- [A CASE OF CHILDHOOD-ONSET EOSINOPHILIC GRANULOMATOUS POLYANGIITIS WITH ASYMPTOMATIC MYOCARDIAL INVOLVEMENT WHO WAS DIAGNOSED AT MORE THAN 5 YEARS AFTER ONSET OF ATOPIC DERMATITIS AND BRONCHIAL ASTHMA]. [Journal Article]
- AArerugi 2019; 68(6):696-700
- Atopic dermatitis and bronchial asthma are common diseases in children. We report the development of eosinophilic polyangiitis granulomatosis (EGPA) in a young girl being treated for both atopic derm…
Atopic dermatitis and bronchial asthma are common diseases in children. We report the development of eosinophilic polyangiitis granulomatosis (EGPA) in a young girl being treated for both atopic dermatitis, diagnosed at 1 year of age, and bronchial asthma, diagnosed at 4 years of age. Her eruption did not result in lichenification and was not fully responsive to corticosteroid ointment. Asthma lightened by treatment of inhalational steroids. Hypereosinophilia was detected at 5 years of age, at least 20% of white blood cells, and 44% at 8 years of age. At 10 years of age, she was diagnosed with anti-neutrophil cytoplasmic antibody-negative EGPA. The diagnosis was based on findings of eosinophil-infiltrating granulomatous vasculitis of the skin accompanied by notable peripheral blood eosinophilia, sinusitis, and pulmonary nodules on radiographic evaluation. Asymptomatic myocardial involvement was also detected utilizing dual perfusion and metabolic scintigraphy with 201Tl/123I-BMIPP, which was relieved by 1-year treatment of glucocorticoid combined with immunosuppressive drugs. EGPA is an extremely rare vasculitis that develops several years after preceding allergic disorders. Pediatric-onset EGPA has a poorer prognosis than adult-onset EGPA, which can be attributed to a high prevalence of cardiac involvement. Therefore, accurate diagnosis is critical for improving prognosis. EGPA should be considered when atypical findings are noted in management of atopic dermatitis and bronchial asthma.
- Erythroderma and Chronic Lichenification Due to Metformin. [Journal Article]
- EJEur J Case Rep Intern Med 2019; 6(6):001119
- We present the case of a 62-year-old man with a 4-year history of pruritus and erythroderma. The patient had been taking metformin for 5 years, so after contact allergies, contact with toxic products…
We present the case of a 62-year-old man with a 4-year history of pruritus and erythroderma. The patient had been taking metformin for 5 years, so after contact allergies, contact with toxic products, and autoimmune diseases were ruled out, the condition was treated as erythroderma secondary to metformin. A skin biopsy subsequently confirmed the diagnosis and lichenification of some areas of the patient's skin.
- Atopic Dermatitis-Like Rash During Evolocumab Treatment of Familial Hypercholesterolemia. [Journal Article]
- JNJ Nippon Med Sch 2019; 86(3):187-190
- Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a serine protease that targets the low-density lipoprotein (LDL) receptor for lysosomal degradation. PCSK9 impedes the receptor-mediated clear…
Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a serine protease that targets the low-density lipoprotein (LDL) receptor for lysosomal degradation. PCSK9 impedes the receptor-mediated clearance of LDL-cholesterol, thereby increasing serum LDL-cholesterol levels. Evolocumab, a human monoclonal antibody against PCSK9, effectively reduces serum LDL-cholesterol levels. We report the first known case of a patient who developed an atopic dermatitis (AD)-like rash during evolocumab therapy. A 43-year-old Japanese man with heterozygous familial hypercholesterolemia was treated with subcutaneous injection of 140 mg evolocumab biweekly, for 16 months. The therapy was then changed to subcutaneous injection of 420 mg evolocumab monthly. A few days after the first dose, the patient experienced pruritus and rash on his extremities. The rash worsened, while the pruritus subsided, then relapsed after the second and third doses. He had erythema and excoriation on his legs, lichenification over his popliteal fossa, xerosis on his forearms, an increased serum IgE level, and a family history of AD in his siblings. We made a provisional diagnosis of AD characterized by enhanced type 2 helper T (Th2) activity and treated him with topical corticosteroids and oral anti-histamines. His rash improved and did not relapse after the fifth dose; however, his LDL-cholesterol level increased. PCSK9 or oxidized LDL activates macrophages or dendritic cells, respectively, and enhances their activity to induce Th1 cells antagonizing Th2 cells. We hypothesized that high-dose evolocumab may suppress Th1 activity to antagonize Th2, and unmask Th2 disposition based on the patient's atopic diathesis, triggering the rash mimicking AD. Clinicians should be aware of rash development during evolocumab therapy.
- Emerging Methods to Objectively Assess Pruritus in Atopic Dermatitis. [Review]
- DTDermatol Ther (Heidelb) 2019 Jun 29
- CONCLUSIONS: The variety of new and improved methods to evaluate pruritus in AD is welcomed by clinicians, researchers, and patients alike. Future directions include next-generation smart devices as well as exploring new territories, such as identifying biomarkers that correlate to itch and machine-learning programs to identify itch processing in the brain. As these efforts continue, it will be essential to remain patient-centered by developing techniques that minimize discomfort, respect privacy, and provide accurate data that can be used to better manage itch in AD.
