Gynecological Endocrinology
ISSN: 0951-3590 (Print) 1473-0766 (Online) Journal homepage: http://www.tandfonline.com/loi/igye20
An unusual cause of cardiothyreosis Lucien Marchand, Paul Chabert, Elise Chaudesaygues, Mélanie Grasse, Stephan Bretones, Julia Graeppi-Dulac & Jean-François Aupetit To cite this article: Lucien Marchand, Paul Chabert, Elise Chaudesaygues, Mélanie Grasse, Stephan Bretones, Julia Graeppi-Dulac & Jean-François Aupetit (2016) An unusual cause of cardiothyreosis, Gynecological Endocrinology, 32:2, 107-109, DOI: 10.3109/09513590.2015.1111328 To link to this article: http://dx.doi.org/10.3109/09513590.2015.1111328
Accepted author version posted online: 11 Nov 2015. Published online: 16 Nov 2015. Submit your article to this journal
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Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=igye20 Download by: [Orta Dogu Teknik Universitesi]
Date: 15 February 2016, At: 11:39
http://informahealthcare.com/gye ISSN: 0951-3590 (print), 1473-0766 (electronic) Gynecol Endocrinol, 2016; 32(2): 107–109 ! 2015 Taylor & Francis. DOI: 10.3109/09513590.2015.1111328
CARDIOTHYREOSIS
An unusual cause of cardiothyreosis Lucien Marchand1, Paul Chabert1, Elise Chaudesaygues1, Me´lanie Grasse1, Stephan Bretones2, Julia Graeppi-Dulac3, and Jean-Franc¸ois Aupetit1 Department of Cardiology, 2Department of Obstetrics and Gynecology, St. Joseph and St. Luc Hospital, Lyon, France, and 3Department of Endocrinology, Nord-Ouest Hospital, Villefranche-Sur-Saoˆne, France
Downloaded by [Orta Dogu Teknik Universitesi] at 11:39 15 February 2016
1
Abstract
Keywords
Severe hyperthyroidism can cause cardiac complications, such as severe rhythm disturbances, heart failure and angina. Gestational trophoblastic disease (GTD) is a rare complication of pregnancy, ranging from benign hydatidiform mole to malignant form. Clinical hyperthyroidism may occur in GTD, as human chorionic gonadotropin (hCG) secreted by molar tissue is structurally similar to thyroid-stimulating hormone. Cardiothyreosis in this context is exceptional. We report the case of a nulligravida 42-year-old woman without thyroid or cardiac history who presented to the emergency department for dyspnoea. Examinations revealed an acute pulmonary oedema and sinus tachycardia. Serum hCG concentration was abnormally high (762 878 UI/l, N55). CT scan showed a voluminous uterine mass and eliminated pulmonary embolism. Cardiac output was increased in echocardiography. Complementary blood tests showed a peripheral hyperthyroidism. GTD was evoked in the context of uterine mass and high hCG concentration, which was responsible for inducing clinical hyperthyroidism and cardiothyreosis. A total hysterectomy was performed and histopathological examinations concluded to a non-invasive complete hydatidiform mole (begnin form). hCG fell to normal within 12 weeks, cardiac and thyroid functions normalized after mole evacuation.
Cardiothyreosis, human chorionic gonadotropin, hydatiform mole, hyperthyroidism, thyroid-stimulating hormone
Introduction Thyrotoxicosis is a clinical state that results from inappropriately high thyroid hormone levels (free triiodothyronine, T3; free thyroxine, T4) [1]. Thyrotoxicosis can occur if the thyroid is inappropriately stimulated by trophic factors, or if there is constitutive activation of thyroid hormone synthesis and secretion leading to autonomous release of excess thyroid hormone, or if the thyroid stores of hormone are passively released in excessive amounts, or if there is an extra-thyroidal sources of thyroid hormone [1]. The most common causes of hyperthyroidism include Graves’ disease, toxic multinodular goiter and toxic adenoma [2]. Severe hyperthyroidism can cause cardiac complications, such as severe rhythm disturbances, heart failure and angina. These complications appear mainly on a cardiac disease background but also in healthy individuals [3]. The presence of one of these complications in a context of thyrotoxicosis settles the diagnosis of cardiothyreosis. We report here the case of a 42-year-old woman without any cardiac or thyroid history who presented a cardiothyreosis. The cause of thyrotoxicosis appeared to be unusual.
