Advances in Digestive Medicine最新文献

A 56-year-old male had a history of tongue and hypopharyngeal cancers following surgery as well as early esophageal squamous cell neoplasm detected after endoscopic submucosal dissection (ESD). His head and neck cancers and esophageal neoplasm stabilized and he underwent esophagogastroduodenoscopy (EGD) follow-up annually. During one such follow-up, a Type 0-Isp whitish protruding mucosal lesion, 1.5 cm, below esophagogastric junction (EG junction) (Figures 1A,B) was discovered. One month later, during follow-up EGD (Figure 1C), the lesion appeared more fragile and irregular with its texture revealed as having a rigid base after endoscopic biopsy. Computed tomography (CT) revealed subtle gastric mucosa thickening (Figure 1D). Despite six endoscopic biopsies, histological examination only showed ulcer and atypical cells.

What is the next step? What is the diagnosis?

Due to suspicion of malignancy, a diagnostic treatment with ESD was performed for a complete pathology examination. During the ESD procedure, performed using Dual knife, an IT-nano knife, a polypoid lesion with fragility was noted below the EG junction, extending to the cardiac region. The procedure revealed that the lesion was separated from the muscular propria (Figure 2A). En-bloc resection was achieved without major complication. Pathologic examination revealed interlacing fascicles of spindle-shaped cells with increased cellularity (Figures 2B,C). The special stain showed SMA(+) (Figure 2D), focal positivity for Desmin and caldesmon, and negativity for CD34, CD117, S-100 and Dog-1. Based on these morphological and immunohistochemical studies, leiomyosarcoma was considered. Surgical esophagectomy was suggested but the patient rejected this; as a result, adjuvant radiotherapy with a dosage of 6000 cGy/30fr was administered. Subsequent years of treatment involved endoscopy and CT follow-ups, and complete remission was achieved.

Leiomyosarcomas of the stomach are rare malignant tumors derived from smooth muscle tissue,¹ derived not only from muscularis propria, but could also be from muscularis mucosa. Image surveillance with endoscopic ultrasound and computed tomography would be helpful for clarification.² Surgical treatment such as esophagectomy is often the preferred choice³; however, based on our experience, ESD has been found to be useful for proper pathological examination, and salvage radiotherapy is a reasonable option if patient is unsuited for esophagectomy.

The authors declare no conflicts of interest.

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

Gastroesophageal reflux disease (GERD) exhibits a global prevalence ranging from 8% to 33%.¹ Esophagogastroduodenoscopy serves as a crucial diagnostic tool for providing objective evidence of GERD, such as erosive esophagitis and Barrett's esophagus, and for excluding other potential causes. It is the preferred initial modality for GERD surveillance as mandated by the national health insurance policy in Taiwan.² GERD diagnosis is typically established through a synthesis of clinical, endoscopic, and physiological criteria, as recently outlined in the Lyon Consensus 2.0. GERD is conclusively diagnosed based on the endoscopic evidence of esophagitis (Los Angeles grades B, C, and D), Barrett's esophagus, or peptic stricture. Additionally, a diagnosis of GERD can be confirmed by acid exposure time (AET) exceeding 6% during pH impedance testing, or over 2 days with AET exceeding 6% as determined by wireless pH monitoring.²

Symptomatic relapse frequently occurs swiftly among patients with GERD symptoms following the discontinuation of treatment. Previous prospective studies have indicated that up to 30.4% of GERD patients experience symptom recurrence within the first year of follow-up, with symptom recurrence associated with the initial symptom burden.³ A severe GERD phenotype, characterized by advanced-grade esophagitis (Los Angeles grade C or D), and/or AET exceeding 12.0%, or a DeMeester score greater than 50, has been identified. Management of this phenotype often necessitates continuous long-term proton pump inhibitor (PPI) therapy or invasive anti-reflux procedures, alongside lifestyle optimization.⁴ According to the AGA clinical practice update on a personalized approach to GERD evaluation and management, clinicians should assess the appropriateness and dosing of PPI therapy within 12 months of initiation for patients with unproven GERD, and should consider offering endoscopy along with prolonged wireless reflux monitoring off PPI therapy to validate the long-term use of PPIs.⁴ In this context, it is recommended that endoscopy coupled with prolonged reflux monitoring be ideally conducted after withholding PPI therapy for 2 to 4 weeks, whenever feasible.⁵ This approach is vital for shared decision-making, as it helps patients understand the necessity for potential chronic lifelong maintenance therapy.⁴

