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Hashimoto’s thyroiditis versus Hashimoto’s encephalopathy

Is Hashimoto’s encephalopathy related to Hashimoto’s thyroiditis?

• Hashimoto’s thyroiditis is an autoimmune disease in which the thyroid gland is gradually destroyed, resulting in chronic hypothyroidism.
• Hashimoto’s encephalopathy is a rare neurological condition characterized by encephalopathy and thyroid autoimmunity. It shows a good clinical response to corticosteroids.

Hashimoto’s thyroiditis, so named because it was first described in a medical publication by Hakaru Hashimoto (1881-1934) in 1912, is an autoimmune disease. Typically the autoantibodies include antibodies against thyroid peroxidase (TPO). TPO is an enzyme expressed in the thyroid gland that is essential for the production of thyroid hormones. In Hashimoto’s thyroiditis, the thyroid gland is gradually destroyed, resulting in chronic hypothyroidism unless treated with thyroid hormone replacement. It is the most common form of hypothyroidism, affecting about 5% of people.

Hashimoto’s encephalopathy, also known as steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT), is an extremely rare (2.1 in 100,000) neurological condition characterized by encephalopathy and thyroid autoimmunity, which shows a good clinical response to corticosteroids. First described by Brain, Jellinek and Ball in 1966, the condition was named for its association with Hashimoto’s thyroiditis, but the pathogenic autoantibodies are thought to be against alpha-enolase, a ubiquitous enzyme invovled in glycolysis. Glycolysis is the metabolic pathway that converts glucose to pyruvic acid releasing energy in the form of adenosine triphosphate (ATP).

Levothyroxine and cancer?

September 10, 2021 / phcdgs / 0 Comments

Is there an association between levothryoxine and breast cancer?

The short answer is that there is not sufficient evidence to draw any conclusion at this time. Patients who require levothyroxine should continue to take their medication as prescribed by their doctor. The risk of ultimately fatal myxedema due to severe untreated hypothyroidism is proven and real. The risk of cancer is speculative and not definitively proven.

When this question came up at the end of the lecture, my initial thought was that an association between levothryoxine and cancer is highly improbable. Oral levothyroxine essentially replaces your own endogenous thyroxine (T4). Treatment normalises T4 levels but should not cause supraphysiological levels of T4. Even the route of absorption is largely physiological as endogenous T4 is recycled through enterohepatic circulation and is absorbed in the small intestine after being excreted in the bile. The only potentially “unnatural” exposure is as the levothryoxine tablet passes from the mouth to the stomach. In theory, there is no reason why taking levothyroxine should expose anyone to greater risk than having physiologically normal thyroid function would.
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Does hyperthyroidism cause constipation or diarrhoea?

March 14, 2018 / phcdgs / 0 Comments

Hyperthyroidism causes sympathetic overactivation such that many of the symptoms of thyroid storm can be alleviated by beta-blockers. The sympathetic nervous system “fright, flight or fight” response opposes the parasympathetic nervous system “rest and digest” response and shuts down gastrointestinal function. So hyperthyroidism causes constipation, correct?

Sorry, not correct. Yes, hyperthyroidism can stimulate overactivation of the sympathetic nervous system. Yes, symptoms of thyroid storm can be treated with sympatholytic beta-blockers. But no, hyperthyroidism does not cause constipation. Hyperthyroidism causes diarrhoea. Conversely, hypothyroidism causes constipation.

So, next, you will ask “What is the mechanism?”. Unfortunately, the mechanism is not known. Recent reviews have speculated that it might be due to beta-2 adrenoceptor-mediated effects on gastrointestinal motility and secretions (Daher et al., 2015; Kyriacou et al., 2015) but the evidence for this is very limited. For example, a case report on one patient has suggested that propranolol can control intractable diarrhoea in hyperthyroidism (Bricker et al., 2001) but another study on ten hyperthyroid patients found no effect of propranolol on the gastrointestinal transit time (Bozzani et al., 1985).

For the moment, as we do not know the underlying mechanism, it is just one of those exceptions that you have to remember. In nearly every other respect, hyperthyroidism has a sympathomimetic effect and hypothyroidism has a sympatholytic effect. But for the gastrointestinal system, it is the opposite.

References:

Bozzani A, Camboni MG, Tidone L, Cesari P, Della Mussia F, Quatrini M, Ghilardi G, Ferrar L, Bianchi PA (1985) Gastrointestinal transit in hyperthyroid patients before and after propranolol treatment. Am J Gastroenterol. 1985 Jul;80(7):550-2.

