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Postpartum thyroiditis is a benign, often self-limited cause of thyroid dysfunction. This report describes the first case of papillary carcinoma arising in a woman with postpartum thyroid disease. Both clinicians and pathologists must keep a high index of suspicion in postpartum patients with persistent thyroid abnormalities, even when a previous biopsy may have disclosed benign disease.
Postpartum thyroiditis is the most common endocrinologic disorder, with an incidence that varies geographically from 5% to 10%. It has important clinical sequelae including symptoms of hyperthyroidism, hypothyroidism, and depression. Long-term follow-up of women who experience postpartum thyroiditis reveals a high recurrence rate in subsequent pregnancies. Postpartum thyroiditis is an autoimmune disorder, and thyroid antibody-positive women in the first trimester have a 33% to 50% chance of developing thyroiditis in the postpartum period. Whether or not to screen for postpartum thyroiditis remains controversial.
Postpartum thyroiditis (PPT) is the occurrence, in the postpartum period, of transient hyperthyroidism and/or transient hypothyroidism, with most women returning to the euthyroid state by 1 year postpartum. The prevalence of PPT varies from 1.1 to 16.7%, with a mean prevalence of 7.5%. Women with type I diabetes mellitus have a three-fold increase in the prevalence of PPT. PPT is an autoimmune disorder which is a transient form of Hashimoto's thyroiditis occurring postpartum as a consequence of the immunologic flare following the immune suppression of pregnancy. Women experience symptoms in both the hyperthyroid and hypothyroid phase, but the association between PPT and postpartum depression remains undefined. Approximately 25% of women with a history of PPT will develop permanent hypothyroidism in the ensuing 10 years. Treatment for the hyperthyroid phase, when required, is a short dose of beta-blockers. Women with a TSH greater than 10 mU/l, or between 4 and 10 mU/l with symptoms or attempting pregnancy, require thyroid hormone replacement. Whether or not to screen for PPT remains controversial.
Postpartum thyroiditis (PPT) affects half of the 10% of women who have elevated circulating thyroid autoantibodies during the postpartum year. Because of the similarities between PPT and Hashimoto's thyroiditis, the pathogenic role of complement in PPT has been investigated. Complement fixation by thyroid peroxidase antibodies (TPO Abs) (expressed as log reciprocal titer) in serum from euthyroid TPO Ab-positive women (n = 29) was 0.91 at 1 month postpartum and increased to 1.45 by 12 months postpartum; complement C3 activation, measured by enzyme-linked immunosorbent assay, in a similar group of women (n = 75) was 0.05 at delivery and increased to 0.33 by 6 months postpartum. In women with PPT, there was greater TPO Ab-related complement activation during the postpartum year; complement fixation increased from 1.00 at 1 month postpartum to 1.48 at 4 months postpartum (P < 0.005) (n = 25), and C3 activation increased from 0.11 at delivery to 0.63 at 6 months postpartum (P < 0.005) (n = 73). Bioactive TPO Ab (TPO Ab x C3 index) was significantly higher in PPT women (55 kilo international units of activity (kIU)/L at 6 months postpartum) (Hashimoto range, 30-108 kIU/L) compared with euthyroid TPO Ab-positive women (< 9 kIU/L at all time points; P < 0.005). Serum samples from TPO Ab-negative control women showed no interaction with complement in either assay at any time during the postpartum year (complement fixation < 0.7; complement C3 activation index < 0.01). This detailed examination of the role of complement in the pathogenesis of PPT shows that TPO Ab-driven complement fixation is a marker for thyroid dysfunction in TPO Ab-positive women. The levels of bioactive TPO Ab in PPT fall within the range seen in Hashimoto's thyroiditis, suggesting similarities in their pathology.
