The PALM Technique: histological findings of masked phototherapeutic keratectomy on rabbit corneas

BACKGROUND: To compare the corneal healing response between conventional and phototherapeutic keratectomy through a masking agent, in rabbit corneas. METHODS: 24 adult rabbits underwent phototherapeutic keratectomy. Animals were divided in two groups: 12 received photoablation through a masking agent (PALM gel) and the remaining 12 received conventional phototherapeutic keratectomy of equal depth and served as control. Light and transmission electron microscopy was performed in specimens of both groups obtained: immediately after, four hours, one week, one, three and six months after treatment. RESULTS: Reepitheliazation was complete within five days in all eyes. Light and transmission electron microscopy did not reveal any differences of the healing process in the experimental eyes compared to the controls. CONCLUSION: Photoablation through the PALM technique did not result any evident alterations of the reepithelisation and stromal healing process

ANCA-associated vasculitis.

The anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides (AAVs) are a group of disorders involving severe, systemic, small-vessel vasculitis and are characterized by the development of autoantibodies to the neutrophil proteins leukocyte proteinase 3 (PR3-ANCA) or myeloperoxidase (MPO-ANCA). The three AAV subgroups, namely granulomatosis with polyangiitis (GPA), microscopic polyangiitis and eosinophilic GPA (EGPA), are defined according to clinical features. However, genetic and other clinical findings suggest that these clinical syndromes may be better classified as PR3-positive AAV (PR3-AAV), MPO-positive AAV (MPO-AAV) and, for EGPA, by the presence or absence of ANCA (ANCA+ or ANCA-, respectively). Although any tissue can be involved in AAV, the upper and lower respiratory tract and kidneys are most commonly and severely affected. AAVs have a complex and unique pathogenesis, with evidence for a loss of tolerance to neutrophil proteins, which leads to ANCA-mediated neutrophil activation, recruitment and injury, with effector T cells also involved. Without therapy, prognosis is poor but treatments, typically immunosuppressants, have improved survival, albeit with considerable morbidity from glucocorticoids and other immunosuppressive medications. Current challenges include improving the measures of disease activity and risk of relapse, uncertainty about optimal therapy duration and a need for targeted therapies with fewer adverse effects. Meeting these challenges requires a more detailed knowledge of the fundamental biology of AAV as well as cooperative international research and clinical trials with meaningful input from patients