Suspicious brush cytology is an indication for liver transplantation evaluation in primary sclerosing cholangitis

AIM To investigate markers for high-grade dysplasia for the optimal timing of liver transplantation in patients with primary sclerosing cholangitis (PSC). METHODS Earlier data support a dysplasia-carcinoma sequence, even low-to high-grade dysplasia, in PSC-associated cholangiocarcinoma (CCA). Surveillance using endoscopic retrograde cholangiography (ERC) and brush cytology aims to detect cases of biliary dysplasia, and liver transplantation is an option in cases with suspicion of malignancy in brushing. This study investigated markers to identify patients with high-grade biliary dysplasia for optimal timing in early liver transplantation. Patients undergoing surveillance using ERC and brush cytology during 2008-2014 and who were diagnosed with biliary dysplasia in explanted liver or CCA until February 2016 were included in the study. Demographic data, cholangiography findings, laboratory values, cytological morphology and DNA ploidy were analysed. RESULTS Thirty PSC patients had biliary neoplasia in the explanted liver during the study period. Sixteen of these patients had low-grade dysplasia, 10 patients had high-grade dysplasia, and 4 patients had CCA. Fifteen PSC patients diagnosed with CCA were not transplanted. Patients with low-grade dysplasia were younger. Alkaline phosphatase or carcinoembryonic antigen values did not differ between groups during surveillance, but carbohydrate antigen 19-9 was higher in CCA patients. No difference in PSC duration, ERC scores, suspicious cytology, or ploidy analysis was found between groups. No difference was observed between fibrosis stage in explanted livers. Low-and high-grade dysplasia could not be differentiated before liver transplantation based on liver enzymes, tumour markers, ERC scores, brush cytology or DNA ploidy. CONCLUSION Repeated suspicion of neoplasia in brush cytology should be an indication for evaluations of liver transplantation prior to the development of CCA.Peer reviewe

Matrix metalloproteinases and their tissue inhibitors after selective laser trabeculoplasty in pseudoexfoliative secondary glaucoma

<p>Abstract</p> <p>Background</p> <p>The aim of this study was to assess changes in metalloproteinases (MMP-2) and tissue inhibitor of metalloproteinases (TIMP-2) following selective laser trabeculoplasty (SLT) in patients with pseudoexfoliative glaucoma (PEXG).</p> <p>Methods</p> <p>We enrolled 15 patients with PEXG and cataracts (PEXG-C group) and good intraocular pressure (IOP) controlled with β-blockers and dorzolamide eye drops who were treated by cataract phacoemulsification and 15 patients with pseudoexfoliative glaucoma (PEXG-SLT group). The PEXG-SLT patients underwent a trabeculectomy for uncontrolled IOP in the eye that showed increased IOP despite the maximum drug treatment with β-blockers and dorzolamide eye drops and after ineffective selective laser trabeculoplasty (SLT). The control group consisted of 15 subjects with cataracts. Aqueous humor was aspirated during surgery from patients with PEXG-C, PEXG-SLT and from matched control patients with cataracts during cataract surgery or trabeculectomy. The concentrations of MMP-2 and TIMP-2 in the aqueous humor were assessed with commercially available ELISA kits.</p> <p>Results</p> <p>In PEXG-SLT group in the first 10 days after SLT treatment a significant reduction in IOP was observed: 25.8 ± 1.9 vs 18.1.0 ± 1.4 mm/Hg (p < 0.001), but after a mean time of 31.5 ± 7.6 days IOP increased and returned to pretreatment levels: 25.4 ± 1.6 mm/Hg (p < 0.591). Therefore a trabeculectomy was considered necessary.</p> <p>The MMP-2 in PEXG-C was 57.77 ± 9.25 μg/ml and in PEXG-SLT was 58.52 ± 9.66 μg/ml (p < 0.066). TIMP-2 was 105.19 ± 28.53 μg/ml in PEXG-C and 105.96 ± 27.65 μg/ml in PEXG-SLT (p < 0.202). The MMP-2/TIMP-2 ratio in the normal subjects was 1.11 ± 0.44. This ratio increase to 1.88 ± 0.65 in PEXG-C (p < 0.001) and to 1.87 ± 0.64 in PEXG-SLT (p < 0.001). There was no statistically significant difference between the PEXG-C and PEXG-SLT ratios (p < 0.671).</p> <p>Conclusion</p> <p>This case series suggest that IOP elevation after SLT can be a serious adverse event in some PEXG patients. The IOP increase in these cases would be correlated to the failure to decrease the TIMP-2/MMP-2 ratio.</p> <p>Trial registration</p> <p>Current Controlled Trials <b>ISRCTN79745214</b></p

Prostaglandin-inhibitor naproxen does not affect contact lens-induced changes in the human corneal endothelium

A randomized, double-masked, placebo-controlled study was conducted to determine the effect of the prostaglandin-inhibitor naproxen on the bleb response of the corneal endothelium during hydrogel contact lens wear. Naproxen did not significantly alter the bleb response. This finding suggests that the endothelial bleb response is not prostaglandin-mediated

Effect of prostaglandin-inhibitor naproxen on the corneal swelling response to hydrogel contact lens wear

Previous studies have demonstrated that the prostaglandin-inhibitor naproxen can reduce post-surgical corneal oedema, which is largely due to an inflammatory process. To determine whether there is an inflammatory component in the oedematous response of the cornea to contact lens wear, we conducted a randomized, double-masked, placebo-controlled study on the effect of naproxen on contact lens-induced corneal swelling. This drug did not have a significant effect, suggesting that prostaglandins are not involved in the hypoxic oedema response. The discrepancy between the effect of naproxen on lens- and surgically-induced corneal oedema can be attributed to the different aetiologies of these oedema responses

Prostaglandin-inhibitor naproxen does not affect contact lens-induced changes in the human corneal endothelium

A randomized, double-masked, placebo-controlled study was conducted to determine the effect of the prostaglandin-inhibitor naproxen on the bleb response of the corneal endothelium during hydrogel contact lens wear. Naproxen did not significantly alter the bleb response. This finding suggests that the endothelial bleb response is not prostaglandin-mediated