Postpartum thyroiditis (PPT) is a form of painless lymphocytic thyroiditis which is thought to be caused by an exacerbation of underlying subclinical autoimmune thyroid disease during a postpartum period of immune rebound. The purposes of this study were to analyze natural killer cell (NK) functional activity and antibody-dependent cell-mediated cytotoxicity (ADCC) of peripheral blood mononuclear cells in patients with PPT compared to those in normal nonpostpartum and postpartum women. NK activity and ADCC were determined by specific lysis of 51Cr-labeled K562 human erythroleukemia tumor cells at varying effector (mononuclear cell) to target cell ratios. Nineteen PPT patients between 4-9 months [mean, 6.5 +/- 0.4 (+/- SE)] postpartum were compared to 20 nonpostpartum women, 31 healthy women between 4-9 months (6.7 +/- 0.3) postpartum, and 14 women 2 days after delivery. There were significant differences in the NK functional activities of the 4 groups (F = 7.95; P = 0.0002). The mean NK activities, as measured by percent specific lysis at an effector to target cell ratio of 10:1, were 31.1 +/- 3.3%, 20.9 +/- 2.3%, 22.5 +/- 2.8%, and 11.5 +/- 2.0% in the nonpostpartum, PPT, postpartum, and 2-day postpartum groups, respectively. Specific lysis by ADCC was not significantly different from lysis by NK activity in any group. The PPT, postpartum, and 2-day postpartum groups had significantly lower NK activity compared to that in nonpostpartum women (P less than 0.05). Both the PPT and postpartum women had higher NK activities than the 2-day postpartum women (P less than 0.05). However, there were no significant differences in the NK activities of the PPT patients compared to those of the healthy postpartum women. Patients with PPT were also found to have associated autoimmune dysfunction. The PPT group had significantly higher serum antinuclear antibody titers; 8 of 24 patients (33%) had titers of 1:160 or greater compared to only 2 of 29 healthy postpartum women (7.4%; P less than 0.05). Seven of the PPT patients had serum immune complexes, and 3 had TSH receptor antibodies. We conclude that functional NK activity and ADCC in peripheral lymphocytes of PPT patients are not different from those in healthy postpartum women; however, the postpartum women had significantly decreased activity compared to that in nonpostpartum women. These data emphasize the importance of studying healthy postpartum women in investigations of PPT, since the immunological changes in pregnancy and the postpartum period remain largely undefined.
In a retrospective study 716 consecutive newly diagnosed and untreated hyperthyroid patients were examined in regard to the frequency of silent thyroiditis and postpartum thyroiditis. Six patients (0.8%) had possible silent thyroiditis (24-hour radioiodine uptake less than or equal to 5% and hyperthyroidism without anterior neck pain). None occurred within one year postpartum. We conclude that silent thyroiditis is a rare cause of hyperthyroidism in our thyroid clinic. The fact that none occurred postpartum suggests that postpartum thyroiditis is oligosymptomatic and that screening programmes are needed if one wants to diagnose the earliest phases of this condition.
Postpartum thyroiditis (PPT) is a syndrome of transient thyroid dysfunction occurring in the first postpartum year. A thyrotoxic phase may be brief and unnoticed before a more long-lasting hypothyroid phase occurs. The incidence is variably reported, ranging from 1.9% to 16.7%, perhaps reflecting racial or geographical differences in the distribution of genetic or environmental risk factors such as the titre of thyroid antibodies and the dietary intake of iodine. The syndrome is an autoimmune disorder, strongly associated with the presence of thyroid microsomal antibody in serum. The thyrotoxic phase may be distinguished from Graves' disease by the finding of low, rather than high, uptake of radioactive iodine or technetium in the thyroid. Screening may be valuable in women with other autoimmune disorders such as Type 1 diabetes mellitus. Treatment should be tailored to the symptoms. Significant thyrotoxic problems should be managed with beta-blocking agents, but severe hypothyroid symptoms should be treated with the short-term replacement thyroxine. A small proportion of affected women will remain permanently hypothyroid. There is also a significant risk of recurrent disease after a subsequent pregnancy.
Postpartum thyroiditis is a disorder which is morphologically similar to Hashimoto's thyroiditis, but differs clinically. The disorder presents with a transient period of thyrotoxicosis which may be so mild that it is clinically missed. Many of these patients subsequently develop hypothyroidism which also spontaneously resolves. Documentation that the hypothyroidism is transient would be necessary to establish the diagnosis. There is a proclivity for this disorder to develop in the postpartum period. Two patients are presented with this disorder, one with a transient hypermetabolic state and one with a transient hypothyroid state.
Postpartum thyroiditis (PPT) is a reversible form of lymphocytic thyroiditis which has been attributed to an aggravation of preexisting subclinical autoimmune thyroiditis. In this study no differences in circulating lymphocyte subsets were found between 9 thyrotoxic and 18 hypothyroid PPT patients and normal subjects. We obtained sufficient numbers of thyroid-infiltrating lymphocytes for surface marker characterization in 3 women in the thyrotoxic phase and in 10 women in the hypothyroid phase of PPT. Cells were identified by conventional T and B cell markers as well as by monoclonal antibodies (OKT) directed against different T cell subsets in a microscale immunofluorescence assay. In the hypothyroid patients a relative accumulation of B cells (31% vs. 17%; P less than 0.01 by the Wilcoxon signed rank test) was found within the thyroid when compared to peripheral blood. A relative decrease in intrathyroidal supressor-cytotoxic (OKT 8+) T cells (19% vs. 28%; P less than 0.01) resulted in an increased intrathyroidal helper to suppressor-cytotoxic (OKT 4+/OKT 8+) T cell ratio (3.0 vs. 2.0; P less than 0.01). Intrathyroidal lymphocyte subsets in the thyrotoxic patients were comparable to those in the hypothyroid patients. These findings, which are similar to those we previously obtained in patients with chronic Hashimoto's thyroiditis, may indicate that local synthesis of thyroid-directed autoantibodies is of primary importance in all stages of autoimmune thyroiditis.
