Clinics in dermatology最新文献

Tuberculosis (TB) is a socially significant disease caused by Mycobacterium tuberculosis (MT). Latent tuberculosis (LTB) represents a state of continuous immune response to stimulation by MT and its antigens without the clinical signs of TB. Biologic agents could trigger LTB into active TB, which is the reason why psoriasis patients should be screened for LTB before initiating biologic therapy. The data of the efficacy of Rp in severe psoriasis patients treated for their coexisting active TB, along with the data of psoriasis remission following Rp therapy in subjects with no active TB, raise the question of whether there is a link between psoriasis and TB. There is a question of the efficacy of the date from rifampicin (Rp), when used for treating patients having severe psoriasis as well as coexisting active TB. Is there a link between psoriasis and TB?

The practice of iconodiagnostics requires careful observation, as well as knowledge of the biographic details of the subject and the artist's style, to avoid making excessive diagnoses. We have analyzed the portraits of Rachel Furtado and her husband from the 19th century displayed at the Museum of Art and History of Judaism in Paris. A thorough examination and knowledge of their way of life allows us to distinguish pigment disorders from the painter's stylistic effects and avoid diagnostic pitfalls.

Prurigo nodularis (PN) is a chronic skin condition that profoundly impacts quality of life. Histopathological studies of itchy hyperkeratotic nodules show dense infiltrates of T lymphocytes, mast cells, and eosinophils. A robust inflammatory response is implicated, coupled with key changes in neuronal plasticity that affect nerve fiber architecture and function. The microbial community in PN lesions exhibits a distinct composition, marked by decreased alpha diversity and a prominent increase in Staphylococcus aureus (S. aureus). This alteration appears to contribute to the disease's pathophysiology, causing further disruption of the skin barrier, immune dysregulation, and neuronal plasticity. There is ample evidence that virulence factors of S. aureus promote Th2, Th17, and Th22 cytokine production, which are key to PN. In addition, S. aureus V8 protease (Endoproteinase Glu-C) has recently been identified to trigger robust itch by activating protease-activated receptor 1 (PAR1) on sensory neurons. Overall, this review underscores the complex interplay between the altered microbiome and the itch-scratch cycle of PN, providing insights into potential therapeutics targeting the skin microbiome. A multidisciplinary approach is crucial for providing relief to individuals suffering from this skin condition.

Prurigo nodularis (PN) is a chronic inflammatory skin condition characterized by firm, itchy nodules and relentless itch. PN was first described in the 19^th century. Following observations of various dermatologists, the clinical presentation was officially given a name in 1909 by James Nevins Hyde. Throughout the 1900s, PN gained pockets of attention concerning its histopathologic features, epidemiology, and pathophysiology, although it existed as a largely ambiguous disease for many years. Only at the turn of the 21^st century was the recognition of PN reignited, prompting extensive research and leading to striking advancements in our understanding of the mechanisms that had contributed to PN during the last decade. Despite a long and inconsistent course, there are now definitive immune and neural pathways that can be selectively targeted with novel therapies, suggesting a promising future for managing this debilitating condition.

Prurigo nodularis (PN) of Hyde is a highly pruritic condition that results from the vicious cycle of itching and scratching. An increasing number of case studies report PN-mimicking lesions in patients with confirmed autoimmune bullous dermatoses (AIBDs). The PN lesions usually precede the blister formation and thus raise the question about the pathogenic relation between the two conditions and the possible role of PN as a trigger of AIBDs. We shed light on PN in the context of AIBDs, especially about the clinical characteristics and the pathogenesis of the PN-like phenotype of bullous pemphigoid, linear IgA bullous dermatosis, and dermatitis herpetiformis, as well as in the hereditary bullous dermatoses setting, namely epidermolysis bullosa pruriginosa.

Prurigo nodularis (PN) is a distinct inflammatory dermatosis. It is characterized by intensely pruritic, firm nodules, typically 1-2 cm in diameter, which usually develop on the extensor surfaces of the extremities. Histopathologically, the following characteristics are observed in PN lesions: (1) dermal cellular infiltrates composed of type 2 inflammation-associated immune cells with lesional overexpression of type 2 cytokines (including IL-4, IL-13, and IL-31); (2) dermal fibrosis; and (3) epidermal hyperplasia with hyperkeratosis. Additionally, functional and structural alterations of cutaneous sensory nerve fibers profoundly contribute to itch in cooperation with type 2 inflammation. This abnormal interaction is referred to as neuroimmune dysregulation. The scratching behavior induced by itching from neuroimmune dysregulation initiates the development of prurigo nodules. This distinctive pathogenic feature of "itch-first" in PN is distinct from "inflammation-first" in atopic dermatitis, another pruritic skin disease with type 2 inflammation. In atopic dermatitis, the skin initially exhibits type 2 inflammation, which is subsequently followed by itching. The interplay between the four elements, namely type 2 inflammation, epidermal hyperplasia, dermal fibrosis, and itch resulting from neuroimmune dysregulation, appears to be pivotal in the pathogenesis and pathophysiology of PN.

Prurigo nodularis (PN) is a chronic inflammatory dermatologic condition that is often incredibly itchy and imposes a debilitating burden on patient quality of life. Historically, patients have faced the hurdles of limited knowledge regarding the mechanisms underlying PN, physician awareness, and effective therapies. Many of the conventional treatments offer minimal benefit or are accompanied by adverse effects. Fortunately, over the last several years, striking advancements in the understanding of the pathogenesis contributing to PN have allowed for the development of novel treatments. The first and only medication approved by the U.S. Food and Drug Administration is dupilumab, a biological agent targeting interleukins 4 and 13, that has revolutionized management for patients with moderate to severe PN. Several other drugs are on the horizon that have the potential to become widely available. This article aims to review the current and emerging therapies for prurigo nodularis, and address the challenges that may hinder effective treatment.

Prurigo nodularis (PN) has been reported in itchy chronic kidney disease (CKD) patients, in particular, in end-stage renal failure. Acquired perforating dermatitis (APD) associated with CKD and diabetes is a group of disorders where dermal materials are eliminated through the epidermis and is characterized by itchy papules and nodules. We focus on the relationship between PN and APD in CKD and provide data to support that both entities share many of the same clinical and histologic features. These cutaneous diseases often go underreported in this patient population, leading to inadequate treatment and suboptimal patient outcomes. Our review of the literature suggests a relationship between PN/APD and CKD, presumably driven by uremic pruritus, changes in the renin-angiotensin-aldosterone system, a predisposing immune dysregulation with increased IL-31 expression, and opioid system imbalances. A variety of pharmacologic therapies may be efficacious. The use of the new targeted biologics for PN and whether they are also helpful for CKD and APD are welcome..