Case description A 42-year-old woman with a medical past of functional colopathy and without medication presented to the emergency department of
Address for correspondence: Jean-Franc¸ois Aupetit, Department of Cardiology, St. Joseph and St. Luc Hospital, Lyon, France. Tel: +33 4 78 61 83 05. E-mail: [email protected]
History Received 30 July 2015 Revised 18 October 2015 Accepted 18 October 2015 Published online 16 November 2015
our hospital for dyspnoea and asthenia. Her vital signs showed a temperature of 37 C, blood pressure of 180/120 mmHg and pulse rate of 160 beats/min. Physical examination and chest X-ray objectivized an acute pulmonary oedema. Electrocardiogram showed a sinus tachycardia. Blood tests showed an elevation of Nt-pro BNP (27 000 ng/l, N [0–300]). There was no sign of inflammation (CRP and leukocytes were normal). Haemoglobin was slightly decreased at 9.7 g/ dl. Serum human chorionic gonadotropin (hCG) concentration was measured at 762 878 UI/l (N55). She was initially treated by furosemide, isosorbide dinitrate and non-invasive ventilation. A thoracic and abdominal CT scan showed a voluminous uterine mass (mean diameter of 13.5) (Figure 1) and eliminated pulmonary embolism. Cardiac cavities were not dilated and left ventricular ejection fraction (LVEF) was 52% on echocardiography. Cardiac output was increased at 7.4 l/min. Transvaginal US showed a mass including vesicular areas in the heterogeneous echogenicity filling the uterine cavity and a snow-storm appearance. Gestational trophoblastic disease (GTD) was evoked in the context of highly elevated serum hCG concentration and the echographic aspect of the uterine mass. Complementary anamnesis reported amenorrhea and signs of thyrotoxicosis for past several weeks (weight loss of 5 kg, nervousness, fine tremor and diarrhoea). Thyroid function tests showed peripheral hyperthyroidism with an undetectable thyroidstimulating hormone (TSH), T4f elevated at 45 pmol/l (N [12– 22]) and T3f elevated at 20 pmol/l (N [3.1–6.8]).
Downloaded by [Orta Dogu Teknik Universitesi] at 11:39 15 February 2016
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Gynecol Endocrinol, 2016; 32(2): 107–109
Figure 1. Uterine mass at CT scan in sagittal view (left) and transversal view (right).
Figure 2. Evolution of hCG and thyroid function in post-surgery.
Antithyroidal antibodies were negative. Ultrasonography showed a normal thyroid gland, with a slight hypervascularization. Thus, the complete diagnosis was a cardiothyreosis in the context of hCG-induced hyperthyroidism. A beta-blocker (propranolol) and antithyroid agent (carbimazole 20 mg/day) were administered until a successful total hysterectomy was performed, without surgical complication. There was a rapid decrease of serum hCG concentration and in parallel spontaneous normalization of thyroid blood tests after evacuation of uterine mass (Figure 2). Control echocardiography showed a normalization of cardiac output.
Final histopathological examinations of the uterine mass showed a non-invasive complete hydatidiform mole (benign form) of 10.5 cm, which did not require additional treatment. After 3 months, hCG had reached normal ranges, thyroid function tests and echocardiography were also normal.
Discussion Hyperthyroidism can increase cardiac output (by 50–300%) because of the combined effect of increases in cardiac contractility, resting heart rate and blood volume [4,5].
