eMedicine Specialties > Emergency Medicine > Toxicology

Toxicity, Thyroid Hormone

Lisandro Irizarry, MD, MPH, FAAEM, Chair, Department of Emergency Medicine, Brooklyn Hospital Center; Assistant Professor, Department of Emergency Medicine, Weill Cornell School of Medicine
Nadine A Youssef, MD, Assistant Professor of Emergency Medicine, Tufts University, Department of Emergency Medicine; Anton A Wray, MD, FACEP,, Clinical Assistant Professor of Emergency Medicine, Weill Cornell Medical College; Attending Physician, Department of Emergency Medicine, Brooklyn Hospital Center

Updated: Jun 3, 2009

Introduction

Background

Iodine is absorbed from the GI tract and is transferred to the thyroid gland where oxidization and incorporation into tyrosyl residues of thyroglobulin occurs. Tyrosine is further oxidized to form monoiodotyrosine (MIT) and diiodotyrosine (DIT). The combination of 2 molecules of DIT forms thyroxine (T4). Triiodothyronine (T3) is made by the combination of MIT and DIT and by the monodeiodination of T4 in the periphery.

T3 is 4 times more active than the more abundant T4. The half-life of T4 is 5-7 days; the half-life of T3 is only 1 day. Approximately 99% of the circulating thyroid hormone is bound to plasma protein and is metabolized primarily by the liver.

Levels of thyroid hormones in the serum are tightly regulated by the hypothalamic-pituitary-thyroid axis. Thyroid-releasing hormone (TRH) is secreted by the hypothalamus, and stimulates the release of thyroid-stimulating hormone (TSH) from the pituitary gland. Mature TSH reaches the thyroid gland and stimulates thyroid hormone production and release. The main hormone secreted from the thyroid gland is T4, which is converted to T3 by deiodinase in the peripheral organs. Secreted thyroid hormone reaches the hypothalamus and the pituitary, where it inhibits production and secretion of TRH and TSH, thereby establishing the hypothalamic-pituitary-thyroid axis.¹

The most common thyroid hormone used clinically is levothyroxine (LT4), which is available in intravenously and orally administered forms to treat hypothyroidism and myxedema coma. Usual dosage ranges from 25-500 mcg/d. The higher doses can be used intravenously to treat myxedema coma.

For related information, see Medscape's Hypothyroidism Resource Center.

Pathophysiology

Pharmacokinetics

Oral absorption of thyroid hormone is erratic (40-80%) and decreases with age. The time for peak serum levels is 2-4 hours. The onset of action for oral administration is 3-5 days and 6-8 hours for IV administration. Thyroid hormone is more than 99% protein-bound, and it is hepatically metabolized to triiodothyronine (the active form). Half-life elimination varies from 6-7 days for euthyroid, 9-10 days for hypothyroid, and 3-4 days for hyperthyroid states. It is excreted in both urine and feces, and this also decreases with age.

Mechanism

Levothyroxine's delayed onset of toxicity is thought to be secondary to the delay in conversion of T4 to T3 and the distribution of T3 into tissues. As a result, symptoms may be delayed, developing anyway from 6 hours to 11 days after ingestion. If the ingested preparation contains T3, clinical symptoms may begin within 24 hours of ingestion. Mixtures of T4 and T3 have immediate and delayed clinical effects. Thus, symptoms can occur anywhere from 6 hours to 11 days after ingestion. 

Mechanism of toxicity involves stimulation of the cardiovascular (CV), GI, and neurologic systems through presumed activation of the adrenergic system. Although the exact mechanism of action is unknown, the metabolic effects of thyroid hormone are thought to be mediated by the control of DNA transcription and protein synthesis. Thyroid hormone is integral to the regulation of normal metabolism, growth, and development. It promotes gluconeogenesis, controls the mobilization and utilization of glycogen stores, increases the basal metabolic rate, and increases protein synthesis at a cellular level.

Frequency

United States

According to the Annual Report of the American Association of Poison Control Centers’ National Poison Data System, in 2007, 12,291 exposures to thyroid hormone preparations were documented; of the total listed, 8,525 were single substance exposures. The breakdown by age for single substance exposures are as follows; 4,823 were associated with children younger than 6 years; 537 were associated with persons aged 6-19 years; and 2715 were associated with those aged older than 19 years. Overall, no major adverse outcomes, and no deaths were reported.²

Mortality/Morbidity

One large retrospective study reported 27,680 cases of thyroid hormone ingestion. Of these cases, 2516 (9.1%) were secondary to suicidal intentions, with only 3 (0.01%) being fatal. Co-ingestants were believed to be the major cause of these fatalities. Among all groups, incidence of a major outcome (described as symptoms that are life threatening or resulting in significant residual disability) was 0.02%.

