{"paper_id":"97a0df0f-3945-4ddb-9fd7-4a8cc79f83f9","body_text":"Case Report\nVolume 4 Issue 4 -  December  2017\nDOI: 10.19080/JOJUN.2017.04.555640\nJOJ uro & nephron\nCopyright © All rights are reserved by João Bernardo Almeida\nBladder Endometriosis an Improbable Cause of \nHematuria\nJoão Bernardo Almeida*, Ana Paula Urbina, Maria Murgui Rodríguez, Paula Manzi Orezzoli, Ana Belén Ferrer, \nMiguel Rodriguez Romero, Gabriel Alejandro Machado , Jesus Angel Olivares Del Olmo and Inmaculada Bravo \nDepartment of Urology, Complex Hospitalário Universitário de Cáceres, Cáceres, Spain\nSubmission: November 03, 2017;  Published: December 19, 2017\n*Corresponding author: João Bernardo Almeida, Department of Urology, Complex Hospitalário Universitário de Cáceres, Cáceres, Spain,  \nTel: , Email: \nIntroduction\nEndometriosis is a fairly frequent condition defined as the \npresence of endometrial tissue outside the uterine cavity [1]. \nIt is a disease that affects mainly young fertile women being \nextremely rare in postmenopausal individuals [2] as endometrial \ntissue dwells on estrogen to grow. \nLocations of endometriosis are essentially the ovaries, \nuterosacral ligaments, fallopian tubes, cervical neck and vagina \n[3]. Urinary tract involvement is rare (around 1-2%), with urine \nbladder involvement in roughly 84% of cases. \nBladder Endometriosis (BE) can be classified as primary \nor secondary according to the onset type: primary BE is a \nspontaneously occurring disease, while secondary BE is defined \nas a iatrogenic lesion, ocurring after pelvic surgery such as  \nc-section [4,5]. Up to 50% of patients with BE have a history of \npelvic surgery.\nNowadays BE pathogenesis is still unclear and object of \ndebate, although three main etiologic hypothesis are supported: \nthe Embryonal theory states that BE might originate from the \nMullerian remnants [6]; the Migratory theory which postulates \nthat products of menstruation reach the pelvis through the \nfallopian tubes in a retrograde fashion [4,5] and the Metaplasia \ntheory in which metaplasia transformation of the peritoneum or \nvesical mucosa would be accountable for BE. \nClinical case\nA 27- year- old non smoker woman was referred from \nthe General practitioner to our unit presenting suprapubic \ndiscomfort and pain during micturition as well as urinary tract \nvoiding symptoms for the last 4 months. The urine examination \npresented microhematuria while urinary citology was negative \nfor malignant cells. CA 125 biomarker was within normal \nJOJ uro & nephron 4(4): JOJUN.MS.ID.5555640 (2017) 001\nAbstract\nEndometriosis is a fairly frequent gynecological condition (it affects 10-15% of fertile women) defined as the implantation of endometrial \ntissue outside the uterine cavity. Seldom does it affect the urinary tract, being the bladder the most frequent site of implantation. A late \ndiagnosis may convey high patient morbidity. \nClinical case: A 27 years old woman was directed from the GP to our unit presenting suprapubic pain and urinary storage symptoms \nconcomitant with menstruation. After a thorough physical examination and battery of tests, a bladder mass was found and resected the \nhistology result being stromal endometrial tissue. \nDiscussion: Bladder endometriosis is a rare condition representing 1% of all endometriosis cases. It may be defined as primary or \nsecondary, depending on its etiology. Patients may present cyclic urinary storage symptoms, with predominance during premenstrual period \nand may be asymptomatic as well. Menouria is not very common, appearing in only 20-25% of cases. It is of the utmost importance to rule \nout tumoral etiology by performing urinary tract ultrasound, cytology and cystoscopy. Currently the treatment is mainly surgical, eventually \nassociated with hormonal therapy. The overall recurrence rate is about 30%. \nConclusion: The bladder is the most common affected site in urinary tract endometriosis. Urologists should know its main features in \norder to achieve correct diagnosis and treatment. We think a combined approach, both surgical and medical, seems to be the best course of \ntreatment\nKeywords: Endometriosis; Bladder endometriosis; Hematuria \nAbbrevations: BE: Bladder Endometriosis; TUR: Transurethral Resection; GnRH: Gonadotrophin Releasing Hormone; US: Ultrasound\n\n\nJOJ Urology & Nephrology\nHow to cite this article: João B A, Ana P U, Maria M R, Paula M O, Ana B F, et al. Bladder Endometriosis an Improbable Cause of Hematuria. JOJ uro \n& nephron. 