China
Africa
Explore chapters and articles related to this topic
Monographs of Topical Drugs that Have Caused Contact Allergy/Allergic Contact Dermatitis
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
A 62-year-old man presented with widespread numerous symmetrically distributed non-follicular pustules on an erythematous base, primarily on his forearms and antecubital fossae and a crusted dermatitis affecting his right foot, thighs and both hands. No bacteria or fungi were cultured from the pustules. Histopathology was consistent with acute generalize exanthematous pustulosis (AGEP) and it was suspected that this had been caused by the antibiotics that the patient had received for the lesions on his foot. He was treated with topical betamethasone valerate and oral prednisolone and 4 days later the skin had recovered almost completely. Patch tests were positive to budesonide and hydrocortisone butyrate, pustules were not observed. The patient now told that, in addition to the oral antibiotics, he had used a topical corticosteroid containing hydrocortisone butyrate from the early onset of the skin symptoms. Tests for penicillin allergy were negative and it was concluded that the patient’s AGEP-like eruption was a manifestation of allergic contact dermatitis to hydrocortisone butyrate (45).
Management of Difficult Vitiligo (Acral, Genital, Lips, Palms, and Soles)
Published in Vineet Relhan, Vijay Kumar Garg, Sneha Ghunawat, Khushbu Mahajan, Comprehensive Textbook on Vitiligo, 2020
Sanjeev Gupta, Swetalina Pradhan
Topical corticosteroids are the first-line therapy for localized vitiligo. High-potency fluorinated corticosteroid (e.g., clobetasol propionate ointment, 0.05%) are given for 1–2 months. Treatment can be gradually tapered to a lower potency corticosteroid (e.g., hydrocortisone butyrate cream, 0.1%). It is very important to observe the side effects of topical steroids during treatment.
Introduction
Published in John Y. M. Koo, Ethan C. Levin, Argentina Leon, Jashin J. Wu, Mark G. Lebwohl, Mild to Moderate Psoriasis, 2014
Unfortunately, advances in topical therapy lag behind the exciting new developments in systemic treatments. Some new topical therapies are in development and the efficacy of older topical therapies have been enhanced. For example, vehicles have been advanced. Previously, only triamcinolone acetonide was available in spray form. Now, clobetasol and desoximetasone are both available as sprays. The combination of calcipotriene and betamethasone dipropionate has been available in an ointment form for years. Most recently, a suspension has been approved for the scalp and body. Previously, there were only a few topical corticosteroids approved for pediatric use, but in recent years, fluticasone lotion and hydrocortisone butyrate lotion have also been approved for use in pediatrics. There are no new topical calcineurin inhibitors, but much information is available about the safety of calcineurin inhibitors, thereby reducing some of the concerns that emerged when a black box warning was added to the package inserts of tacrolimus ointment and pimecrolimus cream. Both of these agents have been successfully used for psoriasis of the face and intertriginous sites, but neither of them is approved for psoriasis. Numerous topical vitamin D analogs and topical tazarotene are still available for psoriasis. Topical tar preparations and anthralin are still in use. In terms of new agents, topical Janus kinase inhibitors and a combination product consisting of calcipotriene and nicotinamide are in development.
Safety and efficacy of Pimecrolimus in atopic dermatitis among Chinese infants: a sub-group analysis of a five-year open-label study
Published in Journal of Dermatological Treatment, 2023
Xia Dou, Lingling Liu, Xuejun Zhu, Weijing Wen, Chunya Ni, Yi Zhao, Zhixin He, Hongchun Li, Qiuning Sun, Qinping Yang, Xinfen Sun, Yifeng Guo
This is a sub-group analysis of the PETITE study (www.clinicaltrials.gov identifier NCT00120523) published by Sigurgeirsson et al. (11). Patients were randomized in a 1:1 ratio to either PIM 1% cream or TCS (low potency, e.g., hydrocortisone 1%; or medium potency, e.g., hydrocortisone butyrate 0.1% cream/ointment used according to the country’s label with potency selected by the investigator). Randomization was stratified by center and age group (3–6 and 6–, 12 months) using a validated Interactive Voice Response System. Study medication was started immediately after randomization and continued until complete AD clearance or for as long as allowed by the label of the specific TCS. Medication was reinitiated at the occurrence of first signs and symptoms of AD flares. In both the treatment groups, investigators explained to caregivers of patients what constituted disease worsening and, to patients in the PIM group, when to stop PIM and start using a TCS, as a rescue medication for an exacerbation not controlled by PIM. The study was conducted in accordance with Good Clinical Practice and the Declaration of Helsinki. The study protocol was approved by the Independent Ethics Committee or Institutional Review Board for each center. Caregivers provided written informed consent for infants’ participation in the study.
An overview of drug discovery efforts for eczema: why is this itch so difficult to scratch?
Published in Expert Opinion on Drug Discovery, 2020
Kam Lun Hon, Steven Loo, Alexander K. C. Leung, Joyce T. S. Li, Vivian W. Y. Lee
Children and adults with AD suffer from sleep loss/disturbance, daytime tiredness, irritability, lowered self-esteem, emotional stress and psychological symptomatology [148]. Quality of life is often impaired in both the patients and their family members [148–151]. Pruritus is a hallmark of AD. It is induced by various mediators. Pruriceptive primary sensory nerves (i.e. C-fibers) transmit the histamine-dependent and independent pruritogen-induced signal of itch through cutaneous afferent fibers to the spinal cord. Immune cells release histamine and activate the histamine receptors H1R and H4R. Mas-related G protein–coupled receptors and gastrin-releasing peptide receptor mediate the itch sensation in the C-fiber and dorsal spinal cord, respectively for histamine-independent pruritus. Also, neural sensitization causes an increase in the sensitivity of itch-selective neurons leading to chronic itch [152,153]. Itch induced by hyperinnervation is due to an imbalance of nerve repulsion factors (e.g. semaphorin 3A) and nerve elongation factors (e.g. nerve growth factor and IL-31). In an NC/Nga AD mouse model, topical application of semaphorin 3A ointment inhibited the behavior of scratching and ameliorates skin inflammation [154]. Dysfunctional and attenuated inhibitory neurons in spinal cord, in addition to structural and functional changes in brain, also contribute to itch sensation in chronic itching [152,153,155]. Scratching activates signal transducer and activator of transcription 3 (STAT3) in spinal dorsal horn astrocytes. Lipocalin 2 then sensitizes a pruritus-processing neuronal network and contributes to the vicious cycle of chronic pruritus. In mice and human subjects, Th2 cells and IL-31 receptor A produce IL-31. In a phase 2 clinical trial, monthly injections of an anti–IL-31 receptor A antibody (Nemolizumab) significantly inhibits pruritus in patients with moderate-to-severe AD [87]. Nemolizumab further decreased the use of topical hydrocortisone butyrate and improved sleep efficiency in the trial [87].