Background

Endometriomas are a type of ovarian cyst composed of degenerated blood products from hemorrhage of ectopic endometrial tissue. Endometriomas can rupture, causing hemoperitoneum, and present with signs and symptoms similar to other, more common abdominal emergencies. Therefore, they are not often diagnosed preoperatively. Ultrasound and cross-sectional imaging can assist in diagnosis of endometriomas. We present a case of ruptured endometrioma causing massive hemoperitoneum that was initially suspected to represent malignancy with carcinomatosis.

Case presentation

A 32-year-old Hispanic woman presented with sharp abdominal pain and 15-pound unintentional weight loss over 6 months. Laboratory work was significant for a negative pregnancy test and elevated cancer antigen-125. Computed tomography of the abdomen and pelvis demonstrated a 13-cm complex cystic mass in the left adnexa with moderate hyperdense ascites and omental nodularity. Ultrasound demonstrated a large left adnexal complex cystic structure with internal echoes, and chest computed tomography showed no signs of intrathoracic neoplastic or infectious processes. Her presentation was concerning for malignancy with carcinomatosis. Fluid from a paracentesis was sent for culture and cytology. Diagnostic laparoscopy revealed that the left ovary had been completely replaced by an endometrioma, which had a small ruptured area superiorly. Brown deposits of endometriosis were present on the cyst, omentum, and various peritoneal linings. Tissue samples of the endometrium, myometrium, cervix, ovaries, fallopian tubes, peritoneum, omentum, and paracolic spaces were taken and showed no hyperplastic, dysplastic, or malignant cells on pathology.

Conclusions

Ruptured endometrioma and ruptured hemorrhagic cyst should be included in the differential diagnosis when a premenopausal female presents with hemoperitoneum in combination with complex adnexal cystic masses in the absence of trauma. Cancer antigen-125 and cancer antigen 19-9 can be falsely elevated in the setting of ruptured endometrioma.

The capacity of the colon to absorb microbially produced amino acids (AAs) and the underlying mechanisms of AA transport are incompletely defined. We measured the profile of 16 fecal AAs along the rat ceco-colonic axis and compared unidirectional absorptive AA fluxes across mucosal tissues isolated from the rat jejunum, cecum, and proximal colon using an Ussing chamber approach, in conjunction with ¹H-NMR and ultra-performance liquid chromatography-mass spectrometry chemical analyses. Passage of stool from cecum to midcolon was associated with segment-specific changes in fecal AA composition and a decrease in total AA content. Simultaneous measurement of up to 16 AA fluxes under native luminal conditions, with correction for endogenous AA release, demonstrated absorptive transfer of AAs across the cecum and proximal colon at rates comparable (30-80%) to those across the jejunum, with significant Na⁺-dependent and H⁺-stimulated components. Expression profiling of 30 major AA transporter genes by quantitative PCR revealed comparatively high levels of transcripts for 20 AA transporters in the cecum and/or colon, with the levels of 12 exceeding those in the small intestine. Our results suggest a more detailed model of major apical and basolateral AA transporters in rat colonocytes and provide evidence for a previously unappreciated transfer of AAs across the colonic epithelium that could link the prodigious metabolic capacities of the luminal microbiota, the colonocytes, and the body tissues.NEW & NOTEWORTHY This study provides evidence for a previously unappreciated transfer of microbially generated amino acids across the colonic epithelium under physiological conditions that could link the prodigious metabolic capacities of the luminal microbiota, the colonocytes, and the body tissues. The segment-specific expression of at least 20 amino acid transporter genes along the colon provides a detailed mechanistic basis for uniport, heteroexchange, Na⁺-cotransport, and H⁺-cotransport components of colonic amino acid absorption.

Prostate cancer genomic subtypes that stratify aggressive disease and inform treatment decisions at the primary stage are currently limited. Previously, we functionally validated an aggressive subtype present in 15% of prostate cancer characterized by dual deletion of MAP3K7 and CHD1. Recent studies in the field have focused on deletion of CHD1 and its role in androgen receptor (AR) chromatin distribution and resistance to AR-targeted therapy; however, CHD1 is rarely lost without codeletion of MAP3K7. Here, we show that in the clinically relevant context of co-loss of MAP3K7 and CHD1 there are significant, collective changes to aspects of AR signaling. Although CHD1 loss mainly impacts the expansion of the AR cistrome, loss of MAP3K7 drives increased AR target gene expression. Prostate cancer cell line models engineered to cosuppress MAP3K7 and CHD1 also demonstrated increased AR-v7 expression and resistance to the AR-targeting drug enzalutamide. Furthermore, we determined that low protein expression of both genes is significantly associated with biochemical recurrence (BCR) in a clinical cohort of radical prostatectomy specimens. Low MAP3K7 expression, however, was the strongest independent predictor for risk of BCR over all other tested clinicopathologic factors including CHD1 expression. Collectively, these findings illustrate the importance of MAP3K7 loss in a molecular subtype of prostate cancer that poses challenges to conventional therapeutic approaches. IMPLICATIONS: These findings strongly implicate MAP3K7 loss as a biomarker for aggressive prostate cancer with significant risk for recurrence that poses challenges for conventional androgen receptor-targeted therapies.