Una paciente con fenómeno de Raynaud del pezón e hipertiroidismo / A patient with Raynaud's phenomenon of the nipple and hyperthyroidism

Introducción: el fenómeno de Raynaud del pezón es una patología poco frecuente. Puede presentarse asociada a hipertiroidismo o enfermedades autoinmunes del tejido conectivo. Presentamos un caso asociado a hipertiroidismo.Caso clínico: mujer, de 39 años, que consulta por dolor en pezón que se agrava con la lactancia 1 mes después del parto. Se diagnosticó fenómeno de Raynaud del pezón, que mejoró con la toma de nifedipino. Tres meses después, la paciente presentó fiebre. El análisis de sangre mostró hormona estimulante del tiroides (TSH) 0,0008 mU/L (normal: 0,55-4,75 mU/L) y T4 libre 48 pg/mL (normal: 2,30-4,20 pg/mL). Los anticuerpos antitiroglobulina fueron > 500 UI/mL. La T3, los anticuerpos antiperoxidasa (TPO) y la inmunoglobulina estimulante del tiroides fueron normales. Se diagnosticó tiroiditis posparto (TPP). Dos meses después, los niveles de TSH y T4 libre volvieron a la normalidad.Conclusión: nuestra paciente presenta una TPP asociada a un fenómeno de Raynaud.(AU)

Introduction: Raynaud's phenomenon of the nipple is a rare pathology. It can occur associated with hyperthyroidism or autoimmune connective tissue diseases.We report a case associated with hyperthyroidism.Case study: a 39-year-old woman consulted for nipple pain, which worsened with breastfeeding, one month after childbirth. Raynaud's phenomenon of the nipple was diagnosed, which improved with nifedipine. Three months later the patient developed fever. Blood test revealed thyroid stimulating hormone (TSH) 0.0008 mU/L (normal 0.55-4.75 mU/L) and free T4 48 pg/mL (normal 2.30-4.20 pg/mL). Antithyroglobulin antibodies were >500 IU/mL. T3, antiperoxidase antibodies (TPO), and thyroid-stimulating immunoglobulin were normal. Postpartum thyroiditis (PPT) was diagnosed. Two months later, TSH and free T4 levels returned to normal.Conclusion: our patient presented PPT associated with Raynaud's phenomenon.(AU)

An update on thyroid disorders in the postpartum period.

PURPOSE: To review the pathophysiology, diagnosis and management of postpartum thyroid dysfunction, and related management of thyroid disorders during lactation. METHODS: We reviewed the literature on postpartum thyroid dysfunction and management of thyroid disorders during lactation. RESULTS: The postpartum period is characterized by a rebound from the immunotolerance induced by pregnancy. Routine thyroid function screening is not recommended for asymptomatic women in the postpartum period. Testing thyroid function should be considered at 6-12-week postpartum for high-risk populations, including women with a previous episode of postpartum thyroiditis, Graves' disease, or those with Hashimoto's thyroiditis on thyroid hormone replacement, known thyroid peroxidase antibody positivity, type 1 diabetes mellitus, other nonthyroidal autoimmune disease, or chronic hepatitis C. A serum TSH should also be checked in the setting of postpartum depression or difficulty lactating. If patients have thyrotoxicosis, new-onset or recurrent Graves' disease must be differentiated from postpartum thyroiditis, because the management differs. Periodic thyroid function testing is recommended following recovery from postpartum thyroiditis due to high lifetime risk of developing permanent hypothyroidism. Levothyroxine, and the lowest effective dose of antithyroid drugs, (propylthiouracil, methimazole, and carbimazole) can be safely used in lactating women. The use of radiopharmaceutical scanning is avoided during lactation and radioactive iodine treatment is contraindicated. CONCLUSIONS: Diagnosing postpartum thyroid dysfunction is challenging, because symptoms may be subtle. A team approach involving primary care providers, endocrinologists, and obstetricians is essential for transitioning thyroid care from the gestational to the postpartum setting.

Targeted Antenatal Screening for Predicting Postpartum Thyroiditis and Its Evolution Into Permanent Hypothyroidism.

