Biomedical subjects
Publications and source records attributed to L B Svendsen.
The brown bowel syndrome (BBS) is a rare disease characterized by malabsorption and accumulation of lipofuscin in the smooth muscle cells of the muscularis externa of the small intestine. Recently, we incidentally observed a case of BBS in a colon operated on because of a neoplasm. Our ultrastructural investigation, which demonstrated changes in the mitochondria, further supports the significance of mitochondrial damage in BBS.
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Based on extensive clinical and clinical chemical information (107 different items) from 1002 jaundiced patients, we developed a diagnostic algorithm which was evaluated on a test sample of another 110 jaundiced patients. A primary classification into categories of obstructive jaundice (probability of obstruction greater than or equal to 0.80), non-obstructive jaundice (probability of obstruction less than or equal to 0.20), and of doubtful causes of jaundice (probability of obstruction: 0.20-0.80) was attempted. Among 234 patients in the data base who were classified as obstructive, 220 (94%) proved to be so, as did 36 (97%) of 37 in the test sample. The corresponding figures for non-obstructive jaundice were 463 (96%) of 483 patients correctly classified in the data base and 47 (92%) of 51 patients in the test sample. Altogether 69% of the patients in the data base and 75% of those in the test sample were correctly classified, in 27% and 20% the cause of jaundice was doubtful, and only 4% and 5%, respectively, were misclassified. A slight majority of the patients in whom the algorithmic diagnoses were doubtful proved obstructive. A close correlation was found between the preliminary diagnoses made by the algorithm and by the clinicians. A secondary classification of the patients by the algorithm into benign versus malignant causes of obstructive jaundice performed equally well in the data base and the test sample.
Pancreatic tissue pressure (PTP) was measured during surgery in six patients with a normal pancreas and in six patients with chronic pancreatitis. The pressures were obtained by insertion of a tiny transducer-connected cannula into pancreas. PTP probably reflects acinus and small-duct pressure. PTP was significantly higher in patients with chronic pancreatitis than in patients with a normal pancreas, but it decreased significantly after drainage. A high degree of linear relationship between PTP and intraductal pressure (r = 0.99) indicates that PTP measurements are valuable when the main duct is difficult to cannulate. Chronic pancreatitis might be a compartment syndrome due to impeded drainage and an inelastic capsule.
The relation between liver function and an oral testosterone load was examined in 42 consecutive patients with alcoholic liver cirrhosis. Administration of an oral load of 400 mg micronized free testosterone increased the serum concentration of testosterone (range, 31.9-694.4 nmol/l; median, 140.8 nmol/l) in male patients with alcoholic liver cirrhosis to significantly (P less than 0.01) higher levels than in male subjects without liver disease (range, 25.4-106.6 nmol/l; median, 61.5 nmol/l). The increase of testosterone after the load (log delta testosterone) in patients correlated inversely with galactose elimination capacity (r = 0.54; P less than 0.001), serum albumin (r = -0.53; P less than 0.001), plasma factor II + VII + X (r = 0.62; P less than 0.001), indocyanine green clearance (r = -0.71; P less than 0.001), and hepatic blood flow (r = -0.61; P less than 0.01) and correlated directly with wedged-to-free hepatic vein pressure (r = +0.54; P less than 0.01). The increase of testosterone after the load did not correlate significantly with sex hormone-binding globulin (r = +0.35; P greater than 0.05). It is concluded that the hepatic extraction of testosterone is significantly decreased in patients with alcoholic cirrhosis. This decrease seems to be due to decreased liver function, decreasing hepatic blood flow, and increased portosystemic shunting. Oral testosterone loading may therefore be of prognostic significance in patients with alcoholic liver cirrhosis.
Serum concentrations of oestrone, oestradiol, follicle-stimulating hormone (FSH), luteinizing hormone (LH), and sex hormone-binding globulin (SHBG) were significantly (P less than 0.01) raised in men with alcoholic liver cirrhosis (no. = 42) compared with age-matched controls (no. = 20). No significant difference was observed when comparing serum testosterone concentrations. Patients were divided into three groups in accordance with the severity of liver cirrhosis, using biochemical and clinical criteria. Patients with the best-preserved liver function (no. = 11) and patients with moderately affected liver function (no. = 18) had significantly (P less than 0.05) raised serum concentrations of testosterone, FSH, and LH when compared with both controls and patients with severely affected liver function (no. = 13). Serum concentrations of testosterone, FSH, and LH in the latter group showed no significant differences from the controls. Serum concentrations of oestrone and oestradiol were significantly (P less than 0.05) increased in all patient groups, and serum oestrone increased with decreasing liver function. No significant differences were observed concerning SHBG concentrations in the three groups of patients. Dexamethasone suppression did not change the concentration of testosterone significantly, but oestrone and oestradiol concentrations decreased significantly (P less than 0.01) in controls and patients. In patients, but not in controls, a significant (P less than 0.01) increase in FSH and LH concentrations was observed after dexamethasone suppression. The mean percentage increase of FSH and LH was higher the greater the severity of liver cirrhosis.
