Survival after vagotomy: Results of the Aarhus county vagotomy trial

Ditlevsen, S

doi:10.1007/bf01658433

Cited by 12 publications

(3 citation statements)

References 10 publications

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“…However, poorer survival in ulcer perforation survivors seem to be related to excess mortality due to smoking-related disorders (C. Svanes, unpublished data). Similar findings have been reported for subjects who survived a bleeding ulcer [61] and for patients treated with elective ulcer surgery [62][63][64].…”

Section: Prognosissupporting

confidence: 84%

Trends in Perforated Peptic Ulcer: Incidence, Etiology, Treatment, and Prognosis

2000

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After increasing steeply at the beginning of the twentieth century, ulcer perforation incidence during the last decades has declined in the young and in men, and it has risen among the elderly and in women. These changes can be attributed to a cohort phenomenon: Ulcer perforation risk is particularly common in the cohorts born after the turn of the twentieth century and is less common in previous and succeeding birth cohorts. A decline in total incidence is expected with the death of the high risk cohorts. Most ulcer perforations among subjects < 75 years of age can be attributed to smoking. Subjects with a history of ulcer perforation therefore have poorer long-term survival than the general population, most pronounced for younger generations. About one of four ulcer perforations can be attributed to the use of nonsteroidal antiinflammatory drugs, a risk factor of particular importance in the elderly. Ulcer perforation was frequently treated by gastric resection in former days, whereas suture, being the first method introduced in 1887, is the method of choice today. The introduction of antibiotics improved the prognosis of ulcer perforation surgery greatly. Postoperative lethality decreased until 1950 but has remained stable since then. Lethality is higher in the elderly and is higher after gastric than after duodenal perforation. The delay before surgical treatment is a strong determinant for lethality, complication rates, and hospital costs. Treatment delay seems to have increased during the last

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Section: Prognosissupporting

confidence: 84%

Trends in Perforated Peptic Ulcer: Incidence, Etiology, Treatment, and Prognosis

2000

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“…This is in contrast with previous reported smaller studies, which showed an up to 3.3-fold death risk from gastric cancer [66,73,[92][93][94]. However, most of these patients were probably operated for duodenal ulcer disease associated with a decreased risk of stomach cancer.…”

Section: Vagotomycontrasting

confidence: 80%

“…A population-based Swedish study of 7198 vagotomized patients followed for 9 to 18 years showed a standardized incidence ratio of 1.33 (95% CI 0.92-1.86) [91]. This is in contrast with previous reported smaller studies, which showed an up to 3.3-fold death risk from gastric cancer [66,73,[92][93][94]. However, most of these patients were probably operated for duodenal ulcer disease associated with a decreased risk of stomach cancer.…”

Section: Vagotomymentioning

confidence: 74%

Risk of Stomach Cancer in Patients with Peptic Ulcer Disease

Hansson

2000

World j. surg.

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Abstract. The relation between peptic ulcer and stomach cancer has long been disputed, but there is accumulating evidence that gastric ulcer disease is positively associated and duodenal ulcerations negatively associated with the risk of developing stomach cancer. As Helicobacter pylori infection is associated with both types of ulceration and stomach cancer, the varying outcomes of the infection indicate that factors other than the infection must be of importance. At present, there is no convincing evidence that pharmacologic inhibition of acid secretion for treatment of peptic ulcer increases the risk of stomach cancer. However, some recent studies indicate that prolonged treatment with proton pump inhibitors may accelerate the development of atrophic gastritis, a risk factor for stomach cancer, in individuals infected with H. pylori. It has repeatedly been shown that there is an at least twofold increased risk of stomach cancer 15 years after gastric resection for peptic ulcer disease, and that the risk increases with the passage of time. Whether vagotomy has the same risk-increasing effect is still unclear.

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Etiology of gastric remnant cancer with special reference to the effects of denervation of the gastric mucosa

Kaminishi¹,

Shimizu²,

Shiomoyama³

et al. 1995

Cancer

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Background. Gastric mucosal blood flow, secretion of mucin, and renewal of the gastric mucosal cells are considered to be defensive factors against gastric mucosal injuries. These factors are regulated by the nervous system and neuropeptides. Gastrectomy may affect this regulation and induce gastric mucosal changes, such as atrophic gastritis and carcinoma. The effects of denervation of the gastric mucosa on tumorigenesis of the remnant stomach were investigated. Methods. Using male Wistar rats, four groups of Bill‐roth I (B‐I) gastrectomy, Billroth II (B‐II) gastrectomy, and those with denervation were conducted. Subdiaphragmatic truncal vagotomy was performed in the denervated group. Thirty weeks after the operations, histologic examination and periodic acid‐Schiff—Alcian blue (PAS‐AB) staining of the gastric mucosa, analysis of cell kinetics of the gastric mucosa by immunohistochemistry of proliferating cell nuclear antigen, and measurement of intragastric pH, intragastric bile acid concentration, and serum gastrin levels were performed. No carcinogenic agents were given. Results. The B‐I group showed no remarkable gastric mucosal changes, but B‐I with denervation showed a significant increase in the development of tumor (67%) and carcinoma (42%). In the B‐II groups, the denervation induced a significant increase in tumorigenesis, from 22% to 58%. Analysis of cell kinetics revealed a significant increase of labeling index in those groups that developed tumors. PAS‐AB staining showed a decrease of PAS positive mucin but an increase of acidic mucin‐producing cells in the denervated groups, suggesting an increase in the number of immature cells that are more susceptible to atrophic gastritis and carcinoma. There was no close relationship between tumorigenesis and intragastric pH, intragastric bile acid concentration, or serum gastrin levels. Conclusions. After gastrectomy, not only duodenogastric reflux, but also the denervation of the gastric mucosa play an important role in the etiology of gastric remnant cancer. Cancer 1995;75:1490‐6.

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Survival after vagotomy: Results of the Aarhus county vagotomy trial

Cited by 12 publications

References 10 publications

Trends in Perforated Peptic Ulcer: Incidence, Etiology, Treatment, and Prognosis

Trends in Perforated Peptic Ulcer: Incidence, Etiology, Treatment, and Prognosis

Risk of Stomach Cancer in Patients with Peptic Ulcer Disease

Etiology of gastric remnant cancer with special reference to the effects of denervation of the gastric mucosa

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