A case-control study of drug risk factors for age-related macular degeneration.

OBJECTIVE: To investigate the association between age-related macular degeneration (AMD) and exposure to antacids, antithyroids, thyroid hormones, and thiazide diuretics. DESIGN: Matched case-control study. PARTICIPANTS: Population-based participants were selected from the United Kingdom General Practice Research Database. A total of 18,007 people with diagnosed AMD were compared with 86 169 controls matched for age, gender, and general practice. METHODS: Conditional logistic regression was used to determine the association between exposure to each drug group of interest and a diagnosis of AMD, adjusting for relevant confounding variables. MAIN OUTCOME MEASURES: The primary outcome was the odds ratio for the association between exposure to antacids, antithyroids, thyroid hormones, or thiazide diuretics and AMD. Secondary analyses were conducted to assess the effect of recent exposure to the drugs of interest, the total number of prescriptions received, and restricting the data set to participants with more than 2 years of observation time. RESULTS: The crude odds ratios for association between any record of drug exposure and AMD were as follows: 1.34 (95% confidence interval [CI], 1.29-1.39) for antacids; 1.15 (95% CI, 0.92-1.44) for antithyroids; 1.34 (95% CI, 1.29-1.39) for thyroid hormones; and 1.13 (95% CI, 1.08-1.17) for thiazide diuretics. After adjusting for consultation rate, observation time, diabetes, heart failure, hyperlipidemia, cardiovascular drug use, atherosclerosis, hypertension, aspirin use, hormone replacement therapy use, body mass index, alcohol consumption, and smoking, the odds ratios reduced to: 1.06 (95% CI, 1.02-1.10) for antacids, 0.98 (95% CI, 0.78-1.24) for antithyroids, 0.99 (95% CI, 0.92-1.06) for thyroid hormones, and 0.98 (95% CI, 0.94-1.02) for thiazides. Secondary analyses were consistent with these findings for all 4 drug categories. CONCLUSIONS: No association was detected between short- and medium-term use of antithyroids, thyroid hormones, and thiazide diuretics and the risk of AMD. Short- and medium-term use of antacids seems to be associated with a small increase in the risk of this disease. However, this increased risk is likely the result of residual confounding by smoking or uncontrolled confounding resulting from socioeconomic status. No conclusions could be drawn regarding longer-term use of each drug category

Imbalance between thyroid hormones and the dopaminergic system might be central to the pathophysiology of restless legs syndrome: a hypothesis

Data collected from medical literature indicate that dopaminergic agonists alleviate Restless Legs Syndrome symptoms while dopaminergic agonists antagonists aggravate them. Dopaminergic agonists is a physiological regulator of thyroid-stimulating hormone. Dopaminergic agonists infusion diminishes the levels of thyroid hormones, which have the ability to provoke restlessness, hyperkinetic states, tremors, and insomnia. Conditions associated with higher levels of thyroid hormones, such as pregnancy or hyperthyroidism, have a higher prevalence of Restless Legs Syndrome symptoms. Low iron levels can cause secondary Restless Legs Syndrome or aggravate symptoms of primary disease as well as diminish enzymatic activities that are involved in dopaminergic agonists production and the degradation of thyroid hormones. Moreover, as a result of low iron levels, dopaminergic agonists diminishes and thyroid hormones increase. Iron therapy improves Restless Legs Syndrome symptoms in iron deprived patients. Medical hypothesis. To discuss the theory that thyroid hormones, when not counterbalanced by dopaminergic agonists, may precipitate the signs and symptoms underpinning Restless Legs Syndrome. The main cause of Restless Legs Syndrome might be an imbalance between the dopaminergic agonists system and thyroid hormones

TSH-CHECK-1 test: diagnostic accuracy and potential application to initiating treatment for hypothyroidism in patients on anti-tuberculosis drugs.

Thyroid-stimulating hormone (TSH) promotes expression of thyroid hormones which are essential for metabolism, growth, and development. Second-line drugs to treat tuberculosis (TB) can cause hypothyroidism by suppressing thyroid hormone synthesis. Therefore, TSH levels are routinely measured in TB patients receiving second-line drugs, and thyroxin treatment is initiated where indicated. However, standard TSH tests are technically demanding for many low-resource settings where TB is prevalent; a simple and inexpensive test is urgently needed

The potential usage of thyroid hormones as sport doping - a mini-review

A thyroid gland is one of the most important organs of a human body. Thyroid hormones, at least in physiological concentration, have anabolic features. The aid of this review is to summarize knowledge on potential usage of thyroid hormones in sport doping.             Thyroid hormones play a crucial role in skeletal muscles physiology. The exposition to T3 and T4 may improve myogenesis, muscles regeneration and muscles blood blow. In a long-time perspective, those hormones may help in reducing body weight.             According to those mechanisms, thyroid hormones may be considered as a plausible agent in sport doping. However WADA guidelines does not include T3 or T4 in a list o sport doping substances, the debate on their inclusion is on-going, and the physicians should be aware of thyroid hormones effects on human metabolism from sports medicine perspective

Thyroid hormone status within the physiological range affects bone mass and density in healthy men at the age of peak bone mass