An unusual cardiothyreosis
Downloaded by [Orta Dogu Teknik Universitesi] at 11:39 15 February 2016
DOI: 10.3109/09513590.2015.1111328
Atrial fibrillation (prevalence in hyperthyroidism ranges between 2% and 20%), angina (mainly in patients with underlying coronary disease) and heart failure (exaggerated sinus tachycardia or atrial fibrillation can produce rate-related left ventricular dysfunction, but pre-existent ischemic or hypertensive heart disease may also predispose) are well-known cardiac complications of thyrotoxicosis [3]. The effects of increased levels of hCG on TSH and on the thyroid are well described in normal pregnancy [6,7] and in GTD [8]. The effect on the thyroid is due to molecular mimicry between hCG subunits and TSH [9]. HCG is a glycoprotein composed of alpha and beta subunits. The alpha subunit is identical to that found in TSH, luteinizing hormone and folliclestimulating hormone, and the beta subunit of hCG has homology with the beta subunit of TSH. The affinity of HCG for TSH receptors is 4000 times less than TSH and so high levels of hCG are usually needed to affect thyroid function. Unlike the normal pregnancies with hCG levels inferior to 100 000 IU/l, the values in molar pregnancies are often superior to 200 000 IU/l. GTD is a rare complication of pregnancy, ranging from the pre-malignant conditions of complete and partial hydatidiform moles through to the malignant invasive mole, choriocarcinoma and very rare placental site trophoblastic tumour/epithelioid trophoblastic tumour. Hydatidiform mole is the most common form, which is composed of villi with excess of paternal genetic material [10]. Molar pregnancies are classified as complete or partial based on gross morphology, histopathologic features and karyotype. The incidence of GTD is 0.57–1.1 per 1000 pregnancies (North America, Australia, New Zealand and Europe), whereas studies in Southeast Asia and Japan have suggested an incidence as high as 2.0 per 1000 pregnancies [11]. In the British study of Walkington [12], 14 (7%) of 196 patients with gestational trophoblastic had biochemical hyperthyroidism. Of these, 4 (2%) had evidence of clinical hyperthyroidism and 1 (0.5%) presented heart failure. Thyrotoxicosis is therefore a rare complication of GTM, and cardiothyreosis is exceptional in this context. In all cases, thyroid function normalized rapidly with treatment of underlying GTD. The originality of this case report is that the cardiac presentation preceded the discovery of the hydatidiform mole and the hCG-induced hyperthyroidism. In our case, the patient did not have cardiac or thyroid history. She was nulligravida but sexually active without regular contraception. She had presented amenorrhea for several weeks. Levels of T4 and T3 were not exceptionally high (45 pmol/l (N [12–22] and 20 pmol/l (N [3.1–6.8], respectively), but in absence of other acceptable hypothesis and in presence of an increased cardiac output, cardiothyreosis was the only valuable diagnosis for the heart failure. The negativity of thyroid antibodies and the normality of thyroid echography precluded the likelihood of an underlying thyroidopathy. A differential diagnosis was a heart failure associated with pregnancy, also called peripartum cardiomyopathy (PC), which is
109
defined as a cardiomyopathy first presenting during the third trimester of pregnancy or the first 6 months of postpartum, in the absence of pre-existing cardiovascular disease [13]. Some cases with myocarditis of pregnancy were published [14]. However, our patient did not have chest pain and pathological ECG abnormalities. She had a sub-normal LVEF, no dilatation of cavities and high cardiac output (whereas women with PC usually have decreased cardiac output) [13]. Therefore, we eliminated this diagnosis. This article figures out the rare case of a heart failure efficiently treated by total hysterectomy, consisting into removing a hydatiform mole causing hCG induced cardiothyreosis. As a conclusion, one should always think about dosing HCG in a sexually active woman.
Declaration of interest The authors report no declaration of interest.