Race

No scientific data demonstrate that outcomes following a toxic thyroid hormone ingestion are based on race.

Sex

No scientific data demonstrate that outcomes following a toxic thyroid hormone ingestion are based on sex.

Age

Inadvertent excessive thyroid hormone ingestion occurs primarily in pediatric patients.

Clinical

History

Access to thyroid hormone, especially in pediatric or unknown ingestions, is important. 

Physical

Focus the physical examination on findings consistent with symptoms of increased adrenergic activity and on the following signs:

• Acute
  • Abdominal pain
  • Nausea or vomiting
  • Diarrhea
  • Increased appetite
  • Insomnia
  • Anxiousness
  • Agitation
  • Tremor
  • Seizures
  • Weakness
  • Diaphoresis
  • Tachycardia
  • Palpitations
  • Hypertension or hypotension
  • Hyperpyrexia/heat intolerance
  • Confusion
  • Psychosis
  • Hypoglycemia
  • Skin flushing
  • Transient systolic ejection murmurs
  • Pulmonary edema
  • Adrenal insufficiency
• Chronic
  • Weight loss
  • Menstrual irregularities
  • Supraventricular tachycardia (SVT)
  • High-output left ventricular failure
  • Hypotension
  • Hemiparesis
  • Delirium
  • Coma
  • Pneumonia
  • Sepsis
  • Hyperthermia
  • Acute renal failure
  • Myopathy
  • Palmar and plantar desquamation
  • Premature epiphyseal closure in children
  • Craniosynostosis (infants)

Causes

Long-term abuse of thyroid supplements has been reported in obese patients as a method of weight control.

Differential Diagnoses

Workup

Laboratory Studies

• Complete blood count
• Electrolytes (eg, calcium, magnesium, phosphorous)
• Urinalysis
• Urine drug screen
• Arterial blood gas (ABG)
• T3, T4, and T3 resin uptake (RU) levels may be sent 2-6 hours postingestion; however, remember the following:
  • These levels offer no aid in the acute phase of clinical management.
  • These levels are of no value in determining prognosis.

Other Tests

• ECG is indicated to evaluate for myocardial ischemia, infarction, and cardiac dysrhythmias (eg, atrial fibrillation, SVT).

Treatment

Prehospital Care

Prehospital management includes gathering evidence of ingestion, a full initial assessment, oxygen, and IV access as necessary.

Emergency Department Care

Litovitz and White developed the following approach to acute levothyroxine ingestion³ :

• If the ingestion is 0.5 mg or less, discharge the patient home because no gastric decontamination is indicated.
• Ipecac syrup–induced emesis at home is recommended for ingestions occurring within 30 minutes if the amount was between 0.5 and 3 mg. Telephone follow-up daily for the next 5 days.
• Administer activated charcoal in the ED for ingestions more than 3 mg.
• Admit all symptomatic patients and place them on cardiac monitoring.
• Thyroid hormones undergo enterohepatic recycling and significant overdoses have been treated with cholestyramine, a bile sequestrant.

Important treatment points

• Ipecac syrup is no longer recommended for home or hospital treatment.
• Chronic overdose — withdraw drug.
• Use acetaminophen for fever control; aspirin is contraindicated because it displaces T4 from thyroid-binding globulin (TBG), increasing free T4.
• Because of the delayed conversion to T3 and distribution to tissues, patients must be observed and managed for a longer period of time, especially with large overdoses.
• The hypothalamic-pituitary-thyroid axis will return to normal in 6-8 weeks.

Consultations

Consult the regional poison control center or local medical toxicologist (certified through the American Board of Medical Toxicology or the American Board of Emergency Medicine) for additional information and patient care recommendations.

Medication

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

GI decontaminant

Empirically used to minimize systemic absorption of the toxin. May only benefit if administered within 1-2 h of ingestion.

Activated charcoal (Liqui-Char)

Emergency treatment in poisoning caused by drugs and chemicals. Network of pores present in activated charcoal adsorbs 100-1000 mg of drug per gram of charcoal. Does not dissolve in water.
Most useful if used within 4 h of ingestion. Repeated doses may be used, particularly with ingestions of sustained-released agents. May repeat dose q4h at 0.5 g/kg. Alternate with and without cathartic, if used.

