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Monographs of Topical Drugs that Have Caused Contact Allergy/Allergic Contact Dermatitis
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
A 65-year-old woman was treated for chromomycosis due to Phialophora verrucosa with systemic antifungal treatment supplemented with topical luliconazole 1% cream. Two days later, itchy erythema and papules appeared at the application site. Patch testing showed a positive reaction to luliconazole 1% pet. at D2 (++) and D3 (++). Since the patient also reported a history of contact dermatitis from lanoconazole cream used for the treatment of tinea pedis, she was patch tested with lanoconazole 1% and 10% pet. and a battery of other antimycotic creams, which yielded ++ reactions to both concentrations of lanoconazole only. Because luliconazole and lanoconazole have a similar chemical structure, the patient was considered to have been sensitized with lanoconazole and to have cross- reacted with luliconazole, resulting in the allergic contact dermatitis. The authors suggest that the dithioacetal structure was essential for inducing contact allergy to luliconazole and lanoconazole (2).
Fluorinated vectors for gene delivery
Published in Expert Opinion on Drug Delivery, 2022
Yu Wan, Yuhan Yang, Mingyu Wu, Shun Feng
It is well known that the stability of the vector/gene complex is crucial, as is the gene releasing capacity. Therefore, the synthesis of block copolymers containing responsive linkers to enable fluorine-containing polymers to release nucleic acids in specific conditions is also important for gene delivery vehicles. A bioreducible fluorinated PEI was constructed by disulfide linkages, which can be reduced by intracellular glutathione [50] (Figure 2c). The thiol-containing polymer was obtained after being treated with Traut’s reagent, which was then attached to the polymer through a disulfide exchange reaction with a fluorocarbon chain bearing an N-(2-(2-pyridyldithio)ethyl) moiety [50,51]. Additionally, a thioketal-crosslinked fluorinated PEI has been developed to produce ROS-responsive gene delivery vectors [30]. Furthermore, fluorobenzene-substituted polycations with thioacetal linkage were prepared to confer ROS-responsiveness to this vector [52] (Figure 2c). Besides, orthoester linkages were introduced into fluorinated polycations to obtain pH-responsive degradability [38] (Figure 2c). Overall, the introduction of responsive cleavage properties can further improve the transfection performance of the vectors.
Evaluation of formaldehyde as an ocular irritant: a systematic review and Meta-analysis
Published in Cutaneous and Ocular Toxicology, 2019
Pedro Vazquez-Ferreiro, Francisco Javier Carrera Hueso, Belén Alvarez Lopez, Marta Diaz-Rey, Xavier Martinez-Casal, Maria Auxiliadora Ramón Barrios
Formaldehyde is one of the most widely used industrial chemicals in the world, with an annual production of approximately 20 million tons1. It has multiple uses in both industry and domestic environments (furniture, cosmetics, dyes, etc.). However, it is a known carcinogen and also causes respiratory and eye irritation. Eye reactions to formaldehyde are an early marker of exposure; these reactions are followed by a dose–response effect that varies according to the tissue’s ability to eliminate the substance. Although the tissues themselves produce small amounts of formaldehyde as a result of metabolism, the main source of entry into the organism is the respiratory pathway, where after interacting with water, it reacts with glutathione (GSH) to form thioacetal that can be transported by the circulation. The excretion is produced both by the respiratory route, as by the urinary route through the transformation in its metabolites, among which the formic acid is the most important. At the level of the ocular mucous membranes, the absorption is more irregular and includes successive steps in which the first one involves alterations of the corneal epithelium. This process could include changes in cell membranes and the cytoskeleton, which would function as a first step in a cascade of events that would trigger tissue inflammation. The sensitive terminals would be activated directly or through receptors of cytokines (IL-1β, TNF-α) released in response to histic damage, which would function by modulating the pain in response to inflammation and triggering damage linked to the immune response. Early response levels are not cytoxic, but they are sufficient to stimulate the trigeminal nerves, leading to irritation of the upper and then lower respiratory tract and ultimately a cytoxic response.