My heart rate has been quite elevated for some time, and now I know why. The half life of T4 is 5-7 days. So, if you take it at low dose (100mcg) everyday for an extended period of time, you will get a toxic buildup that could easily lead to serious health problems including heart seizure.
Read on.
http://www.emedicine.com/EMERG/topic800.htm
Toxicity, Thyroid Hormone
Last Updated: January 5, 2006
Synonyms and related 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
Author: Lisandro Irizarry, MD, MPH, FAAEM, Chair and Program Director, ***artment of Emergency Medicine, Brooklyn Hospital Center; Assistant Professor, ***artment of Emergency Medicine, Weill Cornell School of Medicine Coauthor(s): Andrew Lawrence, MD, Consulting Staff, ***artment of Emergency Medicine, Great Plains Regional Medical Center
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 Editor(s): Jeffrey Glenn Bowman, MD, MS, Consulting Staff, ***artment of Emergency Medicine, Mercy Springfield Hospital; John T VanDeVoort, PharmD, Clinical Assistant Professor, College of Pharmacy, University of Minnesota; Fred Harchelroad, MD, FACMT, Chair, ***artment of Emergency Medicine, Director of Medical Toxicology, Associate Professor, ***artment of Emergency Medicine, Allegheny General Hospital; John Halamka, MD, Chief Information Officer, CareGroup Healthcare System, Assistant Professor of Medicine, ***artment of Emergency Medicine, Beth Israel Deaconess Medical Center; Assistant Professor of Medicine, Harvard Medical School; and Raymond J Roberge, MD, MPH, FAAEM, FACMT, Clinical Associate Professor of Emergency Medicine, University of Pittsburgh School of Medicine; Consulting Staff, ***artment of Emergency Medicine, Magee-Women's Hospital of the University of Pittsburgh Medical Center
Disclosure
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography
Background: Iodine absorbed from the GI tract 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 form 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.
Thyroid-stimulating hormone (TSH), secreted by the anterior pituitary, causes release of T3 and T4. Thyrotropin-releasing hormone (TRH) and a negative feedback mechanism regulate TSH.
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.
Pathophysiology: Mechanism of toxicity involves stimulation of the cardiovascular (CV), GI, and neurologic systems through presumed activation of the adrenergic system.
Clinical effects of acute LT4 ingestion occur approximately 1 week postexposure. Conversion of T4 to the more potent T4 produces this lag time. 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.
Frequency: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%.
- In the US: According to the annual report of the American Association of Poison Control Centers, published in the September 1999 issue of the American Journal of Emergency Medicine, 6844 exposures to thyroid hormone preparations were documented in 1998; of those exposures, 4110 were associated with children younger than 6 years. A total of 1895 exposures were reported in persons older than 19 years. Overall, 13 people had major adverse outcomes, and 2 deaths were reported.
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.
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography
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
- Palpitations
- Hypertension or hypotension
- Hyperpyrexia
- Chronic
- Supraventricular tachycardia (SVT)
- High output left ventricular failure
- Hypotension
- Hemiparesis
- Delirium
- Coma
- Pneumonia
- Sepsis
- Hyperthermia
- Acute renal failure
Causes: Long-term abuse of thyroid supplements has been reported in obese patients as a method of weight control.
- Myopathy
- Palmar and plantar desquamation


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