A 77 year old male patient with multiple cardiopathogenic factors, and the only urological history was benign prostatic hypertrophy. He was admitted to the Internal Medicine Department for the study of constitutional symptoms of 4 months' evolution with anorexia and loss of about 15 kg of weight, accompanied by generalised weakness and epigastric cramping pain lasting minutes. She had no other accompanying symptoms. A gastrointestinal examination (gastroscopy, colonoscopy, echoendoscopy) was performed and was normal. The physical examination was normal, except for an increase in the size of the genitalia, for which an ultrasound was performed, with the result of a bilateral hydrocele, more marked on the left side, with multinodular morphology destructuring in the left teste, which made it necessary to rule out an underlying malignant process. On examination, in addition to presenting positive bilateral transillumination, a 4 cm hard nodule was palpable in the upper pole of the left teste, suggestive of a solid mass. Remote imaging tests (CT, MRI) were negative. Germinal tumour markers and LDH were requested and were negative. Left inguinal radical orchiectomy was performed. The macroscopic description of the specimen, measuring 9 x 6.5cm, showed scarce healthy testicular parenchyma adjacent to the upper pole, in which a solid, multinodular, whitish tumour mass with some brownish areas was found, measuring 4cm in diameter. Microscopic analysis showed areas of sarcomatoid pattern and sheet-like growth together with areas where the cells were arranged in a chordate pattern or forming trabeculae with the presence of vascular structures. The cells were pyramidal, with large cytoplasm, nuclear pleomorphism and prominent nucleoli acquiring in areas a very clear, lipidified cytoplasm. The mitotic index was high, being higher than 5 mitoses x 10 HPF in the areas of sheet-like growth. The tumour contacted the albuginea and infiltrated the epididymis with virtually no viable seminiferous tubules remaining. There were also images highly suggestive of vascular invasion. In the sections of respected testicular parenchyma, the tubules showed hyalinised basement membrane, with an atrophic appearance. Immunohistochemical techniques showed positivity for Inhibin, keratin, CK8, CK18, Vimentin, EMA and S-100. Ki67 showed intense positivity in approximately 30-40% of tumour cells. It was negative for Progesterone, PLAP, AFP, HCG, Chromogranin and HMB45. With all these findings, the diagnosis was malignant Sertoli cell tumour, with variation of histological patterns, classified as Classical type. Twelve months later, the general symptoms persisted, which led to a new admission to Internal Medicine, with suspicion of Systemic Inflammatory Disease. The serum and imaging controls in relation to the testicular process remain within normal parameters.