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PubMed1999

Clinical manifestations of postpartum thyroid disease.

Postpartum thyroiditis (PPT) occurs in 5%-9% of unselected postpartum women; hyperthyroidism and hypothyroidism develop, the latter being permanent, in up to 25 %-30% of women. PPT is strongly associated with antithyroid peroxidase (anti-TPO) antibodies, but 50% of anti-TPO positive women do not develop thyroid dysfunction. Symptom analysis has shown that lack of energy and irritability were the most frequent hyperthyroid symptoms whereas lack of energy, aches and pains, poor memory, dry skin, and cold intolerance were the significant hypothyroid features. Some of these symptoms were more frequently observed than in antibody-negative controls even when these patients were euthyroid and in anti-TPOAb positive women who did not develop PPT at all. The diagnosis of PPT is based on the observation of abnormal thyroid function tests in a postpartum anti-TPOAb-positive woman: transient hyperthyroidism occurs at 14 weeks and hypothyroidism at 19 weeks postpartum. Diffuse or multifocal hypoechogenicity of the thyroid is seen on echography and a thyroid destructive process is evidenced by an increase in serum thyroglobulin and urinary iodine excretion. In addition to the 25%-30% of women who develop permanent hypothyroidism at 3 years, recent data indicate that 50% of women who have developed PPT will be hypothyroid 7-9 years later. The long-term risk is only 5% for those anti-TPOAb positive women not developing thyroid dysfunction postpartum. The risk of recurrent PPT is 70% if previous PPT was experienced and 25% if the patient was euthyroid after the first pregnancy.

Female↗
PubMed1998

Postpartum psychosis and postpartum thyroiditis.

The term postpartum psychosis refers to a group of severe and heterogeneous disorders with psychotic symptoms that occur most frequently in the context of a mood disorder during the postpartum period. We report a case of 'postpartum psychosis' possibly associated with postpartum thyroiditis in a 29 year-old woman. The appearance of psychotic symptoms was chronologically related to the onset of postpartum thyroiditis and resolution of psychosis synchronized with the achievement of biochemical euthyroidism. The patient had typical symptoms of 'classic postpartum psychosis' (a historical term not included in DSM-IV, but used frequently by many physicians to describe diagnostic and therapeutic challenges posed by puerperal psychoses). Three months postpartum, the patient began to believe that she was pregnant with the Christ child, although she was not pregnant. Her delusions resolved around the 'pregnancy' and harm to her 'unborn' child. She also believed that her child (Jesus) was going to be killed. Other key symptoms included hallucinations, mixed mood symptoms, agitation and transient disorientation. Her DSM-IV diagnosis on admission was major depression with psychotic features and her discharge diagnosis (most likely diagnosis) was psychotic disorder due to thyrotoxicosis caused by postpartum thyroiditis. The differential diagnosis of co-occurring psychosis and postpartum thyroiditis can be examined relative to four possibilities: (1) psychosis due to thyrotoxicosis caused by postpartum thyroiditis; (2) a coincidence (no association between psychosis and postpartum thyroiditis); (3) precipitation of psychotic symptoms and disorientation related to a postpartum thyroiditis in a woman with a pre-existing mood disorder; or (4) both psychosis and thyroiditis caused by a pre-existing defect in autoimmunity. The authors stress the importance of early diagnosis and prompt treatment of postpartum psychosis. They discuss the indications for thyroid screening in postpartum psychoses. Further research is needed to clarify the nosology and mechanisms of severe postpartum disorders and to elucidate treatment-relevant and etiologically-distinct subsets of postpartum psychosis.

Adult↗
PubMed1997

Clinical aspects of recurrent postpartum thyroiditis.

