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Objective: The aim of the study is to identify patient- and care-related factors associated with time to treatment for acute testicular torsion and the likelihood of testicular loss., Methods: Data were retrospectively collected for patients 18 years and younger who had surgery for acute testicular torsion between April 1, 2005, and September 1, 2021. Atypical symptoms and history were defined as having abdominal, leg, or flank pain, dysuria, urinary frequency, local trauma, or not having testicular pain. The primary outcome was testicular loss. The primary process measure was time from emergency department (ED) triage to surgery., Results: One hundred eleven patients were included in descriptive analysis. The rate of testicular loss was 35%. Forty-one percent of all patients reported atypical symptoms or history. Eighty-four patients had adequate data to calculate time from symptom onset to surgery and time from triage to surgery and were included in analyses of factors affecting risk of testicular loss. Sixty-eight patients had adequate data to evaluate all care-related time points and were included in analyses to determine factors affecting time from ED triage to surgery. On multivariable regression analyses, increased risk of testicular loss was associated with younger age and longer time from symptom onset to ED triage, while longer time from triage to surgery was associated with reporting atypical symptoms or history.The most frequently reported atypical symptom was abdominal pain, in 26% of patients. These patients were more likely to have nausea and/or vomiting and abdominal tenderness but equally likely to report testicular pain and swelling and have testicular findings on examination., Conclusions: Patients presenting to the ED with acute testicular torsion reporting atypical symptoms or history experience slower transit from arrival in the ED to operative management and may be at greater risk of testicular loss. Increased awareness of atypical presentations of pediatric acute testicular torsion may improve time to treatment., Competing Interests: Disclosure: The authors declare no conflict of interest., (Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.)

Introduction: Most case series describing surgical repair for pelvic organ prolapse (POP) after radical cystectomy (RC) focus on transvaginal repairs. We present our experience of POP after RC repaired by abdominal mesh sacrocolpopexy (ASC) with long-term follow-up., Methods: Two women with previous RC with ileal conduit diversion underwent open ASC for repair of apical prolapse with concomitant enterocele. Prolapse severity was assessed using the POP quantification staging system, whereas pelvic imaging was performed with magnetic resonance imaging defecography., Results: One patient had no POP recurrence at follow-up of 45 months after ASC. The other patient had anterior enterocele recurrence at 11 months after ASC and was treated with a limited outpatient transvaginal repair. She had no POP recurrence at 12 months after secondary repair. Both ASC procedures had technical challenges related to pelvic dissection of adhesed loops of bowels, access to the promontory, and retroperitonealization requiring the assistance of a general surgeon. Neither case had perioperative complications., Conclusion: In women with large enterocele or vaginal vault prolapse after RC, repair with ASC, although technically challenging, can offer durable POP outcomes.

Oversecretion of apoB and decreased removal of apoB-containing lipoproteins by the liver results in hyperapobetalipoproteinemia, which is a risk factor for atherosclerosis. We investigated how dexamethasone, a synthetic glucocorticoid, affects the synthesis, degradation, and secretion of apoB-100 and apoB-48. Primary rat hepatocytes were incubated with dexamethasone for 16 hours. Incorporation of [35S]methionine into apoB-48 and apoB-100 was increased by 36% and 50%, respectively, with 10 nmol/L dexamethasone, despite a 28% decrease of incorporation into total cell proteins. However, Northern blot analysis revealed that dexamethasone (1 to 1000 nmol/L) did not significantly alter the steady-state concentrations of apoB mRNA, suggesting that the net increase in apoB synthesis may involve increased translational efficiency. The intracellular retention and the rate and efficiency of apoB secretion were determined by pulse-chase experiments in which the hepatocytes were labeled with [35S]methionine for 10 minutes or 1 hour, and the disappearance of labeled apoB from the cells and its accumulation in the medium were monitored. Degradation of labeled apoB-100 after a 3-hour chase in both protocols was decreased from about 50% to 30%, whereas degradation of apoB-48 was decreased from 30% to 10% to 20% by treatment with 10 or 100 nmol/L dexamethasone. Additionally, the half-life of decay (time required for 50% of labeled cell apoB-100 to disappear from the peak of radioactivity following a 10-minute pulse) was increased by treatment with 10 nmol/L dexamethasone from 77 to 112 minutes, and the value for apoB-48 increased from 145 to 250 minutes. Treatment with 100 nmol/L dexamethasone also stimulated secretion of 35S-labeled apoB-100 and apoB-48 by twofold and 1.5-fold, respectively. The increased secretion of apoB-100 and apoB-48 after dexamethasone treatment was confirmed by immunoblot analysis for apoB mass, and the effect was relatively specific since albumin secretion was not significantly changed. We conclude that glucocorticoids promote the secretion of hepatic apoB-containing lipoproteins by increasing the net synthesis of apoB-100 and apoB-48 and by decreasing the intracellular degradation of newly synthesized apoB. An increased action of glucocorticoids coupled with a decreased ability of insulin to suppress these effects in insulin resistance can lead to hyperapobetalipoproteinemia and an increased risk of atherosclerosis.