Post-partum thyroiditis in South Brazil presenting as thyrotoxicosis: Prevalence and risk factors

Furlanetto, Tânia Weber; Premaor, Melissa Orlandin; Caramori, M. Luiza; Frantz, Bárbara; Patta, Giuliano; Tatto, Erica; Vaz, Alessandro G.

doi:10.1007/bf03343764

Cited by 12 publications

(9 citation statements)

References 17 publications

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“…Most studies (10-26) had a prospective cohort design. Two studies had a cross-sectional design (27,28) and one study summarized the results of a case-control study (29) Two studies were conducted in the United States (14,22). Two studies were conducted in Sweden (24,25), The Netherlands (13,16), and Asia (21,26).…”

Section: Yield Of Relevant Articlesmentioning

confidence: 99%

Prevalence of Postpartum Thyroid Dysfunction: A Quantitative Review

Nicholson

Robinson²,

Smallridge

et al. 2006

Thyroid

189

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Estimates of the prevalence of postpartum thyroid dysfunction (PPTD) vary widely because of variations in study design, populations, and duration of screening. Our objective was to estimate the prevalence of PPTD among general and high-risk women, across geographical regions and in women with antithyroid peroxidase antibodies (TPOAbs). We conducted a systematic review and pooled analysis of the published literature (1975-2004), simultaneously accounting for sample size, study quality, percentage follow-up, and duration of screening. Data sources were MEDLINE and the bibliography of candidate studies. Two reviewers independently extracted data. Of 587 studies identified, 21 articles (8081 subjects) met the study criteria. The pooled prevalence of PPTD, defined as an abnormal thyroid-stimulating hormone (TSH) level, for the general population was 8.1% (95% confidence interval [CI] 6.6%-10.0%). The risk ratios for the development of PPTD among women with TPOAbs compared to women without TPOAbs ranged between 4 and 97 with a pooled risk ratio of 5.7 (95% CI: 5.3-6.1). Global prevalence varied from 4.4% in Asia to 5.7% in the United States. Prevalence among women with type 1 diabetes mellitus was 19.6% (95% CI 19.5%-19.7%). PPTD occurs in 1 of 12 women in the general population worldwide, 1 of 17 women in the United States and is 5.7 times more likely to occur in women with TPOAbs. The high prevalence may warrant routine screening TPOAbs, but the benefits, cost, and risks related to subsequent therapy must be weighed.

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Section: Yield Of Relevant Articlesmentioning

confidence: 99%

Prevalence of Postpartum Thyroid Dysfunction: A Quantitative Review

Nicholson

Robinson²,

Smallridge

et al. 2006

Thyroid

189

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“…The association of smoking with increased risk of PPT and other postpartum autoimmune disorders has been presented in some studies [16,[57][58][59]. The contradictory results of other researchers are probably due to differences in study design, sample size, and definitions of cigarette smoke exposure [60,61].…”

Section: Influence Of Cigarette Smoking On Maternal and Foetal Thyroimentioning

confidence: 99%

Wpływ palenia papierosów na tarczycę — aktualizacja

Sawicka‐Gutaj¹,

Gutaj²,

Sowiński³

et al. 2014

Endokrynologia Polska

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Many studies have shown that cigarette smoking exerts multiple effects on the thyroid gland. Smoking seems to induce changes in thyroid function tests, like decrease in TSH and increase in thyroid hormones. However, these alterations are usually mild. In addition, tobacco smoking may also play a role in thyroid autoimmunity. Many studies have confirmed a significant influence of smoking on Graves' hyperthyroidism and particularly on Graves' orbitopathy. Here, smoking may increase the risk of disease development, may reduce the effectiveness of treatment, and eventually induce relapse. The role of smoking in Hashimoto's thyroiditis is not as well established as in Graves' disease. Nonetheless, lower prevalence of thyroglobulin antibodies, thyroperoxidase antibiodies and hypothyroidism were found in smokers. These findings contrast with a study that reported increased risk of hypothyroidism in smokers with Hashimoto's thyroiditis. Moreover, cigarette smoking increases the incidence of multinodular goitre, especially in iodine-deficient areas. Some studies have examined cigarette smoking in relation to the risk of thyroid cancer. Interestingly, many of them have shown that smoking may reduce the risk of differentiated thyroid cancer. Furthermore, both active and passive smoking during pregnancy might modify maternal and foetal thyroid function. This review evaluates the current data concerning the influence of cigarette smoking on thyroid gland, including hormonal changes, autoimmunity and selected diseases. These findings, however, in our opinion, should be carefully evaluated and some of them are not totally evidence-based. Further studies are required to explain the effects of smoking upon thyroid pathophysiology. StreszczenieWyniki wielu badań dowodzą, że palenie papierosów wywiera istotny wpływ na gruczoł tarczowy. Wykazano, że nikotynizm modyfikuje parametry hormonalne tarczycy, w szczególności prowadzi do obniżenia stężenia TSH. Sugeruje się, że może również powodować nieznaczny wzrost stężenia wolnych hormonów tarczycy. Ponadto, palenie papierosów odgrywa istotną rolę w procesach autoimmunologicznych związanych z gruczołem tarczowym. Dowiedziono, że nikotynizm wywiera negatywny wpływ na przebieg choroby Gravesa i Basedowa oraz orbitopatii Gravesa i Basedowa. Palenie papierosów nie tylko zwiększa ryzyko rozwoju powyższych schorzeń, ale zmniejsza również skuteczność terapii i zwiększa ryzyko nawrotu. Wpływ palenia papierosów na chorobę Hashimoto nie jest tak jednoznacznie dowiedziony, jak w chorobie Gravesa i Basedowa. Sugeruje się, że palenie papierosów może negatywnie korelować z mianem przeciwciał przeciwko tyreoglobulinie oraz tyreoperoksydazie, zmniejszając w konsekwencji ryzyko rozwoju hipotyreozy. Palenie papierosów zwiększa ryzyko wystąpienia wola guzkowego szczególnie na obszarach niedoboru jodu. Interesująco przedstawiają się również wyniki badań nad wpływem palenia papierosów na ryzyko wystąpienia raka tarczycy. Wiele z nich dowodzi, że u palaczy ryzyko raka zróżnicowanego tarczycy jest mn...

