This is a 56-year-old patient, whose personal history of interest included pulmonary tuberculosis that had resolved; angina pectoris operated on with four aorto-coronary by-passes in 1997, and on antiplatelet treatment, with good control at present; digestive haemorrhage secondary to a duodenal ulcus caused by H. Pylori, treated with triple therapy, in remission with negative breath test controls, and on treatment with proton pump inhibitors (Omeprazole); history of typhoid fever, prostatic syndrome on treatment with a-blockers, with an episode of acute prostatitis, which required admission in 2002; obstructive sleep apnoea syndrome, on treatment with CPAP; cholelithiasis; and tonsillectomy in childhood. Recently, and as a result of an abdominal ultrasound, celiac adenopathy was diagnosed, pending filiation. As family history, her father had died of colon cancer.
He went for a check-up, presenting prostate symptoms with severe impairment of his quality of life (IPSS:22; L:4), a PSA of 1.6 ng/ml, a firmboelastic prostate, non-painful, without palpable indurations, for which transurethral resection (TUR) of the prostate was recommended. The patient delayed it because a laparoscopic cholecystectomy and a lymph node biopsy were performed to filter the celiac lymphadenopathy, with a diagnosis of reactive lymphoid hyperplasia.
Subsequently, a prostate CT scan was performed, which passed without incident. The histological study showed areas of normal prostate tissue, with dilated glands and normal stroma, muscle and tissue, as well as alterations in coagulation by TUR. Other areas with higher glandular density and lower stromal density, diagnostic of Nodular Hypertrophy of the Prostate. Other areas were seen in which prostatic glands were visualised, absence of normal stroma, very dense cellular proliferation in the stroma, which with higher magnification allowed the visualisation of small round cells. This led to a differential diagnosis between lymphoma, anaplastic small cell anaplasia and a primitive neuroectodermal tumour. Immunohistochemistry techniques were therefore performed. The markers CD 20+; CD 10+, BCL2+, BCL6+, typical of B lymphocytes, follicular origin and non-Hodgkin's lymphomas, were positive. A molecular study was carried out by PCR, in which translocation 14-18 typical of B lymphomas was observed, and another translocation characteristic of follicular lymphomas.

With the anatomopathological diagnosis of diffuse small-medium cell lymphoma type b (CD 20+; CD 10+, BCL2+, BCL6+) and benign prostatic hyperplasia. The study was completed by bone marrow biopsy, with no evidence of tumour infiltration. Thoracic-abdominal CT and PET. The CT scan showed laterocervical adenopathy, a paravertebral mass, right lower paratracheal adenopathy, signs of cholecystectomy, and in the PET scan there was uptake of the mediastinal adenopathy (right paratracheal), left inguinal and submandibular lymph nodes, uptake at presacral, subpleural (D8) and axillary level. A karyotype was performed with a result of 46XY.

With the diagnosis of Stage IIIEA follicular non-Hodgkin's lymphoma of the prostate IPI:1 FLIPI:1; treatment was proposed with first-line polychemotherapy with FMD 6 cycles/ 4 weeks (Fludarabin, Mitoxantrone, Dexamethasone) associated with anti-CD20 monoclonal antibodies (rituximab), as prophylactic treatment of Pneumocystis carinii secondary to Fludarabin, followed by treatment with Seprin (Trimetropin sulfamethoxazole). For six cycles.
Subsequently, she attended check-ups without evidence of recurrence, presenting a good response to treatment. Follow-up imaging studies were performed, using CT and PET scans, showing the disappearance of the lymphadenopathies. After a 24-month check-up, the patient remained asymptomatic with no evidence of recurrence.