BACKGROUND: Postpartum thyroiditis (PPT), characterized by transient hyperthyroidism and transient hypothyroidism, occurs in 5-9% of women. It is accompanied by the presence of circulating antithyroid peroxidase antibodies (TPOAb) which have been associated with an increase in depressive symptomatology compared with TPOAb-negative women. AIM: To assess the frequency and nature of the syndrome in patients studied in detail after more than one pregnancy, as there are only sparse data on recurrence of PPT. METHOD: Fifty-four patients were identified who had participated in at least two of three detailed postpartum studies of thyroid and psychiatric function during the past 12 years in the Caerphilly and Cardiff regions of South Wales. They included two women who had had three pregnancies. All patients had been followed monthly postpartum for at least six months, and 44 had been followed for 12 months. RESULTS: Of the 13 patients who developed PPT after their first pregnancy, nine had a recurrence of dysfunction after a further pregnancy and four remained TPOAb positive. Of the 24 women who were euthyroid anti-TPO positive after the first pregnancy, six developed thyroid dysfunction after a subsequent delivery, 14 remained antibody positive and euthyroid, while four underwent seroconversion and were antibody negative. The control group of 17 women were antibody negative after the first pregnancy; 16 remained negative after a further pregnancy and one became anti-TPO positive. The severity of PPT was slightly, but not significantly worse after the second recorded pregnancy (67% hypothyroid versus 44% hypothyroid). Neither the maximum anti-TPO titre following the first pregnancy, nor the rise in titre during this period were predictive of outcome after a subsequent pregnancy. Data from 26 women showed that recurrent depression was seen in 15.4%; a further six were depressed after the first pregnancy only, and two during a further postpartum period. CONCLUSION: There was a 70% chance of developing recurrent PPT after a first attack, and a 25% risk even in women who were only anti-TPO positive without thyroid dysfunction during the first postpartum period. The recurrence of postpartum depression was not related to thyroid function. Patients noted to have thyroid dysfunction or just to be euthyroid but anti-TPO positive after pregnancy should be assessed carefully after a subsequent pregnancy.

Autoantibodies↗
PubMed2002

Thyroid dysfunction: reproduction and postpartum thyroiditis.

Thyroid function during pregnancy is characterized by changes in circulating thyroid hormone concentrations related to alterations in thyroxine binding globulin (TBG), human chorionic gonadotropin (hCG), and iodine status. The immunology of normal pregnancy shows a reduction in antibody titer during gestation and an increase in T helper-2 (TH2) immune responses. Thyroid dysfunction may cause menstrual disturbances in hyper- and hypothyroidism but less marked disturbances of sexual function in men. Fertility is reduced in hypo- and hyperthyroid females. Accumulating evidence suggests a strong association between the presence of thyroid antibodies and fetal loss, although the data relating to recurrent abortion are not so convincing. Asymptomatic maternal gestational hypothyroidism may occur in up to 2.5% of women; studies have shown a significant impact of this condition in causing a decrease of child IQ, suggesting that screening for maternal hypothyroidism with intervention may be justified. Postpartum thyroid disease occurs in 5 to 9% of women and thyroid dysfunction postpartum is seen in 50% of thyroid peroxidase antibody positive (TPO Ab+ve) women. There is a significant rate of hypothyroidism in long-term follow-up of women who have transient postpartum thyroid dysfunction.

Autoantibodies↗
PubMed1997

Evaluating and Managing Postpartum Thyroid Dysfunction.

Postpartum thyroid dysfunction (PTD) occurs in approximately 5% to 10% of all women within 1 year following delivery and is usually due to intrinsic thyroid disease rather than hypothalamic or pituitary lesions. The most common etiology of PTD, which may resemble postpartum depression, is autoimmune thyroid disease (chronic or Hashimoto's thyroiditis). Women with Graves' disease who experience symptom exacerbation in the postpartum period account for a small percentage of cases. Clues to PTD include nonspecific symptoms such as tiredness, fatigue, depression, palpitations, and irritability. On physical examination, tachycardia may be noted. Goiters are detected in the majority of cases. The disease course varies; most patients experience a phase of hypothyroidism that takes 2 to 6 months to resolve, but some develop permanent hypothyroidism within 5 years of the diagnosis.

