Advances in Digestive Medicine最新文献

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).

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.