Shih et al. have demonstrated that within a 12-week period following the initial administration of PPIs, the cumulative incidence of symptom relapse among patients diagnosed with Los Angeles grade A and B erosive esophagitis can reach up to 50.2%. Additionally, advanced age and smoking have been identified as independent predictors of symptom relapse. This study underscores the significant reliance on PPIs even among patients with mild erosive

In recent years, epidemiological studies found a notable change in the occurrence and prevalence of certain types of digestive system malignancies. Specifically, there is a shift in these cancers being diagnosed at a younger age, which is commonly referred to as “early-onset cancer.” This is especially noticeable in colorectal cancer and to a lesser extent in other malignant digestive tumors, primarily in the gastric and to a lesser extent in the pancreas and biliary tract.¹ In this issue, Tran² et al described the clinical and endoscopic characteristics of this group of individuals from a Vietnamese population. Nine percent of the study population were categorized as early-onset gastric cancer (EOGC), with a diagnosis occurring before the age of 40.

Approximately 90% of gastric cancer is attributable to Helicobacter pylori (H. pylori) infection, and the global incidence of gastric cancer declined in both male and female individuals globally, like the declining trend of H. pylori prevalence.³ However, the incidence of EOGC increased and now comprises 30% of gastric cancer^{4, 5} in the United States. Only a minority of them are being associated with a genetic disease such as the hereditary diffuse gastric cancer or the Lynch syndromes and the remaining majority being sporadic.⁶ Higher prevalence of alcohol drinking and unhealthy dietary habits but not smoking are associated with higher prevalence of EOCG.⁷ EOGC is predominantly found in the stomach body and is more prone to manifesting as a diffuse infiltrative pattern.² A higher proportion of early-onset gastric cancers were associated with an unfavorable tumor biology and advanced stage at presentation compared with those that occur later in life.^{2, 5, 6}

The identification of gastric cancer in young adults poses a considerable difficulty from both personal and societal viewpoints, especially due to the unfavorable prognosis linked to this ailment. The absence of recommendations for screening for these younger population hinders early detection.⁸ Screening endoscopy is the main technique employed for early detection and curative resection of gastric cancer.^{9, 10} A trained endoscopist must thoroughly prepare the endoscope by employing defoamers and mucolytics and examine the stomach body to identify any infrequently overlooked anomalies, such as pale or depressed patches.²

In conclusion, EOGC presents unique challenges due to its nonspecific symptoms and rapid disease progression.² Prior research has demonstrated that eliminating H. pylori infection reduces the occurrence and death rate of gastric cancer.¹¹ Further investigation is required to identify

Wisteria floribunda agglutinin-positive Mac-2 binding protein (WFA⁺-M2BP) is a novel biomarker for evaluating hepatic fibrosis and hepatocellular carcinoma (HCC) development. However, no previous study has compared its diagnostic accuracy with that of FIB-4 or APRI nor explored its clinical application for predicting esophageal varices bleeding in HCC patients. In this study, we explored these biomarkers and compared their clinical roles. Total 459 HCC patients who underwent curative operation were enrolled in this study. WFA⁺-M2BP level was evaluated using stored blood samples that were collected during surgery, and liver fibrosis was diagnosed based on findings of surgical specimen analysis. Esophageal or gastric varices were evaluated in 207 patients who underwent esophagogastroduodenoscopy (EGD). The correlation between the markers was also determined. Our study showed WFA⁺-M2BP level, FIB-4, and APRI had a similar high accuracy of approximately 73% for liver cirrhosis diagnosis. Their levels were significantly correlated with the liver fibrosis stage (p < .0001). WFA⁺-M2BP level, FIB-4, and APRI also had high diagnostic accuracy for varices formation (accuracy, 76.8%–80.2%) and high predictive accuracy for variceal bleeding (accuracy, 73.9%–76.3%). The correlation between WFA⁺-M2BP level and FIB-4 or between WFA⁺-M2BP level and APRI was weak (Pearson r < 0.5, p < .0001) but that between FIB-4 and APRI was very strong (Pearson r > 0.9, p < .0001). Our study demonstrated WFA⁺-M2BP level, FIB-4, and APRI have all shown to be very useful noninvasive methods for evaluating liver fibrosis and predicting esophageal varices bleeding to avoid risky liver biopsy and EGD examination.

