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Pneumonitis induced by non-cytotoxic agents
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
Umair A Gauhar, J Allen D Cooper
Oral and parenteral gold salts (auranofin, gold sodium thiomalate, and gold aurothioglucose) have been used in the treatment of rheumatoid arthritis for over 50 years but are rarely used today because of the availability of safer and more effective therapeutic modalities. However, parenteral gold is a therapeutic option for patients refractory to other antirheumatic drugs. Gold salts are also used in selected cases of juvenile rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis and pemphigus.53,54 Gold may also be used in Felty’s syndrome (associated with anaemia and thrombocytopenia), since in such cases methotrexate may cause further bone marrow suppression.39 Gold salts exert an immunomodulatory effect through a decrease in neutrophil chemotaxis, decreased monocyte responsiveness and reduction in the release of proteolytic enzymes in the synovial fluid.53 They have also been shown to have a dose-dependent effect on cell proliferation by affecting thymidine incorporation and collagen synthesis.55
Tattooing in Vitiligo
Published in Vineet Relhan, Vijay Kumar Garg, Sneha Ghunawat, Khushbu Mahajan, Comprehensive Textbook on Vitiligo, 2020
Tattooing in vitiligo is most suitable for mucosal and mucocutaneous vitiligo or recalcitrant patches of vitiligo on glabrous skin not responding to or suitable for surgical therapy. Vitiligo limited to mucosal and mucocutaneous areas of lips, visible area of inside of lip, gums or gingiva, etc. are best treated with micropigmentation (Figure 44.1) [7–14]. Genital vitiligo involving the glans penis, shaft of the penis, scrotum, vulva, and perineal and perigenital areas, umbilicus, etc. (Figure 44.2), which are normally darker than the other parts of the skin, are best suited for tattooing for micropigmentation. The present evidence also indicates its use in recalcitrant lesions of vitiligo, especially over the distal digits, lips, umbilicus, hands, wrists, axillae, elbows, perianal areas, lower legs, mucosae, and mucocutaneous junctions. Micropigmentation has also been used for nipple areola reconstruction, enhancement of eyebrows and eyelashes, permanent repigmentation of achromic burn scars, reconstitution of eyebrows following recalcitrant alopecia areata, and aesthetic improvements of scars and skin grafts, especially to camouflage hairless patches. It is useful adjunctive therapy for camouflaging disturbing discolorations and scars of the head and neck, reports of which have included color matching of vermilionplasty after radial forearm free flap reconstruction of the lower lip, cleft lip, and cleft palate scars, senile lip rejuvenation, and an alternative treatment for disturbing corneal scars [15–20]. Until 1984, tattooing was mainly performed as a permanent eyeliner for enhancing eye expression. Micropigmentation or dermatography has been used in the fields of craniomaxillofacial, reconstructive, and cosmetic surgery. Tattooing has also been done with gold salts, such as 20% aurothioglucose in sesame oil for vitiligo. Others have used this procedure for implanting various earth-tone color pigments to the base of the eyelash as cosmetic eyeliner. Excellent color matching has been reported in cutaneous, mucosal, and mucocutaneous vitiligo; contact leukoderma; and postinflammatory depigmentation and scarring in various studies, especially in dark individuals [21–24]. The latest Cochrane review on treatment of vitiligo, however, fails to find well-controlled studies on this the subject of micropigmentation as a treatment option for vitiligo [1].
