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S Bülow

Publications and source records attributed to S Bülow.

At least 91 records · Page 5Linked to original sources
PubMed1989

Familial adenomatous polyposis.

Familial adenomatous polyposis is an autosomal dominant disease that includes early development of up to thousands of colorectal adenomas and several extracolonic manifestations. All untreated patients will develop colorectal adenocarcinoma. The treatment of choice is colectomy and ileorectal anastomosis, but restorative proctocolectomy may be considered in selected cases. Polyposis patients treated with ileorectal anastomosis should be followed for life, with regular proctosigmoidoscopy and destruction of new adenomas. Furthermore, regular gastroduodenoscopy should be carried out because of frequent occurrence of premalignant duodenal adenomas. The prognosis is good after prophylactic colectomy in patients without carcinoma. All first degree relatives of affected family members should be examined regularly with proctosigmoidoscopy from the age of ten, and prophylaxis should be organised using a national or regional polyposis register. The recent detection of a specific gene for familial adenomatous polyposis is a long step forward, and several problems may be solved by increasing international cooperation.

Adenomatous Polyposis Coli↗
PubMed1989

Psoas abscess complicating Crohn's disease.

Six cases of psoas abscess complicating Crohn's disease are presented. The most common manifestations were weight loss, pain, fever and a palpable mass in the flank or iliac fossa. CT-scan confirmed the diagnosis. The treatment of choice in this condition is either laparotomy with drainage and primary resection of affected bowel or initial ultrasound-guided percutaneous drainage followed by early resection of the affected bowel.

Abscess↗
PubMed1988

Hepatoblastoma and familial adenomatous polyposis.

Eleven children have been identified as having hepatoblastoma and a family history of adenomatous polyposis, and 14 additional instances of this association have been collected from the literature. Among the 11 survivors of hepatoblastoma in the combined series, adenomatous lesions have been sought in seven and detected in six patients at ages 7 to 25 years. Five of these patients also have congenital hypertrophy of the retinal pigment epithelium, a marker for carriers of the polyposis gene. These findings strengthen the association between hepatoblastoma and familial adenomatous polyposis and have led to the establishment of the Hepatoblastoma-Adenomatous Polyposis Registry.

Adenomatous Polyposis Coli↗
PubMed1988

Effect of cimetidine on survival after gastric cancer.

The effect of cimetidine on survival was investigated in 181 patients with gastric cancer. Immediately after operation or the decision not to operate, the patients were randomised in double-blind fashion to placebo or cimetidine 400 mg twice daily for two years or until death, with review every three months. Median survival in the cimetidine group was 450 days (range 1-1826) and in the placebo group 316 days (1-1653). The relative survival rates (cimetidine/placebo) were 45%/28% at 1 year, 22%/13% at 2 years, 13%/7% at 3 years, 9%/3% at 4 years, and 2%/0% at 5 years. Survival in the cimetidine group was significantly longer than in the placebo group.

Actuarial Analysis↗
PubMed1988

Papillary thyroid carcinoma in Danish patients with familial adenomatous polyposis.

All patients from the nationwide Danish Polyposis Register have been followed up with regard to thyroid carcinoma. During the period 1943-1985, 2/107 Danish women and 0/138 men developed papillary thyroid carcinoma after the diagnosis of familial adenomatous polyposis. The expected number among females was 0.02 resulting in a observed/expected ratio of 100 (95% confidence limits 12-361). Consequently, thyroid carcinoma should be included among the extracolonic lesions, which may develop in any female polyposis patient. However, regular thyroid examination is not indicated, as thyroid carcinoma is uncommon and as the prognosis is excellent.

Adenomatous Polyposis Coli↗
PubMed1988

Prognostic significance of hereditary predisposition on the outcome of colorectal cancer as expressed by increased in vitro tetraploidy.

Seventy colorectal cancer patients operated on in the period 1981-1984 were consecutively investigated for in vitro tetraploidy in dermal fibroblasts, as an increased number of tetraploids is considered a marker of genetic predisposition for colorectal cancer. The difference in disease-free survival rates of increased (IVT+) and normal (IVT-) in vitro tetraploidy was not statistically significant (0.1 less than p less than 0.2), but the decrease in the disease-free survival rate of IVT+ was 1.6 times that of IVT-. To exclude the influence of other prognostic factors, a Cox multivariate regression analysis was used, with Dukes C carcinoma and poor differentiation as co-variables for IVT+. In this analysis IVT+ did not show any independent prognostic significance. A genetic predisposition for colorectal cancer, as expressed by the presence of IVT+ in skin fibroblasts, does not seem to influence the survival of patients with colorectal cancer.

