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<b><i>Introduction:</i></b> This study aimed to report the visual acuity outcomes and complications of sutured scleral fixation of posterior chamber intraocular lens (IOL) in children under 9 years old with congenital ectopia lentis. <b><i>Methods:</i></b> Twenty-six children (47 eyes) with congenital ectopia lentis were included in this study. The mean age at surgery was 61.6 ± 22.3 months (range, 32–94). Patients underwent lens extraction, anterior vitrectomy, and sutured scleral fixation of posterior chamber IOL. The implanted IOL included rigid polymethyl methacrylate (PMMA) IOL (CZ70BD, <i>n</i> = 36) and foldable IOL (SA60AT, <i>n</i> = 9, and LI61SE, <i>n</i> = 2). The outcome measures used to assess the benefits were uncorrected visual acuity (UCVA), best-corrected visual acuity (BCVA), refraction, intraocular pressure, and any associated complications. Median follow-up was 33.0 months (range, 4–129). <b><i>Results:</i></b> After surgery, the median UCVA (1.30 vs. 0.35 logMAR) and BCVA (0.82 vs. 0.15 logMAR) improved significantly (<i>p</i> &#x3c; 0.001). The median absolute spherical values decreased considerably (9.00 vs. 0.75 D; <i>p</i> &#x3c; 0.001). The median astigmatism was lower in foldable IOL compared to rigid PMMA IOL (1.0 vs. 2.5 D; <i>p</i> = 0.026), but neither the UCVA nor BCVA was significantly different. There was no intraoperative complication. Postoperative complications included pupillary capture in 4 eyes (9%), IOL decentration in 4 eyes (9%), choroid edema in 1 eye (2%), and subretinal hemorrhage in 1 eye (2%). The rate of secondary surgery was 9%, caused by IOL decentration of IOL haptics which was broken in 3 eyes and suture degradation in 1 eye. <b><i>Conclusion:</i></b> Sutured scleral fixation of posterior chamber IOL provided good visual outcomes in children under 9 years of age with congenital ectopia lentis. Although there were some risks of secondary surgery, the complications were acceptable.

Periprostatic adipose tissue (PPAT) abundance correlates with prostate cancer progression, but the mechanism remains unexplained. Here, we used a statistical approach to define abundant PPAT by normalizing PPAT volume to prostate volume in a cohort of 351 patients with a linear regression model. Applying this definition, we find tumors specifically from patients with abundant PPAT exhibit several hallmarks of aggressiveness, suggesting that PPAT abundance might be used to improve risk stratification. We show that abundant PPAT expands by adipocyte hypertrophy but this does not result in inflammation. Extensive extracellular matrix remodeling, notably of the collagen network, and decreased expression of mechano-sensing proteins in adipocytes explains this inflammation-free expansion by decreasing the mechanical constraints on the adipocytes. Moreover, collagen VI degradation in abundant PPAT is associated with production of endotrophin, a matrikine that promotes cancer progression. We find high levels of endotrophin specifically in the urine of patients with abundant PPAT, indicating the clinical relevance of our findings.