Does preoperative enhanced CT predict requirement of intestinal resection in the patients with incarcerated myopectineal hernias containing small bowel?

PURPOSE: Bowel wall enhancement on CT imaging is considered one of the useful features for the prediction of the presence of irreversible ischemic change in patients with small bowel obstruction. However, the applicability of CT imaging in patients with incarcerated hernias has not been investigated in detail. The aim of this retrospective study was to evaluate the feasibility of preoperative CT findings for the prediction of the presence of irreversible ischemic change in patients with incarcerated hernias containing small bowel. METHODS: Included in this study were 76 patients who underwent surgery for preoperatively diagnosed incarcerated hernias containing small bowel (27 inguinal hernias, 37 femoral hernias and 12 obturator hernias) at our hospital between January 2011 and June 2020. The preoperative clinicoradiological features were compared between the groups, and predictors for intestinal resection were evaluated. RESULTS: Nineteen patients required intestinal resection (Resection group), and the other 57 patients did not require intestinal resection (Nonresection group). Multivariate analyses revealed that age ≥ 80 years (p = 0.018, odds ratio = 6.604) and the absence of bowel wall enhancement (p = 0.032, odds ratio = 51.200) were independent predictors for intestinal resection. In resected specimens, all patients with an absence of bowel wall enhancement on preoperative enhanced CT had ischemic changes extending beyond the muscularis propria. CONCLUSIONS: Preoperative enhancement CT yields useful information for the prediction of the presence of irreversible ischemic change in patients with incarcerated hernias containing small bowel.

Laparoscopic repair is a treatment of choice for selected patients with incarcerated obturator hernia.

PURPOSE: The feasibility and potential advantages of laparoscopic diagnosis and repair of incarcerated obturator hernia (OH) is debated. The aim of this retrospective study was to compare short-term complications comparing laparoscopic to open repair of OH. METHODS: A total of 29 preoperatively diagnosed patients underwent surgery for a preoperatively diagnosed OH between January 2006 and July 2017. The patients were divided into a laparoscopic group (11 patients underwent laparoscopic repair; 8 without and 3 with intestinal resection) and an open group (18 patients who underwent open repair; 9 without and 9 with intestinal resection).The outcomes were compared between groups. A risk factor analysis for postoperative complications was performed. RESULTS: The incidence of postoperative complications was fewer in the laparoscopic group [9.0% vs. 61.1%; (p < 0.001)]. The bleeding amount [1.2 g vs. 40.4 g; (p = 0.087)] and postoperative length of stay [13.3 days vs. 17.1 days; (p = 0.072)] showed a tendency to be favorable in the laparoscopic group. Occult contralateral OH was detected in three patients (27.7%) in the laparoscopic group and one patient (5.5%) in the open group (p = 0.099). Open surgery and intestinal resection were independent risk factors for a postoperative complication. One patient in the open group developed an incarcerated OH on the contralateral side 1 year after the first surgery. CONCLUSIONS: Laparoscopic repair for incarcerated obturator hernia demonstrated more favorable short-term outcomes compared with open repair in terms of a lower incidence of postoperative complications and it was potentially beneficial for detecting and repairing an occult OH on the contralateral side.

Impact of anastomotic complications on outcome after laparoscopic gastrectomy for early gastric cancer.

BACKGROUND: The effects of anastomotic complications after laparoscopically assisted gastrectomy (LAG) have not been studied widely. The aims of this observational study were to identify potential factors that predict anastomotic complications and investigate the impact of anastomotic complications in patients undergoing gastrectomy for early gastric cancer. METHODS: The study included consecutive patients with histologically proven T1 gastric adenocarcinoma treated by LAG with regional lymphadenectomy between August 1997 and March 2008, who had not received neoadjuvant chemotherapy. Anastomotic complications included anastomotic leakage, stricture and remnant gastric stasis of grade II or higher (modified Clavien classification) and were identified by clinical assessment and confirmatory investigation. Predictive factors for the development of anastomotic complications were identified by univariable and multivariable analyses. Long-term survival with or without anastomotic complications was examined. RESULTS: Anastomotic complications occurred in 37 (9·3 per cent) of 400 patients. Multivariable analysis indicated surgeon experience as the only independent predictor of anastomotic complications (hazard ratio 4·40, 95 per cent confidence interval 2·04 to 9·53; P < 0·001). Patients with anastomotic complications had a significantly worse overall 5-year survival rate than those without (81 versus 94·2 per cent; P = 0·009). CONCLUSION: Anastomotic complications after LAG lead to worse long-term survival.

