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American Family Physician Jul 2019Erythema multiforme is an immune-mediated reaction that involves the skin and sometimes the mucosa. Classically described as target-like, the erythema multiforme lesions... (Review)
Review
Erythema multiforme is an immune-mediated reaction that involves the skin and sometimes the mucosa. Classically described as target-like, the erythema multiforme lesions can be isolated, recurrent, or persistent. Most commonly, the lesions of erythema multiforme present symmetrically on the extremities (especially on extensor surfaces) and spread centripetally. Infections, especially herpes simplex virus and Mycoplasma pneumoniae, and medications constitute most of the causes of erythema multiforme; immunizations and autoimmune diseases have also been linked to erythema multiforme. Erythema multiforme can be differentiated from urticaria by the duration of individual lesions. Erythema multiforme lesions are typically fixed for a minimum of seven days, whereas individual urticarial lesions often resolve within one day. Erythema multiforme can be confused with the more serious condition, Stevens-Johnson syndrome; however, Stevens-Johnson syndrome usually contains widespread erythematous or purpuric macules with blisters. The management of erythema multiforme involves symptomatic treatment with topical steroids or antihistamines and treating the underlying etiology, if known. Recurrent erythema multiforme associated with the herpes simplex virus should be treated with prophylactic antiviral therapy. Severe mucosal erythema multiforme can require hospitalization for intravenous fluids and repletion of electrolytes.
Topics: Erythema Multiforme; Humans
PubMed: 31305041
DOI: No ID Found -
American Journal of Clinical Dermatology May 2021Erythema nodosum is the most common form of panniculitis and is characterized by tender erythematous nodules mainly in the lower limbs on the pretibial area. The exact... (Review)
Review
Erythema nodosum is the most common form of panniculitis and is characterized by tender erythematous nodules mainly in the lower limbs on the pretibial area. The exact cause of erythema nodosum is unknown, although it appears to be a hypersensitivity response to a variety of antigenic stimuli. Although the etiology is mostly idiopathic, ruling out an underlying disease is imperative before diagnosing primary erythema nodosum. Erythema nodosum can be the first sign of a systemic disease that is triggered by a large group of processes, such as infections, inflammatory diseases, neoplasia, and/or drugs. The most common identifiable causes are streptococcal infections, primary tuberculosis, sarcoidosis, Behçet disease, inflammatory bowel disease, drugs, and pregnancy. We propose a diagnostic algorithm to optimize the initial work-up, hence initiating prompt and accurate management of the underlying disease. The algorithm includes an initial assessment of core symptoms, diagnostic work-up, differential diagnosis, and recommended therapies. Several treatment options for the erythema nodosum lesions have been previously reported; nevertheless, these options treat the symptoms, but not the triggering cause. Making an accurate diagnosis will allow the physician to treat the underlying cause and determine an optimal therapeutic strategy.
Topics: Anti-Inflammatory Agents; Diagnosis, Differential; Drug Therapy, Combination; Erythema Nodosum; Humans; Incidence; Skin; Treatment Outcome
PubMed: 33683567
DOI: 10.1007/s40257-021-00592-w -
American Journal of Clinical Dermatology May 2022Sweet syndrome (SS), or acute febrile neutrophilic dermatosis, is an inflammatory, non-infectious skin reaction characterized clinically by tender, erythematous... (Review)
Review
Sweet syndrome (SS), or acute febrile neutrophilic dermatosis, is an inflammatory, non-infectious skin reaction characterized clinically by tender, erythematous papules/plaques/pustules/nodules commonly appearing on the upper limbs, trunk, and head and neck; histologically, SS is characterized by dense neutrophilic infiltrate in the dermis. SS is accompanied by fever; an elevation of inflammatory markers (e.g., erythrocyte sedimentation rate, C reactive protein) in serum may also be observed. Although most cases of SS are idiopathic, SS also occurs in the setting of malignancy or following administration of an associated drug. SS has also been reported in association with pregnancy and a burgeoning list of infectious (most commonly upper respiratory tract infections) and inflammatory diseases; likewise, the litany of possible iatrogenic triggers has also grown. Over the past several years, a wider spectrum of SS presentation has been realized, with several reports highlighting novel clinical and histological variants. Corticosteroids continue to be efficacious first-line therapy for the majority of patients with SS, although novel steroid-sparing agents have been recently added to the therapeutic armamentarium against refractory SS. New mechanisms of SS induction have also been recognized, although the precise etiology of SS still remains elusive. Here, we catalogue the various clinical and histological presentations of SS, summarize recently reported disease associations and iatrogenic triggers, and review treatment options. We also attempt to frame the findings of this review in the context of established and emerging paradigms of SS pathogenesis.
