|Year : 2012 | Volume
| Issue : 8 | Page : 352-353
Gynaecomastia as the initial presentation of thyrotoxicosis
Triranjan Sanyal, Deep Dutta, KS Shivprasad, Sujoy Ghosh, Satinath Mukhopadhyay, Subhankar Chowdhury
Department of Endocrinology & Metabolism, IPGMER, SSKM Hospital, 244 AJC Bose Road, Kolkata, India
|Date of Web Publication||4-Jan-2013|
Department of Endocrinology & Metabolism, IPGMER & SSKM Hospital, 244 AJC Bose Road, Kolkata-700020
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Gynaecomastia is a well-recognized manifestation of thyrotoxicosis occurring in a widely variable percentage. Some studies have reported the percentage to be high as 40% while others report it being around 10%. The variation can be attributed to the difference in the criteria used to define gynae-comaslia or racial factors. However, thyrotoxicosis presenting with gynaceomastia as an intial manifestation is very rare. Only handful case reports are found in literature. Here we present a case of 35-year-old Indian male, with thyrotoxcosis who presented initially with painful bilateral gynaceomastia.
Keywords: Gynaecomastia, thyrotoxicosis, sex hormone binding globulin
|How to cite this article:|
Sanyal T, Dutta D, Shivprasad K S, Ghosh S, Mukhopadhyay S, Chowdhury S. Gynaecomastia as the initial presentation of thyrotoxicosis. Indian J Endocr Metab 2012;16, Suppl S2:352-3
|How to cite this URL:|
Sanyal T, Dutta D, Shivprasad K S, Ghosh S, Mukhopadhyay S, Chowdhury S. Gynaecomastia as the initial presentation of thyrotoxicosis. Indian J Endocr Metab [serial online] 2012 [cited 2021 Jul 25];16, Suppl S2:352-3. Available from: https://www.ijem.in/text.asp?2012/16/8/352/104089
| Introduction|| |
Gynaecomastia, although a well-recognized manifestation of thyrotoxicosis (10-40% cases of thyrotoxicosis) are not frequently encountered in clinical practice among thyrotoxic subjects. ,,, It is extremely rare for a thyrotoxicosis patient to present with gynaccomastia as an intial presenting feature. Only a few cases (12-13 cases) have reported so far as the review of literature reveals. However, recognition of an uncommon presentation of a common disease like thyrotoxicosis is important to ensure appropriate management and avoid unnecessary investigations.
| Case Report|| |
A 35-year-old Indian male, presented in our outpatient department with a complain of bilateral painful breast enlargement for 1 month. On further questioning, a history of weakness, weight loss, and excessive eating were revealed. The patient was married and had two children. He had no addiction, no history of any drug therapy, recently developed insomnia, anxiety, decreased libido, but no erectile dysfunction. On physical examination, he was mildly anemic, thin built (BMI-18 kg/m 2 ) with a just palpable thyroid. His resting pulse rate was 122/m, and he had fine-tremor in his hands. He was normotensive. No orbitopathy or dermopathy detected. He had bilateral tender gyncecomastia (disc diameter 2.5 cm). His deep tendon reflexes were brisk. He was a well-virillised men with prominent adamisapple, pubic hair of tanner stage 5, stretched penile length of 12 cm and testicular volume of 20 ml bilaterally.
His laboratory investigation revealed normal haemogram, fasting plasma glucose: 101 mg/dl, 2-h PP plasma glucose: 167 mg/dl, normal renal and liver function tests, FT4: 3.9 mg/dl (normal 0.58-1.64 mg/dl), FT3: 8.3 pg/ml (normal 2.39-6.79 pg/ml), HS-TSH (3 rd gen.): 0.03 mIU/ml (normal 0.34-3.50 miu/ml). Testosterone (total): >1600 mg/dl (normal 250-1600 mg/dl) Beta human chorionic gonadotropin (HCG): 2 miu/ml (<5 Miu/ml), Estradiol 95 mg/l (normal <50 mg/l), sex hormone binding globulin (SHBG): 132 nmol/l (normal 7-50 nmgl/l) luteinizing hormone (LH) 19.7 mlu/ml (normal 0.8-7.6 mlu/ml) follicle stimulating hormone (FSH) 8.06 mlu/ml (normal 0.7-11.1 miu/ml), Prolacton 10.4 mg/dl (normal 2.5-17 mg/ml).
Imaging studies like ultrasonography (USG) abdomen and st. X-ray chest failed to defect any abnormality.
Based on these reports a provisional diagnosis of thyrotosicosis with gynaceomastia was made and given a treatment with carbinazole and propranoloe.
| Discussion|| |
Gynaecomastia is believed to develop in hyperthyroidism as a result of increased level of free (achive) esfrogen to androgen ratio. Hyperthyroiddism causes increased production of SHBG due to direct hepatic stimulation by thyroid hormones. , As testostesone binds to SHBG with greater affinity compared to estogens free testosterone starts falling in spite of a higher total testostenone in the body. This in turn increases free (active) estrogen level in blood which is finally responsible for glandular proliferation of breast tissue leading to clinical gynaecomastia. Pituitary response to this situation by increasing LH secretion which in turn stimulates leydig cells to produce testosterone and estradiol until unbound testosterone returns to normal. This however, may lead to increased level of unbound (free) estradiol. Peripheral tissue aromalisalion of androgens is also increased in hyperthyroidism, which may also contribute to develop a high free estrogen level In the blood. ,
| Conclusion|| |
Hyperthyroidism may be associated with or rarely can be presented with gynaecomastia as an initial and only manifestation. Recognition of this unusual presentation of hypothyroidism will help to avoid and reduce unnecessary investigations or surgical procedure as the condition is completely reversible with anti-thyroid treatment.
| References|| |
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