A case of non-occlusive mesenteric ischaemia caused by pelvic fracture due to fall trauma.

BACKGROUND: Non-occlusive mesenteric ischaemia (NOMI) is a condition in which intestinal ischaemia arises due to spasms of peripheral blood vessels; however, there is no obstruction of the main arteries. Risk factors include hypertension, diabetes, and increasing age, but the traumatic injury triggering NOMI onset is rarely reported. We report a case of NOMI caused by a pelvic fracture due to a fall injury. CASE PRESENTATION: A 77-year-old man was transported to the hospital due to a fall injury. CT revealed a pelvic fracture and a haematoma in the pelvic extraperitoneal space. The next day, the patient developed shock, and CT revealed an increase in haematoma size. Both internal iliac arteries were embolized by transcatheter arterial embolization (TAE). The next day's CT revealed intestinal necrosis of the ascending colon, and emergency surgery was planned. During surgery, necrosis was identified in the serosa of the ascending, transverse, and sigmoid colon. We performed subtotal excision from the ascending colon to the sigmoid colon. On postoperative day 10, melena was observed, and CT revealed partial thickening of the small intestine and a decrease in the contrast effect. Considering the post-total colectomy and general condition, we proceeded with conservative treatment. Over time, the patient developed liver and renal dysfunction and died 16 days after surgery. CONCLUSIONS: We experienced a case of NOMI caused by bleeding from a pelvic fracture. It is important to keep in mind the risk of developing NOMI in traumatic bleeding to avoid missing this diagnosis.

Going back to home to die: does it make a difference to patient survival?

BACKGROUND: Many patients wish to stay at home during the terminal stage of cancer. However, there is concern that medical care provided at home may negatively affect survival. This study therefore explored whether the survival duration differed between cancer patients who received inpatient care and those who received home care. METHODS: We retrospectively investigated the place of care/death and survival duration of 190 cancer patients after their referral to a palliative care consultation team in a Japanese general hospital between 2007 and 2012. The patients were classified into a hospital care group consisting of those who received palliative care in the hospital until death, and a home care group including patients who received palliative care at home from doctors in collaboration with the palliative care consultation team. Details of the place of care, survival duration, and patient characteristics (primary site, gender, age, history of chemotherapy, and performance status) were obtained from electronic medical records, and analyzed after propensity score matching in the place of care. RESULTS: Median survival adjusted for propensity score was significantly longer in the home care group (67.0 days, n = 69) than in the hospital care group (33.0 days, n = 69; P = 0.0013). Cox's proportional hazard analysis revealed that the place of care was a significant factor for survival following adjustment for covariates including performance status. CONCLUSIONS: This study suggests that the general concern that home care shortens the survival duration of patients is not based on evidence. A cohort study including more known prognostic factors is necessary to confirm the results.

Evaluation of A Novel Information-Sharing Instrument for Home-Based Palliative Care: A Feasibility Study.

AIM: To examine the feasibility and usefulness of a novel region-based pathway: the Regional Referral Clinical Pathway for Home-Based Palliative Care. METHOD: This was a feasibility study to evaluate the frequency of variances and the perceived usefulness of pathway using in-depth interviews. All patients with cancer referred to the palliative care team between 2011 and 2013 and received home care services were enrolled. RESULT: A total of 44 patients were analyzed, and pathway was completed in all the patients. The target outcome was achieved in 61.4% while some variances occurred in 54.5%. Nine categories were identified as the usefulness of the pathway, such as reviewing and sharing information and promoting communication, education, motivation, and relationships. CONCLUSION: This novel pathway is feasible and seems to be useful.

[Breast cancer during pregnancy--a case report].

Pregnancy-associated breast carcinoma is generally defined as cancer that occurs during pregnancy or within 1 year of delivery, although treatment options are the most complicated when the disease is diagnosed during pregnancy. We report the case of a 30-year-old woman who was diagnosed with breast cancer at her 9th week of pregnancy. The patient initially had mastectomy with axillary lymph node dissection. She began adjuvant therapy with 3 courses of epirubicin/cyclophosphamide at 19 weeks of gestation. After delivery of a healthy child, she received one course of epirubicin/cyclophosphamide and 4 courses of docetaxel. Although the data are limited, pregnant patients with cancer can be treated with systemic chemotherapy with minimal risks to the fetus during the second or third trimester. Management of breast cancer during pregnancy requires an interdisciplinary care team and careful consideration of the patient's stage of disease, the gestational age of the fetus, and the preferences of the patient and her family.

[A case of recurrent breast cancer with life-threatening multiple lung metastasis markedly responding to CMF as third-line chemotherapy].

A 35-year-old woman with taxane and anthracycline-resistant recurrent breast cancer with multiple lung metastasis and carcinomatous lymphangitis was treated with CMF as third-line chemotherapy. A complete response was achieved,and the toxicities were tolerable. We thought that CMF could be a useful regimen as third-line chemotherapy for metastatic breast cancer.

