Postpartum thyroiditis is a transient inflammatory disease of the thyroid gland that develops within a year after childbirth. The basic symptoms are fatigue, the formation of a painless goiter, a reduction in breast milk volume, dry skin, increased hair loss, depression. The thyrotoxicosis phase is accompanied by muscle weakness, irritability, palpitations, tremor, weight loss, diarrhea; the hypothyroidism phase is accompanied by lethargy, chilliness, apathy, puffiness. Diagnostics includes examination of the level of antibodies and hormones (blood), ultrasound and thyroid scintigraphy. Medical treatment, symptomatic agents, thyroxine are prescribed.
ICD 10
O90.5 Postpartum thyroiditis
Meaning
Postpartum thyroiditis (PT) develops on an autoimmune basis. For the first time, the symptoms of thyroid dysfunction in a recently born woman were described and published in 1948. Currently, PT is considered as a variant of autoimmune thyroopathy, “silent” pain-free thyroiditis. The disease may debut in the next year after the birth of a child, but it is more often manifested from the 8th to the 14th week of the postpartum period. Data on the prevalence of postpartum thyropathies vary significantly (from 1.1 to 21%), due to differences in diagnostic criteria, research methods used in different countries. In the USA, epidemiology accounts for 1-2% of all pregnancy cases.
Causes
The disease occurs against the background of natural fluctuations in the activity of the immune system during pregnancy. The cause of postpartum thyroiditis is autoaggression to the thyroid gland, provoked by the restoration of immune cell functions after a period of suppression necessary for the preservation of the fetus. The high risk of developing an autoimmune reaction is due to the following factors:
- Repeated pregnancies. The frequency of thyroiditis is higher among repeat births. The probability of an autoaggressive process increases with each subsequent pregnancy, which is associated with an increase in the number of antibodies.
- Type 1 diabetes mellitus. In patients with type 1 diabetes, the nocturnal secretion of thyroid-stimulating hormone is reduced, the conversion of T4 to T3oo is insufficient. The functions of the thyroid gland are weakened, with the formation of an autoimmune response, thyroopathy occurs more easily.
- Increased titer of ab-TH. 25% of women with a positive test result for AT to thyroglobulin develop thyroiditis. Specific immunoglobulins provoke a violation of the hormone-secreting function of the gland.
- High titer of anti-TPO. In 50% of patients with high titers of autoantibodies to TPO, postpartum autoimmune thyroopathy is diagnosed. Under the action of antibodies, the formation of the active form of iodine, necessary for the synthesis of thyroid hormones, is suppressed.
- Postpartum thyroiditis in the anamnesis. Mothers who have had the disease after previous pregnancies have a greater risk of re-debut. The immune system “remembers” the features of hormonal shifts.
Pathogenesis
There is a relationship between the development of postpartum thyroiditis, the presence of markers of autoimmune thyropathies (ab-TPO, ab-TH) and several HLA haplotypes characteristic of diffuse goiter, autoimmune thyroiditis. At the morphological level, the phenomena of lymphocytic infiltration and diffuse destructive changes of the thyroid gland are found, similar to those in pain-free and autoimmune thyroiditis. In the pathogenesis of PT, the phenomenon of immune reactivation or “rebound phenomenon” is distinguished. An increase in the amount of anti–TPO in the postpartum period is the result of a general increase in the synthesis of immunoglobulins after prolonged natural immunosuppression. Thyrotoxicosis is caused by the effect of the complement system on thyrocytes. As a result of the immune attack, the gland cells are partially destroyed, reserves of iodized hormones are released into the bloodstream, thyrotoxicosis occurs. With a prolonged autoimmune process, thyrocytes are completely destroyed, hypothyroidism is formed.
Symptoms
As a rule, thyroiditis develops after pregnancy, which ended in childbirth on time. Less often, the disease is diagnosed after premature birth, spontaneous termination in the first or second trimester. The most common option is a three–phase course: first, transient thyrotoxicosis occurs, then short-term euthyroidism, and finally, passing hypothyroidism. The thyrotoxic phase most often debuts 8-12 weeks after the birth of the child and lasts 1-2 months. The absence of pronounced clinical signs is characteristic. Patients note increased nervousness, irritability, weakness, fatigue, weight loss, trembling in the hands, palpitations. Often these symptoms are regarded as the result of lack of sleep, increased workload associated with the birth of a baby.
