Tag: Graves’ disease

Does hyperthyroidism cause constipation or diarrhoea?

March 14, 2018 / / 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 / / 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.

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Myxoedema in hypothyroidism versus pretibial myxoedema in Graves’ disease

January 8, 2018 / / 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).

Carbimazole, thiamazole, methimazole – what is the difference?

November 29, 2017 / / 0 Comments

Carbimazole is a pro-drug converted to the active metabolite thiamazole.  Thiamazole and methimazole are the same chemical.  Thiamazole is the international nonproprietary name (INN) while methimazole is the United States adopted name (USAN).

Thiamazole is a thioamide used to treat hyperthyroidism such as in Graves’ disease.  In the USA, thiamazole (known there as methimazole) is the most widely used thioamide. However, in many other parts of the world carbimazole is the preferred thioamide. The half-life of carbimazole is 3 to 6 hours, while the half-life of thiamazole is 6 to 15 hours. As thiamazole is the active compound, when a patient takes carbimazole, the half-life of the drug effect is 9 to 21 hours. Thus carbimazole can be taken once per day while thiamazole usually has to be taken three times per day or twice per day.

 

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