In several studies on patients with rheumatoid arthritis, an association of bone loss with a persistently high disease activity has been found. The aim of our study was to investigate the relation between disease activity and serum levels of vitamin D metabolites, parathyroid hormone (PTH), and parameters of bone turnover in patients with rheumatoid arthritis. A total of 96 patients (83 women and 13 men) were divided into three groups according to disease activity measured by serum levels of C-reactive protein (CRP). In the whole group, serum levels of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) (P < 0.001) and PTH (P < 0.05) were negatively correlated to disease activity. The urinary excretion of collagen crosslinks--pyridinoline (Pyd) (P < 0.001) and deoxypyridinoline (Dpd) (P < 0.05)--showed a positive correlation with disease activity. The inverse correlation between serum 1,25(OH)2D3 and disease activity was separately evident in patients with (P < 0.001) and without (P < 0.01) glucocorticoid treatment, in pre- (P < 0.01) and postmenopausal (P < 0.001) women, and in men (P < 0.01). 1,25(OH)2D3 and PTH serum levels were positively correlated to serum bone alkaline phosphatase (ALP) (P < 0.01). The results indicate that high disease activity in patients with rheumatoid arthritis is associated with an alteration in vitamin D metabolism and increased bone resorption. The decrease of 1,25(OH)2D3 levels in these patients may contribute to a negative calcium balance and inhibition of bone formation. Furthermore, low levels of 1,25(OH)2D3 as an endogenous immunomodulator suppressing activated T cells and the proliferation of cells may accelerate the arthritic process in rheumatoid arthritis.

The are various opinions about the optimal therapy of endemic goiter in adolescents. From 106 patients (75 girls) suffering from endemic goiter 50 patients (group A) were treated with 300 micrograms iodine per day and 56 patients (group B) with 100 micrograms iodine plus 100 micrograms levothyroxine per day. Before therapy and after 172 days of therapy on average the thyroid volume, the thyroid hormones (TSH, T3, T4) and the lipidparameters (cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides) were measured. Within the period of treatment the thyroid volume (measured by ultrasound) decreased by 11.3% in group A and by 23% in group B. The iodine deficiency was corrected completely in both groups. However, investigations in both groups proved that patients undergoing combined therapy excrete the iodine administered additionally. Analogously to studies of the intrathyreoidal iodine metabolism it can be concluded that combined therapy on the basis of the dose mentioned above does either not result in an increase in the intrathyreoidal iodine contents or in a minor increase only. Iodine treatment as well as combined treatment cause a decrease in TSH-levels and an increase in T4-levels. The changes are only significant in group B. In the total group the percentage of T3-increases was reduced from 45% to 33% during treatment. The initially elevated plasma concentration of cholesterol, LDL-cholesterol and triglycerides - compared to the control group - decreased significantly in both groups during therapy. Both groups does not differ significantly with respect to the decrease in lipids. It is to be concluded that combination therapy is preferable to iodine therapy with respect to the SD-volume reduction as well as the lipid metabolism. The primary cause of endemic goiter, i.e. the intrathyreoidal iodine deficiency, can presumably not be eliminated by means of the dose of 100 micrograms iodine combined with 100 micrograms LT4.

An investigation was carried out in to thyroid hormones (TSH, T3, T4) and lipid parameters (total cholesterol, LDL cholesterol, HDL cholesterol, triglyceride) in 136 adolescents (94 femals, average age 13 years). An iodine deficiency (grade II-II) with respect to the daily urine excretion per 1,73 m2 BSA was found in 75%. With few exceptions the serum levels of TSH and T4 were in the normal range. In 36% of the patients we noticed compensatory elevated T3 levels. Correlations between thyroid hormones TSH, T4, renal iodine excretion and the volume of thyroid glands were not detectable, only T3 showed a dignificant positive correlation to the thyroid gland volume. The average values of lipids in patients were found to be higher than in normals. We consider the changed lipids as a sign of a disturbed efficacy of thyroid hormones. The regional insufficient iodine supply causes goiters and to a high degree the observed hyperchole-sterolemia, too. Our results underline the necessity of a common iodine salt prophylaxis as well as the treatment of "harmless" goiters in puberty.

In 1988 and in 1991, i.e. two and five years after the introduction of a general iod salt supply (32 mg KJO2/kg salt) in our region, we investigated the frequency of goiters and the level of iodine excretion in urine in 504 and 336 school children of 11 to 16 years of age. In 1988 the assessment of goiter size was made by inspection and palpation according to the recommendation of WHO. 36% of the school children were found to have goiters of type I b or II. The average urine excretion of iodine amounted to 46.2 +/- 37.2 micrograms Iod/g creatinine (n = 353). In 1991 we selected school children with goiters by the same criteria and found frequency (34%) to be nearly unchanged compared to 1988. Furthermore we investigated these goiters with ultrasound and confirmed the diagnosis in 100 from 107 children. The average daily urine excretion of iodine was significantly higher in 1991 (57.7 +/- 24.8 micrograms/Iod/g creatinine, n = 328) than in 1988. However this value is below the level recommended by the WHO (minimum 75 micrograms Iod/g creatinine). Despite the increase of the iodine intake over the last years, the frequency of goiters in pubertal school children in the Jena region is endemic. This fact supports the demand for a general and sufficient iodine supply.