Postpartum thyroiditis (PPT) is common and occurs in 1.7 to 16.7% of pregnant women, depending upon the study population. Most of these women develop transient hypothyroidism and thyroid function usually returns to normal. We have studied 11 euthyroid women with a previous history of PPT to determine the incidence of subtle defects in thyroid function measured by iodide-perchlorate (I-ClO4) discharge tests and TRH tests and to determine whether these women would develop iodide-induced hypothyroidism. Seven (64%) had positive I-ClO4 discharge tests and 5 (46%) had an abnormally high TSH response to TRH. Thyroid antimicrosomal and antithyroid peroxidase were positive in 8 women (73%) with a previous episode of PPT. The administration of pharmacological amounts of iodide (10 drops of saturated solution of potassium iodide daily) for 90 days to these 11 women resulted in elevated basal and TRH stimulated serum TSH concentrations in 8 (72.7%) compared to TSH values during iodide administration to women who had never been pregnant. Antimicrosomal and antithyroid peroxidase concentrations did not change during iodide administration. These findings strongly suggest that euthyroid women with a previous episode of PPT have permanent subtle defects in thyroid hormone synthesis and are inordinately prone to develop iodide-induced hypothyroidism, similar to findings previously reported in euthyroid subjects with Hashimoto's thyroiditis, with a previous episode of painful subacute thyroiditis, or previously treated with radioactive iodine or surgery for Graves' disease.
Various studies have reported a spectrum of thyroid dysfunction in the postpartum period. Postpartum thyroiditis is a syndrome of thyroid dysfunction that occurs in the first year after parturition. Prevalence of postpartum thyroiditis has been reported to vary from 3 to 6 percent in different regions of the world. Kashmir Valley is inhabited by a relatively homogeneous racial group and the Valley has been documented to have significant iodine deficiency. We studied the prevalence and pattern of postpartum thyroiditis in an urban region of this Valley. 120 women were registered within first month of postpartum period for the study along with one hundred controls. Of these 120 women, 104 reported for follow-up at 3 months postpartum and 106 reported for follow-up at 6 months postpartum. Initial and subsequent clinical details at follow-up were recorded on a pre-determined questionnaire. Overall, postpartum thyroiditis (PPT) was seen in 8 (7%) study subjects. Of these 8 patients with PPT, 4 had biochemical evidence of thyrotoxicosis at first month, 3 developed biochemical thyrotoxicosis at 3-month follow-up while as one study subject developed thyrotoxicosis at 6 months. Most of these subjects were antithyroid antibodies (anti-microsomal and anti-thyroglobulin) positive. We conclude that iodine deficient status of the community doesn't seem to influence the incidence of PPT.
OBJECTIVE: Six cases of silent thyroiditis are described. Clinical, analytical, therapeutical and prognostical features are reviewed. DESIGN: Descriptive and retrospective study. SETTING: Outpatient endocrinological clinic of a General Hospital PATIENTS OR OTHER PARTICIPANTS: Six women (age 26-41 years) that fulfil clinical and analytical criteria of silent thyroiditis. In 4 patients thyroiditis was diagnosed in the postpartum period and in the remaining 2 there was no relationship with pregnancy. MAIN MEASUREMENTS AND RESULTS: Serum levels of thyroid hormones and thyroglobulin and thyroid peroxidase antibodies were measured in all patients. Follow-up period was between 12 and 41 months. The 2 patients with the sporadic form of silent thyroiditis showed clinical and analytical data of thyrotoxicosis that spontaneously resolved. The remaining 4 patients presented with hypothyroidism. In one of them the hypothyroidism spontaneously resolved, in 2 it became permanent and in a further one it developed to subclinical hypothyroidism. CONCLUSIONS: Silent thyroiditis (sporadic or postpartum) is a frequent disorder, usually benign and transient. It can present in different clinic forms and evolve to resolution of permanent thyroid dysfunction.
