Endocrine Abstracts

Case history: 73-year-old male was seen in breast clinic for right breast lump which was noted 6 weeks back with no nipple discharge. Mammogram and ultrasound confirmed bilateral gynaecomastia more on right side. Referred to endocrine clinic with abnormal hormone profile. He is a retired builder. He was a heavy smoker for 50 years and has stopped smoking 1 year back. He drinks socially and has never used illicit drugs. His only past medical history was GORD for which he takes lansoprazole. Clinical and ultrasound examination of testes were normal.

Investigations : FSH 0.3 IU/l, LH <0.3 IU/l, 17 beta oestradiol 416 pmol/l, testosterone 29.7 nmol/l, TSH 1.6 mU/l, beta-HCG 69.8 IU/l, Alpha-fetoprotein 1.5 kU/l. Whole-body CT showed 5.7×6.4 cm malignant appearing mass in left lung lower lobe with mediastinal lymphadenopathy and nodular lesion in right adrenal gland suspicious for metastases. Radiological staging T4 N2 M1c.

Results and treatment: He was seen in respiratory clinic as priority. His performance status is 1 and his spirometry is normal with only moderate diffusion defect. Flexible bronchoscopic biopsy and bronchial washings with immunohistochemical stains favoured diagnosis of squamous cell carcinoma. He had another rigid bronchoscopic biopsy and is awaiting its results.

Conclusions and discussion: Gynecomastia results from oestrogen to androgen imbalance. Gonadal and extragonadal tumours can present with gynaecomastia. Gonadal tumours causing gynaecomastia could originate from sertoli cells, granulosa cells, Leydig cells or germ cells. Sertoli cell tumours and granulosa cell tumours produce excess of oestrogen whereas Leydig cell tumours produce oestrogen and testosterone. Gonadal germ cell tumours (both seminomatous and non-seminomatous type) produce hCG. The non-seminomatous tumours (embryonal carcinoma, yolk sac carcinoma, choriocarcinoma and teratoma) produce AFP in addition to hCG. Extra-gonadal germ cell tumours that ectopically express hCG can be lung, stomach, head/neck, ovary, leiomyosarcoma, renal-cell and hepato-cellular cancers (20–40% of all common epithelial cancers). The increased hCG acts as LH analogue to stimulate Leydig cells to produce more of oestrogen and less testosterone leading to gynaecomastia. Though paraneoplastic syndromes are common in lung cancer (10%), gynaecomastia occurs as a paraneoplastic syndrome only in 2.4% cases. Though hCG expression occurs in 12–14% of small cell lung cancers, it is exceedingly rare in non-small cell lung cancers (NSCLC). Among NSCLC types, adenocarcinomas express hCG more frequently than squamous cell carcinomas. Prognosis for hCG producing tumours are poor as they are generally aggressive and chemo resistant.