Journal Article↗
PubMed1990

Thyroid size and function in healthy pregnant women with thyroid autoantibodies. Relation to development of postpartum thyroiditis.

In a study of postpartum thyroiditis, thyroid function and ultrasonically determined thyroid size were evaluated in 36 thyroid autoantibody positive healthy women during pregnancy and the first postpartum year. Twelve women (33%) developed postpartum thyroiditis with permanent thyroid dysfunction in three. However, only one woman had symptoms and needed treatment. The most common type of thyroid dysfunction was a transient hyperthyroid phase as seen in 7 women. A significant increase by 20-30% in mean thyroid volume during pregnancy was demonstrated independent of development of postpartum thyroiditis. We conclude that initial thyroid volume or changes during pregnancy and post partum are not useful indicators of the development of postpartum thyroiditis. The fact that the condition is oligosymptomatic suggests that screening procedures are necessary if one wants to diagnose the earliest phases of postpartum thyroiditis.

Adult↗
PubMed1992

Postpartum thyroid dysfunction.

Postpartum thyroid dysfunction (PPTD) refers to the syndromes of transient hyperthyroidism, transient hypothyroidism, or both, occurring sequentially in the first 12 months postpartum. Approximately 5 to 9% of women develop the disorder in this period. PPTD is most often subclinical but some women will experience symptoms such as lack of energy and depression in the hypothyroid phase. The thyroid gland, which normally enlarges during pregnancy, will remain enlarged or enlarge further in the postpartum period in a significant number of affected women, instead of returning to the prepregnancy size as in unaffected women. The gland is painless and histologically demonstrates lymphocytic infiltration. PPTD is strongly associated with the presence of antimicrosomal and/or antithyroglobulin antibodies, which occur in up to 76% of cases. Antibody activity tends to increase in the postpartum period and to peak at the time of onset of the disorder. TSH receptor antibodies are not seen and the gland has low radioiodine uptake, distinguishing PPTD from Graves' disease. The HLA associations are controversial, as is the role of dietary iodine. The etiology of PPTD is almost certainly immunological, reflecting the phenomenon of rebound from the relative immune tolerance of pregnancy. Detection of the disorder is important in order to reassure or treat those who are symptomatic and because PPTD may recur in subsequent pregnancies. In addition, up to one third of affected women will go on to develop permanent hypothyroidism 2 to 4 years later. The role of screening for PPTD remains to be clarified.

Autoantibodies↗
PubMed1998

Interleukin-6 levels are not increased in women with postpartum thyroid dysfunction.

Postpartum thyroid dysfunction (PPTD) is an autoimmune-mediated thyroid destructive process. Human interleukin-6 (IL-6) is a cytokine found to be increased in subacute thyroiditis, amiodarone-induced thyrotoxicosis, Graves' disease, and other thyroid destructive processes. We report serum IL-6 levels in PPTD in two independent studies. New York Study: In a previous prospective study we demonstrated that PPTD occurred in 25% (7/28) of women with type 1 diabetes mellitus. IL-6 determinations were made on the frozen serum samples of these 28 women during each trimester of their pregnancy and at 1.5, 3, 6, 9, and 12 months postpartum. IL-6 levels were found to be similar in women with PPTD compared with women without PPTD (mean 3.06+/-2.25 vs. 2.51+/-2.21 pg/mL; p = 0.15). No difference in IL-6 levels was found between the pre- and the postpartum periods (mean 2.67+/-1.82 vs. 3.04+/-2.44 pg/mL; p = 0.30) in all 28 women. Cardiff Study: Serum IL-6 levels were measured on frozen serum samples of 30 women with PPTD. IL-6 levels were below the detection limit (25 fmol/L or 0.65 pg/mL) in 94 (67%) of these samples. No significant difference in the mean serum IL-6 levels were found between any time points in the study. There was no correlation between serum IL-6 levels, thyroid peroxidase (TPO)- antibodies and serum thyrotropin (TSH) levels at any time point. IL-6 levels during pregnancy or postpartum were not found to be significantly different in women with PPTD compared with women without PPTD.

