Hypothyroidism, secondary

Increased = Decreased N = Normal X = Contraindicated Pregnancy Primary hypothyroidism Secondary hypothyroidism Hyperthyroidism... 

Mather JL, Baycliff CD, Paterson NAM. Hypothyroidism secondary to iodinated glycerol. Can J Hosp Pharm 1993 46 177-8. 

In 50 women taking levothyroxine either for primary thyroid failure or for hypothyroidism secondary to radioiodine treatment for hyperthyroidism, there was no difference between the two groups in terms of bone density at the hip or spine and no difference from the reference population (31). In addition, there was no correlation between bone density and circulating thyroid hormone concentrations or duration of levothyroxine replacement. These findings are reassuring, although large studies of fracture risk are required, in view of previous evidence of an adverse effect of levothyroxine on bone mineral density, especially in post-menopausal women (32). 

Failure of the thyroid to produce sufficient thyroid hormone is the most common cause of hypothyroidism and is known as primary hypothyroidism. Secondary hypothyroidism occurs much less often and results from diminished release of TSH from the pituitary. Treatment of hypothyroidism is achieved by the replacement of thyroid hormone, primarily T4. A synthetic preparation of T4 is available, levothyroxine (Synthroid ), which has been a popular choice for hypothyroidism because of its consistent potency and prolonged duration of action. No toxicity occurs when given in physiological replacement doses. Desiccated animal thyroid is also available at a lesser cost. Overdoses cause symptoms of hyperthyroidism and can be used as a guide in clinical management. Hypothyroidism is not cured by the daily intake of thyroid hormone it is a life-long regimen. 

A patient with clinical hypothyroidism who does not have an elevated serum TSH concentration must have hypothyroidism secondary to either hypothalamic or pituitary disease. A finding of an undetectable TSH level per se does not distinguish these patients from normal because of the insensitivity of the assay. A TRH stimulation test may identify the site of the primary dysfunction, whether pituitary or hypothalamus (see Section 5.3). 

The TSH stimulation is primarily a test of thyroid reserve and has three main applications (1) to identify those patients with minor impairment in thyroid function where the conventional thyroid function tests produce normal results (2) to determine whether or not a patient, who is receiving thyroid therapy for presumed idiopathic myxedema, requires this therapy (3) to distinguish between idiopathic (primary) myxedema from hypothyroidism secondary to pituitary disease. 

If a patient suspected of developing clinical hypothyroidism is investigated only with routine tests, namely total T4, FTI, and the ETR or a similar estimation, there is no way of determining whether the patient has idiopathic myxedema or hypothyroidism secondary to hypothalamic or anterior pituitary disease. The distinction should be made, however, because it is dangerous to treat pituitary hypothyroidism with thyroid hormone without simultaneously treating with adrenocortical hormones. 

Within a year of giving birth, 5 to 10 percent of women develop hypothyroidism secondary to postpartum thyroiditis. Initially, thyroid hormone levels may rise, then either return to normal or drop to hypothyroid levels. Of those women who become hypothyroid, about 20 percent will require lifelong treatmenL... 

Disorders of lipoprotein metabolism involve perturbations which cause elevation of triglycerides and/or cholesterol, reduction of HDL-C, or alteration of properties of lipoproteins, such as their size or composition. These perturbations can be genetic (primary) or occur as a result of other diseases, conditions, or drugs (secondary). Some of the most important secondary disorders include hypothyroidism, diabetes mellitus, renal disease, and alcohol use. Hypothyroidism causes elevated LDL-C levels due primarily to downregulation of the LDL receptor. Insulin-resistance and type 2 diabetes mellitus result in impaired capacity to catabolize chylomicrons and VLDL, as well as excess hepatic triglyceride and VLDL production. Chronic kidney disease, including but not limited to end-stage... 

Inherited defects in lipoprotein metabofism lead to the primary condition of either hypo- or hyperlipoproteinemia (Table 26-1). In addition, diseases such as diabetes mellitus, hypothyroidism, kidney disease (nephrotic syndrome), and atherosclerosis are associated with secondary abnormal hpoprotein patterns that are very similar to one or another of the primary inherited conditions. Virtually all of the primary conditions are due to a defect at a stage in hpoprotein formation, transport, or destruction (see Figures 25—, 26-5, and 26-6). Not all of the abnormafities are harmful. 

Inherited defects in hpoprotein metabofism lead to a primary condition of hypo- or hyperfipoproteinemia. Conditions such as diabetes meUitus, hypothyroidism, kidney disease, and atherosclerosis exhibit secondary abnormal hpoprotein patterns that resemble certain primary conditions. 

Damage and destruction of the pituitary gland may result in secondary hypothyroidism, hypogonadism, adrenal insufficiency, growth hormone deficiency, hypoprolactinemia, or... 

Pituitary failure (secondary hypothyroidism) is an uncommon cause resulting from pituitary tumors, surgical therapy, external pituitary radiation, postpartum pituitary necrosis, metastatic tumors, tuberculosis, histiocytosis, and autoimmune mechanisms. 

Most patients with pituitary failure (secondary hypothyroidism) have clinical signs of generalized pituitary insufficiency such as abnormal menses and decreased libido, or evidence of a pituitary adenoma such as visual field defects, galactorrhea, or acromegaloid features. 

Pituitary failure (secondary hypothyroidism) should be suspected in a patient with decreased levels of T4 and inappropriately normal or low TSH levels. 

