High (but Not Low) Urinary Iodine Excretion Is Predicted by Iodine Excretion Levels from Five Years Ago

Background: It has not been investigated whether there are associations between urinary iodine (UI) excretion measurements some years apart, nor whether such an association remains after adjustment for nutritional habits. The aim of the present study was to investigate the relation between iodine-creatinine ratio (ICR) at two measuring points 5 years apart. Methods: Data from 2,659 individuals from the Study of Health in Pomerania were analyzed. Analysis of covariance and Poisson regressions were used to associate baseline with follow-up ICR. Results: Baseline ICR was associated with follow-up ICR. Particularly, baseline ICR >300 mu g/g was related to an ICR >300 mu g/g at follow-up (relative risk, RR: 2.20; p < 0.001). The association was stronger in males (RR: 2.64; p < 0.001) than in females (RR: 1.64; p = 0.007). In contrast, baseline ICR <100 mu g/g was only associated with an ICR <100 mu g/g at follow-up in males when considering unadjusted ICR. Conclusions: We detected only a weak correlation with respect to low ICR. Studies assessing iodine status in a population should take into account that an individual with a low UI excretion in one measurement is not necessarily permanently iodine deficient. On the other hand, current high ICR could have been predicted by high ICR 5 years ago. Copyright (C) 2011 S. Karger AG, Base

Merck AG Thyroid Symposium - Subclinical hyperthyroidism

Subclinical hyperthyroidism is defined as a situation where the levels of the peripheral thyroid hormones are normal but serum thyrotropin (TSH) is low. It is not a rare finding; rates between 0.2% and 11.8% have been reported in different groups, according to age, sex, etc. The etiology is usually the same as that of overt hyperthyroidism, The health implications include general symptoms, effects on the cardiovascular system, and decreased bone density. The increased frequency of atrial fibrillation and the increased mortality reported are especially serious. It is not clear whether subclinical hyperthyroidism should be treated or not. Most authors conclude that treatment is required in selected cases or in special circumstances

Experimental nephritis: One of the earliest publications on the subject by a pioneer of neohippocratism

From the beginning of the 20th century, cumulative experimental work has provided considerable evidence for the possible immune mechanisms by which certain diffuse glomerular diseases develop. The first classic well-documented studies are attributed to Masugi and his research team (1933), whose experimental model involved the induction of glomerulonephritis by the administration of antikidney sera. However, 23 years earlier, in 1910, Alexander Cawadias had published a monograph on the same subject, for which he was honored with the Medal of the Paris University School of Medicine. In his study, Cawadias concluded that the mechanism of experimental nephritis was multifactorial and that the progression and the aggravation of uremic disease was caused by the production of nephrotoxins and/or antibodies against renal tissue. Cawadias referred to ‘a new colloid substance’, a kind of autoantibody in the context of anaphylaxis; he can be credited with foreseeing the modern era of the autosensitivity and immunology of renal diseases. Although Cawadias is well-known as a pioneer of Neohippocratism, his contribution to experimental nephritis has not been amply appreciated; he merits better recognition as one of the pathfinders in the field of renal immunopathogenesis

Lack of substantial effects of raloxifene on thyroxine-binding globulin in postmenopausal women: Dependency on thyroid status

Long-term estrogen therapy can modify thyroid hormone kinetics by increasing serum concentration of thyroxine-binding globulin (TBG). Raloxifene is a recently developed selective estrogen receptor modulator (SERM) for the treatment of osteoporosis, which possesses estrogenic and antiestrogenic properties. In a prospective and randomized study, we investigated the effects of raloxifene on TBG levels and on the serum concentrations of free thyroxine (FT4), thyroxine (T-4), triiodothyronine (T-3), and thyrotropin (TSH) in controls and in patients receiving TSH-suppressive doses of levothyroxine (LT4). Twenty-nine postmenopausal osteopenic (n = 14) and osteoporotic (n = 15) women were investigated over a period of 6 months. Group 1 (n = 15) included control patients and group 2 (n = 14) patients receiving TSH-suppressive dose of LT4. All patients were treated with raloxifene hydrochloride, 60 mg/d, for a period of 6 months. Serum basal TBG values were found higher in Group 1 compared to Group 2 (26.2 2 mug/mL vs. 21.4 2.1 mug/ml; p &lt; 0.01). The TBG levels raised slightly in group 1 from 26.2 2 &lt;mu&gt;g/mL to 28.6 3.1 mug/mL; p &lt; 0.05 (in group 2 from 21.4 2.1 &lt;mu&gt;g/mL to 22.2 2.3 mug/mL, not significant) after 3 months of treatment and failed to show any further significant change until the end of the study. Serum concentrations of T-4, FT4, T-3, and TSH levels changed insignificantly in both groups up to the completion of the study. Moreover, patients remained clinically euthyroid. Our findings may provide evidence that TBG levels, and consequently, thyroid function are not substantially affected by treatment with raloxifene. Additionally, TBG levels may also be influenced by small variations of thyroid function as subclinical hyperthyroidism