Topics: Adrenal Cortex Hormones; Humans; Iatrogenic Disease; Neck; Skin; Sweet Syndrome
PubMed: 35157247
DOI: 10.1007/s40257-022-00673-4 -
F1000Research 2020Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are life-threatening diseases characterized by detachment of the epidermis and mucous membrane.... (Review)
Review
Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are life-threatening diseases characterized by detachment of the epidermis and mucous membrane. SJS/TEN are considered to be on the same spectrum of diseases with different severities. They are classified by the percentage of skin detachment area. SJS/TEN can also cause several complications in the liver, kidneys, and respiratory tract. The pathogenesis of SJS/TEN is still unclear. Although it is difficult to diagnose early stage SJS/TEN, biomarkers for diagnosis or severity prediction have not been well established. Furthermore, optimal therapeutic options for SJS/TEN are still controversial. Several drugs, such as carbamazepine and allopurinol, are reported to have a strong relationship with a specific human leukocyte antigen (HLA) type. This relationship differs between different ethnicities. Recently, the usefulness of HLA screening before administering specific drugs to decrease the incidence of SJS/TEN has been investigated. Skin detachment in SJS/TEN skin lesions is caused by extensive epidermal cell death, which has been considered to be apoptosis via the Fas-FasL pathway or perforin/granzyme pathway. We reported that necroptosis, i.e. programmed necrosis, also contributes to epidermal cell death. Annexin A1, released from monocytes, and its interaction with the formyl peptide receptor 1 induce necroptosis. Several diagnostic or prognostic biomarkers for SJS/TEN have been reported, such as CCL-27, IL-15, galectin-7, and RIP3. Supportive care is recommended for the treatment of SJS/TEN. However, optimal therapeutic options such as systemic corticosteroids, intravenous immunoglobulin, cyclosporine, and TNF-α antagonists are still controversial. Recently, the beneficial effects of cyclosporine and TNF-α antagonists have been explored. In this review, we discuss recent advances in the pathophysiology and management of SJS/TEN.
Topics: Apoptosis; Epidermis; Humans; Necrosis; Stevens-Johnson Syndrome
PubMed: 32595945
DOI: 10.12688/f1000research.24748.1 -
Journal of the American Academy of... Mar 2024Seborrheic dermatitis (SD) is a common skin disease with signs and symptoms that may vary by skin color, associated medical conditions, environmental factors, and... (Review)
Review
Seborrheic dermatitis (SD) is a common skin disease with signs and symptoms that may vary by skin color, associated medical conditions, environmental factors, and vehicle preference. Diagnosis of SD is based on presence of flaky, "greasy" patches, and/or thin plaques accompanied by erythema of the scalp, face, ears, chest, and groin and is associated with pruritus in many patients. The presentation may vary in different skin types and hyper- or hypopigmentation may occur, with or without erythema and minimal or no scaling. While the pathogenesis is not certain, 3 key factors generally agreed upon include lipid secretion by sebaceous glands, Malassezia spp. colonization, and some form of immunologic dysregulation that predisposes the patient to SD. Treatment involves reducing proliferation of, and inflammatory response to, Malassezia spp. Topical therapies, including antifungal agents and low potency corticosteroids, are the mainstay of treatment but may be limited by efficacy and side effects. Few novel treatments for SD are currently being studied; however, clinical trials assessing the use of topical phosphodiesterase-4 inhibitors have been completed. Improving outcomes in SD requires recognizing patient-specific manifestations/locations of the disease, including increased awareness of how it affects people of all skin types.
