Facial melanoses: Indian perspective.

Facial melanoses (FM) are a common presentation in Indian patients, causing cosmetic disfigurement with considerable psychological impact. Some of the well defined causes of FM include melasma, Riehl's melanosis, Lichen planus pigmentosus, erythema dyschromicum perstans (EDP), erythrosis, and poikiloderma of Civatte. But there is considerable overlap in features amongst the clinical entities. Etiology in most of the causes is unknown, but some factors such as UV radiation in melasma, exposure to chemicals in EDP, exposure to allergens in Riehl's melanosis are implicated. Diagnosis is generally based on clinical features. The treatment of FM includes removal of aggravating factors, vigorous photoprotection, and some form of active pigment reduction either with topical agents or physical modes of treatment. Topical agents include hydroquinone (HQ), which is the most commonly used agent, often in combination with retinoic acid, corticosteroids, azelaic acid, kojic acid, and glycolic acid. Chemical peels are important modalities of physical therapy, other forms include lasers and dermabrasion.

Clindamycin lotion alone versus combination lotion of clindamycin phosphate plus tretinoin versus combination lotion of clindamycin phosphate plus salicylic acid in the topical treatment of mild to moderate acne vulgaris: a randomized control trial.

BACKGROUND: Acne vulgaris is a common skin disease that affects 85% to 100% of people at some time during their lives. It is characterized by noninflammatory follicular papules or comedones and by inflammatory papules, pustules, and nodules in its more severe forms. AIMS: To compare the efficacy of combination treatment of clindamycin+salicylic acid, versus clindamycin+tretinoin versus clindamycin alone in the treatment of the mild-to-moderate acne vulgaris. METHODS: This was a single-blinded, randomized clinical trial.Forty-two female patients (age range: 15-25 years) with mild-to-moderate acne vulgaris were selected randomly and subsequently randomized to 3 groups. Group A patients were treated with 1% clindamycin lotion (C lotion) twice daily. Group B patients were treated with 1% clindamycin+0.025% tretinoin lotion once nightly (CT lotion). Group C patients were treated with 1% clindamycin+2% salicylic acid lotion twice daily (CS lotion) for 12 weeks. For comparison of efficacy of these treatments, and regarding the skewed distribution of the data, Kruskal-Wallis Test and Mann-Whitney U test were used. SPSS software was used for statistical analysis. RESULTS: There was a significant difference between 3 types of treatment in the respect of the total lesion count (TLC) improvement (P = 0.039). The efficacy of treatment on Acne Severity Index (ASI) was maximum for CS lotion (81.80% reduction in ASI). CT lotion reduced ASI by as much as 73.73% during 12 weeks of treatment. The efficacy of C lotion was calculated to be 37.87% in the reduction of ASI. CONCLUSIONS: Our data suggested that the efficacy of CS lotion was significantly more than C lotion with respect to the TLC and ASI, although there was no significant difference between CS and CT lotion.

Modulation of p53 dependent gene expression and cell death through thioredoxin-thioredoxin reductase by the Interferon-Retinoid combination.

We have shown earlier that the IFN-beta and all-trans retinoic acid (RA) combination, but not the single agents, induces death in several tumor cell lines. Employing a genetic technique we have identified several Genes associated with Retinoid-IFN induced Mortality (GRIM). One of the GRIMs was human thioredoxin reductase (TR), a redox enzyme. Since the overexpressed TR augments IFN/RA stimulated cell death, we explored the mechanisms of TR-mediated death. Here we show that TR augments cell death by upregulating the transcriptional activity of p53 tumor suppressor. This process does not involve a physical increase in levels of p53. Using redox inactive mutants of TR and its substrate, thioredoxin (Trx), we demonstrate that IFN/RA-induced regulation of p53 dependent gene expression requires TR and Trx. In contrast-over-expression of wildtype TR or Trx augment the p53 dependent gene expression in response to IFN/RA treatment. Consistent with these results an increased DNA binding activity of p53 was noted in the presence of TR. These studies identify a novel mechanism of p53 mediated cell death regulation involving redox enzymes.