The next phase is hypothyroid. It starts from 19-24 weeks, lasts from 4 to 6 months. Symptoms of hypothyroidism are observed: drowsiness, chilliness, slowness of movements and thought processes, apathy, depression, lowering body temperature, lowering blood pressure, swelling. Over time, headaches, muscle and joint pains appear, the skin becomes drier, hair falls out intensively. After 6-8 months, the thyroid function normalizes, hypothyroidism is reduced. A paradoxical course of the disease is possible when the hypothyroid phase precedes the thyrotoxic one. In 20% of cases, only thyrotoxicosis is observed, in 40-50% – only hypothyroidism.
Complications
In about a third of patients with PT, against the background of an increase in the titer of antibodies to thyroperoxidase, transient hypothyroidism transforms into permanent (persistent) and requires lifelong hormone replacement therapy with thyroxine. A violation of thyroid function in the postpartum period and an increase in the amount of TSH is assessed as a high risk factor for the development of thyroiditis after the next pregnancy. Recent research in the field of endocrinology is aimed at studying the relationship between the prolonged hypothyroid phase and postpartum depression. Statistical data confirm the presence of a direct correlation between these two pathologies – the prevalence of depression among young mothers with thyroid disorders is higher than in the rest of the population.
Diagnostics
The examination of women with suspected postpartum thyroiditis is carried out by an endocrinologist. Diagnosis is based on the detection of functional disorders and structural changes of the thyroid gland, increased levels of autoantibodies. The main objectives of the research are to determine the state of thyrotoxicosis or hypothyroidism (depending on the phase of the disease), to differentiate PT from Graves’ disease and Hashimoto’s thyroiditis. The correct diagnosis is necessary for the appointment of adequate therapy and prognosis. Clinically, it can be difficult to distinguish between these diseases, although diffuse toxic goiter is characterized by more pronounced symptoms of thyrotoxicosis, and for autoimmune thyroiditis – longer signs of hypothyroidism. Often, the final diagnosis is made based on the results of dynamic monitoring of the patient’s condition. Objective methods of examination include:
- Blood test for antibodies. An increase in the level of ab-TPO is determined in 80% of patients, the ab-rTSH indicator almost always remains normal. In Bazedov-Graves’ disease, both types of antibodies are elevated (85 and 75% of cases, respectively).
- Hormonal blood testing. The phase of thyrotoxicosis is characterized by an increase in the concentration of TSH. The level of thyroxine in some patients is normal, sometimes a slight or moderate increase is detected. With diffuse toxic goiter, T4 and T3 indicators are significantly increased, TSH is reduced.
- Echography. According to the ultrasound of the thyroid gland, the preservation of the previous size or a slight increase in the gland is revealed. There is a decrease in echogenicity and the appearance of diffuse changes. The results of ultrasound examination do not allow differentiating autoimmune thyropathies.
- Radioisotope research. Thyroid scintigraphy is allowed for women who are not breastfeeding. With postpartum thyroiditis, the absorption of the drug is reduced or completely absent, with basal disease – diffusely enhanced.
Treatment
Drug therapy. Specific methods have not been developed. At the stage of thyrotoxicosis, symptomatic drugs are used, the use of thyrostatics is not justified, since there is no hyperfunction of the gland, an increase in the concentration of hormones is due to the destruction of follicles. Hormone replacement therapy is indicated for hypothyroidism. In the classic three – phase variant of the course of the disease , the treatment regimen is as follows:
- Symptomatic drugs. Most patients are prescribed beta-blockers to eliminate tachycardia, irritability, tremor. Glucocorticoids and NSAIDs reduce the severity of inflammatory processes and the activity of autoantibodies.
- Hormonal agents . Hypothyroidism therapy is long-lasting, it is carried out for 9-12 months. Thyroxine preparations are used, for example, levothyroxine. After completing the course of treatment, the ability of the thyroid gland to recover is evaluated. With the preservation of hypothyroidism, the question of lifelong intake of the hormone is solved.
- Iodine-containing preparations. After the main therapy, patients need to monitor the intake of iodine. Foods rich in this trace element are introduced into the diet – sea cabbage, seafood, nuts. Women living in regions with iodine deficiency are shown to take special food supplements.
Prognosis and prevention
With a correct diagnosis and the fulfillment of all medical appointments, the thyroid gland’s functionality is fully restored, the disease goes into a stage of persistent remission. Most patients have an increased risk of hypothyroidism. Prevention should begin at the stage of pregnancy planning. Women with thyroid disorders, hereditary burden, living in areas with iodine deficiency need to be examined by an endocrinologist. If there is a risk of thyroiditis, a specialist prescribes iodine-containing drugs and medications that reduce the activity of antibodies.