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Blistering skin disorders
Published in Rashmi Sarkar, Anupam Das, Sumit Sethi, Concise Dermatology, 2021
Skin lesions respond rapidly to the drug dapsone (50–200 mg per day) in most patients. However, dapsone has several potential toxic side effects, including haemolysis, methaemoglobinaemia, and sulfaemoglobinaemia, and may itself cause rashes such as fixed drug eruption. It should not be given to patients with glucose 6-phosphate dehydrogenase deficiency. A gluten-free diet will improve the gastrointestinal lesion and skin disorder in many patients after some months. Topical superpotent corticosteroids, though not useful alone, may help alleviate pruritus when given along with dapsone.
Infectious Diseases
Published in Paul Bentley, Ben Lovell, Memorizing Medicine, 2019
Medical: Dapsone + clofazimine + rifampicin Duration: 6 months (tuberculoid leprosy); 2 years or more (lepromatous leprosy)Dapsone: Neuropathy, erythema nodosum; N+V; Clofazimine: Blue-black skin lesions, red urineSteroids may be needed if lesions worsen acutely on starting Rx (‘reversal reaction’)
Autologous Stem Cell Transplantation in Relapsing Polychondritis
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Falk Hiepe, Andreas Thiel, Oliver Rosen, Gero Massenkeil, Gerd-Rüdiger Burmester, Andreas Radbruch, Renate Arnold
Nonsteroidal anti-inflammatory drugs can control mild episodes of inflammation in a few cases. Low-dose colchicine may also be helpful.13 In most cases, however, corticosteroids are needed to suppress disease activity. They reduce the frequency, duration and severity of flares, but do not stop the progression of relapsing polychondritis in severe cases.12 Prednisolone (1 mg/kg) is indicated in patient with serious manifestations. Many immunosuppressive drugs have been used in attempts to allow tapering of the steroid dose, to achieve a lower maintenance dose, or to treat refractory cases. These include dapsone.30,31 penicillamine,32 azathioprine12,33 cyclophosphamide,2,29,33 cyclosporine,34 methotrexate,35 and monoclonal anti-CD4 antibody.36,37
D-optimal mixture design for optimization of topical dapsone niosomes: in vitro characterization and in vivo activity against Cutibacterium acnes
Published in Drug Delivery, 2022
Basant A. Habib, Nourtan F. Abdeltawab, Ibtehal Salah Ad-Din
Dapsone (a sulfone class drug) which was discovered in 1908 has a bacteriostatic action and an anti-inflammatory activity in diseases characterized by abnormal accumulation of neutrophils (Sago & Hall, 2002). For these reasons, Dapsone can be used in the treatment of acne which affects most of the teenagers. It can alleviate symptoms associated with this skin disease (Draelos et al., 2007). Unfortunately, its oral use is limited due to its low water solubility and harmful side effects like hemolytic anemia, headache, and nausea (Pickert & Raimer, 2009). Topical delivery of Dapsone removes all barriers that complicate its oral use and at the same time facilitates application to the patients (Schneider-Rauber et al., 2020). Although Allergan Company produces Dapsone gel 7.5% (ACZONE® Gel), yet it is expensive enough to trigger researchers for searching for new formulations. Shamma et al. (2019) prepared Dapsone gel after complexation of Dapsone with cyclodextrin. Also, other literature showed formulation of topical Dapsone by different techniques (El-Nabarawi et al., 2018, 2020).
Genetic markers of drug hypersensitivity in pediatrics: current state and promise
Published in Expert Review of Clinical Pharmacology, 2022
Abdelbaset A. Elzagallaai, Michael J. Rieder
An association between the HLA-B*13:01 allele and dapsone-induced SCARs has been reported [148–150]; however, these studies did not specifically look at these reactions in pediatric population. Satapornpong et al. [124] genotypes 16 dapsone-induced SCARs patients (median age of 45 years; range: 2.5–64 year) and 40 drug-tolerant cohort (median age 41.5 years; range: 4–74 year) and found HLA-B* 13:01 to be significantly associated with dapsone-induced SCARs (OR = 39.00, 95% CI = 7.67–198.21, p = 5.3447 × 10−7) as compared to drug-tolerant controls. In a very recent small study, Park et al. [42] studies 7 dapsone-hypersensitive patients (including an 11-year-old boy) and 8 drug-tolerant controls. HLA-B*13:01 allele was present in 6 out of 7 patients. They also described a new variant of the allele that has not been previously reported in one of the participants. Tempark et al. [148] genotyped 15 Thai patients with dapsone-induced SCARs (11 DRESS and 4 SJS/TEN) and 29 controls including 2-year-old girl with Dapsone-induced DRESS. Compared with the drug-tolerant group HLA-B*13:01 allele was found to be significantly associated with dapsone-induced SCARs (odds ratio: 54.00, 95% confidence interval: 7.96–366.16, P = 0.0001).
Hidradenitis suppurativa for the nondermatology clinician
Published in Baylor University Medical Center Proceedings, 2020
Kavina Patel, Lucy Liu, Benjamin Ahn, Annika S. Silfvast-Kaiser, So Yeon Paek
Other systemic antibiotics include oral dapsone as well as a combination of twice-daily rifampin 300 mg, moxifloxacin 400 mg once daily, and metronidazole 500 mg three times daily. Oral dapsone at 25 to 200 mg for 4 to 12 weeks is recommended for those unresponsive to other antibiotic therapies. A retrospective review of patients with Hurley stage I and II disease showed a response rate of 38% to oral dapsone.26 Dapsone may cause hemolytic anemia, methemoglobinemia, cyanosis of the lips, and neuropathy. The use of dapsone as third-line therapy is supported by all guidelines. A retrospective review of 28 patients taking rifampin-moxifloxacin-metronidazole combination therapy for 1 to 12 months showed that 6 of 6 patients with Hurley stage I disease, 8 of 10 with Hurley stage II disease, and 2 of 12 with Hurley stage III disease had complete remission.27 Longer-term use of this combination, however, may lead to increased risk of hepatotoxicity. The use of rifampin-moxifloxacin-metronidazole is supported by the North American and HS ALLIANCE guidelines as second- or third-line therapy in Hurley stage II/III disease.