Allergic Contact Dermatitis From Mercury Antiseptics and Derivatives: Study Protocol of Tolerance to Intramuscular Injections of Thimerosal

Audícana, M.; Muñoz, D.; Pozo, M. D. Del; Fernández, E.; Gastaminza, Gabriel; Corrés, L. Fernández de

doi:10.1053/ajcd.2002.29945

Cited by 61 publications

(28 citation statements)

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“…6 Local reactions can nevertheless be more frequent among sensitized recipients. 7 Formaldehyde is still used in vaccine preparation, 8 but no IgE-mediated reactions to formaldehyde have been recently described.…”

Section: Allergic Reactions To Vaccinesmentioning

confidence: 99%

Vaccination and allergy: EAACI position paper, practical aspects

Nilsson

Brockow

Alm

et al. 2017

Pediatric Allergy Immunology

136

184

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Immunization is highly effective in preventing infectious diseases and therefore an indispensable public health measure. Allergic patients deserve access to the same publicly recommended immunizations as non‐allergic patients unless risks associated with vaccination outweigh the gains. Whereas the number of reported possible allergic reactions to vaccines is high, confirmed vaccine‐triggered allergic reactions are rare. Anaphylaxis following vaccination is rare, affecting <1/100 000, but can occur in any patient. Some patient groups, notably those with a previous allergic reaction to a vaccine or its components, are at heightened risk of allergic reaction and require special precautions. Allergic reactions, however, may occur in patients without known risk factors and cannot be predicted by currently available tools. Unwarranted fear and uncertainty can result in incomplete vaccination coverage for children and adults with or without allergy. In addition to concerns about an allergic reaction to the vaccine itself, there is fear that routine childhood immunization may promote the development of allergic sensitization and disease. Thus, although there is no evidence that routine childhood immunization increases the risk of allergy development, such risks need to be discussed.

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Section: Allergic Reactions To Vaccinesmentioning

confidence: 99%

Vaccination and allergy: EAACI position paper, practical aspects

Nilsson

Brockow

Alm

et al. 2017

Pediatric Allergy Immunology

136

184

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“…AQP3 and another member of the aquaporin family, AQP7, have recently been found in dendritic cells, which play an important role in the innate immune system (41,42). Mercury, which is well known blocker of AQPs (2-4) and a cause of contact dermatitis (6,43), inhibits the regulatory cell volume decrease after macropinocytosis in dendritic cells (42). Given the finding that nickel blocks the water permeability of AQP3, it is tempting to speculate that perturbation of volume regulation of dendritic cells is an important contributor to nickel dermatitis and to the inflammatory component of nickel pneumoconiosis.…”

Section: Regulation Of Aqp3 By Ni 2ϩ and Ph 30040mentioning

confidence: 99%

Nickel and Extracellular Acidification Inhibit the Water Permeability of Human Aquaporin-3 in Lung Epithelial Cells

Zelenina

Bondar

Zelenin

et al. 2003

Journal of Biological Chemistry

112

110

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Nickel is a common cause of pneumoconiosis. Here, we show that nickel inactivates aquaporin (AQP)-3, the water channel expressed apically in epithelial cells of human terminal airways. Human AQP3 was transiently transfected into human lung cells, and water permeability was measured in transfected and neighboring untransfected cells. Incubation with NiCl 2 rapidly, dosedependently, and reversibly decreased water permeability in AQP3-expressing cells. Acidification of the extracellular medium also caused rapid, dose-dependent, and reversible inhibition of AQP3. Sensitivity of AQP3 to nickel was lower at alkaline pH than at neutral and acidic pH. Cells transfected with human AQP4 and AQP5, which are also expressed in airway epithelia, were insensitive to nickel and extracellular acidification. Zinc and cadmium, other common causes of pneumoconiosis, had no effect on the water permeability of AQP3. were also involved in regulation of AQP3 by extracellular pH. In addition, the aromatic side chain of His 154 was shown to be important for the water permeability of AQP3. Our results imply that nickel and extracellular pH may modulate lung water clearance and that defective water clearance may be an early component of nickel-induced lung disease.Nonenzymatic regulation of ion channels by Ni 2ϩ and other divalent cations or by pH is a well established phenomenon with many important physiological and pathophysiological implications. Less is known about nonenzymatic regulation of water channels, aquaporins (AQPs) 1 (1). Mercury inhibits most mammalian water channels via binding to cysteine residues (2-4) and has been an important tool in studies of AQPs. Gold and silver were recently reported to inhibit a water channel from human erythrocytes, presumably AQP1, but a molecular basis for this inhibition has not been revealed (5). The question of whether Ni 2ϩ and other divalent ions known to regulate the activity of ion channels modulate the activity of AQPs has, to our knowledge, not yet been addressed.Nickel is widely used in modern industry (reviewed in Ref. 6). Inhalation is the primary route of occupational exposure to nickel and other heavy metals, and inhalation of nickel compounds is a common cause of pneumoconiosis (6, 7). AQP3, AQP4, and AQP5 are expressed in the airway epithelia (8 -10). AQP3 is located at the apical membrane of human lung epithelium (10). Here, we have examined the effects of Ni 2ϩ on the water permeability of human AQP3, AQP4, and AQP5 expressed in a human lung cell line. Since AQP3 has, when expressed in oocytes, been reported to be pH-sensitive (11), we also examined the effect of extracellular acidification. We show that Ni 2ϩ and pH regulate the water permeability of human AQP3, but not of human AQP4 and AQP5. We also address the question of whether Ni 2ϩ and pH may interact in the regulation of human AQP3.Identification of the molecular sites responsible for the Ni 2ϩ and pH sensitivity of AQP3 is important for future development of therapeutic agents. Histidine, with a pK a of ϳ6.5, is the ...

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“…Aluminum has been reported to be responsible for 77% to 85% of all DTH to vaccinations. 3, 15 Other reported ingredients include polysorbate, 32 thimerosal, 33,34 phenoxyethanol, 35 formaldehyde, 36 and polymyxin B 37 . Although neomycin and others are known causes of DTH, there have been no reports of vaccine DTH to date.…”

Section: Figurementioning

confidence: 99%

Case Report of Subcutaneous Nodules and Sterile Abscesses Due to Delayed Type Hypersensitivity to Aluminum-Containing Vaccines

Lauren

Belsito²,

Morel

et al. 2016

Pediatrics

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Routine childhood immunizations have resulted in great reductions in vaccine-preventable infectious diseases. Vaccine-related adverse events, albeit rare, can be of significant consequence. Although anaphylaxis, or type I hypersensitivity, is recognized as a potential reaction after vaccination, delayed type hypersensitivity or type IV reactions are less so. We present a case of persistent subcutaneous nodules and sterile abscesses in the setting of delayed type hypersensitivity to aluminum, confirmed by patch testing and recurrence on re-exposure. We review sources of aluminum in common immunizations, principles for treatment, and strategies for management of future vaccinations for this patient.

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Allergic Contact Dermatitis From Mercury Antiseptics and Derivatives: Study Protocol of Tolerance to Intramuscular Injections of Thimerosal

Cited by 61 publications

References 0 publications

Vaccination and allergy: EAACI position paper, practical aspects

Vaccination and allergy: EAACI position paper, practical aspects

Nickel and Extracellular Acidification Inhibit the Water Permeability of Human Aquaporin-3 in Lung Epithelial Cells

Case Report of Subcutaneous Nodules and Sterile Abscesses Due to Delayed Type Hypersensitivity to Aluminum-Containing Vaccines

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