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In forty-two patients with alcoholic liver cirrhosis and without recent alcohol ingestion the pituitary-testicular function was studied in an effort to relate the endocrine abnormalities with the degree of liver cell dysfunction, evaluated on a quantitative basis. Compared with values in twenty-one healthy controls, we found significantly elevated serum oestrone, oestradiol, follicle-stimulating hormone, luteinizing hormone and prolactin (P less than 0.01). Serum dehydro-epiandrosterone and dehydroepiandrosterone sulphate were significantly reduced in the cirrhotics (P less than 0.01), whereas serum testosterone was not significantly different from that in the controls. Raised levels of sex-hormone binding globulin were found in 71% (22/31) of the patients (median 8 x 10(-18) mol/l, range 3-17 x 10(-8) mol/l). The incidence of gynaecomastia (38%), cutaneous spiders (67%), testicular atrophy (24%) and reduced axillary hair (71%) was without significant relation to raised levels of sex-hormone binding globulin or progressively reduced liver function. In the presence of clinical or hormonal hypo-gonadism we found evidence of a state of primary hypogonadism together with an inadequate secretion of gonadotropins. The state of hyperoestrogenaemia and the concentration of gonadotropins were significantly correlated to the hepatic synthesis of coagulation factors.
Serum concentrations of testosterone were measured in 24 male patients with alcoholic cirrhosis during testosterone administration. The purpose was to compare serum concentrations of testosterone during peroral with those during parenteral testosterone administration in these patients. Patients who were injected intramuscularly with a combination of short- and long-acting testosterone (Triolandren, 348 mg testosterone) had median peak values of serum testosterone of about 40 ng/ml, which fell to basal levels after a fortnight. During testosterone propionate injections (84 mg testosterone) every other day, rather constant serum concentrations with median values of about 30 ng/ml were reached after 4 days. Peroral testosterone administration (800 mg micronized free testosterone) each day also resulted in fairly constant serum concentrations after 4 days, and the median values were about 50 ng/ml. No side effects were observed.
To determine the reaction of the gastric mucosa to HP 549 (isoxepac) an oxo-dibenz-oxepine derivative of acetic acid and new non-steroidal antiphlogistic agent in comparison with standard drugs, 12 healthy volunteers received 3 g of Aspirin, 150 mg of indomethacin, or 600 mg of HP 549 (isoxepac) in a double-blind cross-over trial. Before and after each treatment period, all subjects underwent gastroscopy with biopsy of gastric mucosa. The subjects recorded complaints (side effects) before and after each treatment period. Aspirin produced significantly more gross mucosal changes at endoscopy. There was no significant difference between isoxepac and indomethacin. Both produced very few gastric mucosal changes and there were few subjective complaints.
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Assays of in vitro biological properties associated with cellular transformation revealed differences in cultured skin cells within the heritable colon cancer syndromes with and without polyposis coli. Such evidence suggested that an in vitro panel of biological assays could be used to recognize genotypes which increase the risk of colon cancer prior to clinical expression and supported the concept, long assumed on clinical differences, of genetic heterogeneity within the heritable colon cancer syndromes.
During a period of 12 months, 88 patients with severe haemorrhage from gastric or duodenal ulcers or from erosive gastritis completed a double-blind trial of either cimetidine or placebo. Only patients needing immediate blood transfusion were admitted to the trial. It was found that in patients with severe bleeding from gastric or duodenal ulcers neither the severity of bleeding nor the incidence of emergency surgery was reduced by cimetidine. Furthermore, the treatment did not improve the mortality rate. It is concluded that patients with severe bleeding from gastric or duodenal ulcers will not benefit from immediate treatment with intravenous cimetidine.
The effects of glucagon versus placebo were evaluated in a double-blind trial including only patients with a first attack of severe acute pancreatitis not associated with biliary disease. All 22 patients had deterioriation of their clinical condition, elevated serum amylase and pulse rate above 100/min. or shock. An initial dose of 1 mg. glucagon was given as a bolus injection followed by infusion of 6 mg. in 1,500 ml. saline/24 hr. for three days. All were treated with nasogastric decompression, fluids, calcium and antibiotics. Severe complications developed in five of the 10 patients receiving glucagon and in eight of the 12 given a placebo. Three of the 10 (glucagon) and five of the 12 (placebo) died from these complications. Hemorrhagic pancreatitis was found in 11 patients at laparotomy or autopsy. Three of the five with hemorrhagic pancreatitis in the glucagon group and four of the six in the placebo group died. Pooling the data of the present and two other studies makes it probable that glucagon has no effect on mortality from acute severe pancreatitis.
64 patients under forty years of age with appendical carcinoid tumor in Denmark 1943-67 have been followed 10-33 years after the operation. Recurrence is found in one patient with a tumor larger than 2 cm and local metastases. Appendectomy alone is generally a sufficient treatment. Right hemicolectomy is indicated in tumors larger than 2 cm, in cases with local metastases or if the resected appendix-base is not free of tumor in cases with tumor localized near the base. Invasion in the mesoappendix does not increase the frequency of recurrence.
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