Nonalcoholic fatty liver disease (NAFLD) is commonly associated with obesity but is also found in non-obese individuals. The PNPLA3 gene variant (rs738409) is by far the most important genetic determinant of NAFLD. To date, there is no study exploring the differences and associations between gut microbiota and PNPLA3 genotype on lean and obese NAFLD patients. Thus, the aim of this study was to evaluate the association between gut microbiota and lean and obese NAFLD, while considering the role of PNPLA3 variants. This prospective study took place at Kaohsiung Chang Gung Memorial Hospital from December 2019 to November 2020. We recruited 35 lean NAFLD patients, 70 obese NAFLD patients, and 35 healthy individuals. Fecal samples were collected to analyze the V4 region of the 16S rRNA gene for intestinal bacteria composition. Although lean and obese NAFLD groups did not differ in PNPLA3 variant abundance, the lean NAFLD group had a higher percentage of the G allele variant (82.9% vs. 72.9%) than obese NAFLD group. Alpha diversity for gut microbiota was not significantly different among the three groups. Microbiota differed significantly between lean and obese NAFLD groups in a multi-response permutation procedure analysis (p = .005). Although, there were no significant differences between PNPLA3 G and C in alpha and beta diversity, the same phylum, family, and genus dominant microbiota differed between lean and obese NAFLD. Lean and obese NAFLD patients have different predominant gut microbiota, as do PNPLA3 C and G variants, indicating that lean NAFLD patients may be associated with PNPLA3 G allele variant.

This 50-year-old woman had no systemic disease. She received health examination, and colonoscopy found multiple back spots and patches from cecum to descending colon, especially proximal colon (Figure 1A,B). Colonic biopsies were obtained from pigmented lesions, and a representative hematoxylin and eosin stain (Figure 1C) and a Fontana-Masson stain (Figure 1D) were shown. No similar discoloration was noted in upper alimentary tract to the duodenum by endoscopy. Histology of the discolored colonic lesion showed colonic mucosa with scattered nests of melanocytic-like cells in mucosa and submucosa (Figure 1C). The brown pigment was positive for Fontana-Masson stain (Figure 1D) and negative for iron and PAS stain. Therefore, it was melanin. In immunohistochemical study, the pigmented cells were positive for HMB-45, S-100, and Melan-A expression, negative for CD163 expression and Ki-67/MIB-1 labeling index labeling index <2%. Therefore, the diagnosis was melanocytic nevus.

Typical melanocytic nevi are round with a uniform color and a diameter of 5 mm or less on the skin.¹ It is caused by proliferation of melanocytes, and associated with ~30% of melanomas.² Colonic melanocytic nevi are also regarded as potential precursor lesions of malignant melanoma.³ Only one case of colonic melanocytic nevi with completely pathological diagnosis has been reported.⁴ In that case, the lesion is a single brownish flat area occupying a quarter of the colonic wall in the ascending colon. However, we presented the case with diffuse black spots and patches on colonic mucosa.

Unlike melanosis coli, which shows continuous homogeneous black-brownish discoloration of colon mucosa (snake-skin appearance or starry sky appearance), melanosis nevus has round pigmentations with heterogenous distribution.⁵ Microscopically, melanosis coli is characterized by deposition of lipofuscin in histiocytes, while melanocytic proliferation is noted in the melanocytic nevus of colon.

Puo-Hsien Le performed the colonoscopy and drafted the article. Tse-Ching Chen confirmed the diagnosis. Cheng-Tang Chiu revised the article critically for important intellectual content. All authors had final approval of the version to be submitted.

