Thyroxine and triiodothyronine content in commercially available thyroid health supplements.

BACKGROUND: As defined by the Dietary Supplement Health and Education Act 1997, such substances as herbs and dietary supplements fall under general Food and Drug Administration supervision but have not been closely regulated to date. We examined the thyroid hormone content in readily available dietary health supplements marketed for "thyroid support." METHODS: Ten commercially available thyroid dietary supplements were purchased. Thyroid supplements were dissolved in 10 mL of acetonitrile and water with 0.1% trifloroacetic acid and analyzed using high-performance liquid chromatography for the presence of both thyroxine (T4) and triiodothyronine (T3) using levothyroxine and liothyronine as a positive controls and standards. RESULTS: The amount of T4 and T3 was measured separately for each supplement sample. Nine out of 10 supplements revealed a detectable amount of T3 (1.3-25.4 µg/tablet) and 5 of 10 contained T4 (5.77-22.9 µg/tablet). Taken at the recommended dose, 5 supplements delivered T3 quantities of greater than 10 µg/day, and 4 delivered T4 quantities ranging from 8.57 to 91.6 µg/day. CONCLUSIONS: The majority of dietary thyroid supplements studied contained clinically relevant amounts of T4 and T3, some of which exceeded common treatment doses for hypothyroidism. These amounts of thyroid hormone, found in easily accessible dietary supplements, potentially expose patients to the risk of alterations in thyroid levels even to the point of developing iatrogenic thyrotoxicosis. The current study results emphasize the importance of patient and provider education regarding the use of dietary supplements and highlight the need for greater regulation of these products, which hold potential danger to public health.

Lethal thyroid storm after uncontrolled intake of liothyronine in order to lose weight.

Thyroid hormones are sometimes used for purposes for which they are not approved. Reasons for off-label use can be overweight, prevailing depressive mood, or various somatic symptoms. Information about the intake of thyroid hormones in order to lose weight can be easily obtained from inappropriate/nonmedical websites. The objective of this case report is to describe the first case of a lethal abuse of liothyronine. The case was a 29-year-old male (BMI 32) without relevant illnesses. An autopsy was performed and followed by histological, toxicological, and clinical chemistry examinations. The autopsy revealed no relevant pathology. Histology showed multiple areas of focal cell necrosis in the myocardium and signs of acute heart failure including severe edema of the lungs; the follicles of the thyroid gland were markedly plump. Postmortem laboratory results indicated lethal liothyronine intoxication. Despite prevailing opinion, uncontrolled intake of liothyronine can cause lethal thyroid storm in a euthyroid patient without manifested cardiac illnesses.

Redotex ingestions reported to Texas poison centers.

Although the multi-component weight loss supplement Redotex is banned in the United States, the supplement can be obtained in Mexico. The intent of this report was to describe the pattern of Redotex calls received by a statewide poison center system. Cases were all Redotex calls received by Texas poison centers during 2000-2008. The distribution of total calls and those involving ingestion of the supplement were determined for selected demographic and clinical factors. Of 34 total Redotex calls received, 55.9% came from the 14 Texas counties that border Mexico. Of the 22 reported Redotex ingestions, 77.3% of the patients were female and 45.5% 20 years or more. Of the 17 ingestions involving no co-ingestants, 52.9% were already at or en route to a health care facility, 41.2% were managed on site, and 5.9% was referred to a health care facility. The final medical outcome was no effect in 23.5% cases, minor effect in 5.9%, moderate effect in 11.8%, not followed but minimal clinical effects possible in 47.1%, and unable to follow but judged to be potentially toxic in 11.8%. Most Redotex calls to the Texas poison center system originated from counties bordering Mexico.

[Triiodothyronine intoxication. A clinical and phamacokinetic study]. / Intoxicación por triyodotironina. Estudio clínico y farmacocinético.

