[Secondary implantation of retropupillary fixated iris-claw intraocular lenses]. / Sekundärversorgung mit retropupillar fixierten Irisklauenlinsen.

BACKGROUND: There is no standard for the treatment of functional aphakia in cases with a compromised capsular system. Retropupillary fixation of an Artisan iris-claw IOL ("Intraokularlinse") is one of the established procedures. OBJECTIVE: Aim of this study was the evaluation of indications, visual and refractive long-term results and complication rates after retropupillary implantation of an iris-claw lens. MATERIAL AND METHODS: This retrospective study comprised 366 eyes that received a retropupillary Artisan intraocular lens (IOL) in a single center between January 2009 and December 2019. The mean follow-up period was 249 days (8 months) ±516 days. RESULTS: IOL dislocation (68%) was the most common reason for a retropupillary iris-claw implantation. Previous vitrectomy was a significant preoperative risk factor for IOL dislocation (p = 0.0001). Best corrected visual acuity improved from 0.65 ± 0.64 (logMAR) preoperatively to 0.57 ± 0.51 (logMAR) 4-6 weeks after the surgery. The mean deviation from the planned refraction was +0.40 ± 1.37 dpt and 73% of the patients had a deviation within ±1 dpt of the planned refraction. Relevant postoperative complications during the first 4 weeks were pupillary distortion (42%), ocular hypotony (15%) and transient hyphema (14%). Late complications (≥4 weeks after the surgery) included persistent pupillary distortion (20%), cystoid macular edema (13%) and iris-claw disenclavation (6%). CONCLUSION: The retropupillary Artisan implantation is an efficient method for treating aphakia without capsular support and provides good visual and refractive results with an acceptable surgical risk profile.

Hypermethylation of the nel-like 1 gene is a common and early event and is associated with poor prognosis in early-stage esophageal adenocarcinoma.

The nel-like1 (NELL1) gene maps to chromosome 11p15, which frequently undergoes loss of heterozygosity in esophageal adenocarcinoma (EAC). NELL1 promoter hypermethylation was examined by real-time methylation-specific polymerase chain reaction in 259 human esophageal tissues. Hypermethylation of this promoter showed highly discriminative receiver-operator characteristic curve profiles, clearly distinguishing esophageal squamous cell carcinoma (ESCC) and EAC from normal esophagus (NE) (P<0.001). NELL1 normalized methylation values were significantly higher in Barrett's metaplasia (BE), dysplastic Barrett's (D) and EAC than in NE (P<0.0000001). NELL1 hypermethylation frequency was zero in NE but increased early during neoplastic progression, to 41.7% in BE from patients with Barrett's alone, 52.5% in D and 47.8% in EAC. There was a significant correlation between NELL1 hypermethylation and BE segment length. Three (11.5%) of 26 ESCCs exhibited NELL1 hypermethylation. Survival correlated inversely with NELL1 hypermethylation in patients with stages I-II (P=0.0264) but not in stages III-IV (P=0.68) EAC. Treatment of KYSE220 ESCC and BIC EAC cells with 5-aza-2'-deoxycytidine reduced NELL1 methylation and increased NELL1 mRNA expression. NELL1 mRNA levels in EACs with an unmethylated NELL1 promoter were significantly higher than those in EACs with a methylated promoter (P=0.02). Promoter hypermethylation of NELL1 is a common, tissue-specific event in human EAC, occurs early during Barrett's-associated esophageal neoplastic progression, and is a potential biomarker of poor prognosis in early-stage EAC.

Transcriptional profiling suggests that Barrett's metaplasia is an early intermediate stage in esophageal adenocarcinogenesis.

To investigate the relationship between Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC), we determined gene expression profiles of discrete pathological stages of esophageal neoplasia using a sequence-verified human cDNA microarray. Fifty one RNAs, comprising 24 normal esophagi (NE), 18 BEs, and nine EACs were hybridized to cDNA microarrays. Five statistical analyses were used for the data analysis. Genes showing significantly different expression levels among the three sample groups were identified. Genes were grouped into functional categories based on the Gene Ontology Consortium. Surprisingly, the expression pattern of BE was significantly more similar to EAC than to NE, notwithstanding the known histopathologic differences between BE and EAC. The pattern of NE was clearly distinct from that of EAC. Thirty-six genes were the most differentially modulated, according to these microarray data, in BE-associated neoplastic progression. Twelve genes were significantly differentially expressed in cancer-associated BE's plus EAC (as a single combined tissue group) vs noncancer-associated BE's. These genes represent potential biomarkers to diagnose EAC at its early stages. Our results demonstrate that molecular events at the transcriptional level in BE are remarkably similar to BE's-associated adenocarcinoma of the esophagus. This finding alarmingly implies that BE is biologically closer to cancer than to normal esophagus, and that the cancer risk of BE is perhaps higher than we had imagined. These findings suggest that changes modulated at the molecular biologic level supervene earlier than histologic changes, and that BE is an early intermediate stage in the process of EAC.