Abstract
Background Actinic prurigo (AP) is a type of photodermatosis, the pathophysiology of which has not been determined. AP has been suggested to be a hypersensitivity reaction to the presence of eosinophils and the local production of IgE. Material and Methods Descriptive study, using paraffin blocks of tissue that have been diagnosed with AP from the Dermopathology department, Hospital General Dr. Manuel Gea González. In 66 blocks from 63 patients, eosinophils were identified by hematoxylin and eosin staining, and mastocytes were labeled by immunohistochemistry. Three random microphotographs (40x) were used, and cell counts were calculated as the mean count in the 3 microphotographs. Results Forty cases (63.5%) were female, and 23 (36.5%) were male. The mean age was 26.49 ±14.09 years; regarding the evolution time of the disease, the average was 11.93 years ±11.39. In 38 of 63 cases (60%), the lip, skin, and conjunctiva were affected clinically. In 22 of 63 cases (34%), AP cheilitis was the sole manifestation, and in 4 of 63 cases (6%), there were lesions in the skin and conjunctiva. The mean eosinophil count was 9 per case, the average number of mastocytes/field was 28.48 (range 0 to 66) Kruskal-Wallis p=0.001. Conclusions There are elements in AP that mediate the reaction of hypersensitivity type IV b, necessitating the identification of triggering factors. Key words:Actinic prurigo, eosinophil, hypersensitivity IV b, IgE, mastocytes.
Highlights
Actinic prurigo (AP) is a chronic, inflammatory photodermatosis that affects the skin, lip, and conjunctival mucosa
Cheilitis is present in nearly 85% of AP cases, and in 27% of cases, it is the sole manifestation of the illness [12]
Epithelial acanthosis, spongiosis and exulceration, and an abundance of eosinophils are seen in the dermis, and there is an infiltrate of nodular lymphoplasmocytes that can form lymphoid follicles, patognomonic image of APs chelitis [14,15]
Summary
Actinic prurigo (AP) is a chronic, inflammatory photodermatosis that affects the skin, lip, and conjunctival mucosa. Mastocytes participate in inflammatory and allergic reactions They are activated primarily through the highaffinity IgE receptor (FcεRI), which can bind the IgEantigen complex to initiate a complex transduction of signals that culminate in the secretion of proinflammatory mediators and cytokines. The presence of IgE-expressing eosinophils and mastocytes implicates a hypersensitivity reaction in the pathophysiology of AP [30]. The subtype IVb initiates a Th2 immune response in which lymphocytes T secrete IL-4, IL-5, and IL-13, which, through B cells that produce IgE and IgG4, stimulate eosinophils and mastocytes and inactivate macrophages. The high production of IL-5 causes eosinophilic inflammation, a characteristic of type IV hypersensitivity reactions [33,34,35,36,37]. AP has been suggested to be a hypersensitivity reaction to the presence of eosinophils and the local production of IgE. Conclusions: There are elements in AP that mediate the reaction of hypersensitivity type IV b, necessitating the identification of triggering factors
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