Postpartum thyroiditis

Definitions & Key takeaways

Postpartum thyroiditis is an inflammation of the thyroid gland that occurs a few months after giving birth, resulting in either hypothyroidism or hyperthyroidism. The first phase is typically hyperthyroidism. Then, the thyroid either returns to normal or a woman develops hypothyroidism. In some cases, the inflammation may subside without any treatment, but once permanent hypothyroidism develops, there is a need for lifelong treatment with thyroid hormone replacement medications.

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Introduction0:00–0:18

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.

Physiology0:18–2:49

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. So as an example, they might produce more proteins and burn up more energy in the form of sugars and fats.
It’s as if the cells are in a bit of frenzy. 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.

Pathology2:49–5:45

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.
These autoantibodies bind to and block those targets, preventing normal function of the thyroid. In addition, they act like a “tag” on the follicular cells that have these autoantigens, so that they can be targeted and destroyed by natural killer cells.
Meanwhile, CD4+ T-helper cells produce inflammatory cytokines, like interferon-γ, which attract macrophages into the thyroid gland thus causing damage to the follicles.
These cytokines also attract another type of T-lymphocytes, called CD8+ cytotoxic T-cells. CD8+ cytotoxic T-cells directly target and destroy thyroid follicular cells.
Now initially, the destruction of these follicular cells leads to T3 and T4 getting spilled out into the blood, creating a transient hyperthyroid or thyrotoxic state.
But as the thyroid gland gets more and more damaged, the colloid gets depleted over time and follicles atrophy, or get smaller.
This leads to decreased T3 and T4 and cause hypothyroidism. In any case, though, all this inflammation also causes connective tissue to build up, leaving less space for the functional thyroid cells.
In most people with postpartum thyroiditis, the thyroid normally recovers within a year of giving birth, but in some unlucky mothers who experience that hypothyroid stage, the thyroid never recovers, leaving them with a chronic case of hypothyroidism.

Symptoms5:45–6:29

Postpartum thyroiditis usually causes a painless goiter, which is an enlarged thyroid gland. Initially, destruction of the thyroid cells release thyroid hormone and causes hyperthyroidism.
In that phase, the body has an increased metabolism, which can cause weight loss, palpitations, tremors, anxiety, or heat intolerance.
Typically, this'll start off a few months after delivery, and last up to eight weeks. Then, there’s the hypothyroidism phase, where the body has a decreased metabolism, which can cause a lack of energy, constipation, dry skin, or cold intolerance.
Typically, this can last up to six months. The diagnosis of postpartum thyroiditis can be confirmed with thyroid function tests to establish whether someone is in the hyperthyroid or hypothyroid phase and can be confirmed by looking for anti-thyroid peroxidase antibodies.

Diagnosis6:29–6:43

Treatment6:43–6:58

Most of the time, postpartum thyroiditis doesn't require treatment, but sometimes beta blockers like propranolol can help with symptoms like palpitations and tremors, and in hypothyroidism, thyroid hormone replacement can help as well.

Review6:58–7:27

All right, as a quick recap… Postpartum thyroiditis is an inflammation of the thyroid gland that occurs in a woman a few months after she’s given birth.
It's often due to an aggravation of a preexisting autoimmune thyroiditis. Initially, damage to the thyroid gland, can result in hyperthyroidism, but later on, the loss of healthy thyroid tissue can result in hypothyroidism.
In most cases, thyroid activity returns to normal after about a year.