dapsone
Regulatory sources consulted
Approved indications
- Dermatitis herpetiformis and leprosy as part of multidrug therapy.
Contraindications
Absolute
- Hypersensitivity to dapsone or sulfones.
Clinical warnings
- It may cause agranulocytosis, aplastic anemia, and other fatal blood dyscrasias. Obtain weekly blood counts for the first month, monthly for 6 months, then every 6 months; discontinue for a significant decline. — DailyMed, set_id 839d7440-ba0e-4c56-b648-d374b155cf03
- It may cause dose-dependent hemolysis and methemoglobinemia, more severe with G6PD deficiency or cardiopulmonary disease; correct severe anemia before starting. — DailyMed, set_id 839d7440-ba0e-4c56-b648-d374b155cf03
- Discontinue for SCAR, TEN, exfoliative dermatitis, or dapsone hypersensitivity syndrome. — DailyMed, set_id 839d7440-ba0e-4c56-b648-d374b155cf03
Drug interactions
- HighPyrimethamine or other antifolates
Mechanism: They increase hematologic toxicity risk.
Recommendation: Avoid or intensify blood-count monitoring.
DailyMed, set_id 839d7440-ba0e-4c56-b648-d374b155cf03
- HighTrimethoprim
Mechanism: It may mutually increase concentrations and methemoglobinemia.
Recommendation: Monitor blood counts, methemoglobin, and toxicity.
DailyMed, set_id 839d7440-ba0e-4c56-b648-d374b155cf03
- HighRifampin
Mechanism: It may reduce dapsone concentrations 7- to 10-fold.
Recommendation: In leprosy, the label does not require adjustment for this interaction; continue specialist regimen management.
DailyMed, set_id 839d7440-ba0e-4c56-b648-d374b155cf03
Adverse events
Common (≥1%)
Hemolysis, methemoglobinemia, nausea, headache, and rash
Rare but serious
Agranulocytosis, aplastic anemia, TEN, and dapsone hypersensitivity syndrome
Pregnancy and lactation
Use during pregnancy only if clearly needed. The local oral regulatory source does not provide breastfeeding data; confirm the current label before deciding between treatment and breastfeeding.
Recent literature (PubMed)
Objective: IgA vasculitis (IgAV), previously named as Henoch-Schönlein purpura, is the most frequent systemic vasculitis in children. In adults, IgAV is less common although it is associated with more severe disease. In fact, the frequency of glomerulonephritis (referred to as IgAV nephritis) in adults is higher than in children and tends to present more severely, with around 10-30% of those affected eventually progressing to end-stage renal disease. In this review, we describe the pathophysiology, main clinical features, diagnosis of the disease, and latest clinical data regarding IgAV therapy. Methods: A narrative literature review, primarily based on articles published in PubMed, was conducted. In addition to discussing the main aspects of glucocorticoids and conventional disease-modifying drugs used in the management of IgAV, this review focuses on the latest information reported regarding biologics and potential future therapies. Results: Glucocorticoids are the first-line therapy for IgAV, especially in adults with severe manifestations. Colchicine, dapsone, and methotrexate can be useful for controlling minor manifestations. Several immunomodulatory agents, such as cyclosporine A, tacrolimus, and mycophenolate mofetil, have shown favorable results as glucocorticoid-sparing agents. Leflunomide has shown promising results but requires further study. The use of rituximab has demonstrated efficacy in reducing relapse frequency, lowering the cumulative glucocorticoid burden, and achieving long-term remission of the disease in children and adults with IgAV. Immunoglobulins and plasma exchange therapy can also be useful in difficult and life-threatening situations. Other potential therapies with encouraging results include TRF-budesonide, B-cell-directed therapy, B-cell-depleting agents, sodium-glucose cotransporter-2 inhibitors, endothelin receptor antagonists, and complement pathway inhibitors. Conclusions: Glucocorticoids are the first-line therapy for IgAV, espe
Acne is one of the most common dermatological conditions to affect women of childbearing age, so it is important to consider the safety of long-term acne treatments on women who could become pregnant. In this review article, we clarify what management options are available to treat acne during pregnancy. Topical treatments, typically first-line for acne, such as azelaic acid, clindamycin, erythromycin, metronidazole, benzoyl peroxide, salicylic acid, dapsone, and retinoids, were reviewed. Systemic treatments, such as zinc supplements, cephalexin, cefadroxil, amoxicillin, azithromycin, erythromycin, and corticosteroids, typically second-line for acne, were also reviewed. Alternative treatments such as light therapy and cosmetic procedures were also evaluated. Due to recommendation of sunscreen utilization during acne treatments, sunscreen usage during pregnancy was also assessed. Management of acne during unplanned pregnancy was discussed in further detail regarding safety and adverse effects. Through summarized tables and examples of studies demonstrating safety and efficacy of treatments, the following is a resource for providers and patients to utilize for management of acne during pregnancy.
Sweet syndrome is a neutrophilic dermatosis characterized by an autoinflammatory nature and a sterile neutrophilic infiltrate. It presents with tender, erythematous, edematous papules or plaques, often accompanied by fever. Aim of this review is to summarize the most meaningful aspects of Sweet syndrome, critically discussing old paradigms and novel findings. A search of the English-language literature was conducted using the terms "Sweet syndrome" and "acute febrile neutrophilic dermatosis." MEDLINE (via PubMed) and Web of Science (WOS) databases were consulted up to June 30, 2024. Since its first identification, new clinical and histopathological variants of Sweet syndrome have been described, highlighting its heterogeneity. Additionally, a multitude of clinical conditions have been increasingly reported in association with Sweet syndrome, ranging from malignancies, autoimmune and infectious disorders. The pathogenesis of the disease is unclear and varies according to the associated conditions. One unifying mechanism is the aberrant activation, proliferation, and skin homing of neutrophils. The mainstay of treatment remains systemic corticosteroids; alternatives include colchicine, dapsone, and potassium iodide. Traditional immunosuppressants, biologic agents, and small molecules have also been described as effective in treating Sweet syndrome. Sweet syndrome is a heterogeneous condition with an elusive pathogenesis. Most cases resolve with corticosteroids, but some remain refractory to various therapies, representing an unmet medical need. Recent evidence on the pathomechanisms underlying Sweet syndrome suggests that not only innate but also adaptive immunity might play roles. Further experimental studies are needed and may help identify new therapeutic targets in the future.
Pyoderma gangrenosum is a rare neutrophilic dermatosis that results in painful cutaneous ulcers and is frequently associated with underlying hematologic disorders, inflammatory bowel disease, or other autoimmune disorders. Pathogenesis involves an imbalance between proinflammatory and anti-inflammatory mediators, leading to tissue damage from neutrophils. First-line treatment options with the greatest evidence include systemic corticosteroids, cyclosporine, and tumor necrosis factor alpha inhibitors. Other steroid-sparing therapies such as dapsone, mycophenolate mofetil, intravenous immunoglobulin, and targeted biologic or small molecule inhibitors also have evidence supporting their use. Wound care and management of underlying associated disorders are critical parts of the treatment regimen. Dapsone is a sulfonamide related drug used for the therapy of leprosy and dermatitis herpetiformis. Dapsone has been linked with rare cases of idiosyncratic liver injury, similar to that seen with the sulfonamides.