conventional endoscopy. However, pathological findings revealed adenocarcinoma. The patient underwent endoscopic submucosal dissection and pathological findings showed a well-differentiated gastric adenocarcinoma tumor, fundic gland type; the tumor dimension was 0.4 × 0.3 cm, and the greatest invasion depth was 0.1 cm above the muscularis mucosae (Figure 2).

Gastric adenocarcinoma of the fundic gland type (GA-FG), a novel rare variant of gastric adenocarcinoma (accounting for 1% of patients with early gastric carcinoma), presents with atypical cells with differentiation toward the fundic gland and has been added to the 2019 edition of the World Health Organization's list. The most common features of tumors are their whitish appearance, dilated vessels with branching architecture, and background mucosa without atrophic changes. Furthermore, at low magnification, GA-FG can mimic a fundic gland polyp.¹ Some reports showed regular microvascular patterns under magnifying endoscopy in partial cases.²

In our case, the small size and unimpressive endoscopic appearance of the polyp further emphasize that these alone cannot predict the histology of the polyp. Although the majority (70%–90%) of gastric epithelial polyps are fundic gland polyps or hyperplastic polyps and are often incidental findings on endoscopy. Gastric polyp histology cannot be reliably distinguished by endoscopic appearance; therefore, a biopsy or polypectomy is warranted when polyps are detected.³

The authors declare no conflicts of interest.

Written informed consent was obtained from the patient.

We proposed that cancer stem cells (CSCs) survived and presented resistance to radiotherapy (RT) in hepatocellular carcinoma (HCC) cells. Interleukin 6 (IL-6) has been reported to be particularly involved in HCC tumorigenesis. Therefore, we intended to validate that IL-6 downstream STAT3-mediated CSCs formation and immune checkpoint PD-L1 expression in HCC, thus contributing to radioresistance. HBV-positive HCC tumorspheres were formed and exposed with X-ray irradiation, cell viability of which was measured consequently. Specific inhibitors targeting EGFR (by gefitinib), STAT3 (by BBI608), and HCC-targeted therapy sorafenib were investigated to suppress tumorsphere formation. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used for detecting STAT3-downstream PD-L1 and anti-apoptosis MCL1 and BCL2 gene expression in the PLC5-derived tumorspheres and STAT3-knockdown PLC5. We found that RT significantly inhibited HBV-positive Hep3B and PLC5 cell viability but not for HCC-derived stem-like tumorspheres cultured by EGF, IL-6, bFGF, and HGF. It revealed that tumorspheres presented radioresistance compared with the parental cells. Specifically, RT induces IFNs, EGF, and IL-6 expression, resulting in STAT3 phosphorylation. Kaplan–Meier plotter indicated that highly EGF (p = .0024), IL-6 (p = .12), and FGF2 (p = .0041) were associated with poor survival probability in patients with HBV-positive HCC. We further demonstrated that BBI608 and sorafenib significantly suppressed PLC5 cell viability and PLC5-derived tumorsphere formation. To investigate the mechanism of CSC-presented radioresistance, STAT3 and STAT3-downstream genes, including PD-L1 and anti-apoptosis MCL1 and BCL2, were detected using qPCR. We demonstrated higher STAT3, PD-L1, MCL1, and BCL2 in Hep3B- and PLC5-derived CSCs compared to PLC5. In addition, knockdown of STAT3 reduced cell proliferation in PLC5 cells, resulting in down-regulation of IL-6-mediated PD-L1 and BCL-2. Meanwhile, we found that knockdown of STAT3 significantly improved RT-mediated suppression of tumorsphere formation. In conclusion, we found that CSCs presented radioresistance and figured out which may be mediated by STAT3 in HBV-positive HCC.

A 43-year-old woman presented with intermittent lower abdominal sharp pain for 4 months, which radiated to her back and right thigh, especially during menstrual period. She denied fever, weight loss, and change in bowel habits, hematochezia, or dysuria. Due to persistent symptoms, colonoscopy was arranged and showed two protruding lesions at the cecum (Figure 1A) and rectosigmoid junction (Figure 1B), respectively. Endoscopic ultrasound (EUS) was arranged for evaluating the originating layer and echogenicity. EUS with miniprobe showed one 25.7 × 9.6 mm heterogeneous hypoechoic mass outside cecum, which was adjacent to the serosa layer (Figure 1C), and one 22.5 × 9.5 mm homogenous hypoechoic mass arising from muscularis propria layer at the rectosigmoid junction (Figure 1D). The differential diagnosis included gastrointestinal stromal tumors, leiomyomas, and schwannomas, which originate from muscularis propria layer and presented as hypoechoic echogenicity.¹ Symptoms associated with menstrual cycle are an important diagnostic clue for endometriosis, which is detected as hypoechoic lesions on EUS. One 2 × 2 cm cystic lesion in the paracecal area and enlarged appendix were noted during laparoscopy (Figure 2A), and laparoscopic right hemicolectomy was performed due to the will of this patient. Pathological examination is compatible with endometriosis (Figure 2B). Dienogest was used for treatment of rectal endometriosis. The pain improved significantly after surgery and medical therapy.

Bowel endometriosis accounts for 3.8% to 37% of women with endometriosis and is most commonly involved in rectosigmoid colon, followed by ileocecal region, appendix and other parts of bowel.² Patients with bowel endometriosis may present with dysmenorrhea, infertility or gastrointestinal symptoms. Transvaginal ultrasound is the preferred modality for patients suspected of rectovaginal endometriosis, and EUS can discriminate the depth of infiltration and aids in surgical planning. Bowel endometriotic lesions involve the serosa, muscularis propria, submucosa, and mucosa layer in 94.5%, 95.1%, 37.8% and 6.4% of cases, respectively.³

All authors contribute to all stages of article composition: data acquisition and editing, manuscript drafting, and manuscript revision.

The authors declare no conflicts of interest.

The patient authorized the publication of the data and the patient's anonymity is preserved in the article.