Adult↗
PubMed1991

Interference in thyroid-function tests in postpartum thyroiditis.

Three women are described from a study of patients with postpartum thyroiditis whose sera gave spuriously increased concentrations of free thyroid hormone because of antibody binding of radiolabeled thyroxin (T4) and triiodothyronine (T3) analogs. All of the women showed increased serum concentrations of thyroid autoantibodies. The antibody binding of radiolabeled analogs and its effect on free T4 and free T3 assays disappeared by 48 weeks postpartum. Postpartum women who develop thyroid autoantibodies have approximately 2% prevalence of increased binding of radiolabeled analogs, which can result in an interference in thyroid hormone assays involving T4 and T3 analogs.

Autoantibodies↗
PubMed1999

Transient diffuse low thyroid echogenicity in painless postpartum thyroiditis: report of two cases.

We report two cases of chronic autoimmune thyroiditis, one patient with recurrent painless thyroiditis and another with recurrent postpartum thyroiditis. In these two patients, the episode of subacute thyroiditis seemed to be immune mediated. Thyroid ultrasonography showed a diffuse, markedly hypoechogenic gland, coinciding with each of the episodes of transient thyroid dysfunction that reverted to a normal echographic appearance with recovery of normal thyroid function. These two cases show that a diffuse low echogenicity of the thyroid, frequently seen in autoimmune thyroid disorders, can be a reversible event and suggest that the transient nature of certain forms of hypothyroidism may be predicted by a follow-up echographic examination. Further studies with a larger number of patients are required to confirm this observation.

Adult↗
PubMed1990

IgG subclass distribution and relative functional affinity of thyroid microsomal antibodies in postpartum thyroiditis.

An association between the development of postpartum hypothyroidism and high levels of IgG1 subclass microsomal (M) antibodies has been reported. Using an assay designed to detect reasonable levels of all the four IgG subclasses, we found no differences in the proportion of each IgG subclass in M antibodies of patients with postpartum hyperthyroidism or hypothyroidism compared with control postpartum patients with M antibodies but no thyroid dysfunction. However the total amount of M antibody of each IgG subclass was elevated above the controls in the patients with thyroid dysfunction. The relative functional affinity of M antibodies did not differ between controls and patients with hypothyroidism but declined 5 and 10-12 months after delivery compared to values at 2 months. These results do not support the suggestion that the amount of IgG1 subclass M antibodies particularly determines the course of postpartum thyroiditis. Rather, the total M antibody level, in all four subclasses, is associated with clinical outcome. Resolution of the disease, despite persisting M antibodies, may occur in part because the relative functional affinity of these antibodies declines after delivery.

Antibody Affinity↗
PubMed1988

Postpartum thyroiditis.

The special characteristics of postpartum thyroid syndromes are summarized in Table 8. Many of the cases will pass unnoticed, although a higher detection rate is to be expected if postpartum thyroid disease becomes better known among physicians and the general public. Screening in early pregnancy of women with a previous or family history of thyroid disease and in women with other autoimmune disorders (such as diabetes mellitus type 1) may be worthwhile. The initial manifestation of postpartum thyroiditis, often appearing during the first three months postpartum, is a thyrotoxic phase characterized by a low RAIU ('painless thyroiditis' or 'destruction-induced thyrotoxicosis'). Subsequently, a transient hypothyroid phase supervenes. In a small proportion of women hypothyroidism becomes permanent. After a subsequent pregnancy recurrence is the rule. Women who are genetically disposed to Graves' disease may experience thyrotoxicosis with a high RAIU usually appearing later than three months postpartum. As the thyroid function abnormalities are usually mild and transient it is often appropriate to withhold treatment. However, in women with pronounced symptoms treatment should be started. When the postpartum period has passed gradual withdrawal of treatment should be attempted. In women who have experienced postpartum thyroid dysfunction, the risk of developing permanent thyroid disease in later life seems important and therefore long-term follow-up is recommended.

Female↗
PubMed1997

[Postpartum thyroiditis and Basedow disease].

