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Hyperpigmented Lesions (hyperpigmented + lesion)

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Medical Sciences	100%

Selected Abstracts

Effective inhibition of melanosome transfer to keratinocytes by lectins and niacinamide is reversible

EXPERIMENTAL DERMATOLOGY, Issue 7 2005
Amanda Greatens
Abstract:, Skin pigmentation results in part from the transfer of melanized melanosomes synthesized by melanocytes to neighboring keratinocytes. Plasma membrane lectins and their glycoconjugates expressed by these epidermal cells are critical molecules involved in this transfer process. In addition, the derivative of vitamin B3, niacinamide, can inhibit melanosome transfer and induce skin lightening. We investigated the effects of these molecules on the viability of melanocytes and keratinocytes and on the reversibility of melanosome-transfer inhibition induced by these agents using an in vitro melanocyte,keratinocyte coculture model system. While lectins and neoglycoproteins could induce apoptosis in a dose-dependent manner to melanocytes or keratinocytes in monoculture, similar dosages of the lectins, as opposed to neoglycoproteins, did not induce apoptosis to either cell type when treated in coculture. The dosages of lectins and niacinamide not affecting cell viability produced an inhibitory effect on melanosome transfer, when used either alone or together in cocultures of melanocytes,keratinocytes. Cocultures treated with lectins or niacinamide resumed normal melanosome transfer in 3 days after removal of the inhibitor, while cocultures treated with a combination of lectins and niacinamide demonstrated a lag in this recovery. Subsequently, we assessed the effect of niacinamide on facial hyperpigmented spots using a vehicle-controlled, split-faced design human clinical trial. Topical application of niacinamide resulted in a dose-dependent and reversible reduction in hyperpigmented lesions. These results suggest that lectins and niacinamide at concentrations that do not affect cell viability are reversible inhibitors of melanosome transfer. [source]

Linear and whorled nevoid hypermelanosis associated with developmental delay and generalized convulsions

INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 2 2004
Ahmad A. Alrobaee MD
A 2-year-old Saudi boy was seen in our dermatology clinic with symmetrical, brown, linear macules over the legs, trunk, and arms (Figs 1,3). He was a product of a full-term vaginal delivery following an uneventful first pregnancy in a 22-year-old mother. The birth weight was 2.3 kg. The hyperpigmented macules followed the lines of Blaschko and were noticed a few months after birth; they had enlarged with body growth until the age of 18 months. There was no family history of a similar condition and the boy's parents were unrelated. No blistering or inflammatory changes preceded the hyperpigmentation. The palms, soles, nails, scalp, mucous membranes, and teeth were normal. In addition to the hyperpigmented macules, the patient started to have generalized convulsions at the age of 2 months. Figure 1. Linear hyperpigmented macules following the lines of Blaschko Figure 2. Close up view of the hyperpigmented macules Figure 3. Trunk: Hyperpigmented macules in whorled distribution Physical examination revealed delayed developmental milestones, microphthalmia, depressed nose, and high arched palate with no other abnormalities. Blood tests were normal. Magnetic resonance imaging of the brain showed changes suggestive of a demyelinating process at the parieto-occipital white matter. Echocardiography revealed an atrial septal defect. Electroretinography (ERG), visual evoked potentials (VEP), and auditory evoked potentials (AEP) were normal. Electroencephalogram (EEG) showed multifocal epileptic discharge in the posterior region. A punch skin biopsy taken from the hyperpigmented lesions showed an increase in the melanin content of the basal layer with no incontinence of pigment or melanophages in the dermis. [source]

Xeroderma pigmentosum with limited involvement of the UV-exposed areas: a case report

INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 4 2003
Mostafa Mirshams-Shahshahani MD
A 21-year-old woman with skin type IV, who had developed photophobia and brown, spotty, hyperpigmented lesions on her face from early childhood, presented to our center for treatment of her facial lesions. Examination on admission revealed numerous, freckle-like, hyperpigmented macules and actinic keratoses over the central part of the face, with sparing of the forehead, chin, and peripheral area (Fig. 1). The area involved was approximated to be around 2% of the total body surface. The dorsal parts of the hands showed no lesions (Fig. 2), but guttate hypomelanotic lesions were apparent on both forearms. Figure 1. Limitation of xeroderma pigmentosum lesions to the center of the face Figure 2. Hands are devoid of any lesions Histologic examination of biopsies from four different facial lesions revealed them to be keratoacanthoma (1.5 × 2.5 cm ulcerative nodule on the right cheek), sclerosing basal cell epithelioma (nasal lesion), lentigo simplex, and hypertrophic actinic keratosis. Corneal clouding, conjunctival injection, loss of lashes, and atrophy of the lids were apparent on ophthalmologic examination. Other parts of the physical examination, including examination of the oral cavity, were nonsignificant. In addition, except for the presence of mild eczema in a sibling, the patient's family history regarding the presence of any similar problem and also any other important dermatologic or general disorder was negative. [source]

Mechanism of tyrosinase inhibition by deoxyArbutin and its second-generation derivatives

BRITISH JOURNAL OF DERMATOLOGY, Issue 6 2008
S. Chawla
Summary Background, Disorders, such as age spots, melasma and hyperpigmentation at sites of actinic damage, emanate from the augmentation of an increased amount of epidermal melanin. Objectives, The ineptness of current therapies in treating these conditions, as well as high cytotoxicity, mutagenicity, poor skin penetration and low stability of skin-depigmenting formulations led us to investigate new compounds that meet the medical requirements for depigmentation agents. We have shown previously that the tyrosinase inhibitor deoxyArbutin (dA) is a more effective and less toxic skin lightener than hydroquinone (HQ). Methods, The efficacy and reversibility of dA and its derivatives on inhibiting tyrosine hydroxylase and DOPAoxidase was assessed using standard assays. Results, dA and its second-generation derivatives inhibit tyrosine hydroxylase and DOPAoxidase activities of tyrosinase dose dependently thereby inhibiting melanin synthesis in intact melanocytes, when used at concentrations that retain 95% cell viability in culture. This depigmenting effect was completely reversible when the compounds were removed. Tyrosinase inhibition was also observed in vitro when tested using human and purified mushroom tyrosinase, establishing that they are direct enzyme inhibitors. Lineweaver,Burk reciprocal plot analysis using mushroom tyrosinase illustrated that dA and its derivatives are more robust competitive inhibitors than HQ, when tyrosine is used as substrate. Conclusions, Thus, dA and its second-generation derivatives, which inhibit melanogenesis at safe concentrations by specifically acting on the tyrosinase enzyme at a post-translational level, are promising agents to ameliorate hyperpigmented lesions or lighten skin. [source]