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Biomedical subjects

K Bech

Publications and source records attributed to K Bech.

At least 55 records · Page 3Linked to original sources
PubMed1989

Importance of cytolytic activity and dietary iodine in the pathogenesis of postpartum thyroiditis.

The incidence of lymphocytic thyroiditis (LT) has increased since the introduction of iodine prophylaxis, and LT is claimed to represent an adverse reaction to iodine. This theory is supported by animal studies as well as experimental studies in humans. In pregnancy iodine turnover is increased. During the immunological rebound period occurring postpartum the thyroid autoantibodies increase, and may lead to postpartum thyroiditis (PPT). The iodine content within the gland may be important for this reaction. In vitro it has been shown that iodine inhibits the cAMP-dependent events of the thyroid cell function, but iodine may also stimulate the intrathyroidal immuno-competent cells leading to cytokine synthesis. Cytokines have been shown to interfer with the thyroid cell function. Iodine may thus trigger the autoreactive attack and enhance the local autoantibody production, which plays a primary pathogenic role for development of PPT.

Animals↗
PubMed1989

Characterization of the natural killer cell activity in Hashimoto's and Graves' diseases.

Natural killer (NK) cell activity and blood mononuclear cell subpopulations were characterized in patients with Hashimoto's thyroiditis (n = 11), Graves' disease (n = 20), non-toxic goitre (n = 10) and in normal controls (n = 22). NK cell activity against K 562 target cells and the capability of IFN-alpha, Il-2, and indomethacin to enhance NK cell activity in vitro did not differ significantly between the groups. The percentages of large granular lymphocytes, CD5+, CD4+, CD8+ and CD16+ cells were normal in patients with non-toxic goitre, Hashimoto's and Graves' diseases. There was no correlation between NK cell activities and TgAb, MAb and TSAb. Although NK cell activity is suppressed in several autoimmune diseases, NK cell function is normal in patients with autoimmune thyroid disorders.

Adult↗
PubMed1989

Repeated screening for colorectal cancer with fecal occult blood test. A prospective randomized study at Funen, Denmark.

Two screenings with Hemoccult-II were performed in a randomized study, allocating 30,970 persons to screening and 30,968 as controls in a population of 140,000 between 45 and 74 years old on the island of Funen, Denmark. The test was completed in 20,672 initially and in 18,779 of these during rescreening 2 years later. Positive H-II tests were found in 215 and 159 persons during the two screenings, respectively. A total colonoscopy was performed in 187 and 144, and cancer was detected in 37 and 13 and adenomata in 86 and 76, respectively. Interval cancers had developed in 40 persons at the end of the second screening, and 39 non-responders had developed cancer. Cancer was diagnosed in 115 controls and an adenoma in 100 during the same period. Interval cancers presented as rectal cancers more frequently than those detected by screening. Early cancers were more frequent in the screening group, and, accordingly, more patients had curative and also less extensive surgery, with a low postoperative mortality. The total number of deaths from colorectal cancer was 37 in the screening group, including interval cancers and cancers in non-responders and persons who developed cancer before they could be invited, which suggests a reduction in mortality of 27% (51 deaths among controls, compared with 37). The reduction is as yet not statistically significant, and final evaluation must await at least one more screening, ending in 1990, and a follow-up of some years. Removal of more large adenomas during screening makes it possible that the incidence of cancer will decrease.

Adenoma↗
PubMed1988

Thyroid function in patients with Pendred's syndrome.

Thyroid function was studied in 17 unrelated patients with Pendred's syndrome. Fourteen patients had been treated with L-thyroxine, which was withdrawn during the investigation. Eight of the patients had previously had a thyroid resection. Thirteen patients had goiter at the time of study. The serum total thyroxine and serum total triiodothyronine concentrations were normal in 8, of whom 3 had elevated serum TSH concentrations. In the remaining 9 cases the thyroxine levels were below normal with elevated TSH. Serum reverse triiodothyronine concentrations were decreased in 8 out of 11. Median serum thyroglobulin was 973 micrograms/l (range 10.9-3200 micrograms/l) and increased in 13. Three patients had slightly positive thyroglobulin antibodies and one with normal level was thyrodectomized. Thyroid stimulating antibodies as measured by adenylate cyclase stimulation (median 114%, range 85-137%) were slightly increased in 11. When measured as TSH binding inhibiting immunoglobulins none were positive. Thyroid microsomal antibodies were negative in all. All patients with a detectable 131I uptake (n = 15) showed a pathological iodide perchlorate discharge test (median 32%, range 16-46%). These findings indicate an organification defect with impaired hormone synthesis.

