Thyrotoxic Crisis: Thyroid Storm
Thyroid storm (thyrotoxic crisis) is a rare but life-threatening condition in which acute severe thyrotoxicosis leads to organ system decompensation. Prompt diagnosis is based on clinical grounds and biochemical evaluation, although there are no specific
- PDF / 187,859 Bytes
- 21 Pages / 439.37 x 666.14 pts Page_size
- 45 Downloads / 203 Views
Thyrotoxic Crisis: Thyroid Storm John J. Reyes-Castano and Kenneth Burman
Pathogenesis The pathogenesis of thyroid storm is still not fully understood as there is usually no difference in thyroid hormone levels between patients with “uncomplicated” thyrotoxicosis and those undergoing a thyrotoxic crisis [1, 2]. One hypothesis that may explain the pathogenesis of thyroid storm is a possible increase in target cell β (beta)-adrenergic receptor density or post-receptor modifications in signaling pathways [3–5] leading to an increased sensitivity to catecholamines. Another theory to explain the cause of thyroid storm is an increase in the amount of free thyroid hormones. In one study comparing six subjects with thyroid storm to fifteen subjects with more typical thyrotoxicosis, Brooks and colleagues [6] found that the mean free thyroxine (FT4) concentration was higher in subjects with thyroid storm, whereas the total thyroxine (TT4) concentration was similar in both groups.
Etiology (See Table 9.1) Graves’ disease remains the most common cause of thyrotoxic crisis/thyroid storm. Graves’ disease is mediated by the thyrotropin (TSH) receptor antibodies that stimulate excess and uncontrolled synthesis and secretion of thyroid hormones (thyroxine
J.J. Reyes-Castano, M.D. Section of Endocrine, Medstar Washington Hospital Center, 110 Irving St NW Suite 2A-72, Washington, DC 20010, USA K. Burman, M.D. (*) Endocrine Section, Georgetown University Medical Center/MedStar Washington Hospital Center, 110 Irving St NW, Suite 2A-72, Washignton, DC 20010, USA e-mail: [email protected] L. Loriaux (ed.), Endocrine Emergencies: Recognition and Treatment, Contemporary Endocrinology 74, DOI 10.1007/978-1-62703-697-9_9, © Springer Science+Business Media New York 2014
77
78
J.J. Reyes-Castano and K. Burman Table 9.1 Etiology of thyrotoxicosis Thyrotoxicosis with a normal or high radioiodine uptakea Autoimmune thyroid disease (AITD) Graves’ disease (GD) Hashitoxicosis Autonomous thyroid tissue Toxic adenoma (TA) Toxic multinodular goiter (TMNG) TSH-mediated TSH producing pituitary adenoma Non-neoplastic TSH-mediated hyperthyroidism Human chorionic gonadotropin-mediated Hyperemesis gravidarum Trophoblastic disease Resistance to thyroid hormone (T3 receptor mutation)b Thyrotoxicosis with a decreased or near-absent radioiodine uptake Thyroiditis Painless (silent, lymphocytic) thyroiditis Subacute (de Quervain’s, granulomatous) thyroiditis Acute thyroiditis Amiodarone-induced thyroiditis Radiation thyroiditis Palpation thyroiditis Exogenous thyroid hormone intake Iatrogenic thyrotoxicosis Factitious ingestion of thyroid hormone Intentional suppressive therapy Ectopic hyperthyroidism Struma ovarii Extensive metastasis from follicular thyroid carcinoma a Uptake may be low if recent iodine load caused iodine-induced thyrotoxicosis b Patients may not be hyperthyroid Source: Adapted from: Bahn R, Burch H, Cooper D, et al. Hyperthyroidism and Other Causes of Thyrotoxicosis: Management Guidelines of the American Thyroid Association an
Data Loading...