2017; 4(4): 555640. DOI: 10.19080/JOJUN.2017.04.555640 .002\nrange. During a thorough anamnesis, macroscopic hematuria \nwas not found but the patient complained about tenesmus \nand catamenial urinary tract voiding symptoms without \nmenouria. Bearing in mind Bladder Endometriosis as a possible \ndiagnosis, a urinary tract ultrasound was requested, revealing \nthe presence of a thickened wall on the posterior aspect of \nthe bladder (approximately 3.5cm in diameter) which needed \nfurther investigation: flexible urethrocistoscopy described a \nnormal urethra and a blueish non papillary, cystic type of lesion \non the base of the bladder with normal ureteral openings. A \ngynecological evaluation by the OB-GYN unit was performed to \nrule out other sites of Endometriosis; a full clinical gynecological \nexamination and a transvaginal ultrasound proved both normal. \nWe proceeded to perform a Transurethral resection of the \ndescribed lesion (TUR) being able to identify the presence \nof what apparently were old hemorrhage areas interleaved \nwith sane mucosae tissue. Confirmation was obtained after \nmicroscopic tissue analysis in which endometrial stroma with \nthe muscularis propria was identified. At the present moment \nthe patient is asymptomatic following a gonadotrophin releasing \nhormone (GnRH) agonists treatment. \nDiscussion\nTo diagnose and identify a possible BE it is of the utmost \nimportance to know the disease’s manifestations and symptoms. \nThese symptoms may vary considerably (some patients may be \nasymptomatic) and depend on size and location of the lesion [7-\n9]. As a matter of fact, the condition usually manifests itself as an \nacute syndrome with tenesmus, burning sensation, suprapubic \ndiscomfort and dysuria [8,9] all of which present in our patient, \nwhilst hematuria seems to be a less frequent symptom. Menouria \n(hematuria concomitantly with menstruation) is not a common \nmanifestation, appearing around in 20% of cases, usually when \nthe mucosa is affected [10].\nThese symptoms are not specific of BE as they overlap other \nurological conditions such as cystitis or bladder carcinoma. \nMoreover, malignant transformation has been described in \nthe form of adenocarcinoma or adenosarcoma, so follow up is \nimportant [11]. Extensive bladder lesions are not common, \nalbeit 50% can be palpable as a mass on anterior fornix. \nUltrasound (US) is the first step in diagnosis of BE. It is a \nlow cost, readily available and radiation free complementary \nexamination. It can also be performed transvaginally, reaching a \nspecificity value close to 100% and sensitivity around 50% [9]. \nPelvic magnetic resonance and computer tomography \ncan be especially useful as a complementary examination in \ncomplex cases of endometriosis, as they evaluate accurately the \npossibility of other organs being affected [2].\nOn the other hand, cystoscopy is a paramount test, as it \nusually confirms the presence of a bladder lesion and enables the \nurologist to perform a biopsy of the lesion to achieve histologic \nconfirmation. BE lesions might change with the different phases \nof the menstrual cycle, but they are often described as irregular \nand nodular, not ulcerated, with a brown to blue color array. Our \npatient presented a blue, cystic type of lesion, not ulcerated on \nthe base of the bladder, being the surrounding mucosa normal \n[12,13]. \nBE treatment is a combination of both surgical and medical \ntreatment. An accurate preoperative workup is essential for \nplanning a correct approach. It is fundamental to rule out \nmalignancy and to define local extension of the lesion. \nTUR is usually the preferred option when the lesion is \nconfined to the bladder or bladder wall. In this case, there is a \nhigh risk of bladder perforation if the TUR is complete and of \nrelapse if it is incomplete and not enough depth is achieved \nduring the procedure1. Extrinsic forms of the disease, which \nlocally affect other organs and/or peritoneum, need a more \naggressive approach consisting in partial cystectomy which \nshould be performed laparoscopically if feasible. Laparoscopy \nalso allows simultaneous treatment of any extravesical lesions \nand concomitant castration with or without hysterectomy \n(preferable approach in patients without pregnancy desire). \nSmall lesions can be treated using laser therapy [14].