Replacement therapy of hypothyroidism. Whether primary, i.e caused by thyroid disease, or secondary, i.e resulting from TSH deficiency, hypothyroidism is treated by oral administration of T4. Since too rapid activation of metabolism entails the hazard of cardiac overload (angina pectoris, myocardial infarction), therapy is usually started with low doses and gradually increased. The final maintenance dose required to restore a euthyroid state depends on individual needs (approx. 

Hyperlipidemia, secondary causes Prior to initiating therapy, exclude secondary causes of hyperlipidemia (eg, poorly controlled diabetes mellitus, hypothyroidism, nephrotic syndrome, dysproteinemias, obstructive liver disease, other drug therapy, alcoholism) and measure total-C, HDL-C, and triglycerides. 

Thyrotropin-releasing hormone, or protirelin, consists of three amino acids. TRH (Relefact TRH) is used for tests to distinguish primary from secondary hypothyroidism (see Chapter 65). 

Secondary hypothyroidism, or pituitary hypothyroidism, is the consequence of impaired thyroid-stimulating hormone (TSH) secretion and is less common than primary hypothyroidism. It may result from any of the causes of hypopituitarism (e.g., pituitary tumor, postpartum pituitary necrosis, trauma). Patients with secondary hypothyroidism exhibit undetectable or inappropriately low serum TSH concentrations. In secondary hypothyroidism, a normal thyroid gland lacks the normal level of TSH stimulation necessary to synthesize and secrete thyroid hormones. Such patients usually also have impaired secretion of TSH in response to exogenous thyrotropin-releasing hormone (TRH) administration. 

Patients with secondary or tertiary hypothyroidism are also usually treated with thyroxine, but the serum TSH concentration is not a reliable guide to therapy. The efficacy of thyroid hormone replacement in these patients must be assessed clinically and by measurement of the serum T4 concentration. 

Calcium play vital role in excitation - contraction coupling in myocardium. Calcium mediates contraction in vascular and other smooth muscles. Calcium is required for exocytosis and also involved in neurotransmitters release. Calcium also help in maintaining integrity of mucosal membranes and mediating cell adhesions. Hypercalcemia may occur in hyperthyroidism, vitamin D intoxication and renal insufficiency, which can be treated by administration of calcitonin, edetate sodium, oral phosphate etc. Hypocalcemia may occur in hypothyroidism, malabsorption, osteomalacia secondary to leak of vitamin D or vitamin D resistance, pancreatitis and renal failure. Hypocalcemia can be treated by chloride, gluconate, gluceptate, lactate and carbonate salts of calcium. 

Hypothyroidism, a condition in which the circulating concentrations of thyroid hormones are too low, is the most prevalent thyroid disease. Primary hypothyroidism, the commonest form, is an autoimmune disease (Hashimoto s thyroiditis) often associated with goitre. Like other autoimmune diseases, it is more prevalent in women (4 per 1000) than in men (1 per 1000). Other causes include thyroidectomy, radioac tive ablation and, in some countries, iodine deficiency. Hypothyroidism can also be caused by several drugs, including lithium, interleukin-2 and interferon. Secondary hypothyroidism is a disease caused by decreased secretion of TSH by the pituitary. 

The adverse effects associated with tositumomab therapeutic regimen include anemia, thrombocytopenia, neutropenia, infections, hemorrhage and allergic reactions. Increased risk of secondary neoplasia and myelodysplasia has also been reported with this regimen. Other side effects produced by tositumomab therapy include pneumonia, pleural effusion and dehydration, GI discomfort and infusional toxicity. Delayed adverse reactions include hypothyroidism and HAMA. 

Peak serum thyrotropin levels occur 20-30 seconds after intravenous TRH injection in healthy individuals. In hyperthyroidism, the serum thyrotropin level is suppressed. In primary hypothyroidism, thyrotropin levels are high and the thyrotropin response to TRH may be accentuated. In secondary (pituitary) hypothyroidism, serum thyrotropin levels are "inappropriately" normal or low (using a sensitive TSH assay) TSH often fails to rise after TRH administration. In tertiary (hypothalamic) hypothyroidism, the baseline serum thyrotropin level may be normal or low and the thyrotropin response to TRH may be normal or blunted. 

Many of the adverse effects of lithium can be ascribed to the action of lithium on adenylate cyclase, the key enzyme 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, hypothyroidism 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. 

Kelling et al. (1987) assessed the effects of 2,3,7,8-TCDD on cardiac function tests in male Sprague-Dawley rats 7 days after single oral doses of 6.25, 25, or 100 g/kg. At 100 g/kg (near-lethal dose), an increased sensitivity to the inotropic (left atrium) and chronotropic (right atrium) effects of isoproterenol were observed. Three daily oral doses of 40 g/kg caused decreased heart rate, depressed blood pressure, and increased myocardial peroxidase activity in rats (Hermansky et al. 1988). All of these effects may have been secondary to the modulation of adenylate cyclase activity at -adrenergenic receptors as a result of hypothyroidism (Hermansky et al. 1987). 

F, H, Heidenumn, P. Strubbe, and W. Beck. Transient secondary hypothyroidism... 

Secondary hypothyroidism results from an underproduction of thyroid hormones from the thyroid caused by deficient thyroid-stimulating hormone (TSH) stimulation by the pituitary. 

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