References 1. Bahn Chair RS, Burch HB, Cooper DS, et al. Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists. Thyroid 2011;21:593–646. 2. Singer PA, Cooper DS, Levy EG, et al. Treatment guidelines for patients with hyperthyroidism and hypothyroidism. Standards of Care Committee, American Thyroid Association. JAMA 1995;273: 808–12. 3. Klein I, Danzi S. Thyroid disease and the heart. Circulation 2007; 116:1725–35. 4. Biondi B, Palmieri EA, Lombardi G, Fazio S. Effects of thyroid hormone on cardiac function: the relative importance of heart rate, loading conditions, and myocardial contractility in the regulation of cardiac performance in human hyperthyroidism. J Clin Endocrinol Metab 2002;87:968–74. 5. Klein I, Ojamaa K. Thyroid hormone and the cardiovascular system. N Engl J Med 2001;344:501–9. 6. Braunstein GD, Rasor J, Danzer H, et al. Serum human chorionic gonadotropin levels throughout normal pregnancy. Am J Obstet Gynecol 1976;126:678–81. 7. Glinoer D, de Nayer P, Bourdoux P, et al. Regulation of maternal thyroid during pregnancy. J Clin Endocrinol Metab 1990;71:276–87. 8. Hershman JM. Human chorionic gonadotropin and the thyroid: hyperemesis gravidarum and trophoblastic tumors. Thyroid 1999;9: 653–7. 9. Fisher PM, Hancock BW. Gestational trophoblastic diseases and their treatment. Cancer Treat Rev 1997;23:1–16. 10. Allias F, Bolze P-A, Gaillot-Durand L, et al. [Gestational trophoblastic disease]. Ann Pathol 2014;34:434–47. 11. Lurain JR. Gestational trophoblastic disease: epidemiology, pathology, clinical presentation and diagnosis of gestational trophoblastic disease, and management of hydatidiform mole. Am J Obstet Gynecol 2010;203:531–9. 12. Walkington L, Webster J, Hancock BW, et al. Hyperthyroidism and human chorionic gonadotrophin production in gestational trophoblastic disease. Br J Cancer 2011;104:1665–9. 13. Lampert MB, Lang RM. Peripartum cardiomyopathy. Am Heart J 1995;130:860–70. 14. Rizeq MN, Rickenbacher PR, Fowler MB, Billingham ME. Incidence of myocarditis in peripartum cardiomyopathy. Am J Cardiol 1994;74:474–7.
ISSN: 0951-3590 (Print) 1473-0766 (Online) Journal homepage: http://www.tandfonline.com/loi/igye20
An unusual cause of cardiothyreosis Lucien Marchand, Paul Chabert, Elise Chaudesaygues, Mélanie Grasse, Stephan Bretones, Julia Graeppi-Dulac & Jean-François Aupetit To cite this article: Lucien Marchand, Paul Chabert, Elise Chaudesaygues, Mélanie Grasse, Stephan Bretones, Julia Graeppi-Dulac & Jean-François Aupetit (2016) An unusual cause of cardiothyreosis, Gynecological Endocrinology, 32:2, 107-109, DOI: 10.3109/09513590.2015.1111328 To link to this article: http://dx.doi.org/10.3109/09513590.2015.1111328
Accepted author version posted online: 11 Nov 2015. Published online: 16 Nov 2015. Submit your article to this journal
Article views: 22
View related articles
View Crossmark data
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=igye20 Download by: [Orta Dogu Teknik Universitesi]
Date: 15 February 2016, At: 11:39
http://informahealthcare.com/gye ISSN: 0951-3590 (print), 1473-0766 (electronic) Gynecol Endocrinol, 2016; 32(2): 107–109 ! 2015 Taylor & Francis. DOI: 10.3109/09513590.2015.1111328
CARDIOTHYREOSIS
An unusual cause of cardiothyreosis Lucien Marchand1, Paul Chabert1, Elise Chaudesaygues1, Me´lanie Grasse1, Stephan Bretones2, Julia Graeppi-Dulac3, and Jean-Franc¸ois Aupetit1 Department of Cardiology, 2Department of Obstetrics and Gynecology, St. Joseph and St. Luc Hospital, Lyon, France, and 3Department of Endocrinology, Nord-Ouest Hospital, Villefranche-Sur-Saoˆne, France
Downloaded by [Orta Dogu Teknik Universitesi] at 11:39 15 February 2016
1
Abstract
Keywords
Severe hyperthyroidism can cause cardiac complications, such as severe rhythm disturbances, heart failure and angina. Gestational trophoblastic disease (GTD) is a rare complication of pregnancy, ranging from benign hydatidiform mole to malignant form. Clinical hyperthyroidism may occur in GTD, as human chorionic gonadotropin (hCG) secreted by molar tissue is structurally similar to thyroid-stimulating hormone. Cardiothyreosis in this context is exceptional. We report the case of a nulligravida 42-year-old woman without thyroid or cardiac history who presented to the emergency department for dyspnoea. Examinations revealed an acute pulmonary oedema and sinus tachycardia. Serum hCG concentration was abnormally high (762 878 UI/l, N55). CT scan showed a voluminous uterine mass and eliminated pulmonary embolism. Cardiac output was increased in echocardiography. Complementary blood tests showed a peripheral hyperthyroidism. GTD was evoked in the context of uterine mass and high hCG concentration, which was responsible for inducing clinical hyperthyroidism and cardiothyreosis. A total hysterectomy was performed and histopathological examinations concluded to a non-invasive complete hydatidiform mole (begnin form). hCG fell to normal within 12 weeks, cardiac and thyroid functions normalized after mole evacuation.
