Pediatric ocular injuries: a 3-year review of patients presenting to an emergency department in Canada.

BACKGROUND: Ocular traumas represent the most common cause of noncongenital blindness in children. Sports are the second most common cause in children less than 14 years old in Canada. To our knowledge, there have not yet been any reports regarding the causes of pediatric ocular trauma in the Quebec population. The goal of our study was to gather data from the Quebec pediatric population to determine high-risk age groups, sports, or other activities. METHODS: A retrospective study evaluating all patients younger than 18 years who presented with ocular trauma to the Ste-Justine Hospital emergency department between 2007 and 2010. Data obtained included age, sex, activity at the time of injury, mechanism of injury, and visual outcomes. RESULTS: Trauma was more common in males (65%). The mean age was 7.2 years. Injuries occurred more often in the 5-9 year age group, at home, and during free play. Sports-related injuries occurred more often in the 10-18 year age group, with hockey being associated most often with injuries. Visual acuity at presentation was variable, but final acuity was 20/30 or better in 86.7% of cases. In 89% of cases, there was no mention of ocular protection and prevention of injuries in the chart by emergency physicians. CONCLUSION: Our study suggests that ocular injuries may be prevented by better supervision and parental education in the younger population and by mandating ocular protection for sports in high school-aged patients.

Impairment of neutrophil migration to remote inflammatory site during lung histoplasmosis.

Histoplasma capsulatum (Hc) induces a pulmonary disease in which leukotrienes promote activation and recruitment of effectors cells. It is also well-recognized that leukotriene B4 (LTB4) and platelet-activating factor (PAF) induce leukocyte recruitment to inflammatory sites. We investigated the impact of pulmonary Hc infection on PMN migration to a remote inflammatory site. Our results show that pulmonary Hc infection impairs LTB4- or PAF-stimulated PMN recruitment to air pouch. Yet, remote inflammation did not modify PMN numbers in the bronchoalveolar lavage fluid (BALF) of Hc-infected mice. Interestingly, the concomitant administration of PAF and LTB4 receptor antagonists inhibited PMN recruitment to both BALF and the remote site, demonstrating cooperation between both mediators. Along that line, our results show that PAF-elicited PMN chemotaxis was abrogated in 5-lipoxygenase-deficient animals. These results suggest caution in the indiscriminate use of anti-inflammatory drugs during infectious diseases.

Inflammatory disorders of the orbit in childhood: a case series.

PURPOSE: To describe a series of cases of orbital inflammatory disorders in children. DESIGN: Retrospective case series. METHODS: The medical records of pediatric patients diagnosed with orbital inflammation between September 1, 2002, and December 31, 2008, at Texas Children's Hospital were reviewed. Data collected included age at presentation, final diagnosis, treatment, workup and evaluation, need for biopsy and biopsy results, and involvement of lacrimal gland and muscles. RESULTS: Twelve cases were identified. Six cases were males and 6 were females with age at presentation ranging from 1.3 to 16.2 years (mean, 11.9 years). The most common presentation was lacrimal gland enlargement, which was bilateral in 3 cases. Other common presenting signs were proptosis, extraocular motility limitation, and pain on eye movement. Half of our patients had systemic complaints at presentation, the most common of which was fever. Four patients were diagnosed as having a systemic cause and 2 of these patients had systemic symptoms. CONCLUSIONS: Idiopathic orbital inflammatory conditions in children are uncommon, but can be associated with systemic conditions. Patients typically have lacrimal gland involvement, pain with eye movement, proptosis, and motility deficits at presentation. Bilateral cases may have a higher incidence of systemic disease.

Histoplasma capsulatum cell wall {beta}-glucan induces lipid body formation through CD18, TLR2, and dectin-1 receptors: correlation with leukotriene B4 generation and role in HIV-1 infection.

Histoplasma capsulatum (Hc) is a facultative, intracellular parasite of worldwide significance. Infection with Hc produces a broad spectrum of diseases and may progress to a life-threatening systemic disease, particularly in individuals with HIV infection. Resolution of histoplasmosis is associated with the activation of cell-mediated immunity, and leukotriene B(4) plays an important role in this event. Lipid bodies (LBs) are increasingly being recognized as multifunctional organelles with roles in inflammation and infection. In this study, we investigated LB formation in histoplasmosis and its putative function in innate immunity. LB formation in leukocytes harvested from Hc-infected C57BL/6 mice peaks on day 2 postinfection and correlates with enhanced generation of lipid mediators, including leukotriene B(4) and PGE(2). Pretreatment of leukocytes with platelet-activating factor and BLT1 receptor antagonists showed that both lipid mediators are involved in cell signaling for LB formation. Alveolar leukocytes cultured with live or dead Hc also presented an increase in LB numbers. The yeast alkali-insoluble fraction 1, which contains mainly beta-glucan isolated from the Hc cell wall, induced a dose- and time-dependent increase in LB numbers, indicating that beta-glucan plays a signaling role in LB formation. In agreement with this hypothesis, beta-glucan-elicited LB formation was inhibited in leukocytes from 5-LO(-/-), CD18(low) and TLR2(-/-) mice, as well as in leukocytes pretreated with anti-Dectin-1 Ab. Interestingly, human monocytes from HIV-1-infected patients failed to produce LBs after beta-glucan stimulation. These results demonstrate that Hc induces LB formation, an event correlated with eicosanoid production, and suggest a role for these lipid-enriched organelles in host defense during fungal infection.

Involvement of endogenous leukotriene B4 and platelet-activating factor in polymorphonuclear leucocyte recruitment to dermal inflammatory sites in rats.

A critical role for leukotriene B(4) (LTB(4)) and/or platelet-activating factor (PAF) in regulating polymorphonuclear cell (PMN) trafficking to inflammatory sites has been reported in a number of experimental inflammatory models. In vitro, newly synthesized LTB(4) and PAF were shown to act in an autocrine/paracrine or intracrine fashion to enhance intracellular arachidonic acid availability and leukotriene biosynthesis. This suggested potentially cooperative effects of these lipid mediators in regulating PMN extravasation. The present study aimed to elucidate whether endogenous LTB(4) and PAF may both act to regulate plasma extravasation and PMN trafficking to inflammatory sites in experimental inflammation. With this aim, we have used selective and potent PAF and LTB(4) receptor antagonist pretreatments in dermal and pulmonary inflammation models in rats. Our results show additive inhibitory effects of dual LTB(4) and PAF receptor blockade in either PAF- or LTB(4)-elicited cutaneous PMN accumulation compared to single-drug administration. Furthermore, the combined administration of the drugs inhibited the PMN accumulation induced by the chemically unrelated soluble agonists tumour necrosis factor-alpha and C5a. Finally, in a model of pulmonary inflammation induced by the intravenous injection of Sephadex beads, lung neutrophilia was reduced by 63% following the administration of LTB(4) and PAF antagonists, in contrast with the lack of effect of single drug administration. Our results strongly support a role of both endogenous LTB(4) and PAF in regulating PMN trafficking to inflammatory sites in various experimental conditions.