Dosing

Adult

1 g/kg PO; not to exceed 50-100 g

Pediatric

1-2 g/kg PO; not to exceed 15-30 g
<2 years: Cathartic not recommended

Interactions

May inactivate ipecac syrup if used concomitantly; effectiveness of other medications decreases with coadministration; do not mix with sherbet, milk, or ice cream (decreases absorptive properties)

Contraindications

Documented hypersensitivity; poisoning or overdose of mineral acids and alkalies; unprotected airway with absent gag reflex

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor for presence of active bowel sounds before readministration to minimize risk of charcoal ileus; not very effective in poisonings of ethanol, methanol, and iron salts; induce emesis before administration; after emesis with ipecac syrup, patient may not tolerate activated charcoal for 1-2 h; can administer in early stages of gastric lavage; without sorbitol, gastric lavage returns are black

Cardiovascular agents

Beta-blockers are administered to counteract the increase in adrenergic activity and treat serious tachyarrhythmias.

Propranolol (Inderal)

Noncardioselective beta-blocker, widely available. DOC in treating cardiac arrhythmias resulting from hyperthyroidism. Controls cardiac and psychomotor manifestations within minutes.
Important added benefit is the inhibition of peripheral conversion of T4 to T3.

Dosing

Adult

0.01-0.1 mg/kg IV q2-5min; titrate to effect

Pediatric

0.05-0.15 mg/kg IV; administer one-half dose and observe; administer remainder in 2 min prn

Interactions

Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase

Contraindications

Documented hypersensitivity; uncompensated congestive heart failure; bradycardia, cardiogenic shock; AV conduction abnormalities

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor closely; monitor BP and HR

Esmolol (Brevibloc)

A short-acting IV cardioselective beta-adrenergic blocker with no membrane depressant activity. Intravenous agent with half-life of 8 min, which allows for titration to effect and quick discontinuation prn.

Dosing

Adult

50-200 mcg/kg/min IV; titrate to effect

Pediatric

300 mcg/kg/min IV with continuous heart rate and blood pressure monitoring to determine onset of beta-blockade (>10% reductions); titrate upward in 50-100 mcg/kg/min increments q10min prn

Interactions

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; cardiotoxicity may increase when administered concurrently with sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents

Contraindications

Documented hypersensitivity; asthma; COPD; CHF; moderate-to-severe left ventricular dysfunction; hypotension <90 mm Hg; bradycardia <60/min; second- and third-degree AV block

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm may worsen when medication is abruptly withdrawn; withdraw drug slowly and monitor patient closely; because of small doses and rapid onset of effects, use volumetric infusion pump when available

Thyroid agents

Thyroid agents are administered to prevent peripheral conversion of T4 to T3.

The US Food and Drug Administration (FDA) has identified 32 cases (22 adult and 10 pediatric) of serious liver injury associated with propylthiouracil (PTU). Of the adults, 12 deaths and 5 liver transplants occurred, and among the pediatric patients, 1 death and 6 liver transplants occurred. PTU is indicated for hyperthyroidism due to Graves disease. These reports suggest an increased risk for liver toxicity with PTU compared with methimazole. Serious liver injury has been identified with methimazole in 5 cases (3 resulting in death). PTU is considered as second-line drug therapy, except in patients who are allergic or intolerant to methimazole, or for women who are in the first trimester of pregnancy. Rare cases of embryopathy, including aplasia cutis, have been reported with methimazole during pregnancy. The FDA recommends the following criteria be considered for prescribing PTU. For more information see the FDA Safety Alert.⁴

• Reserve PTU use during first trimester of pregnancy, or in patients who are allergic to or intolerant of methimazole.
• Closely monitor PTU therapy for signs and symptoms of liver injury, especially during the first 6 months after initiation of therapy.
• For suspected liver injury, promptly discontinue PTU therapy and evaluate for evidence of liver injury and provide supportive care.
• PTU should not be used in pediatric patients unless the patient is allergic to or intolerant of methimazole, and no other treatment options are available.
• Counsel patients to promptly contact their health care provider for the following signs or symptoms: fatigue, weakness, vague abdominal pain, loss of appetite, itching, easy bruising, or yellowing of the eyes or skin.

Propylthiouracil (Propyl-Thyracil)

Derivative of thiourea that inhibits organification of iodine by thyroid gland. Blocks oxidation of iodine in thyroid gland, thereby, inhibiting thyroid hormone synthesis; inhibits T4 to T3 conversion.

