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We report a woman with hypothyroidism who had anosmia.
Loss of smell is an unusual manifestation of hypothyroidism. This is not recorded even in standard textbooks of endocrinology and of thyroid disorders (1,2). There are reports of disturbances of smell and taste in untreated hypothyroidism (3,4).
We describe a woman with primary hypothyroidism from our prospective computerised database (5) of 1103 hypothyroid individuals. She complained she had lost the sense of smell.
A 38 year-old woman presented with symptoms and signs of hypothyroidism, confirmed by laboratory investigation (weight gain, weakness, body pains, excessive daytime somnolence, paresthesia, puffiness of face, slowed higher intellectual function, hoarse voice and cold intolerance; she had a grade 1 goitre (30 gm), with dry skin. Serum thyrotropin was 22 miu/ml (normal 0.3-6.5 miu/ml). In addition she complained she could not smell.
She became euthyroid with thyroxine replacement (150 ug a day), but anosmia persists even four years after euthyroidism was achieved.
Dysfunction of smell in hypothyroidism is an underreported but perhaps not uncommon condition. In a series of 18 untreated primary hypothyroid individuals, 39% (n:7) were aware of some alteration in their sense of smell. Dysosmia (distortion of smell) and hyposmia (elevated threshold for detection of smell) were both seen (3). These were generally reversible with thyroxine replacement. It was commented that distortions of smell and taste could contribute to anorexia and lack of interest in eating, which are common in hypothyroidism.
Similarly, cacosmia (reported illness from environmental chemical odours) was also more common in women who rated themselves as having been exposed to greater stress earlier in their lives; they also had greater prevalence of physician-diagnosed disorders including hypothyroidism (6).
Experimental induction of hypothyroidism in laboratory animals resulted in development of anosmia (7), as well as delayed development of orientation along the olfactory gradient (8). Propylthiouracil-induced hypothyroidism in mice led to disrupted neural development in the olfactory epithelium, although the mature receptor neurons were not completely lost (9). In addition they showed reduced maturation, lesser epithelial surface area and fewer mature olfactory receptor neurons (10).
In summary we describe a woman with primary hypothyroidism with anosmia which could be due to thyroid deficiency (3), although it could have coexisted independently.
Loss of smell is an unusual manifestation of hypothyroidism. This is not recorded even in standard textbooks of endocrinology and of thyroid disorders (1,2). There are reports of disturbances of smell and taste in untreated hypothyroidism (3,4).
We describe a woman with primary hypothyroidism from our prospective computerised database (5) of 1103 hypothyroid individuals. She complained she had lost the sense of smell.
A 38 year-old woman presented with symptoms and signs of hypothyroidism, confirmed by laboratory investigation (weight gain, weakness, body pains, excessive daytime somnolence, paresthesia, puffiness of face, slowed higher intellectual function, hoarse voice and cold intolerance; she had a grade 1 goitre (30 gm), with dry skin. Serum thyrotropin was 22 miu/ml (normal 0.3-6.5 miu/ml). In addition she complained she could not smell.
She became euthyroid with thyroxine replacement (150 ug a day), but anosmia persists even four years after euthyroidism was achieved.
Dysfunction of smell in hypothyroidism is an underreported but perhaps not uncommon condition. In a series of 18 untreated primary hypothyroid individuals, 39% (n:7) were aware of some alteration in their sense of smell. Dysosmia (distortion of smell) and hyposmia (elevated threshold for detection of smell) were both seen (3). These were generally reversible with thyroxine replacement.
Experimental induction of hypothyroidism in laboratory animals resulted in development of anosmia (6), as well as delayed development of orientation along the olfactory gradient (7). Propylthiouracil-induced hypothyroidism in mice led to disrupted neural development in the olfactory epithelium, although the mature receptor neurons were not completely lost (8). In addition they showed reduced maturation, lesser epithelial surface area and fewer mature olfactory receptor neurons (9).
In summary we describe a woman with primary hypothyroidism with anosmia which could be due to thyroid deficiency (3), although it could have coexisted independently.
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