Topics: Humans; Dermatitis, Seborrheic; Antifungal Agents; Adrenal Cortex Hormones; Erythema; Malassezia
PubMed: 36538948
DOI: 10.1016/j.jaad.2022.12.017 -
Journal of the American Academy of... May 2021Cutaneous photobiology studies have focused primarily on the ultraviolet portion of the solar spectrum. Visible light (VL), which comprises 50% of the electromagnetic... (Review)
Review
Cutaneous photobiology studies have focused primarily on the ultraviolet portion of the solar spectrum. Visible light (VL), which comprises 50% of the electromagnetic radiation that reaches the Earth's surface and, as discussed in Part I of this CME, has cutaneous biologic effects, such as pigment darkening and erythema. Photoprotection against VL includes avoiding the sun, seeking shade, and using photoprotective clothing. The organic and inorganic ultraviolet filters used in sunscreens do not protect against VL, only tinted sunscreens do. In the United States, these filters are regulated by the Food and Drug Administration as an over-the-counter drug and are subject to more stringent regulations than in Europe, Asia, and Australia. There are no established guidelines regarding VL photoprotection. Alternative measures to confer VL photoprotection are being explored. These novel methods include topical, oral, and subcutaneous agents. Further development should focus on better protection in the ultraviolet A1 (340-400 nm) and VL ranges while enhancing the cosmesis of the final products.
Topics: Administration, Cutaneous; Administration, Oral; Erythema; Humans; Injections, Subcutaneous; Radiation-Protective Agents; Skin; Skin Pigmentation; Sunlight; Treatment Outcome; Ultraviolet Rays
PubMed: 33640513
DOI: 10.1016/j.jaad.2020.11.074 -
American Journal of Clinical Dermatology Jul 2023Acute generalized exanthematous pustulosis (AGEP) is a rare, acute, severe cutaneous adverse reaction mainly attributed to drugs, although other triggers, including... (Review)
Review
Acute generalized exanthematous pustulosis (AGEP) is a rare, acute, severe cutaneous adverse reaction mainly attributed to drugs, although other triggers, including infections, vaccinations, ingestion of various substances, and spider bites, have also been described. AGEP is characterized by the development of edema and erythema followed by the eruption of multiple punctate, non-follicular, sterile pustules and subsequent desquamation. AGEP typically has a rapid onset and prompt resolution within a few weeks. The differential diagnoses for AGEP are broad and include infectious, inflammatory, and drug-induced etiologies. Diagnosis of AGEP depends on both clinical and histologic criteria, as cases of overlap with other disease processes have been reported. Management includes removal of the offending drug or treatment of the underlying cause, if necessary, and supportive care, as AGEP is a self-limited disease. This review aims to provide an overview and update on the epidemiology, pathogenesis, reported precipitating factors, differentials, diagnosis, and management of AGEP.
Topics: Humans; Acute Generalized Exanthematous Pustulosis; Diagnosis, Differential; Skin; Exanthema; Erythema
PubMed: 37156992
DOI: 10.1007/s40257-023-00779-3 -
Medicina (Kaunas, Lithuania) Sep 2021Erythema multiforme (EM) is an immune-mediated condition that classically presents with discrete targetoid lesions and can involve both mucosal and cutaneous sites.... (Review)
Review
Erythema multiforme (EM) is an immune-mediated condition that classically presents with discrete targetoid lesions and can involve both mucosal and cutaneous sites. While EM is typically preceded by viral infections, most notably herpes simplex virus (HSV), and certain medications, a large portion of cases are due to an unidentifiable cause. EM can be confused with other more serious conditions like Stevens-Johnson syndrome (SJS); however, clinical research has provided significant evidence to classify EM and SJS as separate disorders. Treatment of EM is highly variable, depending on the etiology, the involvement of mucosal sites, and the chronicity (acute vs. recurring) of the disease. If the etiology or causal medication/infection is identified, then the medication is stopped and/or the infection is treated prior to initiating symptomatic treatment. Treatment for acute EM is focused on relieving symptoms with topical steroids or antihistamines. Treatment for recurrent EM is most successful when tailored to individual patients. First line treatment for recurrent EM includes both systemic and topical therapies. Systemic therapies include corticosteroid therapy and antiviral prophylaxis. Topical therapies include high-potency corticosteroids, and antiseptic or anesthetic solutions for mucosal involvement. Second-line therapies for patients who do not respond to antiviral medications include immunosuppressive agents, antibiotics, anthelmintics, and antimalarials.