Dosing

Adult

Not first-line agent
6-10 mg/kg/d PO divided tid for 5-7 d; not to exceed 1 g

Pediatric

Not first-line agent
<1 year: Not established
1-6 years: 120-200 mg/m²/d PO divided q8h
6-10 years: 50-150 mg/d PO or 5-7 mg/kg/d PO divided q6-8h
>10 years: 150-300 mg/d PO or 5-7 PO mg/kg/d divided q6-8h

Interactions

PTU has antivitamin K activity; may potentiate activity of oral anticoagulants

Contraindications

Documented hypersensitivity; breastfeeding mothers; liver impairment; pediatric patients (unless allergic or intolerant to methimazole and no other treatment is an option)

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Monitor during therapy; may cause hypoprothrombinemia and bleeding; once symptoms of hyperthyroidism have resolved, lower maintenance dose if serum TSH levels are elevated; caution in pregnancy; risk of serious liver injury, including liver failure and death, has been reported in adults and children by the FDA (carefully consider drug therapy, and if PTU initiated, monitor for symptoms and signs of liver injury, especially during first 6 mo of therapy)

Bile acid sequestrants

These agents are utilized to bind thyroid hormone agents, which undergo enterohepatic recycling and reabsorption.

Cholestyramine (Questran)

Forms a nonabsorbable complex with bile acids in the intestine, which, in turn, inhibits enterohepatic reuptake of intestinal bile salts.

Dosing

Adult

3-9 g PO q4-6h (usually 4 g q4h for 4-8 doses)

Pediatric

80 mg/kg PO tid

Interactions

Malabsorption of fat-soluble vitamins and drugs

Contraindications

Documented hypersensitivity; biliary obstruction

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in constipation, phenylketonuria; may cause nausea, abdominal discomfort, steatorrhea, and diarrhea

Antipyretics

Used to treat hyperthermia.

Acetaminophen (Tylenol, Aspirin Free Anacin)

Inhibits action of endogenous pyrogens on heat-regulating centers; reduces fever by a direct action on the hypothalamic heat-regulating centers, which, in turn, increase the dissipation of body heat via sweating and vasodilation.

Dosing

Adult

325-650 mg PO q4-6h or 1000 mg tid/qid; not to exceed 4 g/d

Pediatric

<12 years: 10-15 mg/kg/dose PO q4-6h prn; not to exceed 2.6 g/d
>12 years: 325-650 mg PO q4h; not to exceed 4 g/d

Interactions

Rifampin can reduce analgesic effects of acetaminophen; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity

Contraindications

Documented hypersensitivity; known G-6-PD deficiency

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hepatotoxicity possible in chronic alcoholics following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; contained in many OTC products and combined use with these products may result in toxicity due to cumulative doses exceeding recommended maximum dose

Antihypertensive agents

Used to treat hypertension caused by thyroid hormone toxicity.

Guanethidine (Ismelin)

Blocks the adrenergic actions of norepinephrine by interfering with either its release or distribution. These effects produce a reduction in total peripheral resistance that result in lower blood pressure.

Dosing

Adult

10 mg/d PO initial; can increase gradually to an average of 25-50 mg/d

Pediatric

0.2 mg/kg/d PO initially and increase by 0.2 mg/kg/d at 7- to 10-d intervals to 3 mg/kg/d

Interactions

Tricyclic antidepressants, methylphenidate, thioxanthenes, phenothiazines, sympathomimetics, anorexiants, haloperidol may reduce effects of guanethidine; minoxidil, epinephrine, and norepinephrine may increase the toxicity of guanethidine

Contraindications

Documented hypersensitivity; pheochromocytoma or have taken MAO inhibitors within the last 14 d

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, asthma, peptic ulcer disease, and regional vascular disease

Reserpine

Depletes norepinephrine and epinephrine, which in turn depress sympathetic nerve functions resulting in decreased heart rate and lowering of arterial blood pressure.

Dosing

Adult

Initial: 0.5 mg/d PO for 1-2 wk
Maintenance: Reduce dosing to 0.1-0.25 mg/d PO divided in 1-2 doses

Pediatric

0.01-0.02 mg/kg PO divided q12h; not to exceed 0.25 mg/d

Interactions

Tricyclic antidepressants may decrease antihypertensive effects of reserpine when used concurrently; cardiac arrhythmias may occur when either digitalis or quinidine are administered concurrently with reserpine

Contraindications

Documented hypersensitivity; diagnosed mental depression

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients diagnosed with renal impairment and peptic ulcer disease

Corticosteroids

Used when adrenal crisis suspected.

