Intravitreal triamcinolone acetonide: Pattern of secondary intraocular pressure rise and possible risk factors

Ziad F Bashshur1, Abdallah M Terro1, Christelle P El Haibi1, Akaber M Halawi1, Alexandre Schakal2, Baha’ N Noureddin11The Department of Ophthalmology, American University of Beirut, Lebanon; 2The Department of Ophthalmology, Hotel Dieu de France (St. Joseph University), LebanonPurpose: To determine the pattern of increase in intraocular pressure (IOP) following intravitreal triamcinolone acetonide (IVTA) and identify possible risk factors associated with this rise in IOP.Methods: We carried out a retrospective review of records for 185 patients (226 eyes) who received 4 mg of IVTA at the American University of Beirut Medical Center and Hotel Dieu de France eye clinics between 2003 and 2005.Results: Mean follow-up was 8.17 months (range 6 to 24 months). The mean number of IVTA injections per eye was 1.31 ± 0.69. The mean IOP increased after the first IVTA injection from 15.04 ± 3.18 mmHg at baseline to a mean maximum of 17.20 ± 5.75 mmHg (p < 0.0001, paired t-test) at month 3 of follow-up with a return to mean baseline IOP (15.49 ± 4.79 mmHg) at month 12. Fifty nine of 226 eyes showed IOP higher than 21 mmHg during follow-up. Nine eyes started to have IOP greater than 21 mmHg, 6 to 12 months after a single injection. Intraocular pressure lowering medications were started when IOP exceeded 25 mmHg in 15 of the 226 eyes studied. No risk factors have been found to predict this IOP rise.Conclusions: IOP elevation can occur in a significant number of eyes receiving 4 mg of IVTA. This phenomenon seems to be transient and a small number of eyes required treatment during this period. Eyes that received IVTA need to be monitored for IOP changes especially during the first 3 months, but the IOP may still rise 6 months and even 12 months after a single injection. This study did not show any risk factor that may predict this IOP rise.Keywords: intravitreal triamcinolone acetonide, intraocular pressure elevation, diabetic macular edema, choroidal neovascular membrane due to age-related macular degeneration, central retinal vein occlusion, Branch retinal vein occlusion, Uveiti

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Critical role for lysyl oxidase in mesenchymal stem cell-driven breast cancer malignancy

Mesenchymal stem cells (MSCs) are multipotent progenitor cells with the ability to differentiate into multiple mesoderm lineages in the course of normal tissue homeostasis or during injury. We have previously shown that MSCs migrate to sites of tumorigenesis, where they become activated by cancer cells to promote metastasis. However, the molecular and phenotypic attributes of the MSC-induced metastatic state of the cancer cells remained undetermined. Here, we show that bone marrow-derived human MSCs promote de novo production of lysyl oxidase (LOX) from human breast carcinoma cells, which is sufficient to enhance the metastasis of otherwise weakly metastatic cancer cells to the lungs and bones. We also show that LOX is an essential component of the CD44-Twist signaling axis, in which extracellular hyaluronan causes nuclear translocation of CD44 in the cancer cells, thus triggering LOX transcription by associating with its promoter. Processed and enzymatically active LOX, in turn, stimulates Twist transcription, which mediates the MSC-triggered epithelial-to-mesenchymal transition (EMT) of carcinoma cells. Surprisingly, although induction of EMT in breast cancer cells has been tightly associated with the generation of cancer stem cells, we find that LOX, despite being critical for EMT, does not contribute to the ability of MSCs to promote the formation of cancer stem cells in the carcinoma cell populations. Collectively, our studies highlight a critical role for LOX in cancer metastasis and indicate that the signaling pathways controlling stroma-induced EMT are distinct from pathways regulating the development of cancer stem cells.David & Lucile Packard Foundatio