Hashimoto, thyroiditis

(autoimmune thyroiditis, chronic lymphocytic thyroiditis)

Prevalence estimated at 1.2 %.It is the most common cause of acquired hypothyroidism, with or without goiter, in countries where there is no deficiency in iodine.  Occurs between the age of 11 and 18 years, and is rare before the age of 5 years. Strong female preponderance.

There are two clinical forms which have antithyroid antibodies and thyroid dysfunction of varying importance (nervousness, fatigue, dysphagia, cough, hoarseness, increased sweating):

-         form with goiter (2/3): the most common in the younger where goiter may be the only clinical expression; the goiter is solid with a lumpy surface

-         atrophic form (1/3).

Some children show signs of transient hyperthyroidism (nervousness, increased sweating , irritability, hyperactivity) but the biological results do not necessarily demonstrate a biological hyperthyroidism.

It is an autoimmune disease:

-        the family history is positive in 30-40 % of cases. Some genes predisposing to susceptibility to autoimmune thyroiditis which are genes regulating immunomodulation [HLA - DR, CD40, CTLA-4, PTPN22] or genes that code for the thyroglobulin or TSH receptor. Environmental factors however are needed to initiate the autoimmune process: excess of iodine intake, deficiency in selenium, stress, viral infection, pregnancy, toxic...

-        it is frequently associated with other autoimmune diseases: type 1 diabetes (20% have antithyroid antibodies), celiac disease, Addison's disease

-        it is frequently associated with chromosomal abnormalities: trisomy 21, Di George syndrome (microdeletion chromosome 22 or CATCH 22, see this topic), Turner and Klinefelter syndromes

-        the anti-thyroid antibodies are directed either against thyroid peroxidase (TPO) (> 80%) or thyroglobulin (TG) (20%).

There is a small increased risk of developing papillary cancer of the thyroid.

Diagnosis: classically, clinical or biological hypothyroidism with high TSF, low T4 and antithyroid antibodies.

Treatment: most patients are asymptomatic but evolve gradually to hypothyroidism if their TSH level is above normal. This is why it is recommended to administer an thyroid opotherapy if TSH level is > 10 IU/ml or > 5 IU/ml in presence of a goiter. Regular monitoring is necessary to ensure that the patient remains euthyroidic: about 65 % remain euthyroid (and the treatment can be stopped), 9 % present with subclinical hypothyroidism  and 25 % with clinical hypothyroidism.


Anesthetic implications: 

check for the presence of euthyroidism; in case of hypothyroidism, it is better to restore the euthyroidism before anesthesia; risk of thyroid storm when anesthesia is administered at the onset of the inflammatory process.


References : 


Update: April 2019