Bricker LA, Such F, Loehrke ME, Kavanaugh K (2001) Intractable diarrhea in hyperthyroidism: management with beta-adrenergic blockade. Endocr Pract. 2001 Jan-Feb;7(1):28-31.

Daher R, Yazbeck T, Jaoude JB, Abboud B (2009) Consequences of dysthyroidism on the digestive tract and viscera. World J Gastroenterol. 15(23):2834-8.

Kyriacou A, McLaughlin J, Syed AA (2015) Thyroid disorders and gastrointestinal and liver dysfunction: A state of the art review. Eur J Intern Med. 26(8):563-71.

Does levothyroxine overdose cause exophthalmos and lid lag?

March 14, 2018 / phcdgs / 0 Comments

Graves’ disease, an autoimmune disorder resulting in hyperthyroidism, can be associated with bulging eyes (exophthalmos) and a staring gaze (lid lag). Does overdose of levothyroxine cause the same signs?

Graves’ disease is an autoimmune disease involving production of antibodies against the thyroid-stimulating hormone (TSH) receptor (TSHR), also known as the thyrotropin receptor (Davies, 2017). The autoantibodies to the thyrotropin receptor (TRAb) activate TSHRs. In most patients this results in stimulation of thyroid hormone synthesis and secretion resulting in hyperthyroidism.

Hypothyroidism, for example caused by Hashimoto’s thyroiditis, is often treated with levothryoxine to replace the deficiency in endogenous thyroxine. Overdose of levothyroxine can cause hyperthyroidism.

But Graves’ disease is not synonymous with hyperthyroidism (Davies, 2017). Some patients produce TRAb but do not have hyperthyroidism and, by mechanisms independent of thyroid hormone secretion, TRAb can cause orbitopathy resulting in exophthalmos, and dermopathy due to pretibial myxoedema.

Myxoedema in hypothyroidism versus pretibial myxoedema in Graves’ disease

January 8, 2018 / phcdgs / 0 Comments

Intravenous (IV) liothyronine is used to treat severe hypothyroidism resulting in myxoedema and myxoedematous coma. But Graves’ disease, which causes hyperthyroidism, is also associated with myxoedema in the form of infiltrative dermopathy or pretibial myxoedema. Can liothyronine be used to treat pretibial myxoedema? But, if we give IV liothyronine to someone with Graves’ disease suffering from pretibial myxedema, wouldn’t this cause thyroid storm instead?

Myxoedema refers to a relatively hard oedema (as opposed to a soft, fluid oedema) caused by the accumulation of mucopolysaccharides in the interstitial fluids.

The term “myxoedema” alone refers to generalised myxoedema and is used to describe severe hypothyroidism characterised by myxoedema of cutaneous tissue together with other symptoms including somnolence, slow mentation, dryness and loss of hair, ascites, hypothermia etc. This is a severe condition that can result in coma and death. The accumulation of mucopolysaccharides is a direct result of the hypothyroidism as thyroxines are required for their turnover.

When IV liothyronine is used for the treatment of myxoedema or myxoedematous coma, it is the treatment of this form of severe hypothyroidism that is being referred to.

“Pretibial myxoedema” refers explicitly to infiltrative dermopathy localised in the pretibial area (the shin). In this case, the infiltration and accumulation of mucopolysaccharides (especially the glycosaminoglycan hyaluronic acid) is due to secretion from fibroblasts. The pathogenesis is not caused by thyroid hormone levels. The exact pathogenic mechanism is not known, but it is generally thought that it is due to the autoimmune response. Fibroblasts express TSH receptor protein and are likely targeted by the TSH receptor antibodies produces in Graves disease. Cytokines secreted by Th1 type T cells activated by TSH receptor antigen may also stimulate fibroblasts to secrete glycosaminoglycans.

Pretibial myxoedema is not treated with IV liothyronine as thyroid hormone levels are not responsible for this localised inflammatory myxoedema.

Reference:

Davies, TF. Pretibial myxedema (thyroid dermopathy) in autoimmune thyroid disease. Ross, DS, Mudler, JE ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com (Accessed on January 8, 2018).

Tag: hypothyroidism

Hashimoto’s thyroiditis versus Hashimoto’s encephalopathy

Levothyroxine and cancer?

Does hyperthyroidism cause constipation or diarrhoea?

Does levothyroxine overdose cause exophthalmos and lid lag?

Myxoedema in hypothyroidism versus pretibial myxoedema in Graves’ disease

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