Inflammatory Acne Management With a Novel Prescription Dietary Supplement

December 2012 | Volume 11 | Issue 12 | Original Article | 1428 | Copyright © December 2012

Alan R. Shalita MD,a Ronald Falcon MD,b Alan Olansky MD,c Patricia Iannotta MD,d Arash Akhavan MD,e Doris Day MD,f, Anthony Janiga MD,g Prashant Singri MD,h and John E. Kallal PhDi

Background: Inflammatory acne, particularly in postadolescent women, is increasing in incidence. The most effective therapeutic modality for treatment of this type of acne has been the administration of oral tetracyclines. Long-term acne treatment with such drugs, however, is frequently accompanied by undesirable adverse reactions, including gastrointestinal disturbances, antianabolic effects, headaches, tinnitus, and photosensitivity.
Objective: To assess the usefulness of a novel dietary supplement in the overall management of patients with inflammatory acne vulgaris.
Methods: 235 patients with inflammatory acne vulgaris were enrolled by dermatologists in a multicenter, open-label, 8-week, prospective study evaluating the effects of adding NicAzel, 1 to 4 tablets daily, to their current acne treatment regimen.
Results: A statistically significant (P<.0001) number of patients demonstrated improvement over their previous acne treatment regimens after both 4 and 8 weeks of NicAzel (nicotinamide, azelaic acid, zinc, pyridoxine, copper, folic acid; Elorac Inc, Vernon Hills, IL) use. At week 8, 88% of the patients experienced a visible reduction in inflammatory lesions, and 81% of the patients rated their appearance as much or moderately better compared with baseline. Three-quarters (76%) of the patients thought NicAzel was at least as effective as previous treatment with oral antibiotics.
Conclusion: Patients with inflammatory acne showed significant improvement in acne severity and overall appearance when NicAzel was added to their existing treatment regimen.

J Drugs Dermatol. 2012;11(12):1428-1433.


Acne vulgaris is a chronic, inflammatory disease of the pilosebaceous unit that affects approximately 50 million individuals each year in the United States. The pathophysiology of acne is associated with multiple, complex interactive causative influences, including genetic predisposition. The initial process in the formation of acne begins in the upper portion of the follicle of the pilosebaceous unit and progresses with hyperkeratosis of the follicle lining, increased cohesiveness of corneocytes, and accumulation of keratin and sebum. As the trapped comedo materials expand, the tension on the follicular wall increases, resulting in their rupture and extrusion of the immunogenic keratin and sebum with resultant inflammation. The inflammatory lesions of acne, which originate with comedo formation, expand to form erythematous papules, pustules, nodules, and cysts, and depending on severity, may result in scarring.
Four factors are involved in the etiology of acne: 1) excessive production of sebum, likely due to androgenic factors; 2) bacterial colonization and release of inflammatory mediators; 3) inflammation; and 4) abnormal keratinization within the follicle. Sebaceous follicles are usually colonized with gram-positive, lipase-producing Propionibacterium acnes within inflammatory lesions or open and closed comedones. The presence of P acnes or other bacteria in the sebaceous follicles stimulates the production of proinflammatory cytokines/chemokines via the activation of tolllike receptors on the membranes of inflammatory cells. The role of P acnes is complex, and there is still some uncertainty about its effects on acne—whether through direct microbial action or through stimulation of inflammatory processes in the skin.1 Other inflammatory lesions of acne include nodules, papules, pustules, and cysts, which may lead to lifelong sequelae, including scarring, hyperpigmentation changes, and emotional distress.2