An Outbreak of Thyrotoxicosis Caused by the Consumption of Bovine Thyroid Gland in Ground Beef

Research

Recurrent hamburger thyrotoxicosis

CMAJ September 02, 2003 169 (5) 415-417;

Abstract

RECURRENT EPISODES OF SPONTANEOUSLY RESOLVING HYPERTHYROIDISM may exist caused by release of preformed hormone from the thyroid gland after it has been damaged by inflammation (recurrent silent thyroiditis) or by exogenous administration of thyroid hormone, which might be intentional or clandestine (thyrotoxicosis factitia). Community-broad outbreaks of "hamburger thyrotoxicosis" resulting from inadvertent consumption of beefiness contaminated with bovine thyroid gland have been previously reported. Here nosotros describe a unmarried patient who experienced recurrent episodes of this phenomenon over an 11-yr catamenia and nowadays an approach to systematically evaluating patients with recurrent hyperthyroidism.

Case

A 61-year-old woman with a history of recurrent episodes of transient thyrotoxicosis presented in November 2001 with a 3-week history of weight loss of iv kg, palpitations and increased sweating. She had mild tachycardia (112 beats/minute) and fine tremor of the easily. She had no thyroid enlargement, thyroid bruits, heart signs or pretibial myxedema. A clinical diagnosis of hyperthyroidism was confirmed by elevated costless thyroxine (T₄) (46 [usually 9 to 23] pmol/L) and suppressed thyroid-stimulating hormone (TSH) (0.02 [normally 0.35 to v.0] μIU/L). Her symptoms resolved spontaneously and her gratuitous T_iv returned to normal (12 pmol/L) within 8 weeks.

This was the patient's fifth episode of transient hyperthyroidism over an 11-year period (see Fig. one), each episode lasting 2 to 3 months. Silent thyroiditis had been diagnosed in 1991 after investigations at a third intendance centre, and subsequent episodes had been labelled silent thyroiditis considering of similar presentations. Further investigations in November 2001 showed normal erythrocyte sedimentation rate (ESR), no antinuclear antibody or antithyroid antibodies, normal levels of thyrotropin bounden inhibitor immunoglobulin (TBII) (less than eight.0 IU/L) and low serum thyroglobulin level (0.iv [normally two.3 to 48.0] μg/50). A chart review revealed negative results for antithyroid antibodies in 1990, 1996 and 1998, low uptake of radioactive iodine in 1990, 1993 and 1996, and normal ESR and low serum thyroglobulin level in 1998.

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Fig. 1: Thyroid-stimulating hormone (TSH) and gratuitous thyroxine (T _iv ) levels for a 61-year-one-time adult female show 5 documented episodes of transient hyperthyroidism over a period of xi years, starting in November 1990. Normal levels, indicated by shaded horizontal confined: 0.35 to 5.0 μIU/L for TSH, nine to 23 pmol/L for costless T ₄ .

Low uptake of radioactive iodine, both at the electric current presentation and previously, suggested the possibility of silent (painless) thyroiditis,1 iodide-induced thyrotoxicosis2 or thyrotoxicosis factitia.3 Even so, the combination of low uptake of radioactive iodine with depression serum thyroglobulin level is strongly suggestive of an exogenous cause for the hyperthyroidism, such as hush-hush apply of thyroid supplements. Nosotros therefore questioned the patient about exogenous thyroid intake in whatsoever form (including herbal supplements), simply she denied employ of whatever supplements other than glucosamine sulfate for osteoarthritis. She had no history of psychiatric treatment or access to thyroid medications.

Further questioning into the patient's dietary history revealed that she lived on a farm with her married man and that every couple of years they slaughtered a cow from their herd, which was their principal source of meat. Inquiries to the couple'south local butcher revealed that he was unaware of the prohibition against gullet trimming (a procedure whereby muscles from the bovine larynx are harvested) and had inadvertently been contaminating edible meat with thyroid tissue. He used meat from the neck of the patient's cows to make patties, which were commonly consumed by the patient within a couple of months of butchering. Her husband, who was not affected by whatever thyroid issues, did not eat these patties, preferring other cuts of meat. The patties could not be tested, as the patient had finished the current batch a month before consumption of contaminated beef was suspected as the cause of her thyroid problems. Notwithstanding, the temporal clan of episodes of transient hyperthyroidism with availability of meat from a slaughtered cow over the previous 11 years is highly supportive of hamburger thyrotoxicosis, rather than silent thyroiditis.

Comments

The most mutual cause of recurrent hyperthyroidism is a relapse of previously treated hyperthyroidism,4^,5^,half-dozen but other causes should likewise be considered (Box 1).

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In patients with suspected recurrent hyperthyroidism, a history of thyroid disease, presence of goitre and review of medication lists may be helpful in the diagnosis. Eye signs, proptosis and goitre are usually absent in exogenous hyperthyroidism, just such a combination would not exclude Graves' disease, especially in elderly patients, who commonly present with atypical (apathetic) hyperthyroidism. Normal or high uptake of radioactive iodine suggests Graves' disease or toxic nodular goitre, whereas low uptake is seen in patients with thyroiditis or exogenous hyperthyroidism.

To differentiate endogenous from exogenous causes, information technology is helpful to make up one's mind serum thyroglobulin level. Elevation of thyroglobulin is a marking of endogenous hyperthyroidism, whereas low thyroglobulin in association with hyperthyroidism is a authentication of exogenous thyroid intake or thyrotoxicosis factitia.3 A practical approach to diagnosis for a patient with recurrent hyperthyroidism is shown in Fig. 2.

Community-wide outbreaks of thyrotoxicosis acquired by the consumption of bovine thyroid gland in ground beef in Minnesota, Southward Dakota and Iowa10^,11 in 1984 and 1985 resulted in the prohibition of gullet trimming in all plants that slaughter cattle and pigs. This example emphasizes that sporadic cases of recurrent thyrotoxicosis caused by consumption of thyroid-contaminated beef may still occur and may be diagnosed as silent thyroiditis. For patients with features suggestive of silent thyroiditis, health care providers should consider this cause of hyperthyroidism, peculiarly for anyone who may be slaughtering subcontract animals for their own use and for hunters who may be gullet trimming game.

Footnotes

• This article has been peer reviewed.

  Contributors: Dr. Parmar was responsible for the conception of the report, conquering of references and writing of the draft. Dr. Sturge nerveless the groundwork information and reviewed the draft.

  Competing interests: None alleged.

References

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4. iv.↵

   van Soestbergen MJ, van der Vijver JC, Graafland AD. Recurrence of hyperthyroidism in multinodular goiter afterward long-term drug therapy: a comparing with Graves' illness. J Endocrinol Invest 1992;fifteen(11):797-800.

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   Nader S, Mastrobattista J. Recurrent hyperthyroidism in consecutive pregnancies characterized by hyperemesis. Thyroid 1996;half dozen(v):465-half-dozen.

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    Hedberg CW, Fishbein DB, Janssen RS, Meyers B, McMillen JM, MacDonald KL, et al. An outbreak of thyrotoxicosis acquired by the consumption of bovine thyroid in basis beef. N Engl J Med 1987;316:993-8.

11. 11.↵

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Source: https://www.cmaj.ca/content/169/5/415