Topics: Antiviral Agents; Erythema Multiforme; Humans; Simplexvirus; Skin; Stevens-Johnson Syndrome
PubMed: 34577844
DOI: 10.3390/medicina57090921 -
The Australasian Journal of Dermatology Aug 2020Facial aesthetic treatment with injectable neuromodulators and hyaluronic acid fillers is well established, with favourable safety profiles and consistent outcomes. As... (Review)
Review
Facial aesthetic treatment with injectable neuromodulators and hyaluronic acid fillers is well established, with favourable safety profiles and consistent outcomes. As with any medical treatment, adverse events and complications may occur. Adverse events associated with these products are typically transient and mild to moderate in severity. Serious adverse events, such as infection and intravascular occlusion, are rare. Proper patient selection, consent and counselling, preparation and impeccable injection technique are important risk reduction strategies. Both clinicians and patients must be alert to the signs and symptoms of complications so that appropriate treatment can be started promptly. In this article, the authors review the current literature and provide their consensus recommendations for minimising adverse outcomes when treating patients with botulinum toxin or hyaluronic acid fillers.
Topics: Botulinum Toxins, Type A; Consensus; Contusions; Cosmetic Techniques; Dermal Fillers; Directive Counseling; Edema; Erythema; Face; Hematoma; Humans; Hyaluronic Acid; Injection Site Reaction; Injections; Neuromuscular Agents; Pain; Patient Education as Topic; Patient Selection
PubMed: 32201935
DOI: 10.1111/ajd.13273 -
Ophthalmology Oct 2023To evaluate the safety and efficacy of lotilaner ophthalmic solution 0.25% compared with vehicle for the treatment of Demodex blepharitis. (Randomized Controlled Trial)
Randomized Controlled Trial
PURPOSE
To evaluate the safety and efficacy of lotilaner ophthalmic solution 0.25% compared with vehicle for the treatment of Demodex blepharitis.
DESIGN
Prospective, randomized, double-masked, vehicle-controlled, multicenter, phase 3 clinical trial.
PARTICIPANTS
Four hundred twelve patients with Demodex blepharitis were assigned randomly in a 1:1 ratio to receive either lotilaner ophthalmic solution 0.25% (study group) or vehicle without lotilaner (control group).
METHODS
Patients with Demodex blepharitis treated at 21 United States clinical sites were assigned either to the study group (n = 203) to receive lotilaner ophthalmic solution 0.25% or to the control group (n = 209) to receive vehicle without lotilaner bilaterally twice daily for 6 weeks. Collarettes and erythema were graded for each eyelid at screening and at all visits after baseline. At screening and on days 15, 22, and 43, 4 or more eyelashes were epilated from each eye, and the number of Demodex mites present on the lashes was counted with a microscope. Mite density was calculated as the number of mites per lash.
MAIN OUTCOME MEASURES
Outcome measures included collarette cure (collarette grade 0), clinically meaningful collarette reduction to 10 collarettes or fewer (grade 0 or 1), mite eradication (0 mites/lash), erythema cure (grade 0), composite cure (grade 0 for collarettes as well as erythema), compliance with the drop regimen, drop comfort, and adverse events.
RESULTS
At day 43, the study group achieved a statistically significant (P < 0.0001) higher proportion of patients with collarette cure (56.0% vs. 12.5%), clinically meaningful collarette reduction to 10 collarettes or fewer (89.1% vs. 33.0%), mite eradication (51.8% vs. 14.6%), erythema cure (31.1% vs. 9.0%), and composite cure (19.2% vs. 4.0%) than the control group. High compliance with the drop regimen (mean ± standard deviation, 98.7 ± 5.3%) in the study group was observed, and 90.7% of patients found the drops to be neutral to very comfortable.
CONCLUSIONS
Twice-daily treatment with lotilaner ophthalmic solution 0.25% for 6 weeks generally was safe and well tolerated and met the primary end point and all secondary end points for the treatment of Demodex blepharitis compared with vehicle control.
FINANCIAL DISCLOSURE(S)
Proprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article.
Topics: Animals; Humans; Mite Infestations; Prospective Studies; Ophthalmic Solutions; Blepharitis; Mites; Eyelashes; Erythema; Eye Infections, Parasitic
PubMed: 37285925
DOI: 10.1016/j.ophtha.2023.05.030