Teaching Case

An 89-year-old female patient presented to the emergency department with chief complaints of suprapubic pain, dysuria, and frequency. She had a medical history of chronic kidney disease stage IV, long-standing hypertension, and hypercholesterolaemia. Urinary analysis revealed microscopic pyuria.

Abdominal ultrasonography revealed marked, asymmetric smooth thickening of the right half of the bladder wall with secondary hydroureteronephrosis (Fig 1). Abdominal computed tomography confirmed thickening of the right side of the bladder wall, slightly extending towards the left posterior bladder wall. In the nephrogenic-phase after intravenous (IV) contrast an intense contrast enhancement of the internal margin of the urinary bladder was demonstrated (Fig 2).
T2-weighted MRI revealed diffused thickening of the right lateral half of the urinary bladder wall, with low and high-signal intensities on luminal and peripheral sides, respectively (Fig 3). The low signal intensity region showed marked contrast enhancement (Fig 4). Only a small area of diffusion restriction could be demonstrated in this area.
Cystoscopy revealed bullous and solid tissue, and biopsy was performed to rule out malignancy. Histological analysis showed homogeneous eosinophilic infiltration and oedema throughout the submucosa, with transmural extension into the muscularis propria (Fig 5).

Eosinophilic cystitis (EC) is a rare inflammatory disorder characterised by massive eosinophilic infiltration of all layers of the bladder wall, first described by Edwin Brown in 1960 [1]. The incidence of EC is the same in both sexes. The activated eosinophils may release cytotoxic cationic proteins that could induce tissue damage, which is seen histologically as tissue eosinophilia, hyperaemia, muscle oedema, and muscle necrosis in the acute phase [2]. Misdiagnosis and mistreatment management is common, particularly in cases where urine culture is positive. Hence, deep biopsy is needed for establishing an accurate diagnosis. EC may clinically resemble a bladder tumour. Bladder cancer may be focal or diffuse mural thickening of the bladder wall. Both neoplastic (solitary fibrous tumors, urothelial carcinomas or neuroendocrine tumors) and non-neoplastic (inflammatory, amyloidosis and hamartoma) bladder conditions present as polypoid masses within the bladder. Clinical, cystoscopy and radiological findings in many of these neoplastic and non-neoplastic conditions overlap, hence, significant therapeutic and prognostic implications if misdiagnosed. EC can also mimic as Interstitial cystitis (IC) which is a chronic inflammatory disorder of the bladder characterized by urgency, urethral and suprapubic pain, with or without hematuria. Urine analysis shows red blood cells and white blood cells, while the urinary culture remains negative. Etiology of IC has been suggested to be of an allergic, autoimmune, neurological and infectious origin with bladder infiltration allowing toxic and allergic substances into the underlying bladder tissue. The diagnosis of IC is based on cystoscopy findings, urine analysis and chronic irritating voiding symptoms and exclusion of other bladder diseases. Clinical symptoms, radiological examination, as well as cryptoscopic appearance of the pathology are non-specific. The diagnosis is solely based on histopathological examination. Treatment management is typically based on corticosteroids or non-steroidal anti-inflammatory drugs, sometimes on endoscopic resection of the lesion, and exceptionally on surgery [3]. Most patients have a benign course with spontaneous resolution.

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