OBJECTIVE: Postpartum has been considered as a period of risk for developing postpartum depression (PD) by some but not all authors, and this PD has been linked with postpartum thyroid dysfunction (PPTD). The major aim of this study was to evaluate the relation between the presence of PPTD and PD. DESIGN AND PATIENTS: Six hundred and forty-one healthy Caucasian women recruited between their 36th week of pregnancy and fourth day postpartum underwent clinical and laboratory evaluation and were checked again at 1 (n = 605), 3 (n = 552), 6 (n = 574), 9 (n = 431), and 12 (n = 444) months postpartum. MEASUREMENTS: At baseline and at each clinical evaluation, Beck Depression Inventory (BDI) was administered to screen PD. The definitive diagnoses of PD was performed by a psychiatrist according to the DSM-III-R criteria. At each visit, we determined serum free T4 and TSH concentrations. Thyroperoxidase and thyroglobulin antibodies were determined only in patients with abnormal hormone concentrations. Postpartum thyroiditis (PPT) was considered to be present in women with overt or subclinical transient hyperthyroidism between 1 and 3 months postpartum and/or overt or subclinical hypothyroidism between 3 and 6 months postpartum. RESULTS: Fifty-six women developed postpartum thyroid dysfunction (PPTD), corresponding to an incidence rate of 11%: 45 with PPT [incidence rate 7.8%; confidence interval (CI) 5.6-10%], eight with Graves' disease (incidence rate 1.5%; CI 0.5-2.5%) and three with nonpalpable toxic thyroid adenoma (incidence rate 0.5%; CI 0-1.5%). Five hundred and eighty of the evaluated women (incidence rate 90.5%; CI 95% 88.2-92.8) presented BDI scores below 21 and therefore the PD diagnoses was excluded. In 50 cases (incidence rate 7.8%; Cl 95% 5.7-9.8), we detected a BDI score over 21 in some evaluations, but the PD diagnosis was not confirmed. Another 11 (incidence rate 1.7%; CI 95% 0.7-2.7) were diagnosed as having PD and required psychiatric treatment. None of the PPTD was diagnosed as having PD. The BDI scores frequency over 21 was similar between healthy women and those with PPTD. Patients with a previous history of depression developed PD more often (P < 0.0001). One hundred and ninety women breast fed their babies for more than 2 months, without observing a higher PD rate or BDI scores over 21 (P = 0.5). CONCLUSIONS: We found a general PD incidence rate of 1.7% in our group of patients. This figure is not higher in women with hormone abnormalities caused by PPTD. Women with a past history of depression present a higher risk of PD while those who breast fed did not have an increased risk.
OBJECTIVE: Postpartum thyroiditis (PPT) is an autoimmune thyroid disease which shares immunological and clinical features with autoimmune hypothyroidism and Graves' disease, and is believed to be caused by a combination of genetic and environmental factors. Recently, an association has been described between Graves' disease or autoimmune hypothyroidism and a polymorphism in the CTLA-4 gene, which encodes a T cell receptor for the B7 family of ligands, and we wished to test whether a similar association exists with PPT. DESIGN: A population-based case-control study of a CTLA-4 gene microsatellite polymorphism was performed, to look for an association with PPT. PATIENTS: Caucasoid women (n = 122) were studied; 58 had thyroid antibodies (against thyroglobulin or thyroid peroxidase) alone during the postpartum period (PPT-) and 64 had thyroid antibodies and some form of postpartum thyroid dysfunction (PPT+). RESULTS: There was no significant difference between this whole group of women and 161 local Caucasoid thyroid antibody-negative women for the CTLA-4106 base pair (AT)n microsatellite polymorphism (relative risk = 1.3; P = 0.3), nor did the PPT+ group differ from controls when analysed separately (P = 0.2). When the postpartum women were subdivided in groups according to clinical pattern of PPT and the type of thyroid antibodies, there were no associations within the subgroups. CONCLUSIONS: No significant association exists between postpartum thyroiditis and a polymorphism in the CTLA-4 gene. Furthermore, a natural variation in the prevalence of the polymorphism in healthy UK populations underscores the need to select appropriately matched normal subjects in future case-control studies.
BACKGROUND: Postpartum thyroid dysfunction (PPTD) develops in 50% of pregnant women who have raised levels of circulating thyroid peroxidase autoantibodies (TPOAb) at booking. Although these antibodies are able to activate the complement cascade in vitro, it is not known whether complement activation plays any role in the pathogenesis of this disease. AIM: To investigate potential and actual activation of the complement system in women with postpartum thyroiditis. DESIGN: Complement activation was monitored on a weekly basis in 24 postpartum women who had raised TPOAb at 16 weeks gestation, attending an antenatal clinic in Mid-Glamorgan, Wales. METHODS: ELISA procedures were used to measure both in-vitro complement C3 activation by TPOAb and circulating terminal complement complexes (TCC) in serum. RESULTS: Higher levels of bioactive TPOAb activity were seen in women who developed PPTD when compared to those who did not. However, TCC remained undetectable in serum throughout the period of study. CONCLUSIONS: In PPTD, despite the presence of circulating bioactive TPOAbs, the extent of complement activation is inadequate to cause detectable increases in peripheral blood TCC, suggesting that the complement system may not play a major role in PPTD pathogenesis.
