[The introduction of the Public Health Act of 1860]. / Innføringen av sunnhetsloven i 1860.

The Public Health Act of 1860 introduced modern health legislation in Norway. The act was a consequence of the industrial revolution and was influenced by the European hygienic movement and the English Public Health Act of 1848. The act placed the responsibility for public health measures on the local authorities in accordance with contemporary political philosophy. The local board of health was chaired by the officer of health and made up by politically elected members. This system implied co-operation between professional and political interests in order to improve disease prevention and enforce public health measures. The part of the act that provided for local boards of health was in force until 1982; the chapter on communicable diseases was repealed in 1995. The fact that this legislation remained in force for so long may serve as an indication of the usefulness and flexibility of the act. Its main drawbacks were an insufficient financial basis and lack of the authority to introduce relevant sanctions.

Improved assay for fecal calprotectin.

Fecal calprotectin is a marker of inflammatory and neoplastic disease in the lower gastrointestinal tract. A new fecal sample preparation procedure for the measurement of calprotectin has been developed, with higher calprotectin yield and lower contamination risk. Changes in the new method compared to the original [Roseth AG, Fagerhol MK, Aadland E, Schonsby H. Assessment of the neutrophil dominating protein calprotectin in feces. A methodologic study. Scand J Gastroenterol 1992;27(9):793-798] are smaller sample size, higher dilution of the sample, presence of dissociating agents in the extraction solution and procedure performed in closed disposable tubes. The extraction yield was 78% (41-100%) of total calprotectin, giving an overall five-fold increase compared to the original method. Samples with high calprotectin values were increased to a slightly higher degree, than low calprotectin samples, thus improving the separation between high and low calprotectin levels. Median calprotectin level in healthy subjects was 26 microg/g. Pathological samples with pancolitis showed levels up to 30000 microg/g. The mean C.V. (coefficient of variation) in blended feces was lower than that of unblended, suggesting uneven distribution of calprotectin. However, no significant difference between spot measurements was found when five samples from each of 47 stools were measured. Thus measurements of calprotectin in fecal samples were accurate and reproducible. No interference with foods or relevant oral pharmaceuticals or nutraceuticals was found.

[Growth and stagnation--development of health services during the 20th century]. / Vekst og stagnasjon--utviklingen av helsevesenet på 1900-tallet.

The health services of Norway have changed over the last century in tune with the development of society. The health services are not only the result of scientific and technological progress, but also a product of changes in prevailing political and social conditions and ideologies. Quality assessment and concern for the ethical basis of the health services ought to be given priority in the years to come.

[13C-urea breath test as diagnostic method in Helicobacter pylori infection]. / 13C-urea-pusteprøve som diagnostisk metode ved Helicobacter pylori-infeksjon.

We have evaluated a 13C-urea breath test for the diagnosis of Helicobacter pylori infection. The 13C-test was analyzed with isotope-selective nondispersive infrared spectrometry and compared with a 14C-urea breath test and the urease test in gastric mucosal biopsies. 46 patients were analyzed with breath tests; 23 patients were negative and 22 patients were positive with both methods. One patient was positive with the 14C-method and negative with the 13C-urea breath test. 61 patients were analyzed with the 13C-urea breath test and the urease test. 30 patients were negative and 30 patients were positive with both methods, whereas one patient with a negative urease test had a positive breath test. 13C-urea breath test analyzed with isotope-selective non-dispersive infrared spectrometry is a fast, simple, non-radioactive, non-invasive, convenient and reliable method for the diagnosis of Helicobacter pylori infection.

Fecal calprotectin concentration in patients with colorectal carcinoma.

