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Thyroid lithium

Consider augmentation ) (non-SSRI antidepressant, lithium, thyroid hormone,... [Pg.810]

People with exposure to anti-thyroid drugs (e.g., lithium), thyroid disease, or otherwise compromised thyroid function might have a more pronounced response to PBBs and PBDEs because of their underlying limitations in thyroid hormone production. Similarly, people with compromised function of other organs, such as those with liver or kidney diseases (e g., liver cirrhosis or hepatitis B), could be considered more susceptible to health effects of PBBs and PBDEs. [Pg.253]

Oakley PW, Dawson AH, Whyte IM. Lithium thyroid effects and altered renal handling. J Toxicol Chn Toxicol 2000 38(3) 333-7. [Pg.676]

No significant interactions have been reported when tiie expectorants are used as directed. The exception is iodine products. Lithium and other antithyroid drug may potentiate the hypotliyroid effects of these drug if used concurrently with iodine products. When potassium-containing medications and potassium-sparing diuretics are administered with iodine products, the patient may experience hypokalemia, cardiac arrhythmias, or cardiac arrest. Thyroid function tests may also be altered by iodine... [Pg.354]

Chorionic gonadotropin. Follicle stimulating hormone Urea, Uric add. Bilirubin, Cortisol, n-Maimitol. n-Glucose, Sodium pyruvate, 4-hydroxy-3-methoxy mandelic add, 4-Nitro-phenol, 17 Amino adds in HQ, Angiotensin-I, Tripahnitin, Bone meal (8 elements), Bone ash (8 elements), lithium carbonate Luteinizing hormone. Thyroid stimulating hormone... [Pg.210]

Lithium is concentrated in the thyroid gland and can impair thyroid hormone synthesis. Although goiter is uncommon, as many as 30% of patients develop at least transiently elevated thyroid-stimulating hormone values. Lithium-induced hypothyroidism is not usually an indication to discontinue the drug. Patients can be supplemented with levothyroxine if continuation of lithium is desired.30... [Pg.597]

Describe the potential effects of amiodarone, lithium, and interferon-a on thyroid function. [Pg.667]

Drugs (amiodarone, radiocontrast media, lithium, a-interferon) Silent thyroiditis (including postpartum)... [Pg.671]

Lithium is associated with hypothyroidism in up to 34% of patients, and hypothyroidism may occur after years of therapy. Lithium appears to inhibit thyroid hormone synthesis and secretion. Patients with underlying autoimmune thyroiditis are more likely to develop lithium-induced hypothyroidism. Patients may require LT4 replacement even if lithium is discontinued. [Pg.682]

Lazarus, J. H., McGregor, A. M., Ludgate, M. et al. Effect of lithium carbonate therapy on thyroid immune status in manic depressive patients a prospective study. /. Affect. Disord. 11 155-160,1986. [Pg.907]

Up to 30% of patients on maintenance lithium therapy develop transiently elevated serum concentrations of thyroid-stimulating hormone, and 5% to 35% of patients develop a goiter and/or hypothyroidism, which is dose-related and more likely to occur in women. This is managed by adding levothyroxine to the regimen. [Pg.788]

Others Acetazolamide Lithium Thiaazides Phenytoin Rash, fever, autoimmunity Dermatitis autoimmune thyroiditis, vasculitis Hypersensitivity, photosensitivity autoimmunity (diabetes) Rash drug-induced SLE, hepatitis... [Pg.551]

Thyroid Hormone (Thyroxine, Synthroid). The most common use of thyroxine in bipolar patients is the treatment of lithium-induced hypothyroidism. Approximately 5% of patients receiving long-term lithium treatment ultimately develop hypothyroidism. When this occurs, the patient with bipolar disorder may present with symptoms of a depressive episode. Therefore, periodic thyroid axis monitoring, that is, a serum thyroid stimulating hormone (TSH) test, is required for all patients taking lithium and should always be performed when the bipolar patient experiences a depressive episode. [Pg.87]

When laboratory testing indicates that a patient with BPAD is clinically hypothyroid, even if lithium is the readily apparent cause, we recommend starting thyroid hormone replacement. Lithium should not be discontinued, particularly if it has otherwise managed the BPAD well. Thyroxine should be started at 50 ag/day. TSH levels can then be checked 6-8 weeks later. The daily dose of thyroxine can be increased in 25 g increments every 1-2 months until TSH levels have normalized. [Pg.87]

The next step in the management of the depressed bipolar patient is to evaluate thyroid function. This is especially important for patients treated with lithium in order to rule out lithium-induced hypothyroidism. When this occurs, the addition of thyroid hormone replacement may relieve the depressive symptoms without any additional changes to the bipolar treatment regimen. [Pg.91]

Many of the adverse effects of lithium can be ascribed to the action of lithium on adenylate cyclase, the key enz)nne that links many hormones and neurotransmitters with their intracellular actions. Thus antidiuretic hormone and thyroid-stimulating-hormone-sensitive adenylate cyclases are inhibited by therapeutic concentrations of the drug, which frequently leads to enhanced diuresis, h)rpoth)n oidism and even goitre. Aldosterone synthesis is increased following chronic lithium treatment and is probably a secondary consequence of the enhanced diuresis caused by the inhibition of antidiuretic-hormone-sensitive adenylate cyclase in the kidney. There is also evidence that chronic lithium treatment causes an increase in serum parathyroid hormone levels and, with this, a rise in calcium and magnesium concentrations. A decrease in plasma phosphate and in bone mineralization can also be attributed to the effects of the drug on parathyroid activity. Whether these changes are of any clinical consequence is unclear. [Pg.203]

Finally, some drugs widely used including lithium, ethionamide, sulfonamides carbutamide, p-aminobenzoic acid, p-aminosalycilic acid, ketoconazole, or phenylbutazone have adverse side effects on the thyroid [26]. [Pg.420]

Lithium therapy necessitates the monitoring of thyroid function every 6-12 months in stabilised patients. Occurrence of symptoms such as lethargy, which may reflect hypothyroidism, should be monitored. [Pg.34]

Lithium ions inhibit thyroxine release. Lithium salts can be used instead of iodine for rapid thyroid suppression in iodine-induced thyrotoxicosis. Regarding administration of lithium in manic-depressive illness, see p. 234. [Pg.246]

Hypothyroidism Hypothyroidism may occur with long-term lithium administration. Patients may develop enlargement of thyroid gland and increased thyroid-stimulating hormone levels. [Pg.1142]


See other pages where Thyroid lithium is mentioned: [Pg.181]    [Pg.271]    [Pg.284]    [Pg.464]    [Pg.181]    [Pg.797]    [Pg.797]    [Pg.181]    [Pg.271]    [Pg.284]    [Pg.464]    [Pg.181]    [Pg.797]    [Pg.797]    [Pg.52]    [Pg.189]    [Pg.72]    [Pg.578]    [Pg.603]    [Pg.671]    [Pg.671]    [Pg.677]    [Pg.161]    [Pg.256]    [Pg.368]    [Pg.10]    [Pg.786]    [Pg.559]    [Pg.591]    [Pg.79]    [Pg.355]    [Pg.204]    [Pg.174]    [Pg.351]   
See also in sourсe #XX -- [ Pg.420 ]




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