Long-term survival from adenocarcinoma of the esophagus after transthoracic and transhiatal esophagectomy.

BACKGROUND: The effects of transthoracic or transhiatal esophagectomy on the long-term survival of patients who had adenocarcinoma of the esophagus were compared, as were factors applicable in preoperative stratification of patient treatment. METHODS: A cohort of 147 consecutive patients with adenocarcinoma of the esophagus was evaluated for esophagectomy between 1984 and 2000. The patients were followed prospectively and observed survival rates of patients with a transthoracic or transhiatal approach to esophagectomy were compared by standardized mortality ratio (SMR) and relative mortality ratio (RMR) using the expected survival of a matched Norwegian population. RESULTS: A R0 resection was performed by transthoracic (n = 33) or a transhiatal (n = 55) esophagectomy in 88 (60%) patients with a median age of 61 (range: 35-77) and 70 (42-88) years, respectively (P <0.001). Tumor stages and other possible risk factors were similar in the two groups. Transthoracic or transhiatal esophagectomy resulted in a median survival time of 20.5 (95% confidence interval (CI): 10.4-57.6) and 16.4 (10.6-28.7) months, respectively. The respective survival rates were 31.2% and 27.8% by 5 years, and 21.3% and 16.6% by 10 years with an overall RMR of 1.14 (P = 0.63). Median survival time in the absence or presence of lymph node metastases was 74.0 (95% CI: 17.5-166.4) and 10.7 (7.9-14.9) months. The corresponding survival rates by 10 years with non-involved or involved nodes were 48.9% and 3.8% respectively (RMR 2.22, P = 0.007). Patients with a pT1-tumor were few and the survival rate was not very different from that of the general population (SMR = 1.7, 95% CI: 0.7-4.1). The median survival time of patients with a pT2-tumor was 30.4 (95% CI: 9.0-142) months and with a pT3-tumor 14 (9.2-16.4) months. The survival rates by 10 years among patients with a pT1 tumor were 57.0% (95% CI: 14.9-78.9), pT2 33.3% (11.8-52.2), and pT3 7.1% (1.9-15.5). The relative mortality for T3 stages compared to T1 stages was statistically significant (RMR = 3.22, P = 0.024). CONCLUSION: Transthoracic and transhiatal esophagectomy are both effective approaches for treatment of adenocarcinoma of the esophagus and survival of more than 10 years can be expected without adjuvant chemotherapy. However, increasing depth of tumor invasion and lymph node metastases reduce life expectancy.

Prolapse of the rectum, long-term results of surgical treatment.

AIMS: This study evaluates patency and functional results of abdominal and perineal treatment approaches to prolapse of the rectum. METHODS: A database search identified patients operated upon for prolapse of the rectum. The operations were abdominal or perineal approaches. The patient's records were reviewed, patients alive were contacted, and a self-report form evaluated functional results. Patients were followed until the prolapse recurred. RESULTS: A primary operation for prolapse of the rectum was performed in 56 patients. Median age was 59 years (range 20-87) and 78 (40-91) for abdominal and perineal approaches, respectively (p < 0.001). The average length of the prolapses was 8.7 cm (2-25) and 8.6 cm (2-15) for abdominal or perineal approaches. All prolapses treated with a Thiersch's operation recurred within a few months and all prolapses treated with the Delorme's operation recurred within 5 years, whereas the 5-year patency of the abdominal approach was 93% (p < 0.001). No prolapses recurred after mesh rectopexy and the 5-year patency of resection rectopexy was 86%. The abdominal approaches improved stool evacuation and constipation significantly, and anal leakage improved somewhat (p = 0.065). The median hospital stay was 11 (4-20) and 7 (2-155) days after abdominal and perineal approaches (p = 0.003). Complications occurred in 20% of patients. CONCLUSIONS: The patency of abdominal approach to prolapse of the rectum is better than that of perineal repairs. The abdominal approaches also have a favorable effect on constipation and anal insufficiency. Perineal approaches should be reserved for patients with a very short life expectancy.

Ulceration as a possible link between duodenogastric reflux and neoplasms in the stomach of rats.