- Clinical Review Report: Crisaborole Ointment, 2% (Eucrisa): (Pfizer Canada Inc.): Indication: For topical treatment of mild to moderate atopic dermatitis in patients 2 years of age and older [BOOK]
- BOOKCanadian Agency for Drugs and Technologies in Health: Ottawa (ON)
- Atopic dermatitis (AD) is a chronic, relapsing, and inflammatory skin condition, characterized by eczematous lesions, pruritus, and dry skin. Pruritus of the skin causes frequent scratching and may r…
Atopic dermatitis (AD) is a chronic, relapsing, and inflammatory skin condition, characterized by eczematous lesions, pruritus, and dry skin. Pruritus of the skin causes frequent scratching and may result in lichenification (thickening of the skin) and secondary skin infections. The symptoms of AD wax and wane and disease severity can range from mild to severe disease. AD begins in early childhood with the majority of cases beginning before the age of five years. Although childhood symptoms resolve by adolescence, some patients’ AD symptoms will persist or develop in adulthood. The Canadian Dermatology Association reported that the lifetime prevalence of AD is up to 17%, and there is evidence to suggest that the prevalence has increased over the past 30 years. The goal of AD management is to prevent and manage flare-ups, which are recurrent episodes of worsening of symptoms that require an escalation of treatment. Although there is no cure for AD, there are several therapeutic options available to patients. The majority of patients treat AD using general skin care methods and topical anti-inflammatory therapies. However, if these practices fail to improve AD symptoms, patients may use off-label systemic immune-modulating agents or other therapies, such as phototherapy. The most commonly pharmaceutical topical therapies for patients with AD include topical corticosteroids (TCS) and topical calcineurin inhibitors (TCI). TCS are anti-inflammatory agents that act to control flare-ups and they are considered a first-line therapy for patients with AD. Side effects associated with long-term use of TCS include striae (stretch marks), petechiae (small red or purple spots), telangiectasia (small, dilated blood vessels on the surface of the skin), skin thinning, atrophy, and acne. On the other hand, TCI are steroid-free, anti-inflammatory, immunosuppressant agents. In Canada, TCIs are used in the second-line setting for patients who exhibit steroid phobia or where the use of steroids is not advisable. The most common adverse event associated with TCI therapy is application site–specific burning and irritation. Crisaborole is a low-molecular-weight benzoxaborole, nonsteroidal, topical ointment. Crisaborole inhibits phosphodiesterase type 4 (PDE4), which regulates inflammatory cytokine production. It is applied in a thin layer to the affected area, twice daily. The current CADTH Common Drug Review (CDR) submission for crisaborole is for the treatment of patients two years of age and older with mild-to-moderate AD.
- Safety and efficacy of hydroxytyrosol-based formulation on skin inflammation: in vitro evaluation on reconstructed human epidermis model. [Journal Article]
- DARUDaru 2019; 27(1):283-293
- CONCLUSIONS: In light of these results, Fenolia® Eudermal Cream 15 could be an effective agent to counteract atopic dermatitis. Graphical abstract Safety and efficacy of hydroxytyrosol-based formulation on skin inflammation: in vitro evaluation on reconstructed human epidermis model.
- Control of fly strike dermatitis in dogs with a topically applied combination of imidacloprid and permethrin: a prospective open-label controlled clinical trial. [Journal Article]
- PVParasit Vectors 2019 Mar 21; 12(1):132
- CONCLUSIONS: The combination imidacloprid-permethrin proved safe and helpful in the management of natural canine fly dermatitis. It could also be suggested as a preventive measure with a monthly application during the fly exposition phase.
- Stratum corneum interleukin-33 expressions correlate with the degree of lichenification and pruritus in atopic dermatitis lesions. [Letter]
- CIClin Immunol 2019; 201:1-3
- StatPearls: Lichenification [BOOK]
- BOOKStatPearls Publishing: Treasure Island (FL)
- Basic skin lesions divide into primary, secondary and special types. The term lichenification is classed as a secondary skin lesion wherein the characteristic features of skin thickening, hyperpigmen…
Basic skin lesions divide into primary, secondary and special types. The term lichenification is classed as a secondary skin lesion wherein the characteristic features of skin thickening, hyperpigmentation, and increased skin markings are noted. Lichenification can be further divided into primary and secondary types wherein primary lichenification signifies lichen simplex chronicus, also known as neurodermatitis circumscripta. On the other hand, secondary lichenification occurs in atopic dermatitis, infective eczematous dermatoses, psoriasis, psoriasiform dermatosis, xerosis, pityriasis rubra pilaris, porokeratosis, vegetative growths, anxiety, and obsessive-compulsive disorders.
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- Dermatological aspects of the S2k guidelines on Down syndrome in childhood and adolescence. [Journal Article]
- JDJ Dtsch Dermatol Ges 2018; 16(10):1289-1295
- With an incidence of 1 in 700 births, Down syndrome (DS) is not an uncommon condition. It is associated with various disorders of different organ systems. Serious disorders include cardiac defects an…
With an incidence of 1 in 700 births, Down syndrome (DS) is not an uncommon condition. It is associated with various disorders of different organ systems. Serious disorders include cardiac defects and leukemia. With an onset during the newborn period, the latter does not always progress to classic myeloid leukemia (transient myeloproliferative disorder). Skin manifestations in newborns include pustules/vesiculopustules. In individuals with DS, such lesions should not only prompt suspicion for typical neonatal rashes and infections but also for transient myeloproliferative disorder. However, most dermatoses are benign. They essentially comprise disorders of keratinization that present as xerosis, keratosis pilaris, lichenification, and ichthyosis vulgaris. Also typical but not specific is the four-finger palmar crease (simian crease). Patients frequently develop folliculitides, which - due to elastolysis - subsequently progress to anetoderma. The known immune disturbance in DS patients explains the occurrence of autoimmune diseases such as alopecia areata and vitiligo. Typical skin conditions associated with DS include elastosis perforans serpiginosa, syringomas, milia-like calcinosis cutis, and multiple eruptive dermatofibromas.