Cardiothyreosis, human chorionic gonadotropin, hydatiform mole, hyperthyroidism, thyroid-stimulating hormone
Introduction Thyrotoxicosis is a clinical state that results from inappropriately high thyroid hormone levels (free triiodothyronine, T3; free thyroxine, T4) [1]. Thyrotoxicosis can occur if the thyroid is inappropriately stimulated by trophic factors, or if there is constitutive activation of thyroid hormone synthesis and secretion leading to autonomous release of excess thyroid hormone, or if the thyroid stores of hormone are passively released in excessive amounts, or if there is an extra-thyroidal sources of thyroid hormone [1]. The most common causes of hyperthyroidism include Graves’ disease, toxic multinodular goiter and toxic adenoma [2]. Severe hyperthyroidism can cause cardiac complications, such as severe rhythm disturbances, heart failure and angina. These complications appear mainly on a cardiac disease background but also in healthy individuals [3]. The presence of one of these complications in a context of thyrotoxicosis settles the diagnosis of cardiothyreosis. We report here the case of a 42-year-old woman without any cardiac or thyroid history who presented a cardiothyreosis. The cause of thyrotoxicosis appeared to be unusual.
Case description A 42-year-old woman with a medical past of functional colopathy and without medication presented to the emergency department of
Address for correspondence: Jean-Franc¸ois Aupetit, Department of Cardiology, St. Joseph and St. Luc Hospital, Lyon, France. Tel: +33 4 78 61 83 05. E-mail: [email protected]
History Received 30 July 2015 Revised 18 October 2015 Accepted 18 October 2015 Published online 16 November 2015
our hospital for dyspnoea and asthenia. Her vital signs showed a temperature of 37 C, blood pressure of 180/120 mmHg and pulse rate of 160 beats/min. Physical examination and chest X-ray objectivized an acute pulmonary oedema. Electrocardiogram showed a sinus tachycardia. Blood tests showed an elevation of Nt-pro BNP (27 000 ng/l, N [0–300]). There was no sign of inflammation (CRP and leukocytes were normal). Haemoglobin was slightly decreased at 9.7 g/ dl. Serum human chorionic gonadotropin (hCG) concentration was measured at 762 878 UI/l (N55). She was initially treated by furosemide, isosorbide dinitrate and non-invasive ventilation. A thoracic and abdominal CT scan showed a voluminous uterine mass (mean diameter of 13.5) (Figure 1) and eliminated pulmonary embolism. Cardiac cavities were not dilated and left ventricular ejection fraction (LVEF) was 52% on echocardiography. Cardiac output was increased at 7.4 l/min. Transvaginal US showed a mass including vesicular areas in the heterogeneous echogenicity filling the uterine cavity and a snow-storm appearance. Gestational trophoblastic disease (GTD) was evoked in the context of highly elevated serum hCG concentration and the echographic aspect of the uterine mass. Complementary anamnesis reported amenorrhea and signs of thyrotoxicosis for past several weeks (weight loss of 5 kg, nervousness, fine tremor and diarrhoea). Thyroid function tests showed peripheral hyperthyroidism with an undetectable thyroidstimulating hormone (TSH), T4f elevated at 45 pmol/l (N [12– 22]) and T3f elevated at 20 pmol/l (N [3.1–6.8]).