BACKGROUND: Duodenogastric reflux predisposes to gastric cancer. This study investigates whether ulceration induced by duodenogastric reflux is associated with the development of neoplasms in the stomach. MATERIALS AND METHODS: In a rat experiment, duodenal fluid was directed into the corpus (jejunal reflux) or through the pylorus into the antrum (pyloric reflux). Sham-operated animals served as controls. The animals were sacrificed after 24, 36, or 52 weeks. RESULTS: Ulcerations and neoplasms occurred more frequently in the corpus than in the antrum. In the corpus, ulceration was observed significantly more often in animals with jejunal reflux (62, 55, and 53% at 24, 36, and 52 weeks, respectively) than in animals with pyloric reflux (15, 21, and 30%). The incidence of neoplasm in the corpus increased significantly with time from 38% at 24 weeks to 89% at 52 weeks in animals with jejunal reflux and from 12 to 33% in animals with pyloric reflux. Ulceration and neoplasms shared location in the corpus adjacent to the gastrojejunostomy and by 24 weeks, all but one neoplasm in the jejunal reflux and one in pyloric reflux groups occurred adjacent to ulceration. In the antrum, 37% of the animals had a prepyloric ulceration after 24 weeks of pyloric reflux and only one of these animals had a neoplasm. By 52 weeks 20% of animals with pyloric reflux had a neoplasm that appeared in the prepyloric area. CONCLUSIONS: Ulceration and neoplasm occurred at the same sites in the stomach, and ulcerations preceded the development of neoplasms in the antrum and very likely in the corpus. The results suggest that ulceration plays an important role in the genesis of neoplasms in the stomach and that the vulnerability to duodenogastric reflux is more pronounced in the corpus than in the antrum mucosa.

Gastric mucosa lesions induced by duodenogastric reflux increase penetration of N-[3H]-methyl-N-nitro-N-nitrosoguanidine into corpus mucosa of rats.

The mucosal changes by which duodenogastric reflux may predispose to gastric cancer have not been fully clarified. In this study in rats, duodenal fluid was directed into the stomach through a gastroenterostomy (jejunal reflux, N = 29) or through the pylorus (pyloric reflux, N = 30) and compared with 30 controls. Twenty-four weeks later the stomach was exposed to N-[3H]methyl-N-nitro-N-nitrosoguanidine ([3H]MNNG). The corpus mucosa was examined for proliferating cells (bromodeoxyuridine labeled) and cells at risk of methyl-N-nitro-N-nitrosoguanidine-induced carcinogenesis (cells labeled with bromodeoxyuridine and [3H]MNNG). The number of double-labeled cells increased from 0.8 +/- 0.1/mm mucosa in the control group to 5.2 +/- 0.9 in the jejunal reflux group (P < 0.05) and 2.7 +/- 0.5 in the pyloric reflux group (P < 0.05). An erosion or ulcer appeared at the gastroenterostomy in 52% of animals with jejunal reflux and 17% of those with pyloric reflux (P < 0.006). Within erosions the mean number of double-labeled cells was 9.6 +/- 2.2 in the jejunal reflux group and 7.7 +/- 4.8 in the pyloric reflux group, and significantly higher than in the nonlesion area of the mucosa (0.6 +/- 0.2 and 0.8 +/- 0.3). In erosions the distance between the gastric lumen and the proliferating cells was significantly shorter and the cell proliferation significantly higher than in the nonlesion area of the mucosa. We conclude that duodenogastric reflux increases the penetration of [3H]MNNG into the corpus mucosa of rats and also induces mucosa lesions, which further increase the penetration of [3H]MNNG into the corpus mucosa.

Duodenogastric reflux increases the penetration of N-3H-methyl-N-nitro-N-nitrosoguanidine into the antral mucosa of rats: a possible role for mucosal erosions and increased cell proliferation in gastric carcinogenesis.

Duodenogastric reflux is a risk factor for gastric carcinogenesis, but the pathogenesis is not fully understood. We studied the risk of N-methyl-N-nitro-N-nitrosoguanidine (MNNG)-induced carcinogenesis in the antrum of rats with duodenogastric reflux. Duodenal fluid was directed into the stomach through the pylorus (pyloric reflux group) or through a gastrojejunostomy (jejunal reflux group). After twenty-four weeks, 5-bromo-2-deoxyuridine (BrdU) was injected intravenously and the stomach was exposed to N-(3)H-methyl-N-nitro-N-nitrosoguanidine ((3)H-MNNG). The antral mucosa was examined with immunohistochemistry and autoradiography for identification of proliferating cells (BrdU labelled) and cells at risk of MNNG-induced carcinogenesis ((3)H-MNNG and BrdU-labelled cells). Duodenogastric reflux increased the number of double-labelled cells in the antral mucosa from 4.8 +/- 0.6 per mm in the control group to 11.3 +/- 1.9 in the jejunal reflux group (P < 0.05) and 12.7 +/- 0.9 in the pyloric reflux group (P < 0.05). Mucosal erosions were observed in 15 of 28 animals with pyloric reflux and the number of double-labelled cells in the erosion area (4.3 +/- 0.7) was higher than in the same area of animals without erosion (1.4 +/- 0.5) (P < 0.05). Duodeno-gastric reflux increased the cell proliferation and significantly changed the distance between the surface epithelial lining and the proliferating cells when compared to the controls. These results indicate that duodenogastric reflux increases the penetration of (3)H-MNNG into the antrum mucosa of rats. Increased cell proliferation and erosions increase the number of cells at risk of an initiation process from a penetrating gastric carcinogen.