The authors declare no conflicts of interest.

Yes.

A 67-year-old female had a medical history of type 2 diabetes and hypertension with medical control. She also had a history of acute appendicitis and underwent appendectomy 8 years ago. She had a small right abdominal wall mass later and it can easily be pushed into the abdominal cavity. She did not pay much attention to it. She had mentioned a growing palpable mass in the right lower abdominal area since 3 weeks ago and it cannot be pushed into the abdominal cavity. In addition, constipation was noted recent 3 days with increased emesis for 1 day. Physical examination revealed generalized severe abdominal tenderness with a fixed, non-mobile 10-cm hard mass palpable on the right abdominal wall. The laboratory data revealed an elevated white blood cell count of 13 200 per microliter. Abdominal CT determined short segmental, small bowel loops trapped in a lower right abdominal wall defect, and an incarcerated abdominal hernia was diagnosed (Figure 1). The surgeon performed an emergency laparoscopic repair of the incarcerated hernia using a 10 × 15 cm anatomic mesh within 6 h. Following the surgery, the patient's recovery was gradual.

Abdominal wall hernias are suspected based on patient history and confirmed by examination and imaging. Pain caused by the trapping of the bowel and omentum (i.e., fat) is common. In abdominal wall hernia with incarceration justifies an emergency as they are associated with higher morbidity and mortality rates. Older age, high BMI, ASA class III–IV, ascites, and constipation were associated with an incarcerated hernia.¹ In addition, unfavorable outcomes were associated with older age, severe coexisting diseases, and late hospitalization.²

I declare that I have participated in the preparation of the article “Incarcerated hernia in an elderly.” Li-Kai Chang wrote this article. Chia-Yuan Liu and Ming-Jen Chen conducted the literature review. Chen-Wang Chang supported this work by performing a critical reading of the manuscript and supervising the final editing. All authors read and approved the final manuscript.

The authors declare no conflicts of interest.

This study was approved by the appropriate ethics review board (IRB number: 22MMHIS105e).

An 83-year-old bed-ridden female, who underwent percutaneous endoscopic gastrostomy (PEG) 2 months ago, received a colonoscopy as part of a survey for her anemia. Findings of colonoscopy at 50 cm above the anal verge were shown in Figure 1. Key images from a subsequently done CT scan were presented in Figure 2.

In Figure 1, a plastic tube penetrated the colonic wall with granulation seen at the entry and exit site. Figure 2 showed a gastrostomy tube penetrating the redundant colon into the stomach. Laparotomy arranged confirmed penetration of the gastrostomy tube through sigmoid colon. Perforation repair and gastrostomy revision were done. No lasting complication was noted afterwards.

PEG is a procedure to percutaneously place a feeding tube into the stomach via endoscopic guidance.¹ Although being generally safe, PEG carries risks of complications,² and colonic injury is a serious, rare (<1%) one.¹ In these cases, the PEG tube usually penetrates transverse colon which more commonly lie in front of stomach before entering the latter³; this type of injury is usually asymptomatic and remains undiagnosed until tube replacement, while in symptomatic cases, patient would suffer from diarrhea immediately after feeding, or more seriously, symptoms of peritonitis.² In the presented case, the PEG tube penetrated the redundant sigmoid colon (Figure 2, arrow), which was even rarer. Surgical repair is the management of choice, while endoscopic repair has been reported.⁴ To avoid this complication,⁴ it is important to manually palpate the abdomen, observe the location of indentation endoscopically within the stomach, and also ensure evident trans-illumination by endoscope from within the stomach through the abdominal surface is observed. Methods such as placing the patient in anti-Trendelenburg position to prevent displacement of the colon anteriorly to the stomach, using pilot needles to detect potential gushing of air or feces while penetrating colon before reaching the stomach, were proposed. We aim to highlight the importance of recognizing and addressing this potential complication through this case report.

The authors declare no conflicts of interest.

Written informed consent was obtained from the patient, and the patient's anonymity is preserved in the article.