Adult↗
PubMed1988

Increased in vitro tetraploidy and mandibular osteomas in patients with and without colorectal diseases.

One hundred and seventy-six individuals with various colorectal diseases were investigated simultaneously for increased in vitro tetraploidy in dermal fibroblast cultures and for occult mandibular osteomas. In only 10 of the 176 persons were both presumed markers of colorectal genetic predisposition present in the same individual. No evidence was found that these traits are causally associated. A combination of the two presumed markers showed a tendency towards occurrence in individuals with a positive family history of colorectal cancer among first-degree relatives.

Adolescent↗
PubMed1988

Is epidermal growth factor involved in development of duodenal polyps in familial polyposis coli?

Duodenal adenomas are a frequent extracolonic manifestation in patients with familial polyposis coli (FPC). Epidermal growth factor (EGF), a polypeptide that stimulates cellular growth and differentiation, is localized in Paneth cells in the small intestine. In two patients with FPC, we found EGF immunoreactivity in duodenal adenomas. Numerous EGF immunoreactive Paneth cells were localized, not as usually, in the bottom of the crypts, but scattered along the crypts alone or in clusters. We do not know whether EGF is involved in the development of duodenal polyps in FPC patients, or whether the present findings represent secondary changes in duodenal polyps.

Adenoma↗
PubMed1987

Incidence of associated diseases in familial polyposis coli.

In this review we present diseases associated with hereditary polyposis syndromes. In addition to the known extracolonic manifestations of the so-called Gardner's syndrome, other important diseases are carcinomas of the thyroid and of the small bowel and bile duct adenoma. The incidence of these diseases is discussed.

Adenomatous Polyposis Coli↗
PubMed1987

Dental anomalies in familial adenomatous polyposis coli.

Forty-seven Danish and 50 Finnish patients with familial adenomatous polyposis coli (FPC) were studied by panoramic tomography (PTG) of the mandible, which showed dental abnormalities in 17% of the cases. Eleven patients (11%) had supernumerary teeth and/or compound osteomas, and nine patients (9%) had impacted permanent teeth. The frequency of the dental anomalies was statistically significantly higher in FPC patients than in the normal population; it is therefore concluded that this dental abnormality should be included in the list of extracolonic manifestations that may occur in any FPC patient. The frequency of dental anomalies was higher in Finnish than in Danish patients, probably owing to a higher frequency of extracolonic manifestations in the Finnish series.

Adenomatous Polyposis Coli↗
PubMed1987

In vitro tetraploidy in patients with non-hereditary colorectal adenoma and carcinoma. Support for a genetic influence on the pathogenesis of colorectal carcinoma.

One hundred and seventy-two patients (76 patients with colorectal cancer, 46 with adenoma of the colon or rectum, and 50 controls) were investigated for in vitro tetraploidy in dermal fibroblast monolayer cultures. The incidence of increased in vitro tetraploidy (IVT) among patients with adenoma or carcinoma was significantly different from that of controls. There was no difference in the incidence of IVT between the adenoma patients and those with colorectal cancer. IVT was investigated among different subgroups of adenoma and colorectal cancer patients and was only found to be related to an inherited tendency to colorectal cancer.

Adenoma↗
PubMed1987

In vitro tetraploidy in patients with ulcerative colitis.

One hundred and seven patients (57 patients with ulcerative colitis and 50 controls) were investigated for in vitro tetraploidy (IVT) in dermal fibroblast monolayer cultures. There was no difference in incidence of IVT between patients with ulcerative colitis and controls. We advance the hypothesis that the genetic background of the colorectal cancer type found in ulcerative colitis differs from that found in the colon cancer syndromes and in non-hereditary colorectal cancers. Colorectal cancer in ulcerative colitis is probably only dependent on the degree of inflammatory lesions of the colonic mucosa.

Adolescent↗