Downloaded by [Orta Dogu Teknik Universitesi] at 11:39 15 February 2016
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L. Marchand et al.
Gynecol Endocrinol, 2016; 32(2): 107–109
Figure 1. Uterine mass at CT scan in sagittal view (left) and transversal view (right).
Figure 2. Evolution of hCG and thyroid function in post-surgery.
Antithyroidal antibodies were negative. Ultrasonography showed a normal thyroid gland, with a slight hypervascularization. Thus, the complete diagnosis was a cardiothyreosis in the context of hCG-induced hyperthyroidism. A beta-blocker (propranolol) and antithyroid agent (carbimazole 20 mg/day) were administered until a successful total hysterectomy was performed, without surgical complication. There was a rapid decrease of serum hCG concentration and in parallel spontaneous normalization of thyroid blood tests after evacuation of uterine mass (Figure 2). Control echocardiography showed a normalization of cardiac output.
Final histopathological examinations of the uterine mass showed a non-invasive complete hydatidiform mole (benign form) of 10.5 cm, which did not require additional treatment. After 3 months, hCG had reached normal ranges, thyroid function tests and echocardiography were also normal.
Discussion Hyperthyroidism can increase cardiac output (by 50–300%) because of the combined effect of increases in cardiac contractility, resting heart rate and blood volume [4,5].
An unusual cardiothyreosis
Downloaded by [Orta Dogu Teknik Universitesi] at 11:39 15 February 2016
DOI: 10.3109/09513590.2015.1111328
Atrial fibrillation (prevalence in hyperthyroidism ranges between 2% and 20%), angina (mainly in patients with underlying coronary disease) and heart failure (exaggerated sinus tachycardia or atrial fibrillation can produce rate-related left ventricular dysfunction, but pre-existent ischemic or hypertensive heart disease may also predispose) are well-known cardiac complications of thyrotoxicosis [3]. The effects of increased levels of hCG on TSH and on the thyroid are well described in normal pregnancy [6,7] and in GTD [8]. The effect on the thyroid is due to molecular mimicry between hCG subunits and TSH [9]. HCG is a glycoprotein composed of alpha and beta subunits. The alpha subunit is identical to that found in TSH, luteinizing hormone and folliclestimulating hormone, and the beta subunit of hCG has homology with the beta subunit of TSH. The affinity of HCG for TSH receptors is 4000 times less than TSH and so high levels of hCG are usually needed to affect thyroid function. Unlike the normal pregnancies with hCG levels inferior to 100 000 IU/l, the values in molar pregnancies are often superior to 200 000 IU/l. GTD is a rare complication of pregnancy, ranging from the pre-malignant conditions of complete and partial hydatidiform moles through to the malignant invasive mole, choriocarcinoma and very rare placental site trophoblastic tumour/epithelioid trophoblastic tumour. Hydatidiform mole is the most common form, which is composed of villi with excess of paternal genetic material [10]. Molar pregnancies are classified as complete or partial based on gross morphology, histopathologic features and karyotype. The incidence of GTD is 0.57–1.1 per 1000 pregnancies (North America, Australia, New Zealand and Europe), whereas studies in Southeast Asia and Japan have suggested an incidence as high as 2.0 per 1000 pregnancies [11]. In the British study of Walkington [12], 14 (7%) of 196 patients with gestational trophoblastic had biochemical hyperthyroidism. Of these, 4 (2%) had evidence of clinical hyperthyroidism and 1 (0.5%) presented heart failure. Thyrotoxicosis is therefore a rare complication of GTM, and cardiothyreosis is exceptional in this context. In all cases, thyroid function normalized rapidly with treatment