Use of endoscopic assessment of gastric atrophy for gastric cancer risk stratification to reduce the need for gastric mapping.

Background/Aims: Stratification for gastric cancer risk typically involves histologic grading of gastric biopsies. This study aimed to compare endoscopic assessment of gastric atrophy and histologic gastric mapping for gastric cancer risk stratification in a region with relatively high risk of gastric cancer.Methods: Endoscopic and histologic gastric cancer risk stratification were compared in Vietnamese patients with functional dyspepsia. Endoscopic gastric atrophy was graded according to the Kimura-Takemoto classification. High-risk histologic lesions were defined as gastric dysplasia, Operative Link on Gastritis Assessment (OLGA) gastritis stage III/IV, intestinal metaplasia in both the antrum and the corpus or incomplete intestinal subtype at any site. Two experienced pathologists, blinded to endoscopic information, jointly examined all specimens and reached a consensus. The presence of high-risk histologic lesions was compared among patients with different endoscopic grades of gastric atrophy.Results: There were 280 subjects (mean age, 46.1 ± 10 years, and male, 50%). The numbers of patients with moderate/severe grade of endoscopic gastric atrophy and high-risk histologic lesions were 126 (45.0%) and 46 (16.4%), respectively. The sensitivity, specificity, positive and negative likelihood ratios of moderate/severe endoscopic atrophic grade for detecting high-risk histologic lesions were 93% (95% CI 86%-100%), 65% (95% CI 58%-71%), 2.64 (95% CI 2.18 - 3.18) and 0.10 (95% CI 0.03 - 0.30), respectively.Conclusions: Gastric cancer risk assessment using endoscopic or histologic methods provided similar results such that the absence or a mild grade of endoscopic gastric atrophy would preclude the need for histologic mapping.

Rapidly and Slowly Growing Lineages in Chromosomal Instability-Type Gland-Forming Gastric Carcinomas as Revealed by Multisampling Analysis of DNA Copy-Number Profile.

BACKGROUND: To examine whether gastric carcinoma (GC) with chromosomal instability (CIN-type GC), the largest category in the Cancer Genome Atlas classification, consists of a single genetic lineage, we conducted a multisampling analysis of genomic DNA copy-number profile. METHODS: We performed array-based comparative genomic hybridization using formalin-fixed paraffin-embedded tissues from 54 gland-forming GCs containing a total of 106 DNA samples from mucosal, extramucosal invasive, and lymph node lesions. Microarray data were analyzed by unsupervised hierarchical clustering and penetrance plots. Epstein-Barr virus infection status and mismatch repair (MMR) enzyme-silencing/p53/mucin expression were examined by in situ hybridization and immunohistochemistry, respectively. RESULTS: The samples examined were divided into gain-rich cluster A and loss-rich cluster B, which were different in tumor locus and patient age. The T1/T2-4 ratio, the frequency of small cancers (diameter ≤2-4 cm), and intestinal mucin expression were higher in cluster B than in cluster A, but there were no significant differences in the frequencies of MMR silencing, mutant p53 pattern, and lymph node metastasis between the 2 clusters. CONCLUSIONS: We demonstrated that CIN-type GC could be categorized into 2 genetic lineages which are different in terms of rapidity of local extension but similar in terms of nodal metastasis risk.

Relationship between endoscopic and histologic gastric atrophy and intestinal metaplasia.

BACKGROUND: The severity of endoscopic gastric atrophy (EGA), high-stage Operative Link on Gastritis Assessment (OLGA) gastritis (i.e., stage III or IV), and extensive intestinal metaplasia (IM) with incomplete subtype have been separately reported as high-risk factors of gastric cancer (GC). The aim of this study was to evaluate the associations between these endoscopic and pathologic characteristics. MATERIALS AND METHODS: A cross-sectional study was conducted on 280 patients with functional dyspepsia at the University Medical Center at Ho Chi Minh City, Vietnam. Biopsies were taken according to the updated Sydney System. EGA was assessed according to the Kimura-Takemoto classification, and gastritis stage was assessed according to the OLGA system. RESULTS: All of patients with high-stage OLGA gastritis (i.e., stage III or IV) clustered in the subgroup of patients with moderate-to-severe EGA: 13/126 (10.3%) in patients with moderate-to-severe EGA versus 0/154 (0%) in patients with none-to-mild EGA (p < .001). Moderate-to-severe EGA was also significantly associated with extensive IM (p < .001, OR = 28.1 (CI 95% 6.4-173.3)) and incomplete IM subtype (p < .001, OR = 36.7 (CI 95% 5.1-742.1). Extensive IM was also associated with incomplete IM subtype (p = .01). CONCLUSIONS: High-stage OLGA gastritis, extensive IM with incomplete subtype clustered in patients with moderate-to-severe EGA. Assessing the severity of EGA could potentially help to identify patients who should be taken systemic biopsy for evaluating GC risk.