Postpartum thyroiditis (PPT) has a prevalence of 1-22%, with an ~50% rate of evolution into permanent hypothyroidism (PH). PPT risk is assessed by measuring serum thyroid antibodies during gestation, as 1/3-1/2 of Ab+ve pregnant women will develop PPT. Family and personal history positive for autoimmune non-thyroid diseases (AINTDT), and consumption of swordfish increases while consumption of small oily fish decreases the risk of PPT. Monitoring thyroid function in a very high-risk subgroup avoids the costs of the Ab-based universal screening. We aimed at identifying such subgroup in 412 women followed from week 7-11 of gestation to month 12 postpartum. At study entry, we measured serum TPOAb, TgAb, TSH, FT4, FT3, and evaluated seafood consumption, familial history for thyroid diseases and AINTD, and personal history for AINTD. We measured TSH, FT4, FT3 at 1.5, 3, 6, and 12 months postpartum. PPT occurred in 63 women (15.3%), and PH in 34/63 (54%). Based on positivity/negativity for the three histories, women were classified into 8 categories, with PPT rates of 3.8-100%. Seafood consumption allowed further separation of subgroups having different PPT risks. We considered 11 possible strategies, termed [a] through [k]. Strategy [a] consisted in omitting gestational screening, while performing universal postpartum monitoring with TSH and one thyroid hormone; strategy [k] consisted in selective gestational screening with TPOAb and TgAb, based on history and fish consumption, and selective postpartum monitoring in TPOAb and/or TgAb+ve women. The 100% sensitivity, specificity and diagnostic accuracy of strategy [a] were counterbalanced by the highest costs (Euro 32,960 or 523 per each PPT caught). The corresponding numbers for strategy [k] were 78, 95, 93%, and Euro 8,920 or 182/PPT caught. These savings stem from gestational screening being done in 186 women, and postpartum monitoring done in 65/186 women. One gestational screning-free strategy was the cheapest (Euro 2,080 or 83/PPT caught), because based on postpartum monitoring of only 26 women, but had the lowest sensitivity (40%). Identification of pregnant women having different risks for PPT is feasible, with the costless evaluation of history and seafood consumption driving gestational screening of thyroid antibody status and postpartum monitoring of thyroid function.

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.

Abordaje del manejo de la disfunción tiroidea en la gestación. Documento de consenso de la Sociedad Andaluza de Endocrinología y Nutrición (SAEN) / Thyroid dysfunction in pregnancy. Consensus document. Andalusian Society of Endocrinology and Nutrition (SAEN)

En nombre de la Sociedad Andaluza de Endocrinología y Nutrición (SAEN) se ha elaborado un consenso sobre la atención a la mujer gestante que presenta algún tipo de disfunción tiroidea, basándose en la revisión de la bibliografía actualizada y sobre todo de las guías de buena práctica clínica. Se desarrolla bajo distintos epígrafes o apartados en los que se contempla tanto el diagnóstico como el tratamiento del hipotiroidismo clínico y subclínico, el hipertiroidismo franco y subclínico, la hipotiroxinemia y la tiroiditis posparto, así como la justificación de la realización de cribado universal de la disfunción tiroidea durante la gestación, proporcionando a los profesionales que asisten a estas pacientes un arma de toma de decisiones razonada (AU)

A position statement on the diagnosis and treatment of thyroid dysfunction in pregnancy has been agreed on behalf of The Sociedad Andaluza de Endocrinología y Nutrición (SAEN), based on a review of the literature to date and all good clinical practice guidelines. The document is set out in different sections as regards the diagnosis and treatment of, overt and subclinical hypo- and hyperthyroidism, isolated hypothyroxinaemia and postpartum thyroiditis. It also justifies the implementation of universal screening for thyroid dysfunction in pregnancy, and provides practitioners who care for these patients with tool for rational decision making (AU)

[Thyroid dysfunction in pregnancy. Consensus document. Andalusian Society of Endocrinology and Nutrition (SAEN)]. / Abordaje del manejo de la disfunción tiroidea en la gestación. Documento de consenso de la Sociedad Andaluza de Endocrinología y Nutrición (SAEN).

A position statement on the diagnosis and treatment of thyroid dysfunction in pregnancy has been agreed on behalf of The Sociedad Andaluza de Endocrinología y Nutrición (SAEN), based on a review of the literature to date and all good clinical practice guidelines. The document is set out in different sections as regards the diagnosis and treatment of, overt and subclinical hypo- and hyperthyroidism, isolated hypothyroxinaemia and postpartum thyroiditis. It also justifies the implementation of universal screening for thyroid dysfunction in pregnancy, and provides practitioners who care for these patients with tool for rational decision making.

Changes suggestive of post-partum thyroiditis in women with established hypothyroidism: incidence and predictors.