Adolescent↗
PubMed1988

Interleukin-1 affects the function of cultured human thyroid cells.

Cytokines are peptide hormones essential for cellular communication in the immune response. The purpose of this study was to investigate the influence of cytokines, especially recombinant interleukin 1 beta (rIL-1 beta), on human thyroid cells. Thyroglobulin (Tg) was measured by a double antibody radioimmunoassay, and cyclic AMP (cAMP) by a competitive protein binding assay. Supernatants from unstimulated and phytohaemagglutinin-stimulated blood mononuclear cells were added to human thyroid cells cultured in monolayers. A dose-dependent inhibition of the secretion of Tg and cAMP was demonstrated. Both subcultured and primary cultured cells incubated with rIL-1 beta at pharmacological levels (10(-1)-10(2) U/ml) exhibited an inhibition of Tg and cAMP secretion, while at physiological levels (10(-5)-10(-3) U/ml), the secretion of Tg was enhanced. The similar stimulation of cAMP was demonstrated in subcultures. These in vitro studies suggest that IL-1 beta may play a role in the pathogenesis of autoimmune thyroid diseases. Further, the stimulations at low concentrations indicate that IL-1 beta may regulate the function of the thyroid gland under physiological conditions.

Autoimmune Diseases↗
PubMed1988

Hepatitis B in symptomless Danish homosexual men.

Forty eight symptomless homosexual men attending a sexually transmitted disease (STD) clinic and found by screening to have hepatitis B surface antigen (HBsAg) were followed up for a median of 10 (range six to 26) months to characterise their liver disease. Initially 33/50 (66%) of the men had increased serum liver enzyme activity and 19/47 (40%) had increased serum immunoglobulin G concentrations. Liver biopsy specimens showed acute hepatitis B in 12 (39%) and chronic hepatitis B in 19 (61%) of the 31 patients who underwent liver biopsy. The course of the infection was: acute hepatitis B in 14/48 (29%), chronic persistent hepatitis B in 23/48 (48%), chronic aggressive hepatitis B in 8/48 (17%), and cirrhosis in 3/48 (6%) of the patients. Antibodies against human immunodeficiency virus (HIV) were present in 16/45 (36%) of the patients, but the presence of antibodies to HIV did not influence the course of hepatitis B in the observation period.

Adult↗
PubMed1988

The role of somatostatin and serotonin in the beta-adrenoceptor regulation of gastric function. An experimental study in dogs.

CHAPTER 1. The gastric functions are regulated in a complex manner by the autonomic nervous system, sympathetic and parasympathetic, and hormones and moreover by a system of peptide-containing cells and nerves. The sympathetic influence is mediated by alpha- and beta-adrenoceptors, beta-adrenoceptor agonists in general inhibit the gastric functions. The effects of the beta-adrenoceptors are probably mediated indirectly, and the responsible mechanism may be via release of and endogenous mediator--somatostatin or serotonin. The purpose of the present study, described in the survey, is to examine whether somatostatin or serotonin acts as a mediator for the gastric effects in vivo of beta-adrenoceptor agonists. The proposed mediator must present the following characteristics: A. Inhibitory effects of "physiological" doses in vivo. B. Inhibitory characteristics similar to those of the beta-adrenoceptor agonists. C. A beta-adrenoceptor mediated release. CHAPTER 2. In this chapter the known effects of beta-adrenoceptor agonists on gastric functions (acid secretion, pepsin secretion, antral motility and mucosal blood flow) are presented. The possible mechanisms mediating these effects are mentioned, and the effects of somatostatin and serotonin are reviewed. Beta-adrenoceptor agonists inhibit the acid secretion in vivo in several species, but stimulate in vitro. A similar pattern is probable as for the pepsin secretion, but sufficient results are not available in order to draw a certain conclusion. The antral motility is inhibited both in vivo and in vitro. The mucosal blood flow is increased compared to the acid secretion, however the results points to variable effects depending on the circumstances of the experiments. On the basis of the reviewed effects of somatostatin it is concluded that the effects are inhibitory, but the inhibitory characteristics are not known. A beta-adrenoceptor mediated release of somatostatin has been found, but it has not been examined selectively for the stomach. The gastric effects of serotonin has been sparsely examined and it is not possible to determine the effects as parts of a certain characteristic. It is concluded that neither somatostatin nor serotonin have been examined sufficiently to determine which is the proposed mediator. CHAPTER 3. The materials and methods used are reviewed. Dogs were used and various parameters were measured--acid secretion by titration, pepsin secretion by enzymatic process with haemoglobin as substrate, antral motility by registration of intraluminal pressure, mucosal blood flow by the clearance of neutral red, somatostatin by radioimmunoassay.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic beta-Agonists↗
PubMed1987

Thyroid stimulating antibodies in rheumatoid arthritis: an in vitro phenomenon.

