Inflammatory Myofibroblastic Tumor of the Prostate Gland: A Case Report From North-Central Nigeria

Abstract

Inflammatory myofibroblastic tumors (IMTs) are mesenchyme-derived tumors of undetermined malignant potential, generally considered low-grade tumors. They occur within various organs, with the abdominal cavity as the most common site of occurrence. The male genitourinary system, especially the prostate gland, is among the least common sites of occurrence. IMTs are generally diagnosed in the young, where they present as circumscribed masses with symptoms referable to the location and size. Occasionally, however, they present in the elderly. The etiopathogenesis is postulated to be related to an abnormality in chromosome 2p23.5, and association with anaplastic lymphoma receptor tyrosine kinase (ALK) positivity on immunohistochemistry (IHC) has therapeutic and prognostic implications. Distinguishing IMTs from non-neoplastic mimics like inflammatory pseudotumor (IPT) is important because they have similar microscopic features, characterized by benign spindle and stellate cells of variable cellularity, admixed with mixed inflammatory cell infiltrates in a fibrocollagenous background. Surgery is the treatment of choice, with a favorable outcome in most cases. Targeted therapy with the tyrosine kinase inhibitor (TKI) crizotinib is increasingly touted in recurrent cases or those not amenable to surgery. We present a case of IMT in a 77-year-old Nigerian male who was clinically diagnosed as a case of benign prostatic hyperplasia (BPH), in order to highlight the imperative for a high index of suspicion in the histopathological evaluation of prostatic lesions.

Keywords: alk gene translocation; bladder outlet obstruction; inflammatory myofibroblastic tumor; nigeria; prostate gland.

Figure 1. Inflammatory myofibroblastic tumor of the prostate gland

(A) Note haphazard fascicles of spindled to stellate cells, exhibiting variable areas of hypo- and hypercellularity (blue and red arrows, respectively), set in vascularized fibrocollagenous stroma (H&E, x40). (B) Note prominent vasculature comprising medium- to large-sized, thick-walled vascular channels (brown arrows) in a hypercellular area (H&E, x100). (C) Note prominent vasculature comprising small- to medium-sized, thin-walled vascular channels (yellow arrows) in a hypocellular area (H&E, x100). (D) Note short fascicles of spindle cells with eosinophilic fusiform cytoplasm and slender, often vesicular, bland nuclei (green arrows), admixed with moderate infiltrates of lymphocytes and plasma cells (black arrows), occasional eosinophils (blue arrow), and fibrocollagenous stroma (H&E, x400). H&E: hematoxylin and eosin

Figure 2. IHC profile of inflammatory myofibroblastic tumor of the prostate gland

(A) Diffusely positive SMA stain: note intense and diffuse cytoplasmic staining (golden brown coloration) of lesional cells (SMA IHC, x400). (B) Negative CD34 stain: note lack of staining of lesional cells and intense membranous staining (golden brown discoloration) outlining vascular channels (CD34 IHC, x400). (C) Negative S100 stain: note lack of staining of lesional cells (S100 IHC, x400). IHC: immunohistochemistry; SMA: smooth muscle actin