OBJECTIVE: Post-partum thyroiditis (PPT) is a common phenomenon in the general population. To date there have been few studies examining the incidence of PPT in women with hypothyroidism antedating pregnancy. This study aimed to assess the incidence and potential predictors of PPT in women with treated hypothyroidism antedating pregnancy. DESIGN: Retrospective cohort study. PATIENTS AND METHODS: We compiled a cohort of 97 women with previous hypothyroidism antedating pregnancy seen in the Endocrinology in Pregnancy clinic from 1999 to 2011, collecting data on thyroid function, antibodies and levothyroxine doses post-partum. The incidence of PPT and its predictors were analysed. RESULTS: A total of 66 (68%) women had fluctuations in thyroid function consistent with PPT. Of these, 22 (33%) had a hyperthyroid phase alone, 22 (33%) had a hypothyroid phase alone and 22 (33%) had both a hyper and hypo phase. The majority of women had their dose of thyroid medication adjusted during the PPT episode. Women who were on a full dose of thyroxine post-partum were significantly less likely to have a hypothyroid phase. In multivariable analysis, the only predictor of PPT was the presence of thyroid antibodies, with 83% of antibody positive women having PPT compared to 44% of antibody negative women (P = 0·0001). CONCLUSIONS: In our cohort, 2/3 of women had fluctuations in thyroid function consistent with PPT and most required adjustment of their thyroid dose. Women with hypothyroidism antedating pregnancy are at high risk for PPT and should be closely monitored during the first year post-partum.

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.

Tiroiditis posparto. Revisión / Postpartum thyroiditis. A review

La tiroiditis posparto (TPP) es una disfunción tiroidea transitoria de etiología autoinmune que se presenta de forma típica en el primer año tras el parto en mujeres sin enfermedad tiroidea conocida antes del embarazo. Puede cursar con síntomas de tirotoxicosis seguida de hipotiroidismo y recuperación posterior de la función tiroidea, o como tirotoxicosis o hipotiroidismo aislados. Un gran porcentaje de las pacientes que presentan TPP reproducirán esta enfermedad tras los siguientes embarazos. Una gran proporción de mujeres desarrollará hipotiroidismo permanente durante los 3-10 años siguientes a un episodio de TPP. Es importante para el médico de familia estar familiarizado con esta enfermedad, por su gran prevalencia, y para un correcto diagnóstico e intervención terapéutica. Es fundamental también su papel en el seguimiento de estas pacientes, dadas las implicaciones negativas que el hipotiroidismo establecido tiene sobre la reproducción, en una población en edad genésica. En este artículo se revisan las características principales de la TPP, así como su abordaje diagnóstico y terapéutico (AU)

Postpartum thyroiditis (PPT) is a transient thyroid dysfunction of autoimmune origin that can occur in the first year postpartum in women who have not been previously diagnosed with thyroid disease. It may start with clinical thyrotoxicosis followed by hypothyroidism and the subsequent recovery of thyroid function, or may just appear as isolated thyrotoxicosis or hypothyroidism. PPT recurs in high percentage of patients after subsequent pregnancies. Many women develop permanent hypothyroidism sometime during the 3 to 10 year period after an episode of PPT. It is important for family physicians to be familiar with this disease, due to its high prevalence in order to make a correct diagnosis and therapeutic intervention. Family doctors also play a crucial role in the monitoring of these patients, given the negative implications of established hypothyroidism on reproduction in the female population during their reproductive years. This article reviews the principle characteristics of PPT along with its diagnosis and treatment (AU)

[Postpartum thyroiditis. A review]. / Tiroiditis posparto. Revisión.

Postpartum thyroiditis (PPT) is a transient thyroid dysfunction of autoimmune origin that can occur in the first year postpartum in women who have not been previously diagnosed with thyroid disease. It may start with clinical thyrotoxicosis followed by hypothyroidism and the subsequent recovery of thyroid function, or may just appear as isolated thyrotoxicosis or hypothyroidism. PPT recurs in high percentage of patients after subsequent pregnancies. Many women develop permanent hypothyroidism sometime during the 3 to 10 year period after an episode of PPT. It is important for family physicians to be familiar with this disease, due to its high prevalence in order to make a correct diagnosis and therapeutic intervention. Family doctors also play a crucial role in the monitoring of these patients, given the negative implications of established hypothyroidism on reproduction in the female population during their reproductive years. This article reviews the principle characteristics of PPT along with its diagnosis and treatment.