Hydrocortisone (Cortef, Hydrocort, Hydrocortone, HydroTex, Solu-Cortef)

Can be used to treat the potential adrenal insufficiency occurring secondary to the hypermetabolic hyperthyroid state.
DOC because of mineralocorticoid activity and glucocorticoid effects.

Dosing

Adult

100 mg IV bolus, followed by continuous infusion of 100 mg q8h for 24-48 h; once patient is stable, initiate PO hydrocortisone (50 mg q8h for another 48 h; may taper dose to 30-50 mg/d in divided doses)

Pediatric

<12 years: 1-2 mg/kg IV bolus, followed by 25-150 mg/d divided q6-8h
>12 years: 1-2 mg/kg IV bolus, followed by 150-250 mg/d divided q6-8h

Interactions

CYP450 2D6 and 3A3/4 substrate; corticosteroid clearance may increase with phenytoin, barbiturates, or rifampin treatment or decrease with estrogens; cholestyramine may decrease AUC; corticosteroids may increase digitalis toxicity secondary to hypokalemia; coadministration with potassium depleting agents (eg, diuretics) may increase risk of hypokalemia; corticosteroids may decrease growth-promoting effect of GH; decreases effects of salicylates and vaccines used for immunization; monitor for hypokalemia with coadministration of diuretics or amphotericin B; antagonizes effects of anticholinergics; may increase anticoagulant effects of warfarin; decreases hypoglycemic effects of sulfonylureas and insulin; increases toxicity of cyclosporine

Contraindications

Documented hypersensitivity; viral, fungal, or tubercular skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hyperthyroidism, osteoporosis, peptic ulcer, cirrhosis, nonspecific ulcerative colitis, diabetes, and myasthenia gravis

Dexamethasone (AK-Dex, Alba-Dex, Baldex, Decadron, Dexone)

Used as empiric treatment of shock in suspected adrenal crisis or insufficiency until serum cortisol levels are drawn.
Adverse effects are hyperglycemia, hypertension, weight loss, GI bleeding or perforation synthesis, cerebral palsy, adrenal suppression, and death. Most of the adverse effects of corticosteroids are dose-dependent or duration-dependent.
Readily absorbed via the GI tract and metabolized in the liver. Inactive metabolites are excreted via the kidneys. Lacks salt-retaining property of hydrocortisone.
Patients can be switched from an IV to PO regimen in a 1:1 ratio.

Dosing

Adult

4-8 mg IV, followed by 16-24 mg/d as IV injection q4-6h or as continuous infusion

Pediatric

Not established

Interactions

Effects decrease with coadministration of barbiturates, phenytoin and rifampin; dexamethasone decreases effect of salicylates and vaccines used for immunization

Contraindications

Documented hypersensitivity; active bacterial or fungal infection

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Increases risk of multiple complications, including severe infections; monitor adrenal insufficiency when tapering drug; abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications of glucocorticoid use

Follow-up

Further Inpatient Care

• Inpatient admission is warranted for symptomatic patients. Because symptoms generally revolve around cardiovascular problems, admit to a cardiac monitored bed while appropriate beta-blockade is achieved.

Inpatient & Outpatient Medications

• Patients most frequently are treated on an outpatient basis if good follow-up can be guaranteed and psychiatric evaluation is not required. When symptoms develop, beta-blockade may be initiated and titrated to response.

Prognosis

• Significant toxicity with acute ingestions is rare.
• Serious toxicity is more commonly observed with chronic ingestions of large amounts of T4 than with other thyroid hormone ingestions.

Patient Education

• For excellent patient education resources, visit eMedicine's Drug Overdose Center, Poisoning - First Aid and Emergency Center, and Endocrine System Center. Also, see eMedicine's patient education articles Poisoning, Drug Overdose, Activated Charcoal, Poison Proofing Your Home, and Thyroid Problems.

Miscellaneous

Medicolegal Pitfalls

• Failure to consider co-ingestion, as in other toxic ingestions
• Failure to provide corresponding appropriate emergency medical and psychiatric care and disposition if ingestion may have been a suicide attempt
• Failure to acknowledge the possibility of suicide attempts in older children
• Failure to diagnose ingestion in obese or anorexic patients who have been surreptitiously ingesting thyroid supplements as a means to achieve weight-loss goals

Special Concerns

Because of the delayed effects of thyroid hormone, longer periods of observation and treatment may be required.

