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CASE REPORT
Year : 2014  |  Volume : 11  |  Issue : 3  |  Page : 116-117

A curious case of gynaecomastia!


1 Division of Endocrinology and Metabolism, Mazumdar Shaw Medical Center, Narayana Hrudayalaya Health City, Bangalore, Karnataka, India
2 Division of Breast Oncology, Mazumdar Shaw Medical Center, Narayana Hrudayalaya Health City, Bangalore, Karnataka, India

Date of Web Publication13-Aug-2014

Correspondence Address:
Subramanian Kannan
258/ABommasandra Industrial Area, Hosur Road, Bangalore 560 099, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-0354.138558

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  Abstract 

Gynecomastia is a benign proliferation of the glandular tissue of the male breast and is caused by a relative increase in the ratio of estrogen to androgen activity. Gynaecomastia has been reported in patients with Graves's disease; however, it is unusual in transient thyroid disorders like thyroiditis and thyroid hormone over-replacement. We report a case of a young healthy male who presented with gynaecomastia, elevated levels of testosterone, and elevated-free thyroid hormones. Tc 99m uptake was suppressed. Patient was started on corticosteroids and in a period of 6-8 weeks, gynaecomastia resolved, and his thyroid hormone and testosterone levels normalized.

Keywords: Gynaecomastia, thyrotoxicosis, sex hormone-binding globulin


How to cite this article:
Kannan S, Kunder S, Pais A. A curious case of gynaecomastia!. Thyroid Res Pract 2014;11:116-7

How to cite this URL:
Kannan S, Kunder S, Pais A. A curious case of gynaecomastia!. Thyroid Res Pract [serial online] 2014 [cited 2019 Dec 8];11:116-7. Available from: http://www.thetrp.net/text.asp?2014/11/3/116/138558


  Introduction Top


Gynecomastia is a benign proliferation of the glandular tissue of the male breast, and is caused by a relative increase in the ratio of estrogen to androgen activity. Gynaecomastia has been reported in patients with Graves' disease. However its occurrence in transient thyroid disorders has not been reported.


  Case report Top


A 24-year-old man presented with bilateral painful swelling in the breast area (right > left) which he had noticed for a month. There was no history of galactorrhea. He experienced normal libido, morning erections, and normal shaving frequency. Patient was not on any medications; however, he was taking a supplement called "Megamass 4600" (supplement reported to contain: creatine, glutamine, and taurine). He denied use of any other illicit drugs. Rest of the history was noncontributory. On examination, patient had bilateral gynaecomastia (right 3 cm and left 1.5 cm). There was no expressive galactorrhea. Thyroid was normal in size with no tenderness. Patient had warm extremities with tremors and heart rate of 90/min. He had normal androgenic hair distribution and with normal testicular volumes (bilateral testes 25 cc). Laboratory evaluation revealed serum total testosterone levels to be greater than 1300 ng/dL (normal: 300-1060 ng/dL by chemiluminescence) and nonsuppressed gonadotropins [follicle-stimulating hormone: 3.21 mIU/mL and luteinizing hormone (LH): 5.87 mIU/mL]. His thyroid-stimulating hormone (TSH) was undetectable and free T4 and free T3 were elevated at 3.27 ng/dL (normal value: 0.82-1.57) and 11.13 pg/mL (normal value: 2.3-4.2), respectively. Prolactin was 9.22 ng/mL (3-25) and beta-hCG was 0.2 mIU/mL (normal < 10). His liver enzymes were normal. A Tc 99m uptake was very low (0.1%) consistent with thyroiditis or exogenous thyroid hormone intake. Patient was counseled to stop the nutritional supplement and was started with prednisone taper for 3 weeks along with propranolol. On follow-up after 8 weeks, his gynaecomastia had resolved. His repeat laboratory testing were consistent with euthyroid status (FT4 was 0.87; FT3 2.48; and TSH was 0.97) and his serum total testosterone was normal at 900 ng/mL.


