Postpartum Thyroiditis.

Postpartum thyroiditis (PPT) is an autoimmune-mediated destructive thyroiditis that occurs in the first year postpartum with a prevalence of 5%. In order to appropriately counsel and treat the patient, physicians need to recognize the signs and symptoms of PPT and distinguish PPT from Graves hyperthyroidism. This review of PPT will discuss the etiology, clinical course, risk factors, prognosis, and treatment of PPT. Understanding PPT is important for all physicians taking care of women in the peripartum period as women who have had PPT are at an increased risk of subsequent episodes of PP and at risk of permanent hypothyroidism.

[Postpartum thyroiditis as the first clinical manifestation of autoimmune polyendocrine syndrome type 2 ­ case report].

Postpartum thyroiditis is a form of autoimmune thyroiditis developing during the first 12 months postpartum in 5-10% of women as a consequence of the immunologic flare following the immune suppression of pregnancy. Autoimmune polyendocrine syndromes are rarely diagnosed conditions characterized by the association of at least two organspecific autoimmune disorders, and on the basis of their clinical picture, they may be divided into four different types. The underestimation of their real frequency probable results from physicians' inadequate knowledge of these clinical entities and sometimes their atypical clinical picture. Although autoimmune thyroid disease may be a component of both type 2 and 3 autoimmune polyendocrine syndromes, but the association between postpartum thyroiditis and autoimmune conditions of other endocrine organs has very rarely been described in literature. We report a case of a young woman, who after two subsequent pregnancies developed postpartum thyroiditis of different clinical pictures. After her second pregnancy, postpartum thyroiditis was followed by the development of autoimmune adrenal failure and premature ovarian failure, which allowed to diagnose type 2 autoimmune polyendocrine syndrome. Our case study suggests that every person with postpartum thyroiditis, particularly if this disorder is accompanied by atypical clinical manifestation, should be assessed for the possible presence of autoimmune polyendocrine syndrome.

Postpartum thyroiditis.

Postpartum thyroiditis (PPT) is a syndrome of transient or permanent thyroid dysfunction occurring in the first year after delivery or abortion. It is the most common thyroid disease in the postpartum period with incidence between 5 and 9%. In essence, it is an autoimmune inflammation of the thyroid, caused by changes in humoral and cell-mediated immune response. It has a characteristic biphasic course with an episode of transient thyrotoxicosis followed by transient or permanent hypothyroidism. Of all predisposing factors positive titers of thyroid peroxidase antibodies have the greatest importance. In some of the affected patients the disease course is marked by expressed hormonal disorders causing significant subjective symptoms. This underlines the need for early identification of risk groups aimed at prophylaxis and adequate treatment of thyroid dysfunction in the postpartum period. The frequency of PPT varies between analyses and studies on risk factors do not establish reliable predictive models for progression of the disease. This is due to the different methodology of research and the involvement of a number of genetic and non-genetic factors in different geographic regions. That is why implementation of mass screening programs is now controversial. The discrepancy in the opinions of researchers makes it necessary to have studies of the problem in performed in every clinical center in which the possible risk specific to the region and the population covered might be defined prognostically. The results of these studies can be used to introduce targeted and cost-effective screening for early detection of risk patients and prevention of morbidity and complications of PPT.

Approach to the patient with postpartum thyroiditis.

Postpartum thyroiditis (PPT) is the occurrence of de novo autoimmune thyroid disease, excluding Graves' disease, in the first year postpartum. The incidence of PPT is 5.4% in the general population, and it is increased in individuals with other autoimmune diseases such as type 1 diabetes mellitus. The classic presentation of PPT of hyperthyroidism followed by hypothyroidism is seen in 22% of cases. The majority of women with PPT experience an isolated hypothyroid phase (48%), with the remainder experiencing isolated thyrotoxicosis (30%). Up to 50% of women who are thyroid antibody positive (thyroid peroxidase antibody and/or thyroglobulin antibody) in the first trimester will develop PPT. Symptoms are more common in the hypothyroid phase of PPT and include fatigue, dry skin, and impaired memory. Despite multiple studies exploring the relationship between PPT and postpartum depression, or postpartum depression in thyroid antibody-positive euthyroid women, the data are conflicting, and no firm conclusions can be reached. Long-term follow-up of women who had an episode of PPT reveals a 20-40% incidence of permanent primary hypothyroidism. In a single study, selenium administration significantly decreased the incidence of PPT, but replication of the findings is needed before the recommendation can be made that all pregnant thyroid peroxidase antibody-positive women receive selenium. The indication for treating the hyperthyroid phase of PPT is control of symptoms, whereas treatment of the hypothyroid phase of PPT is indicated for symptomatic relief as well as in women who are either breastfeeding or attempting to conceive.

Significance of (sub)clinical thyroid dysfunction and thyroid autoimmunity before conception and in early pregnancy: a systematic review.

