Goiter after childbirth

Introduction Most patients with postpartum thyroiditis appear to have goiter or increase on the original basis. Postpartum thyroiditis (PPT) is a thyroid dysfunction syndrome that occurs one year after birth and can be temporary or permanent. Its pathological basis is thyroid autoimmune inflammation, which is the most common and most characteristic postpartum autoimmune thyroiditis. The disease can also occur after abortion 5 to 20 weeks of pregnancy. Postpartum thyroiditis and postpartum thyroid syndrome are two different concepts. The latter refers to thyroid dysfunction that occurs after birth or is developing thyroid disease.

Cause

(1) Causes of the disease

Autoimmune

The disease has been shown to be closely related to autoimmunity. In the early pregnancy (first 3 months) TPOAb positive, the incidence of postpartum thyroiditis is as high as 30% to 50%.

2. Genetics

Studies have shown that this disease has HLA antigen polymorphism.

3. Iodine

Excess iodine can induce postpartum thyroiditis.

4. Women with previous history of Graves disease, postpartum asymptomatic thyroiditis is particularly common.

(two) pathogenesis

Autoimmune

The disease has been shown to be closely related to autoimmunity. In the early pregnancy (first 3 months) TPOAb positive, the incidence of postpartum thyroiditis is as high as 30% to 50%. Postpartum TPOAb levels tend to suggest a postpartum immune rebound and immune-mediated thyroid damage. In recent years, it has also been noted that thyroiditis can occur within 1 year after natural or elective abortion (including ectopic pregnancy) in early pregnancy, similar to postpartum thyroiditis, and the risk of miscarriage is higher in pre-pregnancy antibody-positive patients than in antibody-negative patients. Times. In vivo immunological changes in non-term pregnancy are sufficient to cause post-production thyroiditis in patients.

2. Genetics

Studies have shown that this disease has HLA antigen polymorphism. A large number of clinical and laboratory studies have also suggested that Hashimoto thyroiditis and the disease may have a common cause. The explanation for the correlation between HLA antigen and the pathogenesis of postpartum thyroiditis may be:

(1) The disease site is not linked to the HLA site. It is also possible that HLA plays a direct role in the disease process.

(2) The polymorphism of HLA may be an influencing factor for the ability of antigen presenting cells to present a special series of antigenic peptides, thereby modulating the susceptibility of the disease.

3. Iodine

Excess iodine can induce postpartum thyroiditis. Hypothyroidism is most likely to occur in women with a history of the disease with a daily intake of iodine greater than their daily requirements.

The cause of postpartum disease in this disease is generally considered to be immune tolerance (decreased CD4 positive cells, inhibition of NK cell activity, etc.) during pregnancy, allowing fetal transplantation. Problems related to the weakening of maternal immunity after birth, including placental factors and fetal inhibitory T cell activity, have not been known. This weakening of postpartum inhibition increases the immune response, that is, the rebound of body fluids and cellular immunity after birth mediates the occurrence of postpartum thyroiditis. The patient detected more thyroid antibodies during pregnancy, indicating the presence of subclinical autoimmune thyroiditis, which worsened after birth.

an examination

Related inspection

Serum total thyroxine (TT4) free thyroxine (FT4) free triiodothyronine (FT3) total triiodothyronine (TT3) free thyroxine

1, blood thyroglobulin: thyrotoxicosis stage, speculated that low levels of thyroid antibody destruction mechanism caused by thyroid iodine protein leakage into the circulation. The hormone released may be a macromolecular complex that requires enzyme catalysis. This explanation is supported by a marked increase in blood thyroglobulin at this stage and an increase in iodine excretion rate. Or may be interpreted as the result of complement attacking thyroid follicles.

2, thyroid pathological examination showed: local or extensive lymphocytes and plasma cells infiltrated thyroid tissue, sometimes visible central transparent follicles. No germinal center and lymphoid follicles.

3, suffering from this disease after pregnancy and delivery and between 2 pregnancy, can relapse, the recurrence rate of 25% to 40%. This disease can occur in Sheehan syndrome postpartum.