The purpose of the study was to evaluate the frequency of thyroid stimulating immunoglobulins and their possible effect in vivo in patients with rheumatoid arthritis. Thyroid stimulating antibodies (TSAb) were present in 17 (68%) of 25 patients with rheumatoid arthritis, whereas only 2 (8%) had thyrotropin binding inhibiting immunoglobulins (TBII). The groups with and without TSAb were comparable with regard to sex, age, anti-inflammatory drugs, serum thyroglobulin levels, antithyroglobulin and antimicrosomal antibodies, rheumatoid factor, as well as to the serum levels of thyroxine and 3, 5, 3'-triiodothyronine. A possible stimulating effect of TSAb in vivo was evaluated by an ultrasensitive immunoradiometric assay for TSH. Both groups had normal serum TSH levels, and no significant difference was found between the two groups suggesting that the demonstration of TSAb in vitro is not always associated with a stimulation of the thyroid gland in vivo.

Adult↗
PubMed1987

Thyroid function in patients with breast cancer.

Thyroid function was evaluated in 58 patients with breast cancer and compared with data obtained from an age-matched control group of healthy women. Thyroid antibodies at low levels were present in 29 patients (50%): 21 patients (36%) had thyroid stimulating antibodies at low activity. Ten patients (17%) had thyroglobulin antibodies compared with 3 in the control group (P less than 0.05). Nine of 10 patients with thyroglobulin antibodies had microsomal antibodies as well. Two patients had only microsomal antibodies. Additionally 10 autoimmune antibodies were determined. These were, however, either absent or present in low concentrations in serum. Independent of the stage of disease, no differences were demonstrated between patients and controls in serum levels of triiodothyronine, thyroxine, free T3 index, free T4 index, thyroid stimulating hormone, and thyroglobulin. In conclusion, we found an increased frequency of thyroid autoantibodies in euthyroid patients with breast cancer compared with healthy controls suggesting a possible relation between this disease and autoimmune thyroid disease.

Adult↗
PubMed1987

The relationships between serum T3 index, thyroid volume, and thyroid stimulating, TSH receptor binding and thyroid growth stimulating antibodies in untreated Graves' disease.

This study represents an international double-blind collaborative study of abnormal immunoglobulin activity in untreated Graves' disease. Laboratories in two countries participated in a comparison of thyrotrophin binding inhibiting (TBII), thyroid stimulating (TSAb), and growth stimulating (TGI) immunoglobulins with clinical data, including ultrasonically measured thyroid size. The correlation between TGI and thyroid volume (n = 25, Rs = 0.54, P less than 0.05) and the fact that 9 of 10 patients with high range TGI values had large goitres establish the relationship between TGI and goitre, confirming that the in-vitro activity of these antibodies is related to an in-vivo action. In addition, both TBII and TSAb correlated with serum free T3 indices (TBII: n = 60, Rs = 0.46, P less than 0.001, and TSAb: n = 60, Rs = 0.64, P less than 0.001). Moreover, both TBII and TSAb correlated with thyroid volume (TBII: n = 60, Rs = 0.37, P less than 0.01, and TSAb: n = 60, Rs = 0.41, P less than 0.01) suggesting that these antibodies are also important in development of goitre in Graves' disease. Finally, some correlation between the antibodies was observed. TBII correlated with TSAb (n = 60, Rs = 0.47, P less than 0.001), and in the 16 patients with positive TGI results, this activity correlated with TBII (Rs = 0.54, P less than 0.05), but not with TSAb. Also some cases were found with corresponding high range TBII and TGI, while negative for TSAb, suggesting a close relationship between the in-vitro measurement of TSH binding and TGI.

Adult↗
PubMed1986

Exogenous serotonin and histamine-stimulated gastric acid and pepsin secretion in dogs.