Hipotiroidismo y bocio en el embarazo / Hypothyroidism and goiter in pregnancy

A pesar de no ser frecuente, la hipofunción tiroidea no controlada en la gestante, puede traer consigo efectos deletéreos sobre la madre y el feto, fundamentalmente cuando se presenta de forma manifiesta. Si se detecta precozmente y se trata de forma adecuada con levotiroxina, los riesgos se minimizan. Las dosis a emplear serán las suficientes para alcanzar un valor de tirotropina de acuerdo con lo recomendado para cada trimestre, y que por lo general serán mayores que en la etapa preconcepcional. El bocio se tratará en algunas condiciones específicas, y lo mismo sucede con la tiroiditis posparto. Pacientes sin disfunción tiroidea, pero con anticuerpos antitiroideos positivos elevados, también serán tratadas(AU)

Despite the rareness of the uncontrolled thyroid hypofunction in the pregnant woman, it may bring deleterious effects for the mother and her fetus, mainly when it is manifested. If early detected and adequately treated with levothyroxin, the risks are minimal. The doses to be used are enough to reach a thyrotropin level in accordance with the recommendations for each pregnancy trimester and they will be generally higher than those of the preconception phase. Goiter will be treated under some specific conditions and the same is valid for the postpartum thyroiditis. The patients without thyroid dysfunction, but with high positive antithyroid antibodies, should also be treated(AU)

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.

[Thyroid dysfunctions and pregnancy]. / Dysthyroïdies et grossesse.

Advances in understanding the physiology of the thyroid function in normal pregnancy have highlighted the importance of the consequences of abnormal thyroid function on mother and fetal outcomes. Thyroid diseases are common in young women of childbearing age while management of thyroid diseases is relatively straightforward. For each thyroid dysfunction (hypothyroxinemia, hypothyroidism, hyperthyroidism, postpartum thyroiditis), the issues with the obstetric complications of the mother and the fetus are considered. Indeed, early recognition of thyroid diseases during pregnancy and appropriate management has the potential to improve outcome for the mother and the fetus.

Diagnostic value of a chimeric TSH receptor (Mc4)-based bioassay for Graves' disease.

BACKGROUND/AIMS: Graves' disease (GD) is caused by thyroid-stimulating hormone receptor (TSHR) and thyroid-stimulating immunoglobulin (TSI). We used a recently introduced, technically enhanced TSI bioassay to assess its diagnostic value and determine the cut-off in patients in high iodine intake area. METHODS: In a cross-sectional setting, we collected serum from 67 patients with untreated GD, 130 with GD under treatment, 22 with GD in remission, 42 with Hashimoto's thyroiditis, 12 with subacute thyroiditis, 20 with postpartum thyroiditis, and 93 euthyroid controls. TSI was measured using the Thyretain™ bioassay, which is based on Chinese hamster ovary cells transfected with chimeric TSHR (Mc4). TSI levels are reported as a specimen-to-reference ratio percentage (SRR%). RESULTS: The TSI levels in patients with GD (either treated or not) were significantly higher than those of the remaining patients (p < 0.05). The new bioassay showed a sensitivity of 97.0% and a specificity of 95.9% with a cut-off value of 123.0 SRR% for GD. A weak correlation was found between TSI and thyrotropin-binding inhibiting immunoglobulin (TBII) (r(s) = 0.259, p = 0.03), but no correlation was found between TSI and tri-iodothyronine or free thyroxine. CONCLUSIONS: The Mc4-CHO bioassay showed comparable diagnostic value for GD with the conventional TBII assay. We propose a cut-off of 123.0 SRR% in areas where iodine intake is high.

Diagnostic Value of a Chimeric TSH Receptor (Mc4)-Based Bioassay for Graves' Disease

BACKGROUND/AIMS: Graves' disease (GD) is caused by thyroid-stimulating hormone receptor (TSHR) and thyroid-stimulating immunoglobulin (TSI). We used a recently introduced, technically enhanced TSI bioassay to assess its diagnostic value and determine the cut-off in patients in high iodine intake area. METHODS: In a cross-sectional setting, we collected serum from 67 patients with untreated GD, 130 with GD under treatment, 22 with GD in remission, 42 with Hashimoto's thyroiditis, 12 with subacute thyroiditis, 20 with postpartum thyroiditis, and 93 euthyroid controls. TSI was measured using the Thyretaintrade mark bioassay, which is based on Chinese hamster ovary cells transfected with chimeric TSHR (Mc4). TSI levels are reported as a specimen-to-reference ratio percentage (SRR%). RESULTS: The TSI levels in patients with GD (either treated or not) were significantly higher than those of the remaining patients (p < 0.05). The new bioassay showed a sensitivity of 97.0% and a specificity of 95.9% with a cut-off value of 123.0 SRR% for GD. A weak correlation was found between TSI and thyrotropin-binding inhibiting immunoglobulin (TBII) (rs = 0.259, p = 0.03), but no correlation was found between TSI and tri-iodothyronine or free thyroxine. CONCLUSIONS: The Mc4-CHO bioassay showed comparable diagnostic value for GD with the conventional TBII assay. We propose a cut-off of 123.0 SRR% in areas where iodine intake is high.