RESUMEN
Pancreatic heterotopia (PH) involves pancreatic tissue located outside its typical anatomical position, lacking vascular or ductal communication with the pancreas. Despite frequently having acini with the capacity to produce digestive enzymes, PH is usually asymptomatic. When symptoms do occur, they typically present in middle to late adulthood and include abdominal pain, nausea, and diarrhea. This clinical presentation is similar to that of Crohn's disease, an autoimmune inflammatory bowel disease (IBD). The presentation of symptomatic PH varies depending on the location of the ectopic pancreatic tissue and its microanatomical constituents, including exocrine and endocrine tissue as well as a duct system. We present a case of a patient who came to medical attention with abdominal pain and was found on colonoscopy to have a non-obstructing stricture of the transverse colon without an associated mass. Biopsies of the area revealed chronic active colitis, leading to a diagnosis of Crohn's disease. Her gastroenterological symptoms remained stable for several years while receiving infliximab infusions until she presented to the emergency department with severe abdominal pain, diarrhea, and sepsis, meeting the criteria for systemic inflammatory response syndrome. Imaging studies revealed a fistula between the previous colonic stricture and the jejunum, again attributed to Crohn's disease. She underwent surgery to remove the fistula between the small and large bowels. Unexpectedly, the resection specimen showed a mass insinuated between the loops of the large intestine, which histological review revealed to be ectopic pancreatic tissue. Following the resection of the ectopic pancreatic tissue, her symptoms resolved without the need for further treatment. In retrospect, the ectopic pancreatic tissue, which contained acini with digestive enzymes, ducts, and islets, may have also caused seemingly unrelated pathology in the patient. Symptomatic PH should be recognized as a pathology that can mimic IBD, prompting reconsideration of the diagnosis in cases of refractory disease while on biologics.
RESUMEN
Hepatic infarction is uncommon due to the dual blood supply from the hepatic artery and portal vein. The majority of the cases are caused following liver transplant or hepatobiliary surgery, hepatic artery occlusion, or shock. Hepatic infarction is a rare complication of hemolysis, elevated liver enzymes, and low platelet (HELLP) syndrome. HELLP is an obstetrical emergency requiring prompt delivery. The presence of elevated liver enzymes, mainly alanine aminotransferase and aspartate aminotransferase in pre-eclampsia, should warrant diagnosis and treatment in the line of HELLP syndrome. Our patient with underlying sickle cell trait presented with features of HELLP syndrome in her third trimester of pregnancy. She underwent cesarean delivery on the same day of the presentation. The liver enzymes continued to rise following delivery and peaked on postoperative day two. Contrast computed tomography scan showed multifocal hepatic infarctions. Pre-eclampsia by itself is a state of impaired oxygenation and can lead to hepatic hypoperfusion, and appeared to be a clear contributor to the hepatic infarction in this case. However, this case also raises the question of whether the underlying sickle cell trait might have potentiated the hepatic infarction. Although sickle cell disease is well known to cause hepatic infarctions, it is unknown whether the sickle cell trait affects the liver to a similar extent as sickle cell disease. In addition, there have been case reports of sickle cell trait causing splenic infarcts and renal papillary necrosis, but it remains unclear if it can be directly associated with hepatic infarction.