Programmed endoscopic follow-up examinations with eventual retreatment in patients locally injected for an acute or recent hemorrhage from a gastric or duodenal ulcer did not influence their outcome when compared to patients receiving only a second endoscopic intervention upon evidence for recurrent hemorrhage. Scheduled control endoscopies cannot be recommended after an initial successful endoscopic treatment of peptic ulcer bleeding when selection of the patients for second-look endoscopy is directed by the Forrest criteria.

The effects of oral iodide, levothyroxine and of iodide and levothyroxine in combination were studied in three groups of 30 children, age 13–15 years, with euthyroid goitre. As endpoints of this study, we used thyroid volume reduction, thyroid hormones, thyrotropin and thyroid grey-scale histograms by computerized analysis. The three groups were well matched with respect to mean age, body weight and pretreatment thyroid volumes and thyroid hormones. Mean urinary iodide excretion before treatment was in the range of 30 μg/g creatinine, since the study was conducted in an iodine-deficient area. All three treatment regimens led to significant reductions in thyroid volume within one month. After six months on 100 μg of levothyroxine, thyroid volume had decreased from 14.1±4.2 ml to 8.3±2.6 2.6ml (mean±sd);on 150 μg of iodide, from 18.5±6.2 ml to 8.8±2.7 ml; and on 100 μg of iodide plus 50μg of levothyroxine, from 17.2±3.1 ml to 8.3±2.0 ml. When treatment was discontinued for three months, or the dosage reduced, thyroid volume increased again in the levothyroxine (to 11.3±2.5 ml) but not in the iodide group. Grey-scale values (by ultrasound, computer-aided estimation) after nine months were significantly different between the three treatment groups; no change was observed with levothyroxine, but after 150 μg of iodide as well as after combined treatment with levothyroxine and iodide there were marked decreases of grey-scale values; this is interpreted as reflecting a decrease in follicle size and colloid content of the thyroid which takes place after iodide supplementation. In conclusion, iodide treatment as well as combined treatment with levothyroxine and iodide lead to volume reduction of juvenile goitre which is quantitatively similar but qualitatively superior compared to the effects of levothyroxine alone.

Substitution of sodium selenite has no beneficial effect on the clinical outcome of patients with acute pancreatitis.

About 90% of all functional thyroid autonomies (FTA) are euthyroid for a prolonged period of time. It is estimated that more than 10% of goiter patients in iodine deficient regions and less than 10% in iodine rich areas have evidence of FTA. After the age of 40, the risk of hyperthyroidism decompensation gradually increases. This risk rises with increasing thyroid volume, nodularity and patient age. In the elderly, hyperthyroidism also occurs in the absence of goiter. After decades of iodine deficiency, especially the intake of unphysiologically high iodine concentrations may result in increased frequencies of hyperthyroidism. In iodine deficient regions, almost half of all cases of hyperthyroidism are FTA related. Following elimination of iodine deficiency, the rate of hyperthyroidism may be reduced below 10%. This will not affect the prevalence of immunogenic hyperthyroidism. The most reliable evidence of FTA is produced using the TcTU supp. test. The highly sensitive TSH0 and the TRH test are 2.5 times less sensitive. Thus, they may still indicate euthyroidism in scintigraphically compensated or decompensated FTA. The TSH0 screening is only recommended with a view to an improved cost/benefit ratio in the elderly, females above the age of 40, and ill persons. Acutely ill and psychiatric patients should be excluded. Already 1 year after the introduction of iodine into the medical treatment of thyroid disorders, Coindet reported in 1821 his epidemiologically relevant clinical observation of an increase in hyperthyroidism, predominantly of the functional autonomy type. In the meantime, detailed and universally accepted knowledge has become available on the pathogenesis and pathophysiology of functional thyroid autonomy (Gerber et al., 1985). Data on the epidemiology of functional autonomy continue to apply only to the regional population they are based on. They allow to draw conclusions on the prevalence and natural course of functional thyroid autonomy (FTA). The different forms and prevalence rates of hyperthyroidism reflect the severity and duration of the nutritional iodine deficiency on one hand and the quality of iodine prophylaxis on the other.