BACKGROUND: Thyroid dysfunction and thyroid autoimmunity are prevalent among women of reproductive age and are associated with adverse pregnancy outcomes. Preconception or early pregnancy screening for thyroid dysfunction has been proposed but is not widely accepted. We conducted a systematic review of the literature on the clinical significance of thyroid dysfunction and thyroid autoimmunity before conception and in early pregnancy. METHODS: Relevant studies were identified by searching Medline, EMBASE and the Cochrane Controlled Trials Register. RESULTS: From a total of 14 208 primary selected titles, 43 articles were included for the systematic review and 38 were appropriate for meta-analyses. No articles about hyperthyroidism were selected. Subclinical hypothyroidism in early pregnancy, compared with normal thyroid function, was associated with the occurrence of pre-eclampsia [odds ratio (OR) 1.7, 95% confidence interval (CI) 1.1-2.6] and an increased risk of perinatal mortality (OR 2.7, 95% CI 1.6-4.7). In the meta-analyses, the presence of thyroid antibodies was associated with an increased risk of unexplained subfertility (OR 1.5, 95% CI 1.1-2.0), miscarriage (OR 3.73, 95% CI 1.8-7.6), recurrent miscarriage (OR 2.3, 95% CI 1.5-3.5), preterm birth (OR 1.9, 95% CI 1.1-3.5) and maternal post-partum thyroiditis (OR 11.5, 95% CI 5.6-24) when compared with the absence of thyroid antibodies. CONCLUSIONS: Pregnant women with subclinical hypothyroidism or thyroid antibodies have an increased risk of complications, especially pre-eclampsia, perinatal mortality and (recurrent) miscarriage. Future research, within the setting of clinical trials, should focus on the potential health gain of identification, and effect of treatment, of thyroid disease on pregnancy outcome.

Thyroid disease in pregnant women with systemic lupus erythematosus: increased preterm delivery.

Thyroid disease is common in pregnancy and is associated with miscarriage, preterm delivery and postpartum thyroiditis (PPT). Systemic lupus erythematosus (SLE) is associated with miscarriage and preterm delivery. The hypotheses of the study are (1) pregnant women with SLE will have a high prevalence of undiagnosed hypothyroidism and a high prevalence of PPT, and (2) women with SLE and thyroid disease will have an increased incidence of adverse pregnancy outcomes as compared with pregnant women with SLE who do not have thyroid disease. This was a retrospective study of the Hopkins Lupus Cohort. All women had thyroid-stimulating hormone and thyroid antibodies assayed on frozen sera. In total, 63 pregnant women who met the ACR classification for SLE were evaluated. Outcome measures were the prevalence of thyroid disease during pregnancy and postpartum, and pregnancy outcomes. Some 13% of the women were on thyroid hormone prior to becoming pregnant, 11% were diagnosed with hypothyroidism during pregnancy, and 14% developed PPT. The prevalence of preterm delivery was 67% in women with thyroid disease and 18% in women who were thyroid disease free (p = 0.002). The presence of thyroid antibodies was not correlated with preterm delivery. Pregnant women with SLE have an increased prevalence of thyroid disease. Women with SLE and thyroid disease have an increased prevalence of preterm delivery.

High iodine intake is a risk factor of post-partum thyroiditis: result of a survey from Shenyang, China.

The aim of the present study is to obtain the epidemiological data on post-partum thyroiditis (PPT) firstly in Chinese women, and to tryto evaluate whether excessive intake of iodine in post-partum women imposes any danger of occurring PPT. Sixty hundred and ten pregnant women were involved in the cohort just before delivery. Four hundred and eighty-eight (80%) of them accepted taking part in follow-ups more than 6 months post-partum. A blood sample was taken from participants before delivery and every 3 months post-partum for testing of serum TSH, thyroid autoantibodies. Free T3 (FT3), free T4 (FT4) and TSH receptor antibody (TRAb) were detected if TSH was abnormal. The iodine nutrition was evaluated according to the mean level of the fasting urinary iodine excretions at different times during the studying period, and participants were subgrouped into 3 categories with low, adequate and high iodine intake. For those participants who had thyroid dysfunction within 6 months post-partum, the follow-up persisted for 1 yr. Of 488 pregnant women, PPT developed in 11.9% (58/488). Given overt and subclinical PPT, the prevalence was 7.17% (no.=35) and 4.71% (no.=23), respectively. There was a strong association between the presence of thyroid peroxidase antibody (TPOAb) at delivery and the risk of developing PPT [RR=6.76, 95% (CI) 4.42-10.34]. Overt cases had much higher titers of TPOAb than subclinical patients (all p<0.05). The median urinary iodine (MUI) of patients with PPT was significantly higher than that of healthy women (231.93 vs 199.88 microg/l p=0.00153). Both the prevalence of PPT and positive TPOAb rise with the increment of iodine intakes. Pregnant women with high iodine intake had more risk of developing PPT when compared with those with low iodine intake (RR=2.92, 95%CI 1.31-6.50). We concluded that positive TPOAb was of value for predicting the occurrence and severity of PPT, and a high iodine intake was a risk factor triggering PPT.