4, the clinical manifestations of this disease is short-lived, sometimes blurred and easy to be ignored.

5, thyrotoxicosis: about 50% occur, 1 to 3 months after birth, can last for 1 to 2 months. Among them, only 22.2% of those who showed this clinical process. Increased appetite, weight loss, neuroticism, etc. often lack specificity, but palpitations and fatigue may be more prominent and become the main complaint. If the thyrotoxicosis stage is more than 2 months, the symptoms are often obvious and may be accompanied by mental symptoms.

6, 51% thyroid enlargement. It appears as a goiter or increases on the original basis. Mostly mild diffuse enlargement, uniform texture, occasionally only a single isolated nodule, no pressure pain. More avascular murmur. There is no thyroid enlargement in permanent hypothyroidism.

7, transient hypothyroidism: 25% ~ 42.3% only this stage of performance. 35.5% have experienced the above two different stages. Symptoms usually appear 3 to 6 months after delivery: edema, weight gain, chills, loss of appetite, etc. Sometimes showing mental disorders, can be mistaken for depression. The incidence of depression in women with circulating thyroid antibody positive patients increased by 8.8% to 30%.

8, some menstruation or uterine bleeding, or with menstrual-lesion syndrome with increased PRL and mistaken for pituitary lesions. Most patients can return to normal within 5 to 10 months after delivery.

9. Permanent hypothyroidism occurs in 10% to 23% of patients. 50% of women with TPOAb-positive disease develop hypothyroidism in the future, with an annual incidence of about 3% to 5%. Permanent hypothyroidism occurs in 25% to 30% of transient thyroid dysfunction in the early stages of the disease. 92% of people with permanent hypothyroidism developed transient hypothyroidism in the early stages of the disease. The early stage of postpartum dysfunction, TSH>20mU/L, is a predictor of long-term thyroid dysfunction. The TPOAb titer in early pregnancy is a good indicator of long-term hypothyroidism after the onset of the disease. Multiple pregnancies are associated with persistent hypothyroidism after postpartum thyroiditis.

10. The incidence of spontaneous abortion is related to permanent hypothyroidism. It is speculated that these patients have mild hypothyroidism during pregnancy and affect the viability of the fetus. For patients with impaired thyroid function, permanent hypothyroidism should be considered in patients who have symptoms for 1 year after diagnosis. In the sixth month after delivery, 82% of women with this disease developed hormonal abnormalities. Some people had no typical clinical experience and had entered the stage of hypothyroidism at the time of treatment. There are also patients with postpartum hyperfunction and dysfunction that do not appear or appear inconspicuous, only thyroid enlargement during physical examination.

11, the disease generally relieved within 1 year.

12, the disease is easily missed. For postpartum goiter or aggravation, it has been attributed to simple goiter in the past. If you experience fatigue, tachycardia, nervousness, goiter, or persistent amenorrhea within 1 year after delivery, you should consider this disease. In particular, gestational goiter and patients with high titer thyroid antibodies, family history of autoimmune thyroid disease, the risk of developing this disease after childbirth, need to improve the vigilance of this disease. Postpartum goiter or progressive thyroid enlargement, even if there is no functional change may be postpartum thyroiditis. Prospective studies have shown that postpartum thyroiditis with normal thyroid function accounts for 4%.

Differential diagnosis

1. Postpartum pituitary necrosis:

Psilotype anterior hypofunction (also known as "Schiehan's disease") is caused by multiple lesions of the pituitary or hypothalamus involving the endocrine function of the pituitary. When all or most of the pituitary is destroyed, a series of manifestations of endocrine glandular dysfunction can occur, with the main glands involved being the gonads, thyroid, and adrenal cortex. The disease is more common in women, and is associated with pituitary avascular necrosis caused by postpartum hemorrhage.

2, edema in late pregnancy:

Pregnancy edema can be divided into two major categories of physiological and pathological. In the second half of pregnancy, mild edema of the lower extremities often occurs in the lower limbs. After the rest, the reduction is mostly physiological; after the break does not subside, and the worse, the pathological should be considered.

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