Allergic contact dermatitis caused by topical ophthalmic medications: Keep an eye on it!

BACKGROUND: Allergic contact dermatitis (ACD) caused by topical ophthalmic medications is often overlooked. OBJECTIVES: To study the demographic characteristics, lesion locations and associated medical conditions of the patients with ACD caused by ophthalmic drugs, and to identify the most common allergenic culprits, as well as trends in frequencies over the years. METHODS: From January 1990 until December 2016, 16 065 patients were investigated in our clinic; all patients with a positive patch test reaction to an eye medication or its ingredient(s) having caused ACD were assessed. For each allergen identified, the number of positive test results as compared with the total number of those in the total population, as well as trends across three periods, namely 1990 to 1998, 1999 to 2007, and 2008 to 2016, were studied. RESULTS: One hundred and eighteen patients (0.7%) presented with positive patch test reactions to ingredients of and/or topical ophthalmic medications. Aminoglycoside antibiotics, followed by corticosteroids, as pharmacologically active ingredients, as well as wool alcohols, thiomersal, and benzalkonium chloride, as excipients, were the most frequent culprits. Chloramphenicol showed a decreasing trend of positive reactions over time, whereas reactions to tobramycin increased. CONCLUSION: ACD caused by eye medication is mainly attributable to active principles, but other excipient ingredients, beside the products "as is," should be tested as well.status: publishe

Implementing an electronic medication overview in Belgium

BACKGROUND: An accurate medication overview is essential to reduce medication errors. Therefore, it is essential to keep the medication overview up-to-date and to exchange healthcare information between healthcare professionals and patients. Digitally shared information yields possibilities to improve communication. However, implementing a digitally shared medication overview is challenging. This articles describes the development process of a secured, electronic platform designed for exchanging medication information as executed in a pilot study in Belgium, called “Vitalink”. FINDINGS: The goal of “Vitalink” is to improve the exchange of medication information between professionals working in healthcare and patients in order to achieve a more efficient cooperation and better quality of care. Healthcare professionals of primary and secondary health care and patients of four Belgian regions participated in the project. In each region project groups coordinated implementation and reported back to the steering committee supervising the pilot study. The electronic medication overview was developed based on consensus in the project groups. The steering committee agreed to establish secured and authorized access through the use of electronic identity documents (eID) and a secured, eHealth-platform conform prior governmental regulations regarding privacy and security of healthcare information. DISCUSSION: A successful implementation of an electronic medication overview strongly depends on the accessibility and usability of the tool for healthcare professionals. Coordinating teams of the project groups concluded, based on their own observations and on problems reported to them, that secured and quick access to medical data needed to be pursued. According to their observations, the identification process using the eHealth platform, crucial to ensure secured data, was very time consuming. Secondly, software packages should meet the needs of their users, thus be adapted to daily activities of healthcare professionals. Moreover, software should be easy to install and run properly. The project would have benefited from a cost analysis executed by the national bodies prior to implementation

Absence of functional peroxisomes from mouse CNS causes dysmyelination and axon degeneration

Peroxisomal metabolism is essential for normal brain development both in men and in mice. Using conditional knock-out mice, we recently showed that peroxisome deficiency in liver has a severe and persistent impact on the formation of cortex and cerebellum, whereas absence of functional peroxisomes from the CNS only causes developmental delays without obvious alteration of brain architecture. We now report that a substantial fraction of the latter Nes-Pex5 knock-out mice survive into adulthood but develop progressive motoric and coordination problems, impaired exploration, and a deficit in cognition and die before the age of 6 months. Histopathologically, both the white and gray matter of the CNS displayed a region-specific accumulation of neutral lipids, astrogliosis and microgliosis, upregulation of catalase, and scattered cell death. Nes-Pex5 knock-out mice featured a dramatic reduction of myelin staining in corpus callosum, whereas cerebellum and other white matter tracts were less affected or unchanged. This was accompanied by a depletion of alkenylphospholipids in myelin and differentially reduced immunoreactivity of myelin proteins. EM analysis revealed that myelin wrappings around axons did still form, but they showed a reduction in thickness relative to axon diameters. Remarkably, multifocal axonal damage occurred in the corpus callosum. Thereby, debris accumulated between axolemma and inner myelin surface and axons collapsed, although myelin sheaths remained present. These anomalies of myelinated axons were already present in juvenile mice but aggravated in adulthood. Together, loss of CNS peroxisomal metabolism both affects myelin sheaths and axonal integrity possibly via independent pathways