The effects of serotonin on histamine-stimulated gastric acid and pepsin secretion were evaluated in conscious dogs with a gastric fistula. Histamine stimulated the acid secretion dose-dependently, whereas pepsin secretion was decreased by the high doses of histamine. The acid secretion was inhibited slightly by serotonin, with a maximum of 42% with a dose of 10 micrograms/kg/min. The pepsin secretion was only decreased non-significantly by serotonin, 10-15 micrograms/kg/min. The acid inhibition was counteracted by beta-adrenergic antagonists (propranolol, atenolol) and methysergide (serotonergic antagonist). The dose-response analysis showed inhibition of a competitive type. In conclusion, serotonin inhibits histamine-stimulated gastric acid secretion via serotonergic receptors and beta-adrenoceptors, whereas pepsin secretion is unaffected.

Adrenergic beta-Antagonists↗
PubMed1986

Beta-adrenergic agonists inhibit gastric acid and pepsin secretion through somatostatin release in dogs.

The purpose of the present study was to evaluate whether the inhibitory effects of beta-adrenergic agonists on gastric secretory activity in vivo could be mediated through a local release of somatostatin. The gastric secretion was measured during continuous stimulation with pentagastrin (1 microgram/kg/h). The infusion of isoprenaline (beta 1 + beta 2), salmefamol (beta 2), and somatostatin produced inhibitory effects on both acid and pepsin secretion. The reaction patterns were similar for isoprenaline and somatostatin, whereas salmefamol induced an inhibition of longer duration and with dissimilar dose-response kinetics. The gastric somatostatin release was significantly increased after infusion of both beta-adrenergic agonists and somatostatin, with patterns similar to those obtained for the secretory inhibition. There was a significant correlation between the somatostatin release and the acid and pepsin secretion during infusion of the secretory inhibitors but not in the control state. This study shows that beta-adrenergic agonists have inhibitory effects on gastric secretion in vivo similar to those of somatostatin. Both somatostatin and the beta-adrenergic agonists stimulated the release of somatostatin from the gastric mucosa. beta-Adrenergic antagonists were without effects. Somatostatin thereby fulfils the requirements for an endogenous mediator of the beta-adrenergic inhibition.

Adrenergic beta-Agonists↗
PubMed1986

Effect of serotonin on bethanechol-stimulated gastric pepsin secretion in dogs.

The effect of serotonin on bethanechol-stimulated gastric pepsin secretion was evaluated with regard to dose-response kinetics and receptor mediation. A low dose of exogenous serotonin produced a stimulation (0.5 microgram/kg/min), whereas inhibition was found for higher doses (5-10 micrograms/kg/min). The inhibition was non-competitive and could be significantly counteracted by beta-adrenergic blocking drugs. This study confirms results obtained during pentagastrin stimulation and supports the concept that serotonin acts via sympathetic nerves to release noradrenaline.

Adrenergic beta-Antagonists↗
PubMed1986

Effect of serotonin on bethanechol-stimulated gastric acid secretion and gastric antral motility in dogs.

The purpose of the present study was to evaluate the effect of serotonin on bethanechol-stimulated gastric acid secretion and antral motility in conscious dogs with gastric fistula. Bethanechol stimulated the acid secretion dose-dependently and maintained the frequency and strength of the antral contractions at a high level. Serotonin inhibited the acid secretion dose-dependently, whereas the antral motility was stimulated. The acid inhibition was blocked by propranolol, and dose-response analysis showed inhibition of a non-competitive type. This study thereby shows that serotonin inhibits bethanechol-stimulated gastric acid secretion similarly to salmefamol (beta 2-adrenergic agonist)--that is, dose-dependently and non-competitively. Serotonin has been proposed to be a mediator of the beta-adrenergic influence on gastric function in vivo, but the counteracting effect of propranolol and the stimulatory effect of serotonin on motility contradict this hypothesis.

Animals↗
PubMed1986

Effect of somatostatin on histamine-stimulated gastric acid and pepsin secretion in dogs.

The purpose of the present study was to evaluate the effect of somatostatin on gastric acid secretion and pepsin secretion in conscious dogs with gastric fistula. Infusion of histamine stimulated dose-dependently the acid secretion, whereas pepsin secretion was decreased by the high doses of histamine. Somatostatin inhibited dose-dependently the stimulated acid secretion but only with a maximum of 40%. The pepsin secretion was inhibited by somatostatin dose-dependently and with a higher potency. The acid inhibition was of a competitive type and prostaglandin-independent.

Animals↗