ABSTRACT
PURPOSE: To report a case of bilateral iatrogenic pigmentary glaucoma secondary to cosmetic iris-lightening laser treatment. CASE REPORT: A 39-year-old patient presented with bilateral iatrogenic pigmentary glaucoma. She had elevated intraocular pressures (IOPs), scattered iris pitting, and intense angle pigmentation secondary to the cosmetic laser treatment she underwent 4 weeks prior to presentation. Her IOPs were refractory to maximal medical treatment and she subsequently underwent trabeculectomy. CONCLUSION: The true scale of complications related to cosmetic laser treatments is as yet unknown. Robust clinical investigations into its safety profile, including long-term data, are required. Prospective patients should consider this with great care. Clinicians should be aware of the potential risks of this procedure, as early recognition of cosmetic laser-induced pigmentary glaucoma may avert further sequelae.
ABSTRACT
BACKGROUND & AIMS: The transcription factor nuclear factor-kappaB (NF)-kappaB promotes survival of hepatic myofibroblasts and fibrogenesis through poorly defined mechanisms. We investigated the activities of angiotensin II and I kappaB kinase (IKK) in regulation of NF-kappaB activity and the role of these proteins in liver fibrosis in rodents and humans. METHODS: Phosphorylation of the NF-kappaB subunit RelA at serine 536 (P-Ser(536)-RelA) was detected by immunoblot and immunohistochemical analyses. P-Ser(536)-RelA function was assessed using vectors that expressed mutant forms of RelA, cell-permeable blocking peptides, and assays for RelA nuclear transport and apoptosis. Levels of P-Ser(536)-RelA were compared with degree of fibrosis in liver sections from chronically injured rats and patients with hepatitis C virus-mediated fibrosis who had been treated with the AT1 antagonist losartan. RESULTS: Constitutive P-Ser(536)-RelA is a feature of human hepatic myofibroblasts, both in vitro and in situ in diseased livers. Autocrine angiotensin II stimulated IKK-mediated phosphorylation of RelA at Ser(536), which was required for nuclear transport and transcriptional activity of NF-kappaB. Inhibition of angiotensin II, the angiotensin II receptor type 1 (AT1), or IKK blocked Ser(536) phosphorylation and stimulated myofibroblast apoptosis. Treatment of fibrotic rodent liver with the angiotensin converting enzyme (ACE) inhibitor captopril or the IKK inhibitor sulphasalazine resulted in loss of P-Ser(536)-RelA-positive myofibroblasts and fibrosis regression. In human liver samples, increased numbers of P-Ser(536)-RelA-positive cells were associated with fibrosis that regressed following exposure to losartan. CONCLUSIONS: An autocrine pathway that includes angiotensin II, IKK, and P-Ser(536)-RelA regulates myofibroblast survival and can be targeted to stimulate therapeutic regression of liver fibrosis.
