Disease relevance of Melanosis

• While MT-ret transgenic animals develop severe melanosis of the skin and subcutis and subsequent melanomas at an incidence of 80% during their first year of life, MT-ret mice devoid of IL-6 developed preneoplastic melanosis and consecutive melanomas significantly less frequently (47%; P < 0.05) [1].
• Furthermore, melanosis observed in patients with pituitary carcinoma is associated with ACTH levels similar to those occurrring in the ectopic ACTH or Nelson's syndrome [2].
• A case is presented in which a patient with a well-differentiated adenocarcinoma showed high gallium concentration in the segment with melanosis coli proximal to the obstruction [3].
• The possibility exists that in the future a combination of HQ plus cystamine or BSO could be used to treat disorders such as melasma and post-inflammatory hyperpigmentation [4].
• Since dicarboxylic acids are competitive inhibitors of tyrosinase, and effective in treatment of hyperpigmentary disorders, such as chloasma and lentigo maligna, probably due to a cytotoxic effect on abnormal melanocytes, it is of interest to examine their effect on normal melanocytes in tissue culture [5].

Psychiatry related information on Melanosis

• The high incidence of esophageal melanosis may be partially linked to high acetaldehyde exposure, a consequence of drinking alcohol in persons with inactive ALDH2 [6].
• The paper describes a case of neurocutaneous melanosis (NM), with mental retardation, chronic psychosis, and epilepsy possibly due to a temporal focus [7].

High impact information on Melanosis

• We conducted association studies by using markers in candidate pigmentation genes and discovered four mutations in the melanocortin-1-receptor gene, Mc1r, that seem to be responsible for adaptive melanism in one population of lava-dwelling pocket mice [8].
• To investigate the genetic basis, adaptive significance, and evolutionary history of melanistic variants in the Felidae, we mapped, cloned, and sequenced the cat homologs of two putative candidate genes for melanism (ASIP [agouti] and MC1R) and identified three independent deletions associated with dark coloration in three different felid species [9].
• Morphological observation of the intestines also revealed melanosis, crypt abscesses and erosion, becoming more pronounced with length of exposure to the anthraquinone [10].
• In controlled studies, topical azelaic acid demonstrated comparable anti-acne efficacy to topical tretinoin, benzoyl peroxide, erythromycin and oral tetracycline, while in patients with melasma azelaic acid proved at least as effective as topical hydroquinone [11].
• The melasma patients presented statistically significant increased levels of LH (p less than 0.001) and lower levels of serum estradiol (p less than 0.025) than normal controls [12].

Chemical compound and disease context of Melanosis

• Thus, topical azelaic acid, employed either as monotherapy or in combination with other treatments, is likely to prove of value in the management of acne and several hyperpigmentary disorders, most notably melasma [11].
• It is concluded that the pigmentation of chloasma is not due to increased plasma concentrations of immunoreactive beta-MSH [13].
• The monobenzyl ether of hydroquinone should never be used in melasma therapy [14].
• Treatment of melasma with Jessner's solution versus glycolic acid: a comparison of clinical efficacy and evaluation of the predictive ability of Wood's light examination [15].
• Reversible melasma associated with tretinoin [16].

Biological context of Melanosis

• Cell growth and p53 expression in primary acquired melanosis and conjunctival melanoma [17].
• AIMS: To evaluate cell growth and the pattern of p53 suppressor gene expression in atypical primary acquired melanosis (PAM) and in recurrent conjunctival melanoma [17].

Anatomical context of Melanosis

• Aggregates of macrophages containing pigment, identified in a subepithelial location, were reminiscent of melanosis coli, which is caused by abuse of anthracene-containing laxatives [18].
• Transgenic mice overexpressing hepatocyte growth factor/scatter factor (HGF/SF) demonstrate extensive pigmented nevi in both skin and leptomeninges of the central nervous system resembling human neurocutaneous melanosis [19].
• Based on the inhibitor constant on tyrosinase, at least cytotoxic levels of azelaic acid would be required for the direct inhibition of melanin biosynthesis in melanosomes if this mechanism is responsible for depigmentation in the hyperpigmentation disorders lentigo maligna and melasma [20].
• These disorders include ocular surface squamous neoplasia, dry eye syndrome, limbal stem-cell deficiency, specific viral infections, vitamin A deficiency, allergic disorders, conjunctival melanosis, and malignant melanoma [21].
• Studies were performed on the efficacy, residues and in vitro enterocyte toxicity of 4-hexylresorcinol (4-HR), which could be utilized as an inhibitor of shrimp melanosis (black spot) [22].

Gene context of Melanosis

• AIMS: To compare the proliferative activity of intraepithelial melanocytes in primary acquired melanosis (PAM) without atypia and PAM with atypia by immunohistochemical staining for the Ki-67 antigen and the proliferating cell nuclear antigen (PCNA) [23].
• The conserved molecular basis for the evolution of melanism in birds and several other vertebrates is probably related to low pleiotropic effects at the MC1R [24].
• Reconstruction of the evolution of bananaquit MC1R alleles shows that melanism is a derived trait in this species [25].
• MIB-1 and PC-10 immunostaining for the assessment of proliferative activity in primary acquired melanosis without and with atypia [23].
• Eleven of 11 melanomas (95% confidence interval, 72% to 100%) and three of three lesions with primary acquired melanosis with atypia stained positively for NQO1 [26].

Analytical, diagnostic and therapeutic context of Melanosis

• Colorimetry (an objective measure of skin colour) demonstrated a 0.9 unit lightening of tretinoin-treated melasma and a 0.3 unit darkening with vehicle (P = 0.01); these results correlated with clinical lightening (r = 0.55, P = 0.0005) [27].
• CONCLUSION: Both glycolic acid/kojic acid and glycolic acid/hydroquinone topical skin care products are highly effective in reducing the pigment in melasma patients [28].
• A randomized, double-blind, placebo-controlled trial of vitamin C iontophoresis in melasma [29].

References