[A case of primary small intestinal cancer accompanied by virchow lymph node metastasis undergoing TS-1 treatment].

A 72-year-old female was admitted to our hospital with the complaint of left neck lymph node swelling. Abdominal computed tomography (CT) revealed wall thickening of the small intestine and multiple lymph node metastases. Barium meal study of the small intestine showed circular stenosis. The patient was operated on under a diagnosis of tumor of the small intestine and left neck lymph node swelling. Needle biopsy of the left neck lymph node and partial resection of the small intestine was done without regional lymph node dissection because of Virchow lymph node metastasis. On the resected material a 5 x 4 cm type 2 tumor was identified. Pathological findings included poorly-differentiated adenocarcinoma, si (bladder), n 4, P 0, ly 3, v 3, H 0, M(-), Stage IV. The patient received the chemotherapy with TS-1. TS-1(80 mg/body/day) orally administered for 4 weeks followed by a drug-free 2-week period as one course. CT revealed that the metastatic lesion had shrunk markedly after the second course. A complete response (CR) was observed after one year. There were no drug side effects. At present, 3 years and 9 months after the operation, cervical and abdominal CT reveals no evidence of enlargement of the cervical and intraperitoneal lymph nodes.

The profile of hMLH1 methylation and microsatellite instability in colorectal and non-small cell lung cancer.

Microsatellite instability (MSI) is caused mainly by dysfunction of hMLH1, where aberrant hypermethylation (HM) of its promoter region is involved. Previously, we suggested that HM in the proximal region of the hMLH1 promoter plays a critical role in progression of gastric cancer with MSI and this specific region should be analyzed for diagnostic use of hMLH1 HM. We expanded the analyses of hMLH1 HM and MSI phenotype to sporadic colorectal cancer (CRC) and non-small cell lung cancer (NSCLC) to further evaluate the diagnostic value of hMLH1 HM. A total of 174 CRC and 94 NSCLC samples were used for hMLH1 methylation analysis by real-time methylation-specific PCR. Methylation levels were measured in three distinct regions of the promoter, designated as hMLH1-A, hMLH1-B, and hMLH1-C from distal to proximal. MSI phenotype was determined using five microsatellite markers, BAT25, BAT26, D2S123, D5S346, and D17S250. Methylation profile of the hMLH1 promoter varies between CRC and NSCLC. High methylation levels were observed in a group of CRC samples. Consequently, three patterns of methylation in the hMLH1 promoter regions were found: 1) low methylation level in all regions, 2) high methylation level in hMLH1-A with low methylation level in hMLH1-C, 3) high methylation level in all regions. In contrast, only one NSCLC showed high methylation level in hMLH1-A. Of the 134 CRCs examined, 14 (10.4%) showed MSI phenotype. No MSI phenotype was found in the initial 80 NSCLCs analyzed. Eight (57.1%) of 14 CRC with MSI showed HM in hMLH1-C, which was linked exclusively with MSI phenotype. However, the HM in hMLH1-A or -B was not sufficient for MSI. CRC with MSI phenotype was significantly more frequent in older patients and in the proximal colon, and was more evident in cases with hMLH1-C HM. The results suggested that hMLH1 HM cannot be used as an alternative diagnostic marker of MSI phenotype in sporadic CRC and NSCLC. CRC with MSI might have clinicopathologically distinct subgroups according to hMLH1-C HM status. The observed profiles of hMLH1 methylation and MSI in gastric cancer, CRC, and NSCLC were quite different from each other, facilitating the better understanding of the pathogenesis of these cancers.

The association between methylenetetrahydrofolate reductase polymorphism and promoter methylation in proximal colon cancer.

BACKGROUND: Methylenetetrahydrofolate reductase (MTHFR) plays a critical role in folate metabolism, which is an important pathway of the methyl donor for DNA methylation. The MTHFR gene has genetic variants (C667T and A1298C), which cause reduced enzyme activity. Impaired folate metabolism by these genetic variants of MTHFR could change the methylation pattern of DNA including promoter hypermethylation, which has been frequently observed in cancer. In this study, we compared the MTHFR genotypes and haplotype to the features of colorectal cancer focusing on the promoter methylation of tumor DNA. MATERIALS AND METHODS: Genomic DNA was isolated from 194 colorectal cancer tissues and subjected to MTHFR genotyping by PCR-based restriction fragment length polymorphism analysis. The MTHFR haplotype was determined by combination of C667T and A1298C genotype and classified into 2 groups, high (H-haplotype) or low (L-haplotype) enzymatic activity of MTHFR. The methylation level of tumor suppressor genes (CDKN2A, hMLH1, ARF and TIMP3) was measured by a fluorescence-based, real-time methylation specific PCR method. RESULTS: There was no significant association of the clinicopathological features with either C667T genotype, A1298C genotype or haplotype of MTHFR. The methylation level of CDKN2A was higher in cancer with the L-haplotype of MTHFR than in that with the H-haplotype when cancers of proximal origin were considered (p=0.029). hMLH1 methylation also tended to be higher in proximal colon cancers of MTHFR L-haplotype (p=0.059). In addition, the proximal colon cancers showing CpG island methylator phenotype (CIMP) were significantly more frequent in L-haplotype than in H-haplotype. CONCLUSION: These results suggest that the haplotype with low enzymatic activity of MTHFR is linked with promoter hypermethylation and consequently modifies the risk of CIMP(+) proximal colon cancer development in the Japanese people. The relationship between MTHFR polymorphism and DNA methylation in the Japanese is contrary to the previous results in Caucasians. Further study is needed focusing on ethnic variations in the relationships among MTHFR polymorphism, DNA methylation and the development of CIMP(+) colorectal cancer.

