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Classical Greece
Published in Scott M. Jackson, Skin Disease and the History of Dermatology, 2023
The dermatologist pays homage to the Greeks every single day in practice. Epidermis. Rhinophyma. Pityriasis lichenoides. The language of the field of dermatology was in part built by the Greeks. One of the joys of being a dermatologist is speaking the antiquated language that perpetually recognizes the influence of the Greeks (and Romans) in the specialty. Although the meanings of the words may have changed, the dermatologist uses words today that were used by physicians 2000 years ago. The language of dermatology, like the language of medicine, did not stray from its roots as it evolved. Ninety percent of the technical terms used today in medicine have Greek, Latin, or Greco-Latin origins.26
Papulosquamous Diseases
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Melek Aslan Kayıran, Jordan V. Wang, Ayşe Serap Karadağ
Overview: The etiology, prevalence, and incidence of pityriasis lichenoides (PL) are not fully clarified. Disease has been shown to peak in the third decade, and the majority of cases are diagnosed before the age of 50 years. PL typically appears in late childhood and young adulthood; however, it can be seen in all ages, races, and geographic regions. It is thought to be slightly more common in men. Cases of PLEVA can also be seen during pregnancy.
Inflammatory and infectious conditions
Published in Aimilios Lallas, Enzo Errichetti, Dimitrios Ioannides, Dermoscopy in General Dermatology, 2018
Vishal Gupta, Sidharth Sonthalia, Yasmeen Jabeen Bhat, Sonali Langar, Manal Bosseila
Pityriasis lichenoides et varioliformis acuta (PLEVA) in dark-skinned patients shares many dermoscopic features with fair-skinned subjects, namely, purpuric areas in early lesions, a central amorphous brownish crust in mature lesions, and white areas (often diffuse and central) in healing lesions.13 However, in skin of color, there may be additional features seen, including focal bluish-grayish areas due to melanin pigment in the dermis and yellow globules/structures corresponding to spongiosis and basal cell degeneration.14
Immune-related dermatologic toxicities: to make a long story short
Published in Cutaneous and Ocular Toxicology, 2020
Ariadni Angelaki, Dimitra Ioanna Lampropoulou, Gerasimos Aravantinos
To date, the inflammatory toxicities related only to anti-PD1/PD-L1 therapy, are pityriasis lichenoides, exfoliative rash and eczema, whereas Sweet syndrome, dermatomyositis and CD30 lymphomatoid reaction have been linked only with anti-CTLA-4 agents10. As proposed by Brahmer et al.11, the management of this type of skin irAEs, includes the combination of topical emollients and topical steroids for G1 (grade 1) events, while for G2 (grade 2) events the addition of antihistamine and possibly per os prednisone has been suggested. Regarding G3 (grade 3) inflammatory skin toxicity, temporary interruption of immunotherapy and dermatologic consultation have been added to the management algorithm. Additionally, i.v. steroid administration as well as consideration of changing the anticancer treatment instead of resuming treatment with ICPis (especially if the irAE has not improved to at least G1) are proposed for G4 (grade 4) inflammatory toxicities. Furthermore, an interesting suggestion regarding G3/4 pruritus refers to the use of GABA (Gamma-aminobutyric acid) agonists14; however, the exact mechanism of their antipruritic action is not clear yet. At this point, it should also be mentioned that the severity of cutaneous adverse events in terms of grading, is considered to be a topic of great difficulty that combines several factors such as BSA (Body Surface Area), tolerability and duration or morbidity11.
Correlation analysis between IL-35, IL-36γ, CCL27 and psoriasis vulgaris
Published in Journal of Dermatological Treatment, 2021
Jiao Chen, Jiaxi Du, Yiyang Han, Zhiping Wei
The IL-36 subfamily is part of the IL-1 superfamily, which includes three agonists (IL-36α, IL-36β and IL-36γ) and antagonist IL-36Ra (10). IL-36 cytokines and their receptors are usually expressed at low levels, but are significantly induced during inflammation of skin, joints, lungs and intestines (11,12). It has been found that immune cells such as plasma cells, T cells, macrophages and dendritic cells can produce IL-36 under certain conditions (such as inflammation caused by pathological changes) (13). The expression of IL-36 cytokines and their regulation in skin have been well studied. Gene expression analysis showed that all IL-36 family members in psoriatic lesions were upregulated, especially the agonists of IL-36α and IL-36γ (14). IL-36γ subtypes seem to play a special role in psoriasis (12). The protein expression level of IL-36γ in psoriatic lesions is three times higher than that in other inflammatory skin diseases (such as atopic dermatitis [AD, lichen planus, contact eczema, pityriasis lichenoides, subacute cutaneous lupus erythematosus and fungoid diseases) (15). IL-36γ can induce macrophages to produce psoriasis-related cytokines (IL-23 and TNF-α), and this response increases in macrophages of psoriasis patients. This effect is unique to IL-36 gamma and cannot be imitated by other IL-1 family members (16). The expression of IL-36γ is associated with disease activity and decreases during TNF-α treatment, thus improving the disease (17). In this study, we found that the expression of IL-36γ in peripheral blood of patients with psoriasis vulgaris was significantly higher than that of the control group, and its expression level was positively correlated with PASI, suggesting that IL-36γ may participate in the pathogenesis of psoriasis as a pro-inflammatory cytokine.
Type A lymphomatoid papulosis presenting as an eyelid ulcer in a young man
Published in Orbit, 2019
Juan Carlos Sánchez España, Roberto Secondi
A multidisciplinary systemic assessment is crucial to follow-up the disease and to exclude other concomitant tumors. A differential diagnosis6,9 between LP and other conditions sharing the features of histologic evidence of a CD30+ infiltrate and/or a relapsing-remitting clinical course could be necessary. The conditions included in the differential diagnosis of our patient were reactive lymphoid hyperplasia, Churg-Strauss syndrome, leishmaniasis, Pityriasis lichenoides, Wells syndrome, contact dermatitis, Herpes simplex virus, Varicella zoster virus, arthropod infections or drug reactions.