\nThe aim of the medical treatment is to induce regression of \nthe endometrial tissue inside the bladder [15-17]. Different types \nof drugs have been classically used, essentially hormonotherapy \nconsisting in gonadotrophin-releasing hormone (GnRH) agonists \nand antagonists and oral contraceptives. Although these drugs \nmay reduce or alleviate the severity of the symptoms, they are \nnot a definitive solution; moreover, they are associated with \nsuboptimal safety and tolerability and postpone pregnancy \nwishes. \nIn our case, after a thorough examination, endometriosis \nwas confined to the bladder wall, so we decided to perform a \ntransurethral resection of the lesion, with good surgical margins \nand depth followed by oral contraceptives for 6 months. We \nbelieve that a combined therapy, both surgical and medical, \nis the correct option as there is a high probability that TUR \nis incomplete due to the lesions’ characteristics (usually \ntransmural). \nConclusion\nBladder Endometriosis is a rare clinical condition; knowing \nand recognizing its symptoms is of paramount importance \nin order to perform a correct treatment and avoid unwanted \nmorbidity. We think combined treatment; both medical and \nsurgical is the correct approach to the disease. We must always \nbear in mind the possibility (although rare) of a malignant \ntransformation; so a close follow up is mandatory. \nReferences\n1. Casasola CJ, Guti érrez GS, Fernández FR, Guerreiro GR, De Blas GV, et \nal. (2003) Endometriosis Vesical Diagnóstico y Tratamiento. Actas Urol \nEsp 27(5): 394-396 .\n\nJOJ Urology & Nephrology\nHow to cite this article: João B A, Ana P U, Maria M R, Paula M O, Ana B F, et al. Bladder Endometriosis an Improbable Cause of Hematuria. JOJ uro \n& nephron. 2017; 4(4): 555640. DOI: 10.19080/JOJUN.2017.04.555640 .003\n2. Alapont AJM, Andreu GA, Herrero PE, Botella AR, Schiefenbusch ME, \net al. (2004) Endometriosis vesical: Dos nuevos casos. Actas Urol Esp \n28(10): 789-791.\n3. Sánchez JMM, Guillán CM, García JA (2005) Tratamiento de la \nEndometriosis Vesical. Revisió n de la literatura Española. Arch Esp \nUrol 58(3): 189-194).\n4. Vercellini P , Meschia M, De Georgi O, Panazza S, Cortesi I, et al. \n(1996) Bladder detrusor endometriosis: clinical and pathogenetic \nimplications. J Urol 155(1): 84-86.\n5. Somigliana E, Vercellini P , Gattei U, Chopin N, Chiodo I, et al. (2007) \nBladder endometriosis: getting closer and closer to the unifying \nmestastasic hypothesis. Fertil Steril 87(6): 1287-1290.\n6. Donnez J, Van Langendonckt A, Casanas-Roux F, Van Gossum JP , Pirard \nC, et al. (2002) Current thinking on the pathogenesis of endometriosis. \nGynecol Obstet Invest 54(Suppl 1): 52-58.\n7. Nezhat CH, Malik S, Osias J, Nezhat F, Nezhat C (2002) Laparoscopic \nmanagment of 15 patients with infiltrataing endometriosis of the \nbladder and a case of primary intravesical endometrioid adenosarcoma. \nFertil Steril 78(4): 872-875.\n8. Maeda T , Uchida Y, Nakajima F (2009) Vesical endometriosis following \nthe menopause. Int Urogynecol J Pelvic Floor Dysfunct 20(12): 1515-\n1517.\n9. Maccagnano C, Pellucchi F, Rocchini L, Ghezzi M, Scattoni V, et al. \n(2012) Diagnosis and Treatment of Bladder Endometriosis: State of \nthe Art. Urol Int 89(30: 249-258.\n10. Westney OL, Amundsen CL, McGuire EJ (2000) Bladder Endometriosis \nconservative management. J Urol 163(6): 1814-1817.\n11. Allen D, O’Brien T , Pingle P , Chandra A (2005) Endometrioid \nadenocarcinoma of the bladder. Histopathology 46(2): 232-233. \n12. Douglas C, Rotimi O (2004) Extragenital endometriosis - a \nclinicopathological review of a Glasgow hospital experience with case \nillustrations. J Obstet Gynaecol 24(7): 804-808.\n13. Seracchioli R, Mannini D, Colombo FM, Vianello F, Reggiani A, et al. \n(2002) Cystoscopy assisted laparoscopic resection of extramucosal \nbladder endometriosis. J Endourol 16(9): 663-666.\n14. Vicente J, Laguna P , Díaz L y cols (1991) Tratatmiento de la \nendometriosis vesical con Nd-Yag Láser. Arch Esp Urol 44: 169.\n15. Prentice A, Deary AJ, Bland E (2000) Progestagens and anti-\nprogestagens for pain associated with endometriosis. Cochrane \nDatabase Syst Rev 2: CD002122.\n16. Pérez-Utrilla, Aguilera Bazán A, Alonso Dorrego JM, Hernández A, \nde Francisco MG, et al. (2009) Urinary tract endometriosis: clinical, \ndiagnostic, and therapeutic aspects. Urology 73: 47-51.\n17. Schindler AE, Henkel A, Moore C, Oettel M (2010) Effect and safety \nof high dose dienogest (20mg/day) in the treatment of women with \nendometriosis. 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