Context: The hormonal factors involved in the regulation of peak bone mass (PBM) in men have not been fully investigated. Apart from gonadal steroids and somatotropic hormones, thyroid hormones are known to affect bone maturation and homeostasis and are additional candidate determinants of adult bone mass. Objective: We aimed to investigate between-subject physiological variation in free and total thyroid hormone concentrations, TSH, and thyroid binding globulin (TBG) in relation to parameters of bone mass, geometry, and mineral density in healthy men at the age of PBM. Design and setting: We recruited 677 healthy male siblings aged 25-45 years in a cross-sectional, population-based study. Areal and volumetric bone parameters were determined using dual-energy x-ray absorptiometry (DXA) and peripheral quantitative computed tomography (pQCT). Total and free thyroid hormones, TBG, and TSH were determined using immunoassays. Results: Free and total thyroid hormone concentrations were inversely associated with bone mineral density (BMD) and bone mineral content (BMC) at the hip and total body (free triiodothyronine (FT(3)), total T(3) (TT(3)), and total T(4) (TT(4))) and at the spine (FT(3)). TBG was negatively associated with BMC and areal BMD at all sites. At the radius, cortical bone area was inversely associated with TT(3), TT(4), and TBG, and trabecular bone density was inversely associated with free thyroxine, TT(4), and TBG. We observed inverse associations between cortical bone area at the mid-tibia and FT(3), TT(3), TT(4), and TBG. No associations between TSH and DXA or pQCT measurements were found. Conclusion: In healthy men at the age of PBM, between-subject variation in thyroid hormone concentrations affects bone density, with higher levels of FT(3), TT(3), TT(4), and TBG being associated with less favorable bone density and content

Revisiting thyroid hormones in schizophrenia

Thyroid hormones are crucial during development and in the adult brain. Of interest, fluctuations in the levels of thyroid hormones at various times during development and throughout life can impact on psychiatric disease manifestation and response to treatment. Here we review research on thyroid function assessment in schizophrenia, relating interrelations between the pituitary-thyroid axis and major neurosignaling systems involved in schizophrenia’s pathophysiology. These include the serotonergic, dopaminergic, glutamatergic, and GABAergic networks, as well as myelination and inflammatory processes. The available evidence supports that thyroid hormones deregulation is a common feature in schizophrenia and that the implications of thyroid hormones homeostasis in the fine-tuning of crucial brain networks warrants further research.The present work was supported by Grant POCI/SAUESP/58757/2004 from the Portuguese Science Foundation (FCT/FEDER). NCS was supported by the fellowship SFRH/ BPD/51057/2010 by FCT

THE RELATIONSHIP BETWEEN ANTI-THYROIDAL PEROXIDISE ANTIBODIES AND THYROID HORMONES (T3, T4 AND THYROID STIMULATING HORMONE TSH) AMONG PATIENTS WITH AUTOIMMUNE THYROID DISEASE

Objectives: This Study was designed to investigate the role of the auto antibodies against thyroid peroxidise (TPO-Abs) and thyroid Hormones (T3, T4, TSH) in pathogenesis of Autoimmune Thyroid Disease (AITD). Methodology: Blood parameters of (90) individual who were attended to hormonal centre at AlSadder Medical City, in the period from January 2013 to June 2013 were measured, which includes Ttriiodothyronine (T3), Thyroxine or Tetraiodothyronine (T4), Thyroid Stimulating Hormone (TSH) and auto antibodies of thyroid peroxidise (TPO-Abs), the biostatic use difference between the maximum and minimum values (range). Results: the search results showed no significant increase in the rate of thyroid hormones (T3, T4, TSH) (p>0.2). Conclusion: The auto antibodies of thyroid peroxidise has no rule in function of thyroid hormones

THE RELATIONSHIP BETWEEN ANTI-THYROIDAL PEROXIDISE ANTIBODIES AND THYROID HORMONES (T3, T4 AND THYROID STIMULATING HORMONE TSH) AMONG PATIENTS WITH AUTOIMMUNE THYROID DISEASE

Objectives: This Study was designed to investigate the role of the auto antibodies against thyroid peroxidise (TPO-Abs) and thyroid Hormones (T3, T4, TSH) in pathogenesis of Autoimmune Thyroid Disease (AITD). Methodology: Blood parameters of (90) individual who were attended to hormonal centre at AlSadder Medical City, in the period from January 2013 to June 2013 were measured, which includes Ttriiodothyronine (T3), Thyroxine or Tetraiodothyronine (T4), Thyroid Stimulating Hormone (TSH) and auto antibodies of thyroid peroxidise (TPO-Abs), the biostatic use difference between the maximum and minimum values (range). Results: the search results showed no significant increase in the rate of thyroid hormones (T3, T4, TSH) (p>0.2). Conclusion: The auto antibodies of thyroid peroxidise has no rule in function of thyroid hormones

Hyperthyroidism

Excess level of thyroid hormones in blood is thyrotoxicosis, which is responsible for clinical syndrome of hypermetabolism, sympathetic hyperactivity. Hyperthyroidism is the term used to denote the overproduction of thyroid hormones from the thyroid gland. Hyperthyroidism is possible with hyperactive thyroid gland due to multi/solitary nodular thyroid disease or Grave’s disease. Thyrotoxicosis associated with thyroiditis is not hyperthyroidism. Treatment of hyperthyroidism is with anti-thyroid drugs (ATT), radio-active iodine ablation (RAI), or thyroid surgery; whereas, treatment of thyroiditis is symptomatic