PURPOSE: The study contained herein was undertaken to investigate fecal calprotectin excretion in a series of patients with colorectal carcinoma and to determine whether the excretion was influenced by localization or stage of the tumor. Furthermore, the effect of surgical treatment on the concentrations was studied. Fecal calprotectin was also compared with plasma concentrations of calprotectin, carcinoembryonic antigen, and C-reactive protein. METHODS: Fecal calprotectin was measured in 119 consecutive patients admitted for treatment of colorectal carcinoma. In 116 (97.5 percent) patients, resectional surgery was performed. Plasma calprotectin was measured in 90 (76 percent) patients, carcinoembryonic antigen in 88 (74 percent) patients, and C-reactive protein in 82 (69 percent) patients. RESULTS: Median fecal calprotectin concentration in the 119 patients was 50 (range, 2-950) mg/l, which was significantly (P < 0.0001) higher than in 125 control patients (median, 5.2 mg/l). In 23 patients studied also after resection, the excretion fell greatly. There were no significant differences in fecal calprotectin concentration among patients with different tumor stages. Elevated plasma calprotectin concentrations were found in 67 of 90 (73.3 percent) patients with colorectal carcinoma, compared with elevated fecal calprotectin in 111 of 119 (93.3 percent) patients, and there was no significant correlation between plasma and fecal calprotectin concentrations. Plasma calprotectin concentrations were significantly lower in patients with T1 or T2 tumors than in those with more advanced stages (P = 0.0025). CONCLUSION: Measurement of fecal calprotectin may become a diagnostic tool in detecting colorectal carcinoma. The specificity in relation to colorectal carcinoma has not, however, been completely investigated. Both neoplastic and inflammatory conditions may be associated with elevated values; therefore, it is unlikely that calprotectin can predict specific colonic disorders.

Faecal calprotectin: a novel test for the diagnosis of colorectal cancer?

Calprotectin, a prominent cytosol protein in neutrophil granulocytes, was present in increased concentrations in stools from 50 of 53 patients with colorectal cancer, 32 of 40 patients with colorectal polyps, and all of 18 patients with gastric cancer. After radical surgery, faecal calprotectin levels reverted to the normal range in all but one patient with colorectal cancer. Calprotectin determinations are simplified by the stability of this protein in stools. Reliable estimates can be obtained in samples of only 5 g. On the basis of data from the literature, the test for calprotectin seems better than that for occult blood for the detection of gastrointestinal neoplasms.

Assessment of the neutrophil dominating protein calprotectin in feces. A methodologic study.

This study describes methods for extraction and quantification of calprotectin (L1 protein) in feces by enzyme immunoassay. This protein is a prominent antimicrobial component of neutrophils, monocytes, macrophages, and squamous epithelia. Calprotectin was stable in feces during storage for 7 days at room temperature. Small fecal samples taken from a 24-h feces collection gave a reliable estimate of calprotectin. Within-assay precision was 1.9%, and between-assay precision 14.8%. In healthy subjects (n = 33) median fecal calprotectin was 2025 micrograms/l and in hospital controls (n = 40) 10,500 micrograms/l. Median values in patients with Crohn's disease (n = 21) was 43,000 micrograms/l and in ulcerative colitis (n = 17) 40,000 micrograms/l. Fecal calprotectin was significantly correlated to fecal alpha 1-antitrypsin in the patients with Crohn's disease. Ten of 11 patients with gastrointestinal carcinomas had calprotectin level above the suggested reference limit of 6740 micrograms/l.

The inhibitory effect of bile on the binding of vitamin B12 to intrinsic factor. An in vivo study in rats.

To investigate whether bile reduces the amount of vitamin B12 bound by intrinsic factor (IF) in the intestinal juice in vivo, choledochocolic fistulae were made in 9 rats, and 10 rats were sham-operated. Small-intestinal juice was collected 1 h after gastric instillation of 57CoB12. The percentage of 57CoB12 bound by IF in the intestinal juice was markedly increased in fistula rats (median, 86%; range, 75-91%) as compared with sham-operated rats (35%; 12-50%) (p less than 0.001). In a second experiment we investigated whether bile enhances the intestinal uptake of the IF-B12 complex. Aliquots of the radioactive intestinal juice collected from the sham- and fistula-operated rats were separately instilled into tied intestinal loops created in 19 rats. The percentage of the instilled radioactivity taken up per 10 cm of the loop was significantly higher when juice from fistula-operated rats was instilled (median, 12.4; range, 4.3-18.7) than when juice from sham-operated rats was instilled (3.3; 1.4-6.2) (p less than 0.001).

Effect of calcium deficiency on vitamin B12 absorption in rats.

The influence of calcium on vitamin B12 absorption was investigated in two experiments. In the first we investigated whether B12 malabsorption in rats with biliary diversion through choledochocolic fistula is caused by deficiency of calcium in the small intestine. Calcium concentrations were measured in 10 fistula- and 10 sham-operated rats. Fistula rats had steatorrhea, but the concentration of calcium in the intestinal lumen was increased. In the second experiment we studied the effect of calcium deficiency on B12 absorption. Ten young rats were fed a low-calcium diet and 10 rats a control diet for 4 weeks. Rats on the low-calcium diet had moderately reduced calcium concentration in the blood and in the intestinal juice but unaltered calcium concentration in the cytosol fraction of intestinal mucosal scrapings. The absorption of 57CoB12 was unimpaired. This suggests that moderate calcium deficiency does not influence the intestinal absorption of vitamin B12 in the rat.

