Assessing the Effectiveness of Stabilized Cysteamine 5% Cream Compared to Hydroquinone 4%/Ascorbic Acid 3% Combination Cream in Treating Acne-induced Post-inflammatory Hyperpigmentation: A Randomized, Controlled Study.

Objective: Postinflammatory hyperpigmentation (PIH) is a common sequela of acne vulgaris. Topical treatment with hydroquinone is the standard treatment, but may be associated with complications. Cysteamine is a relatively safe depigmenting agent with an observed depigmenting effect.

Topical isoniazid as a novel treatment for melasma: A randomized, double-blind, vehicle-controlled clinical trial.

Introduction: Melasma is a chronic hyperpigmentation disorder, and its treatment poses a challenge to dermatologists due to its chronicity and resistance to conventional therapies. Oral isoniazid is used for the treatment of tuberculosis. One of us had previously showed that topical isoniazid exerts a strong depigmenting action in animal models.

Successful treatment of solar lentigines by topical application of stabilized cysteamine: A vehicle-controlled, double-blind randomized study.

Background: Solar lentigines are common hyperpigmented lesions typically appearing after 50 years of age and associated with negative psychological effects in affected individuals. Topical depigmenting products, such as hydroquinone and even the Kligman's formula, are usually ineffective for treating lentigines. Stabilized cysteamine has been recently shown to be as effective as the modified Kligman's formula for treating melasma.

Comparison of the efficacy of cysteamine 5% cream and hydroquinone 4%/ascorbic acid 3% combination cream in the treatment of epidermal melasma.

Background: Few safe and effective treatments are available for melasma. Cysteamine, a non-melanocytotoxic molecule is a safer alternative to hydroquinone and usable for long-term use.

Aim: To evaluate the effect of cysteamine 5% cream in the treatment of melasma.

Significant therapeutic response to cysteamine cream in a melasma patient resistant to Kligman's formula.

L-Cysteamine is a biological antioxidant produced during the coenzyme A metabolism cycle and is naturally present in all mammalian cells. The efficacy of topical cysteamine for the treatment of melasma has been recently shown in two double-blind, randomized, and placebo-controlled clinical trials. Herein, we report a 44-year-old patient with melasma resistant to Kligman's formula (Pigmanorm cream), who was successfully treated with topical cysteamine as a new depigmenting agent.

Efficacy of cysteamine cream in the treatment of epidermal melasma, evaluating by Dermacatch as a new measurement method: a randomized double blind placebo controlled study.

Background: Melasma is a difficult-to-treat hyperpigmentary disorder. Very few studies have been performed regarding the efficacy of cysteamine in the treatment of melasma.

Objective: To determine the efficacy of cysteamine cream in the treatment of patients with epidermal melasma using Dermacatch as a more accurate skin colorimetric measurement tool.

Correlation between protoporphyrin IX fluorescence intensity, photobleaching, pain and clinical outcome of actinic keratosis treated by photodynamic therapy.

Background: Photodynamic therapy (PDT) with Metvix® is a good therapeutic option to treat actinic keratosis, but it presents drawbacks (pain, lesion recurrences, heterogeneous outcome), emphasizing the possible need to individualize treatment.

Objective: We assessed whether PDT clinical outcome and pain during treatment were correlated with protoporphyrin IX fluorescence intensity and photobleaching.

Methods: 25 patients were treated by Metvix PDT.

Ebselen is a new skin depigmenting agent that inhibits melanin biosynthesis and melanosomal transfer.

We assessed the ability of ebselen, a glutathione peroxidase mimic, to reduce pigmentation in various models. In murine B16 melanocytes, 25 μm ebselen inhibited melanogenesis and induced a depolymerisation of actin filaments. In co-cultures of B16 melanocytes with BDVII keratinocytes, a pretreatment of melanocytes with ebselen resulted in a strong inhibition of melanosome transfer to keratinocytes, as shown under optical and electron microscopy.

D-penicillamine, a potent melanogenesis inhibitor, lacks any depigmenting effect on black guinea pig skin: the first randomized, evaluator-blinded, vehicle-controlled, in vivo study.