Retroperitoneal mucinous cystadenoma: report of two cases and review of the literature.

Primary retroperitoneal cystic tumor is extremely rare, and its histogenesis and biological behavior remain speculative. Two surgical cases of retroperitoneal mucinous cystadenoma (Case 1, an 18-year-old woman; and Case 2, an 85-year-old woman) are reported. The cystadenomas in these cases were mainly lined by a monolayer of columnar or thin flat cells. Case 1 was positive for mucin and epithelial membrane antigen, whereas Case 2 was positive for a mesothelial marker (calretinin). Ciliated epithelium was also interspersed in Case 2. Some parts showed papillary projections, resembling well-differentiated papillary mesothelioma. Within the cyst walls of both cases, ovarian-like stroma that was positive for both estrogen and progesterone receptors was found. Interestingly, focal nodular hyperplasia of the liver was also detected in Case 1. We believe the retroperitoneal mucinous cystadenoma might have arisen from the peritoneum via mucinous epithelial metaplasia with a phenotype of extragenital Mullerian system.

Microsatellite instability in gastric cancer is closely associated with hMLH1 hypermethylation at the proximal region of the promoter.

Most sporadic gastric cancer with the microsatellite instability (MSI) phenotype is linked with hypermethylation (HM) of hMLH1. However, a part of gastric cancer with hMLH1 HM does not show MSI, suggesting a region-specific effect of hMLH1 promoter methylation on developing MSI. To test this possibility, we measured the methylation level in 3 distinct areas of hMLH1 promoter and compared them with MSI in 129 sporadic gastric cancer patients. Three areas of hMLH1 promoter, from distal toward proximal, were designated as hMLH1-A, hMLH1-B, and hMLH1-C, respectively. The methylation level was measured by fluorescence-based real-time methylation specific PCR. MSI status was tested using a panel of 5 microsatellite markers (BAT25, BAT26, D2S123, D5S346, and D17S250). Gastric cancers with no HM in hMLH1-A (n=105, 81.4%) also showed no HM in 2 other regions of hMLH1 promoter. On the other hand, the cancers with HM in hMLH1-A (n=24, 18.6%) showed various levels of methylation in 2 other regions. In most cases, the methylation value was the highest in hMLH1-A and the lowest in hMLH1-C. We found the MSI phenotype in 12 cancers (13%) of 92 tested cases and these cancers were all associated with HM in the region of hMLH1-C. A third of hypermethylated cancers in the hMLH1-A region did not show the MSI phenotype. The survival of the patients with HM in hMLH1-C was significantly better than that of patients without HM (P<0.05). These results suggest that HM in the proximal region of hMLH1 promoter, hMLH1-C in this study, plays a critical role in the progression of gastric cancer with MSI. The complete association between HM in hMLH1-C and MSI phenotype with gastric cancer provides an alternative diagnostic tool for detecting a favorable prognostic subgroup with MSI by using simple methylation analysis.

Hypermethylation of the CDKN2A gene in colorectal cancer is associated with shorter survival.

Promoter hypermethylation of the CDKN2A gene has been suspected to be involved in the carcinogenesis of colorectal cancers. However, the relations between CDKN2A hypermethylation and clinicopathological findings, and patient prognosis, remain inconclusive. We analyzed the CDKN2A methylation status in primary colorectal cancers using real-time methylation specific PCR (MethyLight) which enables quantitative measuring of the methylation level. CDKN2A promoter methylation was detectable in 55 (61.1%) of 90 tumor samples and the median level of the methylation was 0.187 (range 0.00-197.9). The methylation value of CDKN2A was correlated with certain clinicopathological findings, including tumor differentiation (p=0.018), and Dukes stage (p=0.016). In survival analysis, the CDKN2A methylation level was correlated with a poor prognosis of the patient with colorectal cancer for either all cases (p=0.014) or Dukes C (p=0.004) cases that were analyzed. These results suggest that CDKN2A methylation status is a prognostic factor in colorectal cancer and may be of use for the patient specific design of therapy.