ABSTRACT
The swallowed or aspirated foreign body is a common pediatric emergency medicine complaint for which emergency providers must be familiar with the intricacies of management. Most swallowed foreign bodies will harmlessly pass through the GI tract, but children with GI tract abnormalities may have an increased risk of object impaction. There are few reported cases of foreign object ingestion in children with GI tract abnormalities, specifically ostomies. The Foley catheter is a versatile tool that is easily accessible in the ED setting. We present a novel case of foreign body ingestion in an infant with a colostomy secondary to Hirschsprung's disease managed with Foley catheter retrieval through an ileostomy stoma. A 17-month-old infant presented to the ED with a chief complaint of an episode of bloody vomiting. He had a two-day history of increased irritability and intolerance of feeds with emesis after every feed. The child's medical history is pertinent for Hirschsprung's disease, for which the patient had a pull-through procedure shortly after birth and a revision of the pull-through. On physical examination, the patient's ostomy was found to contain brown-green liquid stool. A small ovular mass was visualized at the stoma during crying episodes. Supine posteroanterior radiograph of the abdomen showed an oval-shaped radiolucency consistent with a metallic ingested foreign body at the site of the stoma. The foreign object was removed using a Foley catheter and forceps and was found to be a penny. The patient was observed and discharged without complications later that day. Treatment of a symptomatic ingested foreign object requires careful consideration of the type of object present and its location in the body. In this case report, we discussed the removal of an ingested coin in a symptomatic 17-month-old infant with a history of ileostomy secondary to Hirschsprung's disease using a Foley catheter. In children with ostomies, prompt imaging and non-surgical removal may be an option to manage retrieval of these objects if the patient is stable and symptoms are not severe.
ABSTRACT
Androgen deprivation (AD) therapy failure leads to terminal and incurable castration-resistant prostate cancer (CRPC). We show that the redox-protective protein thioredoxin-1 (TRX1) increases with prostate cancer progression and in androgen-deprived CRPC cells, suggesting that CRPC possesses an enhanced dependency on TRX1. TRX1 inhibition via shRNA or a phase I-approved inhibitor, PX-12 (untested in prostate cancer), impedes the growth of CRPC cells to a greater extent than their androgen-dependent counterparts. TRX1 inhibition elevates reactive oxygen species (ROS), p53 levels and cell death in androgen-deprived CRPC cells. Unexpectedly, TRX1 inhibition also elevates androgen receptor (AR) levels under AD, and AR depletion mitigates both TRX1 inhibition-mediated ROS production and cell death, suggesting that AD-resistant AR expression in CRPC induces redox vulnerability. In vivo TRX1 inhibition via shRNA or PX-12 reverses the castration-resistant phenotype of CRPC cells, significantly inhibiting tumor formation under systemic AD. Thus, TRX1 is an actionable CRPC therapeutic target through its protection against AR-induced redox stress.