D-penicillamine is a melanogenesis inhibitor. This in vivo study on ten black guinea pigs using a 5% D-penicillamine ointment showed its lack of any skin-lightening effect. The potential reasons for this ineffectiveness are discussed in the paper, which could be very helpful for researchers exploring new skin-lightening agents.

A new spectrophotometric method for simple quantification of melanosomal transfer from melanocytes to keratinocytes.

Three major difficulties must be overcome to establish a quantitative method for melanosomal transfer analysis: (i) establishing a three-dimensional co-culture reassuring direct melanocyte to keratinocyte transfer, (ii) separation of melanocytes and keratinocytes following co-culture and (iii) melanosome quantification in each cell population. Melanocytes and keratinocytes are cultured on the opposite sides of the porous membrane of hanging cell inserts (1μm pores, 2×10(6) pores/cm(2) ). Cell separation is performed after 3days of co-culture by simple trypsinisation.

Porokeratosis of Mibelli with mutilation: a case report.

Porokeratosis is a rare keratinization disorder of the skin characterized by annular plaques with an atrophic center surrounded by a raised keratotic wall that spreads centrifugally. We report a case of porokeratosis of Mibelli with mutilation. A 30-year-old woman presented with atrophic plaques on the index fingers of both hands with a keratotic ridge in some margins of the plaques.

Topical captopril as a novel agent against hypertrophic scar formation in new zealand white rabbit skin.

Collagen constitutes the majority of extracellular matrix in tissues such as bone, cartilage, and especially the skin. Over production and/or decreased degradation of collagen fibers could lead to an abnormal wound healing response resulting in hypertrophic scarring or keloid formation. Recently, angiotensin II has been shown to be present in several cutaneous cells and that it stimulates fibroblast proliferation, collagen synthesis, and suppresses matrix metalloproteinase activity.

Retinoic acid synergistically enhances the melanocytotoxic and depigmenting effects of monobenzylether of hydroquinone in black guinea pig skin.

Monobenzylether of hydroquinone (MBEH) has long been utilized for the depigmentation therapy of patients with extensive vitiligo. In this approach, the normally pigmented areas surrounding vitiligo lesions are depigmented to achieve a uniform skin tone. One of the important disadvantages of MBEH therapy, however, is the resistance of a considerable number of vitiligo patients against the depigmenting effect of this agent.

Topical methimazole as a new treatment for postinflammatory hyperpigmentation: report of the first case.

We have previously shown that the peroxidase inhibitor methimazole (1-methyl-2-mercapto imidazole; MMI) is a noncytotoxic inhibitor of melanin production in cultured B16 melanocytes. It was further demonstrated that the topical application of 5% MMI on brown guinea pig skin for 6 weeks causes a significant reduction in the amount of epidermal melanin, resulting in visually recognizable cutaneous depigmentation. Herein, we report a 27-year-old male with postinflammatory hyperpigmentation (due to acid burn), successfully treated with topical MMI as a new skin depigmenting agent.

Pharmacology of RALGA, a mixture of retinaldehyde and glycolic acid.

Background: Retinoids and alpha-hydroxy acids (AHAs) are major compounds in topical therapy. They exert distinct but potentially complementary activities. However, their association is limited by their respective irritating potential.

Enhancement of the depigmenting effect of hydroquinone and 4-hydroxyanisole by all-trans-retinoic acid (tretinoin): the impairment of glutathione-dependent cytoprotection?

Many of the well-known depigmenting agents such as hydroquinone and 4-hydroxyanisole are, in fact, melanocytotoxic chemicals which are oxidized in melanocytes to produce highly toxic compounds such as quinones. These cytotoxic compounds are responsible for the destruction of pigment cells, which results in skin depigmentation. However, cells are capable of protecting themselves against cytotoxic agents by intracellular glutathione (GSH).

Peroxidase-mediated mechanisms are involved in the melanocytotoxic and melanogenesis-inhibiting effects of chemical agents.

Melanogenesis is based on the enzymatic conversion of the amino acid tyrosine, through a series of intermediates, to melanin pigments. The nature of the enzymes involved in the different steps of melanogenesis has been intensely debated. However, it is now believed that tyrosinase is responsible for the conversion of tyrosine to dopa and of dopa to dopaquinone, and that peroxidase accomplishes the oxidative polymerization of the eventually formed indoles to eumelanin pigments.