A woman, thyroidectomised because of a thyroid papillary carcinoma, interrupted temporarily her levothyroxine intake in order to be subjected to an extension study five weeks later. To minimise her symptoms for the first three weeks, a treatment was prescribed consisting of one 25 micro g-capsule of triiodothyronine every 8 hours. Nine days later she complained of abdominal pain, nausea, vomiting, fever of 40 degrees C and chest discomfort. A serum total triiodothyronine of 575.2 nmol/l was measured by chemoluminiscent immunoassay eleven hours after the intake of the latest capsule (normal level: 1.1-2.9 nmol/l). Along the following ten days the patient suffered from delirium, agitation, tachycardia, hypertension, constipation and later diarrhoea, but neither arrythmias nor axillary temperature over 38 degrees C. Fifty-nine measurements of the serum total triiodothyronine were performed in order to determine the kinetics of elimination of this drug. We estimate that the maximal serum concentration after the intake of the latest capsule could be 794.3 nmol/l, i.e. 397 times higher than the mean normal value. The elimination half-life was 24 hours 40 minutes. The charcoal haemoperfusion had no impact on the velocity of elimination. The concentration of triiodothyronine became normal 200 hours after the intake of the latest capsule, but the clinical manifestations still lasted three days more. The pharmacokinetic data suggest that this intoxication could be due to the intake of capsules containing 5 mg of triiodothyronine, i.e. a dose 200 times higher than that prescribed by her physician.

Massive triiodothyronine intoxication: efficacy of hemoperfusion?

A case of massive accidental triiodothyronine intoxication (1000-fold the usual therapeutic dose, for 8 days) is reported with important disturbances of cardiovascular and central nervous systems that required intensive care support. Serum free triiodothyronine levels were 4789 pmol L(-1) on admittance (normal values, 3.5-6.5 pmol x L(-1)). In the absence of a specific treatment, hemoperfusions were performed but failed to accelerate significantly the decay of blood levels of free triiodothyronine (apparent half-life 25.9 hours; 95% confidence interval: 19.8-37.4 hours). The patient, a young woman, made a satisfactory recovery, in spite of important clinical complications.

[Acute factitious hyperthyroidism--moderate clinical symptoms in 3 cases under beta-blocker treatment]. / Hyperthyreosis factitia acuta--Geringe klinische Symptome bei drei Fällen unter beta-Blocker-Behandlung.

The clinical and laboratory findings are described in three patients who ingested large amounts of L-thyroxine (two cases) and L-thyroxine together with L-triiodothyronine and who were treated with propranolol. Serum concentrations of thyroxine (maximum values 75 micrograms/dl, 64 micrograms/dl, and 20 micrograms/dl, respectively; normal range 4-12 micrograms/dl), triiodothyronine (maximum values 837 ng/dl, 453 ng/dl, and 566 ng/dl, resp.; normal range 80-180 ng/dl), reverse triiodothyronine (maximum values 235 ng/dl, 190 ng/dl, and 65 ng/dl, resp.; normal range 10-40 ng/dl) as well as free thyroxine equivalent and free triiodothyronine equivalent were monitored daily until they reached the normal range. Statistical analysis of the kinetics of these parameters indicated that the extreme thyroxine conversion was directed toward reverse triiodothyronine, partly due to the treatment with the beta-adrenergic blocker propranolol. The striking discrepancy between the high concentrations of the active hormones and the moderate clinical symptoms was most likely caused by peripheral effects of propranolol.

Benign course after massive levothyroxine ingestion.

Management of thyroid hormone ingestion is controversial. We present nine children with massive levothyroxine ingestion who experienced a benign course. Their serum thyroxine levels ranged from 19.9 to 84.7 micrograms/dl. Seven were clinically euthyroid, and the other two had mild symptoms. No specific therapy was given. We recommend gastrointestinal decontamination procedures and serum thyroxine levels for an ingestion of greater than 2.0 mg of levothyroxine (or its equivalent). If levothyroxine has been ingested, neither immediate hospitalization nor prophylactic antihyperthyroidism therapy is recommended. If the initial serum thyroxine level is significantly elevated, close outpatient follow-up, especially during days three to 10, is warranted. However, massive ingestion of thyroid extract or triiodothyronine may require immediate hospitalization for observation. Therapeutic interventions aimed at extracorporeal removal of excess thyroid hormones are not recommended. Specific antithyroid therapy should be reserved for those rare patients with significant symptoms of thyrotoxicosis.

[Acute poisoning with L-triiodothyroinine, L-thyroxine and phendimetrazine bitartrate with suicidal intention]. / Akute Intoxikation mit L-Trijodthyronin, L-Thyroxin und Phendimetrazinbitartrat aus suizidaler Absicht

It is reported on an acute intoxication after application of 8 mg L-thyroxin, 2 mg L-triiodotyronine (200 tablets Thyreotom) and 4.5 g hendimetrazine bitartrate (100 tablets Sedafamem). The clinical picture is described. An endangering of the vital function of the organism was not observed. The symptoms disappeared after 4 days. The pharmacological aspects of the intoxication after application of the hormone of the thyroid gland, its significance for the pathogenesis of the thyreotoxic crisis and its therapy are discussed