[Hydrogen breath tests in the diagnosis of primary lactase deficiency]. / Hydrogenpusteprøven i diagnosen av primaer laktasemangel.

The H2 breath test as an indirect method of detecting lactase deficiency was evaluated in 55 patients referred because of abdominal complaints. The patients underwent both jejunal biopsy with determination of enzyme activities and the H2 breath test. 19 patients had lactase deficiency defined as a lactase/sucrase ratio less than 0.33. A rise in breath H2 of more than 20 ppm above base-line at two hours following 50 g lactose given orally was used as the cut off point indirectly suggesting lactase deficiency. The specificity of the H2 breath test in detecting lactase deficiency was 89%. The sensitivity was 74%.

Is vitamin B12 malabsorption in bile fistula rats due to bacterial overgrowth? A study of bacterial metabolic activity in the small bowel.

To investigate whether vitamin B12 malabsorption in rats with choledochocolic fistulae is caused by bacterial overgrowth, we studied intestinal bacterial metabolic activity in choledochocolic fistula-operated rats, self-filling blind-loop-operated rats, and sham-operated rats. Fistula-operated rats had a moderate indicanuria compared with sham-operated ones, whereas the faecal excretion of nitrogen was unchanged. There was no difference in the amounts of radioactivity recovered in sediments of intestinal contents after an oral dose of 57CoB12, indicating unaltered bacterial uptake of vitamin B12 in fistula rats. The 14C-xylose breath test showed bacterial overgrowth in blind-loop rats only. Neomycin treatment of fistula rats diminished the excretion of indican but did not alter the absorption of vitamin B12. The results suggest moderately increased activity of indole-producing bacteria in fistula rats, but they do not support the hypothesis that vitamin B12 malabsorption is caused by bacterial overgrowth.

Effect of gastric anacidity on the release of cobalamins from food and their subsequent binding to R-protein.

Rabbit liver homogenate, labelled in vivo with 57Co, was used to investigate the effect of anacid gastric juice on the release of cobalamins from food and on the cobalamin binding to proteins in humans. The cobalamin release was investigated in vitro by incubating the liver homogenate with native and neutralized gastric juice. The cobalamin release and the amount of cobalamins bound to R-protein were significantly higher with native than with neutralized gastric juice. To investigate the effect of anacidity on cobalamin release in vivo, 14 healthy volunteers were given omeprazole or placebo in a double-blind crossover fashion. 57Co-labelled liver-bound cobalamins were given orally, and aspirates were collected from the stomach and the upper jejunum. After omeprazole gastric anacidity (pH greater than 6.0) was obtained in 11, 12, and 10 individuals after 5, 30, and 60 min, respectively. In the gastric aspirates obtained after omeprazole there was a slight inhibition in cobalamin release after 5 and 30 min (p less than 0.05). In the jejunal aspirates the cobalamin release was close to 90% in both the placebo and the omeprazole experiment, and there was no significant difference in the percentage of cobalamins bound to R-protein in the two groups. The percentage of cobalamins bound to R-protein was much lower in the jejunal aspirates (26.6% and 23.7% in omeprazole and placebo, respectively) than in the gastric aspirates (65.8% and 68.6%).

Intestinal epithelial function and villus surface area in rats with bile fistulae.

We have previously found reduced absorption of vitamin B12 in rats with choledochocolic fistulae. To investigate whether the reduction is caused by epithelial dysfunction or mucosal hypoplasia, choledochocolic fistulae were made in 11 rats, whereas 10 rats were sham-operated. The epithelial function was evaluated 9 days later by measuring the uptake of 57CoB12 and glucose in perfused intestinal segments and by determining the activities of 11 mucosal enzymes. Hypoplasia was investigated by performing morphometric measurements of the villus surface area and by measuring the weight, protein, and DNA in mucosal scrapings. The results suggest that choledochocolic fistulae in rats do not impair the epithelial function or cause mucosal hypoplasia. The urinary excretion of indican was increased in the fistula-operated rats, but further studies are needed to establish the significance of this observation.