Skin
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Zbigniew W. Wojcinski, Lydia Andrews-Jones, Daher Ibrahim Aibo, Rie Kikkawa, Robert Dunstan
Immunologic reactions may involve humoral or cellular components. Humoral reactions include skin anaphylaxis (type I hypersensitivity reaction mediated via IgE) and immunocomplex reactions (type III hypersensitivity reaction mediated via IgG, IgM, complement; Arthus reaction). Cell-mediated immunotoxicity is a delayed-type response (type IV hypersensitivity reactions) often observed 24–96 h after application of the test article or as occurs in graft-versus-host reaction (Figure 21.3c). Contact allergic reactions are delayed-type hypersensitivity reactions and involve the capture and metabolism of antigens by keratinocytes and Langerhans cells and the formation of the hapten-protein complexes (Khan et al. 2006). At the same time, keratinocytes or Langerhans cells secrete cytokines (IL-1β, TNFα, IL-18, etc.) important for the migration of Langerhans cells to the local lymph nodes. These Langerhans cells upregulate receptors (CCR7, etc.) important for interaction with these cytokines and their homing to the lymph nodes. In the lymph nodes, Langerhans cells present the antigen to the resident T cells resulting in their activation and proliferation and migration to the skin. Upon reexposure of the antigen, dermal dendritic cells or keratinocytes present the antigen to the T memory cells in the skin, which then release cytokines (IFN-γ, IL-17, etc.) and recruit macrophages that produce more cytokines and elicit an inflammatory reaction. With lipid-soluble antigens that can cross the cell membrane, intracellular processing and modification lead to their presentation linked to MHC I and elicitation of cytotoxic T cells and the killing of the eliciting cell. Chemicals such as 2,4-dinitrofluorobenzene and picryl chloride are associated with allergic contact dermatitis. Clinical manifestations of delayed hypersensitivity include exanthemas, erythema multiforme, and Stevens-Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN). Erythema multiforme and TEN represent severe, often life-threatening forms of immune-mediated diseases. Inappropriate activation of cytotoxic CD8+ T cells has been implicated as a cause of these diseases (Haschek et al. 2010). A broad spectrum of drugs has been associated with development of erythema multiforme and TEN, including sulfonamides, penicillins, cephalosporins, ivermectin, aurothioglucose, griseofulvin, propylthiouracil, d-limonene, anticonvulsant drugs, minoxidil, and nonsteroidal anti-inflammatory drugs (NSAIDs) (Paul et al. 1998; Karaoui and Chahine-Chakhtoura 2009; Haschek et al. 2010).
Metallo therapeutics for COVID-19. Exploiting metal-based compounds for the discovery of new antiviral drugs
Published in Expert Opinion on Drug Discovery, 2021
Damiano Cirri, Alessandro Pratesi, Tiziano Marzo, Luigi Messori
Such drug repurposing strategy that we propose for AF could be well extended to some other clinically established gold drugs for rheumatoid arthritis, such as aurothiomalate (Figure 2(c)) and aurothioglucose. The AF analogue, chloro(triethylphosphine)gold(I), AF-Cl hereafter, where the thiosugar moiety is replaced by a simple chloride ligand (Figure 2(b)) is another promising candidate. AF-Cl is commercially available and has been clinically tested in comparison with AF for the treatment of arthritis [25]. Notably AF-Cl, through the pharmacologically active cation [Et3PAu]+, is able to bind the catalytically relevant His133 residue of cyclophilin models [26]. This latter feature is of particular interest considering that some molecules interacting with cyclophilin A have been selected as promising drug candidates against COVID-19 [6].
GOLD: human exposure and update on toxic risks
Published in Critical Reviews in Toxicology, 2018
Gold exhibits oxidation states ranging from −1 to +5 and theoretically has the capacity to form a large number of inorganic and organic compounds, but compounds of Au(I) and Au(III) are predominant (Henderson and Raynor 1962; Mohr et al. 2006). Gold chloride (AuCl3) is hygroscopic and highly soluble in water; it decomposes at 160° to form AuCl. Chloroauric acid (HAuCl4.xH20) formed when gold dissolves in aqua regia is also highly soluble, but corrosive and very toxic. The principle compounds listed in formularies for treatment of rheumatoid arthritis include auranofin (Ridaura®) (Figure 1), sodium aurothiomalate (Mycrisin™) sodium aurothiosulphate, aurothiopropanol sulfate (Allocristin™) and aurothioglucose (Solganal™) (Best and Sadler 1996). Auranofin contains 29% gold and is administered orally, whereas the gold thiolates are injectable. Following administration of gold salts, plasma gold is associated with red blood cells and plasma proteins. The exact metabolic fate of sodium aurothiomalate and aurothioglucose is not understood. Pharmacokinetics have shown that with aurothioglucose administration, approximately 85% of plasma gold is metabolized to lymph nodes, bone marrow, liver, skin and bone. Auranofin is metabolized rapidly such that the intact molecule is not detectable in blood (Blocka 1983).