The severity of endoscopic gastric atrophy could help to predict Operative Link on Gastritis Assessment gastritis stage.

BACKGROUND AND AIMS: The aims of the present study were to evaluate the role of moderate-to-severe endoscopic gastric atrophy (EGA) on predicting Operative Link on Gastritis Assessment (OLGA) gastritis stage, and to assess the association of high-stage OLGA gastritis with gastric neoplasia in patients with non-ulcer dyspepsia. METHODS: A cross-sectional study was carried out on 280 dyspeptic outpatients. EGA was assessed according to the Kimura-Takemoto classification. Gastritis stage was established according to the OLGA staging system and gastric neoplasia was assessed according to the Vienna classification. The pathologists who read the specimens were kept blind to the endoscopic results. RESULTS: The mean age of patients was 46.1 years (range 20-78 years) with a male-to-female ratio of 1:1. High-stage gastritis (e.g. stage III or IV) was confirmed in 13 (4.6%) patients. All of these patients were more than 40 years-of-age (P = 0.01), had Helicobacter pylori infection (P = 0.0006) and moderate-to-severe EGA (P < 0.001). Low-grade dysplasia was found in seven patients: 4/13 (30.7%) with high-stage gastritis versus 3/267 (1.1%) with low-stage gastritis (P < 0.001). Six of these patients had moderate-to-severe EGA (P = 0.048). The sensitivity, specificity, positive predictive value and negative predictive value of this endoscopic finding in high-stage gastritis diagnosis were 100%, 57.7%, 10.3% and 100%, respectively. CONCLUSIONS: OLGA high-stage gastritis was associated with gastric dysplasia and was mostly diagnosed in patients with moderate-to-severe EGA. The absence of this endoscopic finding could effectively rule out the possibility of having high-stage gastritis.

Infantile mesenchymal hamartoma of the liver with elevated alpha fetoprotein.

Mesenchymal hamartoma of the liver (MHL) is a benign tumour that most commonly occurs in children. In most cases of MHL, the α fetoprotein (AFP) level is within the normal limits, only in a few cases, increased AFP has been described which usually causes misdiagnosis of hepatoblastoma. We report a case of a 3-month-old paediatric patient who was incidentally detected with a very high level of AFP, at 6388.4 ng ml-1. Ultrasound revealed a right liver tumour, segment VI, measuring at 56 × 53 mm. According to images of ultrasound and MRI, the diagnosis was mesenchymal hepatic sarcoma. The paediatric patient had surgery to remove the entire liver segment containing the tumour. Micropathological examination showed that the tumour was a MHL. The serum AFP level fell rapidly to near normal following the surgery. The MHL benign liver tumour with an atypical presentation caused a very high AFP level. This was a rare clinical case, and it was difficult to diagnose.

The Distribution of Incomplete Gastric Intestinal Metaplasia (GIM) Subtype among Biopsy Sites according to the Updated Sydney System and Its Association with GIM Extension.

BACKGROUND: Current guidelines recommend that extensive gastric intestinal metaplasia (GIM) be considered as a high-risk marker for the development of gastric cancer (GC). But there is emerging evidence that the incomplete GIM subtype is also a high-risk marker. AIMS: To evaluate the performance of biopsy sites according to the updated Sydney system on detecting the incomplete GIM subtype and to assess its association with GIM extension. PATIENTS AND METHODS: A cross-sectional study was conducted on 280 Vietnamese patients with nonulcer dyspepsia. Biopsy specimens were taken from gastric sites according to the updated Sydney system, and sections were routinely stained with Giemsa and hematoxylin and eosin. Biopsy specimens with intestinalization were further evaluated for GIM subtypes with alcian blue 2.5 and periodic acid Schiff stainings. Two experienced pathologists jointly examined all the specimens and reached consensus. RESULTS: The rates of patients with GIM and the incomplete GIM subtype were 81 (28.9%) and 24 (8.4%), respectively. There was no GIM in specimens taken from the greater curvature of corpus. The proportions of the incomplete GIM subtype detected at the incisura angularis, lesser curvature of corpus, lesser curvature of antrum, and greater curvature of antrum were 34.3% (12/35), 34.5% (10/29), 40.5% (17/42), and 31.6 (6/19), respectively, which were not significantly different (p = 0.89). The presence of an incomplete GIM subtype was associated with multifocal GIM (i.e., ≥3 out of 5 biopsy sites with GIM) (OR = 4.02, CI 95%, 1.33-12.16, p = 0.022) and extensive GIM (i.e., GIM in specimens from both of corpus and antrum) (OR = 2.89, CI 95% 1.04-8.02, p = 0.045). CONCLUSIONS: The proportions of an incomplete GIM subtype were not significantly different among gastric biopsy sites with intestinalization. The association between an incomplete GIM subtype and GIM extension, therefore, may be due to an sum accumulation effect.