With postpartum thyroiditis, postpartum means "after birth", thyroid refers to the thyroid gland, and -itis means inflammation, so postpartum thyroiditis is an inflammation of the thyroid gland that women experience after giving birth.
Normally, the hypothalamus, which is located at the base of the brain, secretes thyrotropin-releasing hormone, or ΤRH, into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary gland.
The anterior pituitary then releases a hormone of its own, called thyroid-stimulating hormone, thyrotropin, or simply TSH.
TSH stimulates the thyroid gland, which is a gland located in the neck that looks like two thumbs hooked together in the shape of a “V”.
If we zoom into the thyroid gland, we’ll find thousands of follicles, which contain a sticky substance called colloid, which sits within follicular cells.
Follicular cells convert the protein thyroglobulin into two iodine-containing hormones, triiodothyronine or T3, and thyroxine or T4.
Once released from the thyroid gland, these hormones enter the blood and the majority is bound to circulating plasma proteins, with only a small amount of T3 and T4 traveling unbound in the blood.
Ultimately, these two hormones get picked up by nearly every cell in the body.
Once inside the cell T4 is mostly converted into T3, and it can exert its effect. T3 speeds up the basal metabolic rate.
T3 increases cardiac output, stimulates bone resorption - thinning out the bones, and activates the sympathetic nervous system, the part of the nervous system responsible for our ‘fight-or-flight’ response.
Thyroid hormone is important - and the occasional increase can be really useful when you need a boost to get through the final rounds of a sporting competition or to stay warm during a snowstorm!
Thyroid hormones are also involved in a number of other things, like controlling sebaceous and sweat gland secretion, hair follicle growth, and regulating proteins and mucopolysaccharide synthesis by skin fibroblasts.
For all this to work properly, the levels of thyroid hormones have to stay within the normal range.
To do that, the body uses negative feedback, which means that low levels of thyroid hormones tell the hypothalamus and pituitary gland to increase their secretion of TRH and TSH, respectively.
More TRH increase TSH production in the pituitary and the thyroid gland gets more stimulation to make thyroid hormones, and eventually, T3 and T4 levels go back up to the normal range again.
In postpartum thyroiditis, a woman typically has a preexisting autoimmune thyroiditis like Hashimoto’s thyroiditis, but it’s usually very mild, so they may not have any symptoms.
When that woman gets pregnant, there are a lot of physiologic changes and one of them is to dampen the immune response - perhaps to stop the immune system from reacting to the presence of a baby that makes new proteins because of the father’s DNA.
Then after birth, the immune system returns to its normal level of activity, and that change can sometimes aggravate the pre-existing autoimmune thyroiditis.
Ultimately, the reason our immune system might attack the thyroid is molecular mimicry, where thyroid cell antigens look so similar to antigens of foreign invaders, like viruses, that immune cells actually confuse the two! Any time this happens, the body's cells earn the name of autoantigens.
When that happens, the autoantigens, in this case from the thyroid cells, get picked up by antigen-presenting cells and delivered to a nearby lymph node, activating CD4+ T-helper cells.
T-helper cells stimulate the B-cells in the lymph node to start proliferating, and differentiate into plasma cells, which are able to produce specific autoantibodies against these autoantigens like thyroid peroxidase, thyroglobulin, and TSH receptors.