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“…Prevalence of PPT is variable, ranging from 1.1% in Thailand to 16.7% of parturient women in Great Britain (Table 1) (5,(9)(10)(11)(12)(13)(14). The variability of PPT prevalence may be due to different or inappropriate screening procedures or to different genetic and environment risk factors.…”

Section: Prevalencementioning

confidence: 99%

Post-partum thyroiditis--a clinical update

Roti¹,

Uberti²

2002

European Journal of Endocrinology

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Since the late 1960s, many studies have focused on post-partum thyroiditis (PPT) and 295 papers whose titles mention PPT were recorded on MEDLINE as of August 2001. We refer briefly to some excellent reviews and some original articles in order to update our knowledge on PPT. European Journal of Endocrinology 146 275-279Definition Post-partum thyroiditis (PPT) is an autoimmune disorder characterized by lymphocytic infiltration of the thyroid gland and by transient thyrotoxicosis followed by hypothyroidism or by one or the other occurring in the first year after parturition. It has been the subject of several excellent reviews (1 -8). Thyroid function abnormalities are not due to the presence of thyrotrophin (TSH) receptor antibodies (TRAb) either with stimulating or inhibiting thyroid activity or to a toxic adenoma. PathogenesisSeveral findings strongly suggest that PPT is an autoimmune disease.PPT has been reported more frequently in women with HLA-DR3, DR4 or DR5 phenotypes. These results are similar to those seen in women with Hashimoto's thyroiditis. PPT has been observed also in patients with Graves' disease and primary autoimmune hypothyroidism.In general, PPT occurs in women with positive antithyroid peroxidase antibodies (TPOAb) in early pregnancy. During pregnancy TPOAb titres decline, whereas in the post-partum period they markedly and rapidly increase, similar to all immunoglobulin G. The fact that TPOAb in the post-partum period retain their specificity in recognizing epitopes suggests that PPT is not related to thyroid antigen specific changes but to a non-specific immune phenomenon.TPOAb are often able to fix the complement, thus inducing the initial cell destruction. The role of complement in the development of PPT is confirmed by the observation that positive TPOAb women who develop PPT have higher complement activation than positive TPOAb women without PPT. Lymphocytic infiltration of the thyroid is the most evident pathologic feature of PPT. However, in peripheral blood there is no variation in the ratio of T to B lymphocytes. An increased CD4 + /CD8+ ratio and an increased activation of T lymphocytes has been reported in PPT women. Some authors suggested a possible role of thyroid cell specific T-cell clone with cytolytic activity. It is probable that T-cell clones reactive to thyroglobulin (Tg), TPO and TSH receptor are expanded within the thyroid during the early phase of PPT.All these possible mechanisms, able to induce the development of PPT, are only temporary since in the vast majority of women the disease does not chronicize and normal thyroid function is resumed. Thus, the immune system has to recover normal tolerance by unknown mechanisms. PrevalencePrevalence of PPT is variable, ranging from 1.1% in Thailand to 16.7% of parturient women in Great Britain (Table 1) (5,(9)(10)(11)(12)(13)(14). The variability of PPT prevalence may be due to different or inappropriate screening procedures or to different genetic and environment risk factors. In three different studies it has been ...

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Post-partum thyroiditis in South Brazil presenting as thyrotoxicosis: Prevalence and risk factors

Cited by 12 publications

References 17 publications

Prevalence of Postpartum Thyroid Dysfunction: A Quantitative Review

Prevalence of Postpartum Thyroid Dysfunction: A Quantitative Review

Wpływ palenia papierosów na tarczycę — aktualizacja

Post-partum thyroiditis--a clinical update

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