Central nervous system , thyroid

Toxicology. Disulfiram affects the central nervous system, thyroid, and skin in combination with alcohol it causes an Antabuse-alcohol syndrome. 

It has also been mentioned that salt iodization efficacy, the preferred strategy for IDD, might be influenced by ID, because this disorder impairs thyroid metabolism (WHO, 2001, Zimmermann et al., 2000). It has been observed that two initial steps in thyroid hormone synthesis are catalyzed by Fe-dependent thyroid peroxidase (TPO). One Fe-defl-ciency anemia study in rats showed reduced TPO activity, and decreased plasma T4 and triiodothyronine (T3) levels (Hess et al, 2002). IDA may also alter the central nervous systems thyroid metabolism control, and reduce T4 to T3 peripheral conversion (Beard etal, 1998), modify nuclear T3 binding (Smith et al, 1994), and increase circulating thyrotropin (TSH) (Beard et at, 1990). The therapeutic response to oral iodized oil is impaired in children with IDA compared with Fe-sufficient children (Zimmermann et al, 2000). 

Intermediate-duration inhalation exposure data in rats, mice, and monkeys have identified the lungs, hematological system, liver, central nervous system, thyroid, and possibly the thymus in female rats, as the target organs (Ingle 1953 Khasawinah et al. 1989 Velsicol Chemical Co. 1984). 

All OCPs are polytropic, parenchymatous poisons, afflicting the central nervous system, liver, kidneys, the heart muscle, the stomach and intestines, and the endocrine system (mostly the adrenal glands, thyroid, and ovaries). Morphological changes in warm-blooded creatures poisoned by OCPs vary from insignificant disruptions in circulation and reversible dystrophy to focal necroses these effects depend on the organism, the dose of OCP, how long the OCP remains active, as well as on other factors [9, 39, 40, A47, A79]. 

Substance-Induced Anxiety Disorder. Numerous medicines and drugs of abuse can produce panic attacks. Panic attacks can be triggered by central nervous system stimulants such as cocaine, methamphetamine, caffeine, over-the-counter herbal stimulants such as ephedra, or any of the medications commonly used to treat narcolepsy and ADHD, including psychostimulants and modafinil. Thyroid supplementation with thyroxine (Synthroid) or triiodothyronine (Cytomel) can rarely produce panic attacks. Abrupt withdrawal from central nervous system depressants such as alcohol, barbiturates, and benzodiazepines can cause panic attacks as well. This can be especially problematic with short-acting benzodiazepines such as alprazolam (Xanax), which is an effective treatment for panic disorder but which has been associated with between dose withdrawal symptoms. 

Other Systemic Effects. Studies in animals revealed that a number of other tissues besides liver, kidney, and the central nervous system can be affected by carbon tetrachloride, including the adrenals, pancreas, testes, pituitary, spleen and thyroid (Chatterjee 1966 De Castro et al. 1978 de Toranzo et al. 1978b Itoh et al. 1985 Kalla and Bansal 1975 Reuber and Glover 1970). However, effects on these tissues have been reported only after exposure to relatively high doses of carbon tetrachloride, indicating that these tissues are not as sensitive to carbon tetrachloride as liver, kidney, and brain. 

Angiotensin II, administered into the central nervous system, increases the release of luteinizing hormone, adrenocortical hormone, thyroid-releasing hormone, (3-endorphin, vasopressin, and oxytocin from the anterior pituitary. In contrast, centrally administered angiotensin II inhibits the release of anterior pituitary growth hormone and prolactin. 

Medical history and a physical examination should be completed for every patient. Given the physiological changes during ECT, the physical examination should include assessment of the airway, cardiovascular, pulmonary, and central nervous systems. Eaboratory examinations may include a blood count, liver and thyroid function tests, urine analysis, and electrocardiogram (EKG). Other investigations such as skeletal X-ray, completed tomographic (CT) scan of the... 

There is no such clear cut difTcrcnlialiun as metamorphosis in the mammal, but development is an extremely complex process and has been shown to depend upon the presence of adequate amounts of thyroid hormones. Deficient development, especially of the central nervous system, is marked in ehildren suffering from thyroid deficiency early in life, ansi this inadequacy cannot be overcome completely by medication commenced after the first few weeks. In the adult, thyroxine is important in the maintenance of energy turnover in most of the tissues of the body, such as the heart, skeletal muscle, liver, and kidney, Other physiological functions, most notably brain aclivity and reproduction, are also dependent upon thyroxine, although the metabolic rales of the tissues concerned in these functions do not seem to be altered. 

Fifth, certain kallikreins, such as human kallikrein 6, are highly expressed in the central nervous system. It has previously been shown that hK6, and possibly some other kallikreins, are implicated in inflammatory reactions within the central nervous system that lead to demyelination. The association of hK6 and some other kallikreins with AD and multiple sclerosis points to the possibility that some of these enzymes may play important roles within the central nervous system. In addition, many of these enzymes have been found in endocrine tissues such as the islets of Langerhans, thyroid, pituitary, and others, pointing to the possibility that they may participate in prohormone or hormone processing. 

Such events show how the immune, endocrine and central nervous systems are integrated in their responses to any form of stress. It is well established that physical or psychosocial stress causes increased secretions of prolactin, growth hormones, thyroid, and gonadal hormones, in addition to ACTH. Endogenous opioids are secreted under such conditions and function as immunomodulators, while also elevating the pain threshold. Receptors for such hormones exist on immunocompetent cells, along with receptors for catecholamines, serotonin and acetylcholine. 

B27. Burke, J. S., Waldeyer s ring, sinonasal region, salivary gland, thyroid gland, central nervous system and other extranodal lymphomas and lymphoid hyperplasias. In Neoplastic Hematopathology (D. M. Knowles, ed.), pp. 1351-1389. Lippincott Williams Wilkins, Philadelphia, PA, 2001. 

Cancer is uncommon during the first two decades of life, but is nonetheless a substantial concern. In the United States, cancer is diagnosed in approximately 12 400 children and adolescents annually and is the most common cause of death from any kind of disease between 1 and 19 years of age. In the United States and other developed countries, lymphoid neoplasms (leukaemia, lymphoma) and cancers of the central nervous system are the most common paediatric malignancies. Other kinds of childhood tumours include embryonal tumours of the retina, sympathetic nervous system, kidney, and liver tumours of bone and soft connective tissues and certain gonadal neoplasms. Different kinds of cancer (e.g. carcinomas of liver or thyroid) may predominate in children in parts of the world where specific environmental risk factors are more prevalent. 

In addition to the obvious deactivating role of deiodinases, there has been recent evidence that a relationship exists between regulation of deiodination of thyroid hormones in target cells and the intracellular effects of T4 and T3 on pituitary and hypothalamus function. In the rat pituitary, and probably the human, type-II deiodinase-catalyzed conversion of T4 to T3 is a prerequisite for inhibition of TRH release. rT3, produced from T4 by type-III deiodinase, is a potent inhibitor of type-II deiodinase. In a postulated regulatory circuit, rT3 formed from T4 by type-III deiodinase in surrounding CNS (Central Nervous System) tissue enters the pituitary and inhibits type-II enzyme. The resulting decrease in T3 concentration, in turn, causes an increase in TSH secretion49. 

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