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CodiEsp_corpus / dev /text_files_en /S0004-06142008000700014-1.txt
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A 77-year-old male patient with multiple cardiopathogenic factors and a benign prostatic hypertrophy as the only urological history.
She was admitted to the Internal Medicine Department to study a constitutional picture of 4 months of evolution with anorexia and weight loss of about 15 kg, accompanied by generalized weakness and epigastric colic pain lasting minutes.
There was no other accompanying clinic.
A digestive study (gastroscopy, ultrasound endoscopy) was normal.
Physical examination was normal, except for an increase in size of the genitals, so an ultrasound was performed, with the result of a bilateral hydrocele, more marked on the left side, with underlying non-malignant morphology test ruled out.
On physical examination, a 4 cm hard nodule was found in the upper pole of the left testis, suggesting a solid mass.
Distant imaging tests (DCT, MRI) were negative.
Germline tumor markers and LDH were requested, which were negative.
Left inguinal radical orchiectomy was performed.
The macroscopic description of the specimen, about 9 x 6.5cm, showed little healthy testicular parenchyma adjacent to the upper pole, in which a solid, multinodular, brownish-colored tumour mass of 4 cm diameter was found.
1.
Microscopic analysis showed areas of sarcomatoid pattern and growth on sheets together with areas where cells were arranged in a cordonal pattern or trabecular patterns with presence of vascular structures.
The cells were pyramidal, of great cytoplasm, with prominent nuclear pleomorphism and acquired in areas a very clear, lipidized cytoplasm.
The mitotic index was high, being higher than 5 mitosis x10 HPF in growing areas on sheet.
The tumor contacted the albuginea and the epididymis without practically remaining viable seminiferous tubules.
Images suggestive of vascular invasion were also observed.
In the sections of testicular parenchyma respected, the tubules presented hyalinized basal membrane with atrophic aspect.
Immunohistochemical techniques showed positivity for Inhibina, keratin, CK8, CK18, Vimentin, EMA and S-100.
Ki67 showed intense positivity in approximately 30-40% of tumor cells.
The patient was negative for Progesterone, PLAP, AFP, HCG, Cromogranin and HMB45.
With all these findings, the diagnosis was malignant Sertoli cell tumor, with variation of histological patterns, as classic type.
Twelve months later, the general situation persisted, which led to a new admission to Internal Medicine, suffering from an inherited disorder.
Serum and imaging controls in relation to the testicular process remain within normal parameters.