BACKGROUND: The postpartum period is characterized by a rebound in autoimmunity secondary to immune tolerance induced by pregnancy, creating favorable conditions for flare up of Graves' disease or autoimmune thyroiditis. Postpartum thyroiditis is a recognized clinical entity. CASE REPORT: Six years after onset of Graves' disease treated with antithyroid drugs, a 25-year-old woman had a high serum level of antithyroperoxidase antibodies a few months before she became pregnant. Six weeks after delivery, she developed signs of hyperthyroidism and goiter. The diagnosis of postpartum thyroiditis was retained. Her condition regressed spontaneously to euthyroidism then hypothyroidism. DISCUSSION: The therapeutic options involved underline the importance of distinguishing between Graves' disease and postpartum thyroiditis. The diagnosis of postpartum thyroiditis is based on history taking, clinical findings, and laboratory tests, especially isotope uptake.

Adult↗
PubMed2001

Postpartum thyroiditis and autoimmune thyroiditis in women of childbearing age: recent insights and consequences for antenatal and postnatal care.

Postpartum thyroiditis is a syndrome of transient or permanent thyroid dysfunction occurring in the first year after delivery and based on an autoimmune inflammation of the thyroid. The prevalence ranges from 5-7%. We discuss the role of antibodies (especially thyroid peroxidase antibodies), complement, activated T cells, and apoptosis in the outbreak of postpartum thyroiditis. Postpartum thyroiditis is conceptualized as an acute phase of autoimmune thyroid destruction in the context of an existing and ongoing process of thyroid autosensitization. From pregnancy an enhanced state of immune tolerance ensues. A rebound reaction to this pregnancy-associated immune suppression after delivery explains the aggravation of autoimmune syndromes in the puerperal period, e.g., the occurrence of clinically overt postpartum thyroiditis. Low thyroid reserve due to autoimmune thyroiditis is increasingly recognized as a serious health problem. 1) Thyroid autoimmunity increases the probability of spontaneous fetal loss. 2) Thyroid failure due to autoimmune thyroiditis-often mild and subclinical-can lead to permanent and significant impairment in neuropsychological performance of the offspring. 3) Evidence is emerging that as women age subclinical hypothyroidism-as a sequel of postpartum thyroiditis-predisposes them to cardiovascular disease. Hence, postpartum thyroiditis is no longer considered a mild and transient disorder. Screening is considered.

Adult↗
PubMed1992

The sonographic appearances in postpartum thyroiditis.

During the postpartum period about 50% of women with circulating thyroid autoantibodies develop a transient autoimmune thyroiditis. To determine the sonographic appearances in postpartum thyroiditis (PPT), serial ultrasound (US) scans of the thyroid were performed in 135 postpartum women who were divided into three clinical groups: Group 1, 37 antibody positive subjects who developed PPT; Group 2, 28 antibody positive subjects in whom thyroid function remained normal; Group 3, 70 antibody negative controls. Thyroid hypoechogenicity was observed in 14/31 patients (45%) who were scanned between 4 and 8 weeks postpartum and who subsequently developed PPT (Group 1) compared with 4/24 patients (17%) in Group 2 (P less than 0.05) and 1/65 patients (1.5%) in Group 3 (P less than 0.001). In antibody positive patients, the positive predictive value of an abnormal scan during this period was 78%. Between 15 and 25 weeks postpartum thyroid hypoechogenicity was present in 32/37 patients (86%) in Group 1 compared with 11/28 patients (39%) in Group 2 (P less than 0.001) and 2/70 patients (3%) in Group 3 (P less than 0.001). Sonographic abnormality persisted beyond 32 weeks postpartum in 36/41 antibody positive patients (87%) who had exhibited thyroid hypoechogenicity earlier during the study and who had late scans. The characteristic US appearance in PPT is thyroid hypoechogenicity. The role of sonography in the prediction, diagnosis and follow up of patients with PPT is discussed.

Autoantibodies↗
PubMedDate not supplied

[Postpartum thyroiditis. 31 cases].

