Thyrotoxicosis factitia is a rare disorder characterized by elevated levels of plasma thyroid hormones due to increased intake which can be iatrogenic, accidental, or intentional. Symptoms are similar to those in Grave's disease and diagnosis is based on history, examination findings, and by testing thyroid functions.
Presentation
Thyrotoxicosis factitia (TF) is also known as thyroxine addict or metabolic malingerer [1] [2] syndrome. It occurs in patients who are prescribed a very high dose of thyroid hormones as medication (iatrogenic); or those who consume thyroid hormone medication surreptitiously for weight loss or to increase their energy levels or to decrease sleep but deny taking the medication (intentional); or in children (accidental) or adults who consume meat containing thyroid tissue (accidental).
Clinical presentation of TF is identical to thyrotoxicosis except that patients with TF do not have a goiter (thyromegaly) and unlike patients with Grave's disease, they have neither exophthalmos nor myxedema (thickened skin over their shins). Features of thyrotoxicosis like anxiety, hyperactivity, increased perspiration, dyspnea, intolerance to heat, unexplained weight loss, diarrhea, fine tremors, hyperreflexia, tremulousness, palpitations and atrial fibrillation are seen in TF too. Complications like cardiac arrhythmias, hypermetabolism, hyperpyrexia, thyroid storm and myocardial infarction have been reported in TF [3] [4].
Workup
The initial diagnosis of TF is based on clinical suspicion. A detailed history is essential to determine medicine intake, diet, the degree of symptom progression and underlying psychiatric issues. Physical examination should take into consideration the patient's heart rate, basal metabolic rate, presence or absence of goiter, exophthalmos, and myxedema. Laboratory biochemical tests are required to determine total triiodothyronine (T3), total thyroxine (T4), thyroid-stimulating hormone (TSH), TSH receptor, and thyroglobulin level. An elevated free thyroxine index (ratio of T-4 to T-3) [5], diminished thyroglobulin level [6] with an increased basal metabolic rate are diagnostic of TF. Patients with a positive TSH receptor and hyperthyroidism can be misdiagnosed as Grave's disease [7]. To distinguish TF from other causes of thyrotoxicosis, fecal thyroxine levels can be obtained with elevated levels confirming the diagnosis of TF [8].
An imaging study like color doppler ultrasonography is also useful to diagnose TF as it demonstrates the lack of thyroid blood flow [9]. If a patient has an elevated free thyroid hormone level with low TSH levels but is not able to provide a history of ingesting thyroid hormones, a radioactive iodine I-123 uptake is indicated and a low uptake is suggestive of TF [10].
A psychiatrist referral must be considered to exclude Munchausen syndrome [11] and other psychiatric disorders.
Treatment
The primary treatment for Thyrotoxicosis Factitia is the cessation of the exogenous thyroid hormone intake. Once the source of excess hormone is removed, thyroid hormone levels typically return to normal. In some cases, beta-blockers may be prescribed to manage symptoms such as rapid heartbeat and anxiety until hormone levels stabilize.
Prognosis
The prognosis for patients with Thyrotoxicosis Factitia is generally good, provided that the source of excess thyroid hormone is identified and discontinued. Most patients experience a resolution of symptoms and normalization of thyroid function tests within weeks to months after stopping the hormone intake.
Etiology
The etiology of Thyrotoxicosis Factitia is the ingestion of thyroid hormone medication in amounts exceeding the body's requirements. This can occur intentionally, as in cases of factitious disorder where individuals take the hormone to simulate illness, or unintentionally, due to misunderstanding or mismanagement of prescribed thyroid hormone therapy.
Epidemiology
Thyrotoxicosis Factitia is relatively rare compared to other thyroid disorders. It is more commonly seen in individuals with access to thyroid hormone medications, such as healthcare workers or patients with a history of thyroid disease. The condition can occur in any age group but is more frequently reported in adults.
Pathophysiology
The pathophysiology of Thyrotoxicosis Factitia involves the introduction of exogenous thyroid hormones into the body, leading to elevated circulating levels of these hormones. This suppresses the pituitary gland's production of TSH, resulting in low or undetectable TSH levels. The absence of increased thyroglobulin levels helps distinguish this condition from endogenous hyperthyroidism.
Prevention
Prevention of Thyrotoxicosis Factitia involves careful management and monitoring of thyroid hormone therapy. Patients should be educated about the appropriate use of thyroid medications and the potential risks of taking excessive doses. Regular follow-up and thyroid function tests can help ensure that hormone levels remain within the desired range.
Summary
Thyrotoxicosis Factitia is a condition caused by the excessive intake of thyroid hormone medication, leading to symptoms of hyperthyroidism. Diagnosis involves identifying the source of excess hormone and differentiating it from other thyroid disorders. Treatment focuses on discontinuing the hormone source, with a generally favorable prognosis. Prevention includes patient education and careful monitoring of thyroid therapy.
Patient Information
If you are experiencing symptoms such as rapid heartbeat, weight loss, or nervousness, and are taking thyroid hormone medication, it is important to discuss these symptoms with your healthcare provider. Thyrotoxicosis Factitia is a condition that can occur when too much thyroid hormone is taken, either accidentally or intentionally. Treatment involves stopping the excess hormone intake, and most people recover fully with appropriate management. Regular check-ups and communication with your doctor can help prevent this condition.
References
- Harvey RF. Thyroxine ‘‘addicts.’’ Br Med J (Clin Res Ed). 1973;2:35–36.
- Gorman CA, Wahner HW, Tauxe WN. Metabolic malingerers: patients who deliberately induce or perpetuate a hypermetabolic or hypometabolic state. Am J Med. 1970;48:708–714.
- Yoon SJ, Kim DM, Kim JU, et al. A case of thyroid storm due to thyrotoxicosis factitia. Yonsei Med J. 2003;44 :351–354.
- Locker GJ, Kotzmann H, Frey B, et al. Factitious hyperthyroidism causing acute myocardial infarction. Thyroid. 1995;5:465–467.
- Pearce EN. Diagnosis and management of thyrotoxicosis. BMJ. 2006 Jun 10; 332 (7554): 1369 -1379
- Mariotti S, Martino E, Cupini C, et al. Low serum thyroglobulin as a clue to the diagnosis of thyrotoxicosis factitia. N Engl J Med. 1982;307:410–412.
- Jahagirdar VR, Strouhal P, Holder G, Gama R, Singh BM. Thyrotoxicosis factitia masquerading as recurrent Graves’ disease: Endogenous antibody immunoassay interference, a pitfall for the unwary. Ann Clin Biochem. 2008; 45: 325-7
- Bouillon R, Verresen L, Staels F, Bex M, De Vos P, De Roo M. The measurement of fecal thyroxine in the diagnosis of thyrotoxicosis factitia. Thyroid. 1993;3:101–103.
- Bogazzi F, Bartalena L, Vitti P, Rago T, Brogioni S, Martino E. Color flow Doppler sonography in thyrotoxicosis factitia. J Endocrinol Invest. 1996;19: 603–606.
- Braverman LE. Evaluation of thyroid status in patients with thyrotoxicosis. Clin Chem. 1996;42:174–178
- Mittra ES, Niederkohr RD, Rodriguez C, et al. Uncommon causes of thyrotoxicosis. J Nucl Med 2008; 49:265-278