A 27-year-old woman with no previous personal or family history of thyroid disease was referred to us for the evaluation of thyroid nodule, five months postpartum. Thyroid scintigraphy demonstrated a left cold nodule. Fine needle aspiration cytology of the nodule showed a mixture of colloid, follicular cells and lymphocytes, suggesting lymphocytic thyroiditis. Thyroid function tests were normal and thyroid autoantibodies were negative. After two months the thyroid nodule was not palpated and thyroid scintigraphy returned to normal. Thyroid function tests remained normal twelve months after delivery. These findings suggest that postpartum thyroiditis may present as a localized transient form and should be considered in the differential diagnosis of painless solitary nodule that appears postpartum.
BACKGROUND: Postpartum thyroiditis is a common but frequently unrecognized disorder, affecting approximately 5% of women during the first 12 months after delivery. We investigated whether the antimicrosomal antibody titer could be used to determine which women with positive titers postpartum (1) might develop symptomatic or biochemical abnormalities within the first postpartum year (early disease), (2) might require therapy with thyroid hormone, and (3) might have persistent abnormalities (late disease). METHODS: Women (n = 55) who had positive antimicrosomal antibody titers at delivery were prospectively followed for 11 to 45 months. Titers were evaluated again at 6 to 10 weeks postpartum and approximately every 8 weeks for the first year. RESULTS: Early disease occurred in 40 of 55 (73%) women, late disease occurred in 29 of 55 (53%) women, and treatment was required by 21 of 55 (38%) women. The occurrence of early disease was associated with the occurrence of late disease (P < .05). The chances of developing early disease were 6 to 1 (P = .01) when serum titers of antimicrosomal antibodies were > or = 400 at delivery, and 5 to 1 (P = .02) when titers were > or = 1600 at 6 to 10 weeks postpartum. The chances of being given thyroid hormone therapy were 23 to 1 (P = .006) when titers at delivery were > or = 6400, and 6 to 1 when titers at 6 to 10 weeks postpartum were > or = 6400 (P = .004). Titers were not useful in estimating who would have late disease. CONCLUSIONS: Screening for postpartum thyroid dysfunction after delivery using antimicrosomal antibody titers is highly useful. The titer value can help guide the physician in the care of patients with postpartum thyroiditis whose disease may not be self-limiting and who will probably require thyroid hormone therapy.
Postpartum thyroiditis (PPT) is a transient autoimmune thyroiditis occurring during the postpartum year that is characterized by circulating antithyroid antibodies, abnormal thyroid ultrasound echotexture, and episodes of hyperthyroidism, hypothyroidism, or both. In this study we examined the relationship between lymphocytic thyroiditis, as indicated by echotexture changes, and complement-activating thyroid autoantibodies. Thyroid ultrasound echotexture, thyroid function, and bioactive (complement-activating) thyroid peroxidase (TPO) antibodies have been measured in a group of 63 TPO antibody-positive women during the postpartum year. When the maximum bioactive TPO antibody activity recorded was compared with echogenicity and thyroid status, there was a correlation between hypoechogenicity, elevated antibody activity, and abnormal thyroid status (r = 0.72, p < 0.001). However, 7 cases showed severe ultrasound changes in the absence of any thyroid dysfunction (3 of these cases showed normal bioactive antibody activity), while 4 (all hyperthyroid PPT) showed thyroid dysfunction in the absence of any ultrasound changes. Within the euthyroid ultrasound normal group, bioactive TPO antibody activity remained low throughout the postpartum year. Antibody activity in the hypoechogenic euthyroid women was significantly elevated (p < 0.001) compared with the echo normal group, but was indistinguishable from the activity curve obtained in women whose PPT included a hypothyroid phase. The determination of echotexture by thyroid ultrasonography gives a useful, noninvasive measure of the degree of thyroiditis in these women. However, as a significant number of cases with severe changes in echotexture remained euthyroid, we conclude that the development of thyroid dysfunction is not an inevitable consequence of lymphocytic thyroiditis during the postpartum and suggests that other factors must also be involved in progression to overt thyroid dysfunction.