Postpartum thyroiditis. 31 cases. Between 1977 and 1986, 29 women consulted in three internal medicine and endocrinology departments for clinical disorders which could be ascribed to 31 episodes of thyroiditis developed within 9 months of giving birth. Thyroiditis was diagnosed clinically on the basis of acute diffuse (11 cases) or nodular (7 cases) goitre formation, signs of dysthyroidism (16 cases) revealed by menstrual disturbances and/or galactorrhoea (11 cases). A thyrotoxic episode was observed in 9 patients; it was either without sequelae (5 cases) of followed by transient hypothyroidism (4 cases). In other patients transient hypothyroidism was observed in 11 cases and permanent hypothyroidism in 5 cases. Six patients showed no sign of dysthyroidism, and the diagnosis was made by immunological, cytological and/or histological examination of the thyroid gland. Circulating anti-thyroid antibodies were present in two-thirds of the patients. The results of radioisotope scanning varied according to the stage of the disease. In these patients, only the absence of goitre was predictive, in 4 out of 5 cases, of subsequent permanent hypothyroidism; in all other patients the prognosis was highly favourable, even without specific treatment.

Adult↗
PubMed2005

The occurrence of permanent thyroid failure in patients with subclinical postpartum thyroiditis.

OBJECTIVE: The long-term effect of the subclinical form of postpartum thyroid dysfunction (PPTD) has not been well established. This study was conducted to evaluate the outcome of permanent hypothyroidism in a large cohort of women with PPTD. DESIGN AND METHODS: Of 213 women with PPTD, 172 (81%) returned for follow-up. There were 27 (16%) with subclinical (group 1) and 145 (84%) with overt hypothyroidism (group 2). They were all treated with levothyroxine for 23 +/- 16 months and followed-up for thyroid function after thyroxine (T(4)) withdrawal. RESULTS: In group 1, the time of occurrence of PPTD was longer, serum T(4) was higher and TSH was lower than in group 2. After T(4) withdrawal, 59 and 64% of patients became hypothyroid in groups 1 and 2 respectively; however, serum TSH was increased in group 2 as compared with group 1 (29.7 +/- 8.4 vs 16.4 +/- 15.4 mU/l, P < 0.002). The duration of euthyroidism, serum free T(4) and triiodothyronine indices and thyroperoxidase antibodies were not significantly different between the two groups. CONCLUSION: It was concluded that a high percentage of patients with the subclinical form of PPTD proceed to permanent thyroid failure. The timely recognition of mild to severe cases of PPTD is important for the improvement of life for mothers and infants.

Adult↗
PubMed1993

Postpartum thyroid dysfunction: a viewpoint from Thailand.

Postpartum thyroid dysfunction (PPTD) refers to changes in thyroid function that occur during the first 12 months postpartum. The changes in thyroid function can either be thyrotoxicosis or hypothyroidism which may be transient or permanent in nature. The aetiology is multiple, including postpartum thyroiditis, new onset or exacerbation of Graves' disease, exacerbation of primary hypothyroidism due to Hashimoto's thyroiditis, central hypothyroidism due to postpartum pituitary necrosis or central hypothyroidism due to lymphocytic hypophysitis. There is a paucity of data concerning PPTD in South East Asia. However, available data indicate a seemingly high prevalence of central hypothyroidism due to postpartum pituitary necrosis in Thailand. The alterations in the course of Graves' disease during pregnancy and postpartum are similar to those reported elsewhere. However, the dosage of antithyroid drug used during pregnancy in Thai women is quite small. The lower environmental iodine in Thailand may be one of the responsible factors. Interestingly, the prevalence of PPTD due to postpartum thyroiditis reported from Thailand was only 1.1% which was less than that reported in other countries. The discrepancy in the geographic prevalence of postpartum thyroiditis may result from the interaction of immunogenetic heterogeneity of different ethnic background, environmental iodine intake, and other unidentified environmental factors.

Cross-Cultural Comparison↗