RESUMEN
Intussusception denotes the intricate phenomenon wherein one segment of the bowel undergoes invagination or telescoping into its contiguous distal segment. The ensuing invaginated segment may be propelled forward through peristaltic movements, potentially precipitating bowel obstruction or ischemia, culminating in necrosis of the affected bowel segment. Although the precise etiology of intussusception remains elusive, particularly in cases devoid of an identifiable lead point, dysrhythmic contractions and lymphoid hyperplasia have been implicated in the pathophysiology of this condition. We present the case of an 86-year-old African American female with a past medical history of hypertension and asthma who presented to our emergency room with a seven-day history of worsening abdominal. The pain was described as sharp and intermittent, and it would worsen with every meal or drink. A physical exam demonstrated the right lower quadrant with vague abdominal tenderness, especially below the umbilical region. Computed tomography of the abdomen and pelvis revealed a long segment of ileocolic obstructing intussusception in the ascending colon, with a 2.6 cm solid mass serving as a lead point. Swift intervention ensued with an urgent exploratory laparotomy, culminating in a right hemicolectomy to excise the intussuscepted segment of the bowel. The pathological examination identified a well-differentiated adenocarcinoma of the cecum, categorized as T1N0M0, with all 20 resected lymph nodes yielding negative results. This illustrative case presents a unique insight into a patient with ileocolic obstructing intussusception, caused by a well-differentiated adenocarcinoma acting as the lead point, a relatively uncommon occurrence in adults. Diagnosing intussusception in adults is challenging due to its nonspecific symptoms, which are similar to those of various other gastrointestinal disorders. Therefore, it is crucial for medical providers to be acutely aware of the possibility that adenocarcinoma can trigger obstructing intussusception in various parts of the bowel.
RESUMEN
Placental development is a highly regulated process requiring signals from both fetal and maternal uterine compartments. Within this complex system, trophoblasts, placental cells of epithelial lineage, form the maternal-fetal interface controlling nutrient, gas and waste exchange. The commitment of progenitor villous cytotrophoblasts to differentiate into diverse trophoblast subsets is a fundamental process in placental development. Differentiation of trophoblasts into invasive stromal- and vascular-remodeling subtypes is essential for uterine arterial remodeling and placental function. Inadequate placentation, characterized by defects in trophoblast differentiation, may underlie the earliest cellular events driving pregnancy disorders such as preeclampsia and fetal growth restriction. Molecularly, invasive trophoblasts acquire characteristics defined by profound alterations in cell-cell and cell-matrix adhesion, cytoskeletal reorganization and production of proteolytic factors. To date, most studies have investigated the importance of the matrix metalloproteinases (MMPs) and their ability to efficiently remodel components of the extracellular matrix (ECM). However, it is now becoming clear that besides MMPs, other related proteases regulate trophoblast invasion via mechanisms other than ECM turnover. In this review, we will summarize the current knowledge on the regulation of trophoblast invasion by members of the metzincin family of metalloproteinases. Specifically, we will discuss the emerging roles that A Disintegrin and Metalloproteinases (ADAMs) play in placental development, with a particular focus on the ADAM subtype, ADAM12.
