Advances in Digestive Medicine最新文献

Incidence of early-onset colorectal cancer is on the rise, prompting updated international guidelines recommending screening for average-risk individuals starting at age 45. Adenoma detection rate (ADR) serves as a crucial quality indicator for colonoscopy (CFS), with a current benchmark of 25% for screening CFS starting at age 50. However, the impact of lowering the screening age on ADR remains uncertain. This study aimed to assess the ADR in average-risk individuals who undergo screening colonoscopy at an age older than 40. Participants who underwent a complete colonoscopy for health examination at a medical center between January 2014 and February 2020 were enrolled in this study. We excluded colonoscopies performed on individuals younger than 40 years of age or older than 75 years of age, as well as those conducted for surveillance purposes. ADR was defined as the percentage of colonoscopies with at least one colorectal adenoma detected. We calculated the ADR for different age groups, including 40–44, 45–49, 50–54, and 55–75, to understand the age-specific ADR of screening colonoscopy. Additionally, we evaluated the ADR among participants who started screening colonoscopy at ages ≥40, ≥45, and ≥50 to understand the impact of starting age on ADR. A p value <.05, determined by the chi-square test, was considered significant. Among the 33 073 CFS completed during the study period, 5852 CFS examined in patients aged younger than 40 years, 344 CFS examined in patients aged older than 75, and 6881 CFS with surveillance indication were excluded, leaving 19 996 CFS enrolled for analysis. The mean age of the participants was 53, with 57% being male and 43% being female. The ADR for the age groups of 40–44, 45–49, 50–54, and 55–75 were 28.0% (1058/3778), 31.8% (1191/3741), 35.6% (1387/3891), and 44.2% (3794/8586), respectively, with a statistically significant difference (p < .01). The ADR for age ≥40, ≥45, and ≥50 were 37.2% (7430/19996), 40.1% (6372/15874), and 41.5% (5181/12477), respectively, with a statistically significant difference (p < .01). The findings of our study indicate that there are notable differences in ADR among various age groups. Lowering the screening age might result in a decrease in the overall ADR. However, our results suggest that even if CRC screening begins at age 40 or 45, the current benchmark of 25% ADR for screening colonoscopy may still be maintained. These findings provide valuable insights into the age- and gender-specific prevalence of adenomas in colonoscopy screening and can be used to inform future screening guidelines and recommendations.

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.

Gastroesophageal reflux disease (GERD) characterized by heartburn and/or acid regurgitation symptoms is one of the most common gastrointestinal disorders. The rapid onset of proton pump inhibitors (PPIs) to improve annoying symptom is an essential need in treating GERD. There was no report about the short-term clinical effects comparing lansoprazole 30 mg to rabeprazole 20 mg. This pilot study was designed to compare the initial one-week clinical response of the two drugs in GERD with erosive esophagitis. Total 44 patients with GERD were enrolled in this study and randomized into two groups. The patients had the symptoms of acid regurgitation, heartburn, or feeling of acidity in the stomach and erosive esophagitis proven by endoscopy. They respectively received once-daily dose of lansoprazole 30 mg (n = 23) and rabeprazole 20 mg (n = 21) for treatment of GERD. The primary end point was complete symptom resolution (CSR). The CSR rate was evaluated by questionnaire including acid regurgitation, heartburn sensation and epigastric pain at day 1, 3 and 7. Two patients in the arm of rabeprazole had poor compliance of drugs and were excluded from analysis. The final patient numbers were 23 in the arm of lansoprazole and 19 in rabeprazole. The baseline characteristics of two groups were similar in age, gender, body mass index (BMI), Helicobacter pylori infection, GERD severity, smoking, alcohol, coffee, spicy, sweet food and laboratory data. The ingestion of tea was the only one variable with significant difference between the two groups (65.2% and 31.58%, p = .03). At day 1, 3 and 7, the CSR rate of lansoprazole and rabeprazole were 21.74% and 26.32% (p = 1.000), 34.78% and 31.58% (p = .827), 47.83% and 47.37% (p = .976), respectively. The other clinical factors, including age, gender, BMI, Helicobacter pylori infection, smoking, alcohol, coffee, tea, spicy, sweet food and laboratory data, have also no significant influence on CSR rates at day 1, 3, 7. However, the patients with GERD C and D had significantly higher CSR rate than patients with GERD A and B at day 1 and 7 (CSR rate at day 1: 50.00% vs. 15.63, p = .040; day 3: 60.00% vs. 25.00%, p = .059; day 7: 90.00% vs. 34.38%, p = .003). In multivariate regression analysis, the patients with GERD C and D still had significantly higher CSR rate than patients with GERD A and B at day 7 (Odds ratio: 28.27, 95% CI: 2.10–380.03, p = .012). The CSR rates between lansoprazole group and rabeprazole group at day 1, 3, 7 were not significantly different, so the difference of PPIs did not play the role on the initial clinical response within 1 week for the erosive GERD patients. However, the patients with more severe erosive GERD on endoscopy had higher CSR rate at day 7.