of underlying GTD. The originality of this case report is that the cardiac presentation preceded the discovery of the hydatidiform mole and the hCG-induced hyperthyroidism. In our case, the patient did not have cardiac or thyroid history. She was nulligravida but sexually active without regular contraception. She had presented amenorrhea for several weeks. Levels of T4 and T3 were not exceptionally high (45 pmol/l (N [12–22] and 20 pmol/l (N [3.1–6.8], respectively), but in absence of other acceptable hypothesis and in presence of an increased cardiac output, cardiothyreosis was the only valuable diagnosis for the heart failure. The negativity of thyroid antibodies and the normality of thyroid echography precluded the likelihood of an underlying thyroidopathy. A differential diagnosis was a heart failure associated with pregnancy, also called peripartum cardiomyopathy (PC), which is
109
defined as a cardiomyopathy first presenting during the third trimester of pregnancy or the first 6 months of postpartum, in the absence of pre-existing cardiovascular disease [13]. Some cases with myocarditis of pregnancy were published [14]. However, our patient did not have chest pain and pathological ECG abnormalities. She had a sub-normal LVEF, no dilatation of cavities and high cardiac output (whereas women with PC usually have decreased cardiac output) [13]. Therefore, we eliminated this diagnosis. This article figures out the rare case of a heart failure efficiently treated by total hysterectomy, consisting into removing a hydatiform mole causing hCG induced cardiothyreosis. As a conclusion, one should always think about dosing HCG in a sexually active woman.
Declaration of interest The authors report no declaration of interest.
References 1. Bahn Chair RS, Burch HB, Cooper DS, et al. Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists. Thyroid 2011;21:593–646. 2. Singer PA, Cooper DS, Levy EG, et al. Treatment guidelines for patients with hyperthyroidism and hypothyroidism. Standards of Care Committee, American Thyroid Association. JAMA 1995;273: 808–12. 3. Klein I, Danzi S. Thyroid disease and the heart. Circulation 2007; 116:1725–35. 4. Biondi B, Palmieri EA, Lombardi G, Fazio S. Effects of thyroid hormone on cardiac function: the relative importance of heart rate, loading conditions, and myocardial contractility in the regulation of cardiac performance in human hyperthyroidism. J Clin Endocrinol Metab 2002;87:968–74. 5. Klein I, Ojamaa K. Thyroid hormone and the cardiovascular system. N Engl J Med 2001;344:501–9. 6. Braunstein GD, Rasor J, Danzer H, et al. Serum human chorionic gonadotropin levels throughout normal pregnancy. Am J Obstet Gynecol 1976;126:678–81. 7. Glinoer D, de Nayer P, Bourdoux P, et al. Regulation of maternal thyroid during pregnancy. J Clin Endocrinol Metab 1990;71:276–87. 8. Hershman JM. Human chorionic gonadotropin and the thyroid: hyperemesis gravidarum and trophoblastic tumors. Thyroid 1999;9: 653–7. 9. Fisher PM, Hancock BW. Gestational trophoblastic diseases and their treatment. Cancer Treat Rev 1997;23:1–16. 10. Allias F, Bolze P-A, Gaillot-Durand L, et al. [Gestational trophoblastic disease]. Ann Pathol 2014;34:434–47. 11. Lurain JR. Gestational trophoblastic disease: epidemiology, pathology, clinical presentation and diagnosis of gestational trophoblastic disease, and management of hydatidiform mole. Am J Obstet Gynecol 2010;203:531–9. 12. Walkington L, Webster J, Hancock BW, et al. Hyperthyroidism and human chorionic gonadotrophin production in gestational trophoblastic disease. Br J Cancer 2011;104:1665–9. 13. Lampert MB, Lang RM. Peripartum cardiomyopathy. Am Heart J 1995;130:860–70. 14. Rizeq MN, Rickenbacher PR, Fowler MB, Billingham ME. Incidence of myocarditis in peripartum cardiomyopathy. Am J Cardiol 1994;74:474–7.