References

1. Yamada M, Mori M. Mechanisms related to the pathophysiology and management of central hypothyroidism. Nat Clin Pract Endocrinol Metab. Dec 2008;4(12):683-94. [Medline]. [Full Text].

2. Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Heard SE. 2007 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 25th Annual Report. Clin Toxicol (Phila). Dec 2008;46(10):927-1057. [Medline]. [Full Text].

3. Litovitz TL, White JD. Levothyroxine ingestions in children: an analysis of 78 cases. Am J Emerg Med. Jul 1985;3(4):297-300. [Medline].

4. FDA MedWatch Safety Alerts for Human Medical Products. Propylthiouracil (PTU). US Food and Drug Administration. Available at http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm164162.htm.. Accessed June 3, 2009.

5. Bauer LA. Simulations of Levothyroxine Bioavailability Using a Single-Dose Study Protocol. Am J Ther. Jun 1995;2(6):414-416. [Medline].

6. Berkner PD, Starkman H, Person N. Acute L-thyroxine overdose; therapy with sodium ipodate: evaluation of clinical and physiologic parameters. J Emerg Med. May-Jun 1991;9(3):129-31. [Medline].

7. Bosse GM, Matyunas NJ. Delayed toxidromes. J Emerg Med. Jul-Aug 1999;17(4):679-90. [Medline].

8. Golightly LK, Smolinske SC, Kulig KW, Wruk KM, Gelman CJ, Rumack BH. Clinical effects of accidental levothyroxine ingestion in children. Am J Dis Child. Sep 1987;141(9):1025-7. [Medline].

9. Lehrner LM, Weir MR. Acute ingestions of thyroid hormones. Pediatrics. Mar 1984;73(3):313-7. [Medline].

10. Mariotti S, Martino E, Cupini C, Lari R, Giani C, Baschieri L, et al. Low serum thyroglobulin as a clue to the diagnosis of thyrotoxicosis factitia. N Engl J Med. Aug 12 1982;307(7):410-2. [Medline].

11. Seger D. Endocrine principles. In: Goldfrank L, ed. Goldfrank's Toxicologic Emergencies. 5^th ed. New York, NY: McGraw-Hill; 1994:338-90.

12. Singh GK, Winterborn MH. Massive overdose with thyroxine,--toxicity and treatment. Eur J Pediatr. Jan 1991;150(3):217. [Medline].

13. Tunget CL, Clark RF, Turchen SG, Manoguerra AS. Raising the decontamination level for thyroid hormone ingestions. Am J Emerg Med. Jan 1995;13(1):9-13. [Medline].

14. Veltri JC, Litovitz TL. 1983 annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med. Sep 1984;2(5):420-43. [Medline].

Keywords

thyroid hormone toxicity, tyrosine, monoiodotyrosine, MIT, diiodotyrosine, DIT, thyroxine, T4, triiodothyronine, T3, thyroid-stimulating hormone, TSH, thyrotropin-releasing hormone, TRH, levothyroxine, LT4, thyroid hormone overdose, thyroid hormone, thyroid hormone poisoning, thyroid hormone exposure, thyroid hormone ingestion, hypothyroidism, hyperthyroidism

Contributor Information and Disclosures

Author

Lisandro Irizarry, MD, MPH, FAAEM, Chair, Department of Emergency Medicine, Brooklyn Hospital Center; Assistant Professor, Department of Emergency Medicine, Weill Cornell School of Medicine
Lisandro Irizarry, MD, MPH, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Nadine A Youssef, MD, Assistant Professor of Emergency Medicine, Tufts University, Department of Emergency Medicine
Nadine A Youssef, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Emergency Medicine Residents Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Anton A Wray, MD, FACEP,, Clinical Assistant Professor of Emergency Medicine, Weill Cornell Medical College; Attending Physician, Department of Emergency Medicine, Brooklyn Hospital Center
Anton A Wray, MD, FACEP, is a member of the following medical societies: American College of Emergency Physicians and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Jeffrey Glenn Bowman, MD, MS, Consulting Staff, Highfield MRI, Columbus, Ohio
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals
John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

Fred Harchelroad, MD, FACMT, FAAEM, FACEP, Chair, Department of Emergency Medicine, Director of Medical Toxicology - Allegheny General Hospital, Associate Professor, Department of Emergency Medicine, Drexel University College of Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

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