Lymphomatous involvement of the prostate is rare, accounting for only 0.09% of all prostate neoplasms.
It can manifest as either a primary prostate lymphoma (PPL) or, more commonly, as a secondary involvement (SPL) occurring in 0.1% of all Non Hodgkin Lymphomas (NHL).
Prognosis is usually poor.
Prostate lymphoma has a bimodal clinical distribution: PPL is more frequently seen in elderly patients, with a mean age of 62 years, while SPL occurs in younger patients.[1,2,3] The main criteria to define PPL involvement proposed by Bostwick and Mann consist in: 1) symptoms attributable to prostatic enlargement, 2) the prostate as the predominant site of involvement, and 3) the absence of involvement of liver, spleen, or lymph nodes within one month of diagnosis. [4] Prostate lymphoma usually presents as lower urinary tract obstruction that does not respond to symptomatic medication.
Compared to other prostatic obstructive diseases, it tends to progress rapidly and may show only a slight or no increase in PSA levels.
A history of lymphoid disease, systemic symptoms such as fever, chills, night sweats, weight loss, or peripheral adenopathies can suggest the diagnosis.[5] Transrectal ultrasound (TRUS) of the prostate reveals an enlarged gland and a prostate mass, prompting the need for Multiparametric prostate MRI (mp-MRI). mp-MRI accurately describes the lesions and their potential extension to the surrounding structures (seminal vesicles, periprostatic fat).
It also helps differentiate from aggressive prostate adenocarcinoma, sarcoma, and other rare prostate tumors.
A diagnosis by prostate biopsy is mandatory to initiate chemotherapy.[2] Results: ====== We will describe three types of lymphomatous prostate gland involvement, and their semiology at mp-MRI (fig 1) : a) Localized nodular type ; b) Extensive tissular mass (sarcoma-like) and c) Periprostatic and periseminal involvement.
Localized nodular type: (fig 2, 3) --------------------------- Lymphoma with a nodular pattern involving only the prostate gland is infrequent.
It can be related to follicular subtype, Mantle cell and Burkitt lymphomas, although it can also be an early form of diffuse large B-cell lymphoma (DLBCL), the most frequent subtype.
As clinically they can be indolent, they don’t cause PSA elevation and they can be missed in digital rectal examination, most of these are diagnosed on LUTS material or at MRI due to PSA elevation for concomitant inflammation or synchronously to a prostate adenocarcinoma. [6] At MRI, ther can be a single or multiples nodules, appearing iso - hypointense on T2WI, localized to the gland without causing loss of the regional differentiation or extraprostatic extension.
On DWI there is an important restriction due to the hypercellularity and in DCE they are hypovascularized.
Involvement of the transition zone often causes misdiagnosis and difficulties in giving a PIRADS score.
Extensive tissular intraprostatic mass: (fig 4) --------------------------------------------- This is the most frequent presentation, and in most cases this presentation is related to DLBCL.
It is an aggressive form, that usually comes with urinary symptoms such as acute urinary retention. [7] The prostate volume is increased but with relative conservation of its shape (this is why some authors refers to it as “prostatomegaly”).
Infiltration is heterogeneously iso-hypointense on T2WI but isointense on T1WI and invades almost the whole parenchyma. [8] On DWI there is an important restriction but no clear enhancement.
There can be some areas of necrosis and cystic degeneration. [9] Periprostatic and periseminal involvement: (fig 5, 6) ------------------------------------------------- This type is exceptional, usually reported as SPL and it can be associated with immunosuppression.
The cellular types involved in the literature include follicular lymphoma, Burkitt lymphoma and intravascular large B-cell lymphoma. [4] There is an infiltration of the peri prostatic and seminal fat, with encompassement of vascular and nervous structures.
This tissue has the same characteristics as other forms : mildly low signal intensity on T2WI, restriction on DWI/ADC because of the cellularity, and slow enhancement (hypovascularized).
Key points to differentiate PL from adenocarcinoma (PCa): (table 1) -------------------------------------------------------------------- Patients with PL are usually symptomatic, presenting urgency, frequency, painful urination, hematuria, increased nocturia, dysuria, and acute urinary retention, while specific symptoms associated with lymphoma such as fever, night sweats, and weight are not frequent in early stages.[2] PSA value is generally normal or low in PL in comparison with PCa.[10] T2 signal is intermediate, very homogeneous, lesion shows very low ADC, and enhancement is weak, whereas T2WI signal is usually very low, restriction is variable and enhancement is strong and early in case of PCa.