  Discussion Top


Gynecomastia has been reported in as many as 25%-40% of men with hyperthyroidism due to Graves' disease, although one study suggests that the actual prevalence is less than 10%. [1],[2],[3],[4] The pathogenesis of gynecomastia in patients with Graves's disease is multifactorial. There is several-fold increase in levels of sex hormone-binding globulin (SHBG) as a result of primary hepatic stimulation by thyroid hormones. [5],[6],[7] Higher affinity of testosterone to SHBG relative to estrogen contributes to elevated total testosterone levels, normal or low free testosterone levels, and elevated free estradiol levels. There is also enhanced aromatization of testosterone to estradiol and of androstenedione to estrone in extraglandular tissues. [8] Increased serum LH levels in Graves' disease also contribute to further increased estradiol relative to testosterone production by Leydig cells.

Although the association of gynaecomastia and hyperthyroidism was long noted by von Basedow more than 100 years ago, it was not until 1968 that Becker et al., [9] first reported on the histological findings of the breast tissue in patients before and after treatment of hyperthyroidism. In hyperthyroid men with gynaecomastia, they demonstrated that the ducts were elongated and tortuous, the epithelium hyperplastic and papillary, and the periductal stroma loose and myxomatous. Regression was noted with treatment of hyperthyroidism, with the histology showing the epithelium receded in height, the ducts became less branched, and stroma less dense and collagenous. Subclinical gynaecomastia may assume an even greater prevalence among male patients with hyperthyroidism. [10] They found histologic evidence of gynaecomastia in 15 (83%) of the 18 hyperthyroid men who underwent bilateral breast biopsies at the time of subtotal thyroidectomy, whereas breast enlargement was noted clinically in only six patients (33%).

The occurrence of gynaecomastia as a presenting complaint in patients with transient elevations in thyroid hormone like in the above patient has not been reported. The nonsuppressed gonadotropins in our patient likely rules out the use of exogenous androgens. Although we did not perform free testosterone levels, it was clear that the etiology of gynaecomastia may be either due to a transient thyroiditis or due to the thyroid hormones in the supplement that the patient was taking. In either regards, the primary presentation with gynaecomastia in a patient with transient thyroid hormone elevation was unusual and thus highlights the need for exclusion of thyroid abnormalities in patients presenting with gynaecomastia.

 
  References Top

1.Chopra IJ, Tulchinsky D. Status of estrogen-androgen balance in hyperthyroid men with graves' disease. J Clin Endocrinol Metab 1974;38:269-77.  Back to cited text no. 1
    
2.Ashkar FS, Smoak WM 3 rd , Gilson AJ, Miller R. Gynecomastia and mastoplasia in graves' disease. Metabolism 1970;19:946-51.  Back to cited text no. 2
    
3.Chan WB, Yeung VT, Chow CC, So WY, Cockram CS. Gynaecomastia as a presenting feature of thyrotoxicosis. Postgrad Med J 1999;75:229-31.  Back to cited text no. 3
    
4.Bercovici JP, Mauvais-Jarvis P. Hyperthyroidism and gynecomastia: Metabolic studies. J Clin Endocrinol Metab 1972;35:671-7.  Back to cited text no. 4
    
5.Anderson DC. Sex-hormone-binding globulin. Clin Endocrinol (Oxf) 1974;3:69-96.  Back to cited text no. 5
    
6.Marcus R, Korenman SG. Estrogens and the human male. Annu Rev Med 1976;27:357-70.  Back to cited text no. 6
    
7.Chopra IJ, Abraham GE, Chopra U, Solomon DH, Odell WD. Alterations in circulating estradiol-17 in male patients with graves's disease. N Engl J Med 1972;286:124-9.  Back to cited text no. 7
    
8.Olivo J, Gordon GG, Rafii F, Southren AL. Estrogen metabolism in hyperthyroidism and in cirrhosis of the liver. Steroids 1975;26:47-56.  Back to cited text no. 8
    
9.Becker KL, Winnacker JL, Matthews MJ, Higgins GA Jr. Gynecomastia and hyperthyroidism. An endocrine and histological investigation. J Clin Endocrinol Metab 1968;28:277-85.  Back to cited text no. 9
    
10.Becker KL, Matthews MJ, Higgins GA Jr, Mohamadi M. Histologic evidence of gynecomastia in hyperthyroidism. Arch Pathol 1974;98:257-60.  Back to cited text no. 10
    




 

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