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| MINI REVIEW |
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| Year : 2013 | Volume
: 10
| Issue : 4 | Page : 5-6 |
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Hashitoxicosis: A clinical perspective
AG Unnikrishnan
Department of Endocrinology, Amrita Institute of Medical Sciences, Cochin, Kerala, India
| Date of Web Publication | 2-Feb-2013 |
Correspondence Address:
A G Unnikrishnan
Department of Endocrinology, Amrita Institute of Medical Sciences, Cochin, Kerala
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0973-0354.106803
Chronic autoimmune thyroiditis is the most common cause of hypothyroidism worldwide. Sometimes, it is associated with a transient hyperthyroid phase. This hyperthyroid phase, called Hashitoxicosis (the term generally refers to a combination of thyrotoxicosis/hyperthyroidism in the setting of ongoing autoimmune thyroiditis), is self limiting, and lasts for a period of a few weeks to some months. During this time, classical symptoms of mild to moderate hyperthyroidism may co-exist with a diffuse, firm, painless goiter. Thyroid scintigraphy may show normal or a slightly increased uptake. Anti-thyroid antibodies are often positive, and ultrasound with Doppler is a useful test. A combination of clinical features, thyroid function tests, and appropriate radiology will help make the diagnosis. This mini review will touch upon the clinical aspects of Hashitoxicosis. Keywords: Thyrotoxicosis, hypothyroidism, thyroiditis
How to cite this article:
Unnikrishnan A G. Hashitoxicosis: A clinical perspective. Thyroid Res Pract 2013;10, Suppl S1:5-6 |
| Introduction | |  |
Whenever a patient presents with thyrotoxicosis, common etiologies considered are Grave's disease and toxic goiters. However, destructive/inflammatory conditions may also exist, which may damage the thyroid gland, and cause the classical "leakage" of hormones into the blood, causing transient thyrotoxicosis. Sub acute viral thyroiditis is a classical example of destructive thyroiditis. However, an often overlooked cause of destructive thyroiditis is Hashitoxicosis, which is a term that is given to the transient hyperthyroid phase of chronic autoimmune thyroiditis. In other words, Hashitoxicosis is a transient thyrotoxicosis caused by destructive inflammation due to Hashimoto's thyroiditis damaging the thyroid follicles, and resulting in excess release of thyroid hormone. The term Hashitoxicosis has also been loosely used to imply a combination of hyperthyroidism (especially Graves' disease) with autoimmune thyroiditis, and subjects with this disorder are largely expected to remit or even develop hypothyroidism spontaneously. A combination of clinical features and careful antibody testing may reveal the diagnosis. [1],[2]
| Prevalence and Pathogenesis | | |
In a study of autoimmune thyroiditis, Hashitoxicosis occurred in about 4.47% of subjects, suggesting that the disease is not as rare as commonly perceived. [2] Drugs that may interfere with immunity may also trigger Hashitoxicosis a combination of pegylated interferon-α2b (PEG-IFNα) and ribavirin, given for hepatitis C has been shown to produce Hashitoxicosis, followed by type 1 diabetes. [3] Interferon therapy, it has been postulated, may provoke the Th-1 immune reaction, and thereby CD4 lymphocyte activation- that causes release of interleukin-2, interferon-gamma and tumor necrosis factor. [3],[4] These immune cytokines cause a vigorous stirring of autoimmunity, resulting in Hashitoxicosis as well as type 1 diabetes. Hence, Hashitoxicosis seems to directly result from an over activation of the immune system, simultaneously resulting in clinical features of thyrotoxicosis with pathologic features of autoimmune thyroiditis. [2],[3],[4]
| Clinical Presentation | | |
Classically, patients present with mild or moderate hyperthyroidism. Palpation of the thyroid gland may reveal a goiter that is firm, and non tender. Classically, the painful, tender goiter and the history of antecedent viral infection are both lacking. Unlike the classical diffusely enlarged, lobular, bruit-associated goiter that is described with classical Graves disease the goiter is small, diffuse and often firm in these cases. However, clinical features are only subtle pointers in the diagnosis. [2]
