Short reviewNicotinamide as a potential addition to the anti-atopic dermatitis armamentarium
Section snippets
Overview
Atopic dermatitis (AD) is an intensely pruritic, chronic skin disease that can affect all age groups. Beginning in childhood, AD follows a remitting/flaring course that may continue lifelong [1].
It has been shown that elevated levels of cAMP phosphodiesterase (cAMP PDE) underlie many of the abnormalities of atopic dermatitis (AD), such as increased histamine release and IgE synthesis. In AD, there is a great increase in the potential for proliferation of clones of activated lymphocytes by
Brief definition of atopic dermatitis (AD)
Atopic dermatitis (atopic aczema) is an itchy, chronic, or chronically relapsing, inflammatory skin condition that can affect all age groups. It nearly always begins in childhood and follows a remitting/flaring course that may continue throughout life [1], [2], [3], [4]. The rash is characterized by itchy papules which become excoriated and typically have a flexural distribution. It is estimated to affect 20% of the general population [1].
The disease often moderates with age, but patients carry
Brief review of the pathomechanisms underlying AD
The histologic feature of AD is the same epidermal spongiosis of any eczematous disease, along with varying degrees of epidermal proliferation, lymphocyte infiltration of predominantly CD4+ T cells into the dermis (and sometimes epidermis), and increased numbers of dermal macrophages and eosinophils [6].
A variety of functional abnormalities have been noted in these infiltrating cells as well as in circulating leukocytes.
It is documented that peripheral blood mononuclear cells, particularly
Pharmacological characteristics of nicotinamide relating to the subject
Nicotinamde, also known as niacinamide, is the pyridin-3-carboxylic acid amide of niacin, a component of the vitamin B complex. This agent has no effect on blood pressure, pulse, or body temperature [15], [16].
Nicotinamide has myriad of effects that makes it a potential treatment for AD.
It is an inhibitor of poly (ADP-ribose) polymerase-1 (PARP-1) which is a nuclear enzyme enhancing nuclear factor kappa B-mediated transcription. The latter plays a pivotal role in the expression of adhesion
Conclusion
Since topical steroids which are the most important therapeutic tools in AD [5] are commonly associated with frequent side effects such as skin atrophy and telagiectasia, alternative therapeutic agents have been, and are being, developed to treat this condition.
Given the high safety of nicotinamide and also in view of its anti-inflammatory, antioxidant, nitric oxide synthase inhibition, ceramide synthesis increment, suppression of antigen-induced lymphocyte transformation, and mast cell
References (25)
- et al.
Cellular and immunologic mechanisms in atopic dermatitis
J. Am. Acad. Dermatol.
(2001) - et al.
Elevated leukocyte cyclic AMP phosphodiesterase response in atopic dermatitis; a possible mechanism for cyclic AMP-agonist hyporesponsiveness
J. Allergy Clin. Immunol.
(1982) - et al.
Biochemical and immunologic mechanisms in atopic dermatitis: new targets for emerging therapies
J. Am. Acad. Dermatol.
(1999) - et al.
Analysis of the cytokine pattern expressed in situ in inhalant allergen patch test reactions of atopic dermatitis patients
J. Invest. Dermatol.
(1995) - et al.
Increased oxidative stress in childhood atopic dermatitis
Life Sci.
(2001) - et al.
Nicotinamide inhibits enhanced in vitro production of interleukin-12 and tumor necrosis factor-alpha in peripheral whole blood of people at high risk of developing type 1 diabetes and people with newly diagnosed type 1 diabetes
Diabetes Res. Clin. Pract.
(2000 (Feb.)) Atopic dermatitis
Clin. Dermatol.
(1991)- et al.
- et al.
Biphasic response against aeroallergen in atopic dermatitis showing a switch from an initial TH2 response to a TH1 response in situ: an immunocytochemical study
J. Allergy Clin. Immunol.
(1996) - et al.
Pharmacologic alternatives for severe atopic dermatitis
Int. J. Dermatol.
(2001)