{"paper_id":"ee21abb3-c16f-4d91-89a6-baa7589dfb11","body_text":"A 44-year-old woman with a history of endometriosis was referred to our radiology unit with progressive right upper quadrant pain and vomiting for few months. The pain is periodic and dull in nature. Her surgical history included hysterectomy for endometriosis and cholecystectomy. The patient had a previous ultrasound that reported a 3-cm complex cystic lesion in the right lobe of the liver which was not further characterized.\nHer tumor markers (alfa fetoprotein, CA 19-9, CA 125 and carcinoembryonic antigen) and liver function tests were within normal range.\nComputed tomography (CT) scan of the abdomen demonstrated 3 cm rather well-defined hypodense subscapular lesion in the right lobe of the liver that illustrated heterogeneous peripheral enhancement in the venous and delayed phases ( Fig. 1 ). The primary differential considerations were subcapsular abscess, granuloma, hematoma, or metastasis, further characterization with magnetic resonance imaging (MRI) was suggested.\nMRI examination revealed subcapsular partially cystic focal lesion with intrinsic high-signal intensity in both T1-weighted and T2-weighted images—with and without fat suppression—suggestive of subacute hemorrhagic content. It exhibits heterogeneous peripheral enhancement in multiphasic contrast study ( Fig. 2 ). The differential diagnosis was hematoma, complex hepatic cyst, hepatic adenoma (probably due to blood products), and hemorrhagic metastasis (ie, melanoma).\nDue to nonconclusive imaging findings, CT-guided core biopsy was performed. Histopathology reported endometrioid glands, stroma, and smooth muscle, consistent with adenomyoma. The patient had followed up for 2 years without considerable increase in the size of the endometrioma, but with persistent pain in spite of hormonal treatment, she finally underwent hepatic segmentectomy for segment VII, and histopathology report confirmed the diagnosis of hepatic endometrioma ( Fig. 3 ).\n\nEndometriosis is a common benign disease affecting women of reproductive age usually with an estimated prevalence rate of 17%-47% among infertile women  [8] . Uterine and extrauterine endometriosis was the first described by Rokitansky in 1860  [9] . Endometriosis is usually confined to the pelvis and reproductive organs, the ovaries are the most frequent location; however, other remote sites including the gastrointestinal tract, peritoneum, chest, scar tissue, lymph nodes, and kidneys have been also described  [3] ,  [4] ,  [5] ,  [6] ,  [8] . The clinical presentation of the disease is variable and can be associated with distressing symptoms such as pelvic pain, dyspareunia, infertility, or it may be asymptomatic and incidentally discovered  [8] .\nThe mechanism of extrauterine endometriosis is still uncertain  [7] ,  [8] . However, various theories have been proposed to explain the pathogenesis of endometriosis. In our report, we are discussing 2 of the major theories that strengthen their hypothesis through providing strong supporting evidences. These theories are the implantation theory and the celomic metaplasia theory.\nThe implantation theory suggests that endometrial tissue is transplanted into the peritoneum and pelvic organs through retrograde menstruation, hematogenous and/or lymphatic dissemination, or iatrogenic injury  [7] ,  [8] . Considerable evidences have validated this theory: (1) The menstrual effluent and peritoneal fluid usually have viable endometrial cells, (2) endometrium can experimentally be implanted and grown in a peritoneal cavity, and (3) adequate percentage of female have a degree of retrograde menstruation.\nIn celomic metaplasia theory, few authors considered peritoneal endometriosis, endometriosis of the ovary and endometriosis of rectovaginal septum as 3 separated entities each has a different pathogenesis  [7] ,  [8] . The supporting evidence of this theory proposed that the peritoneal endometriosis originates from the metaplasia of peritoneal mesothelium, ovarian endometriosis results from either invagination of ovarian cortex, or metaplasia of celomic epithelium and the rectovaginal nodule from metaplasia of Müllerian duct.\nHepatic endometriosis, first described by Finkel et al. in 1986, is a rare entity of extra-uterine endometriosis  [1] ,  [2] ,  [3] . Within the reviewed literature, only 21 cases were reported  [4] .\nAlthough ovarian endometriosis usually illustrates classical radiological findings, there is no specific diagnostic sign to distinguish hepatic endometriosis from other hepatic lesions  [4] . Accordingly, the histopathologic examination is considered the gold standard for definite diagnosis.\nWithin the reviewed literature, variable differential diagnosis of hepatic endometriosis was provided depending on clinical presentation and the radiological characteristics of the lesion, for eg, hematoma, complex cyst, metastasis, and hepatocellular carcinoma. Interestingly, they all described it primarily as a complex cystic lesion on ultrasound with distinctive subcapsular location in subsequent imaging. In our case, the lesion was complex cyst in a reported ultrasound and subcapsular in location on CT and MRI images.\nWe summarized the published cases and their respective described findings in ( Table 1 ) below.\n\nThe radiologist should consider hepatic endometrioma on the top of the differential diagnosis of complex hepatic cyst, subcapsular in location with hemorrhagic content in any women, particularly of reproductive age with prior history of endometriosis.","source_license":"CC0","license_restricted":false}