Fluoroscopy is necessary for endoscopic retrograde cholangiopancreatography (ERCP). Occupational radiation exposure of staff (endoscopists, nurses, or assistants) is inevitable. Fluoroscopes with a tube over-couch (OC) rather than under-couch (UC) may have more radiation reflection dosage on the staff's upper body theoretically, where the most vital organs are. In the study, we assessed the radiation exposure on staff by two different types of fluoroscopes in real-world practice. Using a radiation dosimeter to measure the radiation dosage on endoscopists and assistants in each ERCP procedure under two different fluoroscopic systems (UC vs. OC). Forty-one ERCP procedures were enrolled. Dosimeters were used NanoDots for the measurement of personal radiation exposure. Those dosimeters were attached to the left forearm and chest of the endoscopist and only the chest of two assistants, the wall of the ERCP room, and the controlling room in every procedure. Nine-teen ERCPs were performed under the OC unit, and the other 22 ERCPs were UC method. Fluoroscopic time and output of radiation dose showed no significant difference between the two groups. Radiation exposure in endoscopist were 0.0911[0.1041–0.3974] mGy (OC) versus 0.0276 [0.0080–0.2924] mGy (UC), p < .01 for the forearm; and 0.0318 [0.0070–0.2628] mGy (OC) versus 0.0182 [0.0088–0.1628] mGy (UC), p = .04 for the endoscopist's body. There was no difference in radiation exposure from assistants in both groups. For all the ERCP procedures, the measurement of radiation exposure from high to low is endoscopist's hand, endoscopist's body, assistant 1, assistant 2, and ERCP room (p < .01). Radiation detection from ERCP room is slightly higher but close to controlling room (p = .06). For the safety of occupational radiation protection, tube of fluoroscope UC is better than OC for the endoscopists more than assistants. Besides, the assistant 1 took higher radiation exposure than assistant 2 for each ERCP procedure.

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.

Bismuth quadruple therapy is recommended as the choice treatment for Helicobacter pylori (H. pylori) infection in areas of either low or high clarithromycin resistance in the Maastricht VI/Florence Consensus Report. However, the optimal treatment duration and drug dosages of bismuth quadruple therapy remain unclear. The study aimed to search the independent risk factors predicting eradication failure of standard bismuth quadruple therapy in the first-line treatment of H. pylori infection. From July 2014 to June 2022, 274 H. pylori-infected patients who received 10-day or 14-day bismuth quadruple therapy containing a proton pump inhibitor, bismuth, tetracycline and metronidazole were included for the study. Post-treatment H. pylori status was assessed at least 4 weeks after completion of treatment. The relationships between eradication rate and 13 clinical parameters were analyzed by univariate and multivariate analyses. The eradication rates of standard bismuth quadruple therapy were 93.8% and 94.2% by intention-to-treat and per-protocol analyses, respectively. Univariate analysis revealed that patients harboring metronidazole-resistant strains had a lower eradication rate than those harboring metronidazole-susceptible strains (88.7% [55/62] vs. 96.7% [148/153]). The other factors including smoking, treatment duration and drug adherence were not significantly associated with cure rate. Multivariate analysis revealed that metronidazole resistance of H. pylori was the only independent risk factors related to eradication failure of standard bismuth quadruple therapy with an odds ratio of 3.8 (95% CI: 1.2–12.4). In conclusion, metronidazole resistance is an independent risk factor predicting eradication failure of standard bismuth quadruple therapy in the first-line treatment of H. pylori infection. There is no difference in eradication efficacy between 10-day and 14-day bismuth quadruple therapies in Taiwan.

A 63-year-old female presented to our hospital for further management of a rectum lateral spreading lesion discovered by colonoscopy for fecal occult blood survey. Conventional white light colonoscopy showed type 0-IIa + IIb lesion over rectum (Figure 1A). Indigocamine chromoendoscopy showed an irregular mucosal surface pattern (Figure 1B). Subsequent magnifying colonoscopy with narrow-band imaging (NBI) revealed a focal avascular area with scant enlarged, dilated branch-like microvascular pattern on the lesion surface (Figure 1C). 12 MHz endoscopic ultrasound (EUS) showed thickening of mucosal layer (second layer) with preserved muscular propia layer (Figure 1D).

What is the diagnosis?

Biopsy specimen showed colon tissue with atypical lymphocytes proliferation above the lamina propria (Figure 2A–E). Immunohistochemical stain showed CK (scant lymphoepithelial lesions), CD138(−), MNDA focal positive, CD20(+), CD79a(+), and PAX-5(+). Mucosa-associated lymphoid tissue lymphoma (MALToma) is diagnosed.

Primary gastrointestinal non-Hodgkin lymphoma is most often located in the stomach. The large intestine MALToma is rare.¹ Primary colorectal lymphoma accounts for approximal 10% of gastrointestinal lymphoma and 0.2% of colorectal malignancy.² The gross morphology of colorectal lymphoma could be polyposis, subepithelial tumor, epithelial mass, and ulcerated type under white light endoscopy.³ However, flatten type may mimic lateral spreading tumor and be confused with sessile serrated lesion. Image-enhanced colonoscopy was useful for observed microstructure of flatten lesion. Tree-like-appearance blood vessels observed on magnified NBI have been mentioned in colon MALT lymphoma.⁴ In this case, Indogocarmine chromoendoscopy showed irregular mucosal surface pattern, not correlated with EUS finding. NBI magnifying colonoscopy showed Japan NBI Expert Team classification type 3 with branch-like microvascular pattern was the high spot and gave us the hint of colon MALToma.

The authors declare no conflicts of interest.

Informed consent was obtained from the patient to publish this article and images.