Absence of functional peroxisomes from mouse CNS causes dysmyelination and axon degeneration

Peroxisomal metabolism is essential for normal brain development both in men and in mice. Using conditional knock-out mice, we recently showed that peroxisome deficiency in liver has a severe and persistent impact on the formation of cortex and cerebellum, whereas absence of functional peroxisomes from the CNS only causes developmental delays without obvious alteration of brain architecture. We now report that a substantial fraction of the latter Nes-Pex5 knock-out mice survive into adulthood but develop progressive motoric and coordination problems, impaired exploration, and a deficit in cognition and die before the age of 6 months. Histopathologically, both the white and gray matter of the CNS displayed a region-specific accumulation of neutral lipids, astrogliosis and microgliosis, upregulation of catalase, and scattered cell death. Nes-Pex5 knock-out mice featured a dramatic reduction of myelin staining in corpus callosum, whereas cerebellum and other white matter tracts were less affected or unchanged. This was accompanied by a depletion of alkenylphospholipids in myelin and differentially reduced immunoreactivity of myelin proteins. EM analysis revealed that myelin wrappings around axons did still form, but they showed a reduction in thickness relative to axon diameters. Remarkably, multifocal axonal damage occurred in the corpus callosum. Thereby, debris accumulated between axolemma and inner myelin surface and axons collapsed, although myelin sheaths remained present. These anomalies of myelinated axons were already present in juvenile mice but aggravated in adulthood. Together, loss of CNS peroxisomal metabolism both affects myelin sheaths and axonal integrity possibly via independent pathways.status: publishe

Absence of functional peroxisomes from mouse CNS causes dysmyelination and axon degeneration

Bernard Gildas. Gilles Henry, Recherchez vos ancêtres, 1982. In: La Gazette des archives, n°117-118, 1982. pp. 160-161

Peroxisomal and mitochondrial status of two murine oligodendrocytic cell lines (158N, 158JP): potential models for the study of peroxisomal disorders associated with dysmyelination processes

In some neurodegenerative disorders (leukodystrophies) characterized by myelin alterations, the defect of peroxisomal functions on myelin-producing cells (oligodendrocytes) are poorly understood. The development of in vitro models is fundamental to understanding the physiopathogenesis of these diseases. We characterized two immortalized murine oligodendrocyte cell lines: a normal (158N) and a jimpy (158JP) cell line mutated for the proteolipid protein PLP/DM20. Fluorescence microscopy, flow cytometry, and western blotting analysis allow to identify major myelin proteins (PLP colocalizing with mitochondria; myelin basic protein), oligodendrocyte (CNPase and myelin oligodendrocyte glycoprotein), and peroxisomal markers [adrenoleukodystrophy protein, PMP70, acyl-CoA oxidase 1 (ACOX1), l-peroxisomal bifunctional enzyme, and catalase]. Using electron microscopy, peroxisomes were identified in the two cell lines. Gene expression (ATP-binding cassette, Abcd1, Abcd2, Abcd3, and Acox1) involved in peroxisomal transport or beta-oxidation of fatty acids was evaluated using quantitative PCR. 4-phenylbutyrate treatment increases expression of ACOX1, l-peroxisomal bifunctional enzyme, PLP, myelin oligodendrocyte glycoprotein, and CNPase, mainly in 158N cells. In both cell lines, 4-phenylbutyrate-induced ACOX1 and catalase activities while only Abcd2 gene was up-regulated in 158JP. Moreover, the higher mitochondrial activity and content observed in 158JP were associated with higher glutathione content and increased basal production of reactive oxygen species revealing different redox statuses. Altogether, 158N and 158JP cells will permit studying the relationships between peroxisomal defects, mitochondrial activity, and oligodendrocyte functions