Microsatellite instability and K-ras mutations in gastric adenomas, with reference to associated gastric cancers.

Gastric adenomas are often detected in the stomach resected for gastric cancer. Previous investigation have revealed that the prevalence of their malignant transformation is generally low, but the frequent coexistence with carcinoma suggests that they may share some common processes with gastric cancer in tumorigenesis. In contrast to the cumulative information about genetic alterations in gastric cancer, inquiries into the genetic changes of adenoma and coexisting carcinoma in the same individual's stomach are still few. We investigated microsatellite instability (MSI) and K-ras point mutations in codons 12 and 13 in 50 lesions of gastric adenomas in 43 cases, and 31 lesions of gastric cancers that coexisted with these adenomas. In gastric adenomas, we found seven lesions (14.0%) to have microsatellite instability (MSI) at one or more loci, and most of them (six cases) had MSI at only one locus and were not associated with alterations in presumable target molecules. MSI was detected more frequently (11/31, 35.5%) and more extensively (five lesions at multiple loci) in accompanying gastric carcinomas. The prevalence of MSI in adenomas was more frequently found in those with synchronous gastric cancer (6/37, 16.2%, vs. 1/13, 7.6%) than without, and gastric adenoma accompanied by gastric cancer with multiple MSI tended to have MSI more frequently than that accompanied by cancer without MSI (4/5, 80%, vs. 1/24, 4.2%; p = 0. 01). In at least some individuals, MSI appears to represent one step in the pathway of gastric tumorigenesis, shared by adenoma and carcinoma. We found K-ras gene alteration in 8 lesions (16.0%) out of 50 gastric flat adenomas and no difference in its prevalence between adenoma with or without cancer. Only one gastric cancer, which had adenoma without K-ras mutation, had K-ras codon 12 mutation. Adenomas with a higher grade of atypia (p < 0.05) more frequently carried K-ras point mutation, which is consistent with the situation in colorectal adenoma. We conclude that MSI, not K-ras mutation, is a shared genetic alteration in adenoma and carcinoma of the individual stomach.

[A case of stage IV esophageal cancer successfully treated by chemoradiation].

A 63-year-old man was admitted to our institution with a hard tumor on the left side of the neck. He was diagnosed as having advanced esophageal cancer (Stage IV) with a massive supraclavicular lymph node metastasis, and the lesion was thought to be unresectable. He was treated with chemotherapy (CDDP-VDS-5-FU) and radiation therapy, and all the tumors completely disappeared on endoscopic and CT examination. A stricture with scarring was detected in the esophagus at 6 months after treatment. No neoplastic tissue was detected in the lesion, and his dysphagia was relieved by dilation of the stricture. Recurrence on the left side of the neck was detected by CT at 2.5 years after chemoradiation therapy. However, the tumor has not grown over the 2-year interval since then, so it seems to be dormant. He has now survived with a good QOL for 5 years since the first hospital admission. We conclude that advanced esophageal cancer can be treated with chemoradiation therapy if the patient is in sufficiently good overall condition.

Laparoscopic inguinal hernia repair using fine-caliber instruments and polyester mesh.

Laparoscopic inguinal hernia repair (LH) requires similar scar size to traditional open repair. To perform LH with minimal access, finer instruments were used. A 5-mm laparoscope was inserted from the umbilicus, and surgical instruments were inserted through 5- and 3-mm trocars to perform LH by the transabdominal preperitoneal approach. Polyester mesh was placed over the hernia orifice and the peritoneum was closed with 3-0 silk sutures. Sixteen patients underwent smaller access LH and 24 had standard LH. Although smaller access LH took longer (105.7 versus 83.9 min), significantly fewer patients required analgesia after smaller access LH than after standard LH (12.5 versus 70.8%), and the postoperative hospital stay was shorter (4.6 versus 5.6 days). In addition, a better cosmetic outcome was obtained with smaller access LH. In conclusion, access was minimized by using fine-caliber instruments and polyester mesh, making LH less invasive and improving the cosmetic outcome.

RER phenotype and its associated mutations in familial gastric cancer.

