ABSTRACT
OBJECTIVES: To assess long-term postoperative ultrasonographic outcomes of robotic-assisted laparoscopic pyeloplasty (RALP) and of conventional open pyeloplasty (COP) in pediatric patients with ureteropelvic junction obstruction. METHODS: Retrospective review of 312 patients who underwent RALP or COP in a single institution. Preoperative and postoperative ultrasounds were used to determine the grade of hydronephrosis. Postoperative assessment included 3 ultrasounds at 0-6, 6-12 and >12 months intervals. Patients were matched by age, etiology of obstruction, grade of preoperative hydronephrosis and gender for case-matched analysis. RESULTS: We identified 212 pyeloplasties that met inclusion criteria, being 58 RALP and 154 COP. Groups were different in age, gender and etiology, but similar in severity of hydronephrosis and follow-up time. At the end of follow-up, complete resolution and success rates were 62% and 74% in RALP and 45% and 70% in COP, respectively. Matching included 105 patients. Complete resolution was higher in RALP (p = 0.004), while median time before improvement was lower (12.3 months RALP vs 29.9 months COP). There was no difference in success rate at the end of follow-up between the groups. CONCLUSION: RALP shows satisfactory long-term outcomes, comparable to COP. In our cohort, patients who underwent robotic pyeloplasty showed faster resolution of hydronephrosis on ultrasound.
Subject(s)
Hydronephrosis/surgery , Laparoscopy/methods , Robotics , Ureteral Obstruction/surgery , Urologic Surgical Procedures/methods , Child , Child, Preschool , Female , Follow-Up Studies , Humans , Hydronephrosis/diagnostic imaging , Infant , Kaplan-Meier Estimate , Male , Postoperative Complications/diagnostic imaging , Retrospective Studies , Treatment Outcome , UltrasonographyABSTRACT
BACKGROUND: The antiplatelet effect of aspirin is attributed to platelet cyclooxygenase-1 inhibition. Controversy exists on the prevalence of platelet resistance to aspirin in patients with coronary artery disease and effects of aspirin dose on inhibition. Our primary aim was to determine the degree of platelet aspirin responsiveness in patients, as measured by commonly used methods, and to study the relation of aspirin dose to platelet inhibition. METHODS AND RESULTS: We prospectively studied the effect of aspirin dosing on platelet function in 125 stable outpatients with coronary artery disease randomized in a double-blind, double-crossover investigation (81, 162, and 325 mg/d for 4 weeks each over a 12-week period). At all doses of aspirin, platelet function was low as indicated by arachidonic acid (AA)-induced light transmittance aggregation, thrombelastography, and VerifyNow. At any 1 dose, resistance to aspirin was 0% to 6% in the overall group when AA was used as the agonist, whereas it was 1% to 27% by other methods [collagen and ADP-induced light transmittance aggregation, platelet function analyzer (PFA-100)]. Platelet response to aspirin as measured by collagen-induced light transmittance aggregation, ADP-induced light transmittance aggregation, PFA-100 (81 mg versus 162 mg, P < or = 0.05), and urinary 11-dehydrothromboxane B2 was dose-related (81 mg versus 325 mg, P = 0.003). No carryover effects were observed. CONCLUSIONS: The assessment of aspirin resistance is highly assay-dependent; aspirin is an effective blocker of AA-induced platelet function at all doses, whereas higher estimates of resistance were observed with methods that do not use AA as the stimulus. The observation of dose-dependent effects despite nearly complete inhibition of AA-induced aggregation suggests that aspirin may exert antiplatelet properties through non-cyclooxygenase-1 pathways and deserves further investigation.