| Investigations | | |
The thyroid functions show a high T4 and/or T3 and a low TSH. The thyroglobulin level may be high, as in other destructive thyroid lesions. Thyroid scintigraphy is generally useful to distinguish between hyperthyroidism and thyroiditis but not necessarily so in cases of Hashitoxicosis in this situation the uptake may be normal or even slightly high. High antibody titers accompany Hashitoxicosis however, this is not diagnostic. Anti thyroid peroxidase antibody (anti-TPO) antibody may be positive in 45-80% of subjects with Graves' disease (and therefore this does not establish Hashitoxicosis). [2] In addition, TSH-receptor antibodies may be positive in about 6% of patients with Hashimoto's thyroiditis (and thus this test may not distinguish classical Graves' disease from Hashitoxicosis). [2] Ultrasound of the thyroid is a promising test. In Graves' disease, there is a very vascular picture on color Doppler (vascular inferno). If there is Hashitoxicosis, the ultrasound/Doppler would be expected to show only a normal/slightly increased vascularity. The crucial sonological difference between Graves' disease and Hashitoxicosis rests on the assessment of vascularity. [2]
| Treatment Course and Natural History | | |
Hashitoxicosis requires treatment with β-blockers during the active phase of thyrotoxicosis. In case the diagnosis of a transient thyrotoxic phase of autoimmune thyroiditis can not be confirmed with certainty, i.e. if a possibility of Graves' disease is suspected, then a short course of anti-thyroid drugs may be prescribed, while cautiously watching out with periodic testing, for preventing the onset hypothyroidism. Though many features of the disease suggest that ultimately, hypothyroidism may ensue there is no data to substantiate the proportion of subjects with Hashitoxicosis whose thyroid glands succumb to eventual hypothyroidism. In children, a study from Italy recently showed that the hyperthyroid phase eventually resolves, either with persistent euthyroidism or hypothyroidism (all these patients had negative thyrotropin receptor antibodies). [5] Occasionally, the subjects may develop fluctuating thyroid function, with alternating episodes of hypothyroidism and hyperthyroidism, as the thyroid responds to the autoimmune attack. In another study from the United States of America (in children), 8 patients with Hashitoxicosis were followed up. [6] Five patients became euthyroid after an average duration of 112 days. Three patients had persistently high thyroid stimulating immunoglobulin titers, and two subjects had an increased radioiodine uptake on scintigraphy. Hence, most subjects with Hashitoxicosis seem to recover from their hyperthyroidism, while a small proportion may continue to have persistent thyroid dysfunction.
| References | | |
| 1. | Fonseca V, Thomas M, Havard CW. Hashitoxicosis and autoantibody interference with thyroid function tests. J R Soc Med 1988;81:546-7. 
[PUBMED] |
| 2. | Harsch IA, Hahn EG, Strobel D. Hashitoxicosis - Three cases and a review of the literature. Touch Briefings (European Endocrinology) 2008. p. 70-2. Available from: http://www.touchbriefings.com/pdf/3186/strobel.pdf. [Last accessed on 2012 Jan 9].
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| 3. | Yagyu H, Okada K, Sato S, Yamashita Y, Okada N, Osuga J, et al. Pegylated interferon-α2b and ribavirin combination therapy induces Hashitoxicosis followed by type 1 diabetes mellitus. Diabetes Res Clin Pract 2012;95:e52-4.
[PUBMED] |
| 4. | Soultati AS, Dourakis SP, Alexopoulou A, Deutsch M, Archimandritis AJ. Simultaneous development of diabetic ketoacidosis and Hashitoxicosis in a patient treated with pegylated interferon-alpha for chronic hepatitis C. World J Gastroenterol 2007;13:1292-4.
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| 5. | Wasniewska M, Corrias A, Salerno M, Lombardo F, Aversa T, Mussa A, et al. Outcomes of children with hashitoxicosis. Horm Res Paediatr 2012;77:36-40.
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| 6. | Nabhan ZM, Kreher NC, Eugster EA. Hashitoxicosis in children: Clinical features and natural history. J Pediatr 2005;146:533-6.
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