To clarify the genetic background of gastric cancer, we collected 28 familial gastric cancers (FGCs) with reference to the Amsterdam criteria in hereditary non-polyposis colorectal cancer (HNPCC) and investigated the frequency of replication error (RER) at six microsatellite loci and frameshift mutations in its related genes in these tumors. RER was detected in seven (25%) of the 28 gastric cancers. Five (18%) cases showed RER at more than two loci. The apparent increased incidence of RER in FGC was not detected compared with that reported in sporadic gastric cancers previously. Among four cases with RER at more than three loci, frameshift mutations in the (A)8 track of the hMSH3 gene were detected in all the four cases and mutations in the (A)10 track of the transforming growth factor-beta type II receptor (TGF-beta RII) gene were detected in the three of them. Histologically, three of the four cases were of the intestinal type, and the other one was the diffuse type. No mutation was detected in the (C)8 and (GT)3 tracks of the hMSH6 and TGF-beta RII genes respectively. These results indicate that the acquisition of the RER phenotype equally influences the gastric carcinogenesis of both sporadic and familial cases, and that the majority of FGC is pathogenetically distinct from HNPCC.

Mutational analyses of multiple target genes in histologically heterogeneous gastric cancer with microsatellite instability.

It has been recognized that gastric cancer often shows histological heterogeneity in a single tumor. Although microsatellite instability (MSI) has been reported in gastric cancer, the significance of genomic instability in gastric cancers with histological heterogeneity within a single tumor has never been addressed. We investigated MSI at 8 microsatellite loci in 40 normal/tumor DNA pairs from 20 gastric cancers with histological heterogeneity. Six of 20 patients (10 DNAs of 40 tumor DNAs) had severe MSI in more than 3 loci. Four of the MSI-positive cases had frameshift mutations in the poly(A)10 tract of the TGF beta RII gene. This mutation was found only in the MSI-positive component in the 2 cases (cases 4 and 5) in which only 1 component exhibited MSI. The other 4 cases demonstrated homozygous or heteroclonal mutations (1 and 2 base deletions) in the poly(A)8 tract of the hMSH3 gene; no mutation was detected in the poly(C)8 tract of the hMSH6 gene in any of the MSI-positive cases. The profile of alterations in multiple targets was different between the 2 components in most of the cases (5/6). These findings suggest that mismatch repair deficiency in MSI-positive tumors causes multiple gene inactivations through frameshift mutations in short repetitive sequences in a heterogeneous way within a histologically heterogeneous tumor.

Stage-dependent evaluation of microsatellite instability in gastric carcinoma with familial clustering.

Familial clustering of gastric cancer is probably caused by multifactorial processes, both environmental and genetic. In this report, the incidence of microsatellite instability (MSI) in 31 cases of gastric cancer in Japanese (33 lesions) with familial clustering (two or more gastric cancers within second-degree relatives) was compared to MSI in Japanese cases without a family of any cancer in age ( +/- 10 years)-, stage-, and histological subtype-matched case-control study. Although the difference noted was not significant, we noted a strong trend for MSI at any of up to seven loci of CA repeats to occur more frequently in the patients with a family history of gastric than in the control patients in early cancer (intramucosal and submucosal), whereas the prevalence of MSI was similar in both groups in more advanced cases, in which the tumor invaded beyond the proper muscle layer of the gastric wall. Because the contribution of a family history of gastric cancer to MSI apparently differs in early and advanced gastric cancer, interpretation of MSI in familial gastric cancer cases published previously require reevaluation in terms of stage and proper controls. An acquisition of CA repeat alterations in the early stage rather than in the late stage of gastric carcinogenesis may have in common etiological factors, at least in some cases, with the familial clustering of gastric cancer.

Bilateral breast tumors, malignant phyllodes tumor and invasive lobular carcinoma in a 46,XX/46,XY mosaic female with family history of breast cancer.

Bilateral breast tumors, a malignant phyllodes tumor in the right breast and an invasive lobular carcinoma in the left breast, occurred in a 47-year-old woman with 46XX/46XY mosaic karyotype in her peripheral blood lymphocytes and intersex external genitalia. Postmortem examination revealed bilateral ovotestis. Three of the patient's sisters also had breast cancer. In situ hybridization with a Y-specific probe revealed Y-chromosome-specific signal in both tumors, suggesting that the clonal origin of tumors in this patient was Y-containing cells. Androgen-receptor polymorphism also revealed a monoallelic X chromosome pattern in the recurrent phyllodes tumor tissue taken at autopsy, in addition to loss of heterozygosity demonstrated at locus TP53. The slippage of the CA repeats in the tumor was also shown at the loci of D5S82 and D11S527. The mechanistic basis for the occurrence of bilateral malignant tumors of the breast, XX/XY mosaicism, and familial clustering of breast cancer is still unknown. The present study, however, suggests that the sex chromosome abnormality may have modified the cancer phenotype in a manner similar to breast cancer in Klinefelter's syndrome (though phenotypically male) and the Y chromosome may have promoted cell growth.