We present herein a case of sebaceous hyperplasia in a 55-year-old male, who showed multiple asymptomatic yellowish papules on the forehead and the cheeks. Histopathologic examination of a papule revealed numerous sebaceous lobules grouped around several enlarged sebaceous ducts. Three weeks of oral administration. of isotretinoin 40 mg per day brought marked improvement.
Administration, Oral ; Cheek ; Forehead ; Humans ; Hyperplasia* ; Isotretinoin* ; Male ; Middle Aged

Background: Reactive oxygen species (ROS) generated by neutrophils are closely correlated with the pathogenesis of a variety of inflammatory skin diseases. The aim of this study was to investigate whether the amount of reactive oxygen species (hydrogen peroxide) generated by neutrophils from patients with acne inflammation decrease after oral administration of standard doses of isotretinoin. Method: In order to measure neutrophil hydrogen peroxide production, phorbol myristate acetate (PMA, neutrophil stimulant), was added to whole blood. Intracellular dichlorofluorescein (DCF) fluorescence of neutrophils was determined by flow cytometry. In order to assess treatment efficacy, we used a Global Acne Grading Score (GAGS) and assessed the efficacy based on examinations at baseline and week 8. Results: Patients with acne inflammation showed a significantly increased level of hydrogen peroxide produced by neutrophils compared to healthy controls. Patients with acne inflammation treated with isotretinoin showed a significant decrease in the ability of neutrophils to produce hydrogen peroxide in accordance with a clinical improvement of acne lesions. Conclusion: Our result shows that the generation of ROS which induce a chemical insult to the integrity of the follicular epithelium in acne, can be suppressed in isotretinoin-treated acne patients.
Acne Vulgaris* ; Administration, Oral ; Epithelium ; Flow Cytometry ; Fluorescence ; Humans ; Hydrogen Peroxide* ; Hydrogen* ; Inflammation ; Isotretinoin* ; Neutrophils* ; Reactive Oxygen Species ; Skin Diseases ; Tetradecanoylphorbol Acetate ; Treatment Outcome

Acne Vulgaris ; chemically induced ; drug therapy ; Administration, Topical ; Adolescent ; Adrenal Cortex Hormones ; administration & dosage ; therapeutic use ; Anti-Bacterial Agents ; administration & dosage ; adverse effects ; therapeutic use ; Doxycycline ; administration & dosage ; adverse effects ; therapeutic use ; Drug Therapy, Combination ; Humans ; Isotretinoin ; administration & dosage ; therapeutic use ; Male ; Thorax

The growth inhibitory effects of four retinoic acid (RA) derivatives, 9-cis RA, 13-cis RA, N-(4-hydroxyphenyl) retinamide (4-HPR), and all-trans retinoic acid (ATRA) were compared. In addition, the effects of various combinations of these four agents were examined on non-small cell lung carcinoma (NSCLC) cell-lines, and on the expressions of retinoic acid receptors (RARs) and retinoid X receptors (RXRs) on these cells. At the clinically achievable concentration of 1 micrometer, only 4-HPR inhibited the growths of H1299 and H460 cells-lines. However, retinoic acid receptor beta(RAR beta) expression was up-regulated on H460 and H1299 cells treated with 1 micrometer of ATRA, 13-cis RA, or 9-cis RA. All NSCLC cell lines showed growth inhibition when exposed sequentially to 1 micrometer ATRA and 0.1 micrometer 4-HPR. In particular, sequential treatment with 1 micrometer ATRA or 13-cis RA and 4-HPR markedly inhibited H1703 cell growth; these cells exhibited no basal RAR beta expression and were refractory to 4-HPR. However, in NSCLC cell lines that expressed RAR beta, the expressional levels of RAR beta were up-regulated by ATRA alone and by sequential treatment with ATRA and 4-HPR. 4-HPR was found to be the most active of the four agents in terms of NSCLC growth-inhibition. Moreover, sequential treatments with ATRA or 13-cis RA followed by 4-HPR were found to have synergistic growth-inhibitory effects and to regulate RAR expression.
Base Sequence ; Carcinoma, Non-Small-Cell Lung/*drug therapy/genetics/metabolism ; Cell Line, Tumor ; DNA Primers/genetics ; Drug Therapy, Combination ; Fenretinide/administration & dosage ; Gene Expression/drug effects ; Humans ; Isotretinoin/administration & dosage ; Lung Neoplasms/*drug therapy/genetics/metabolism ; Receptors, Retinoic Acid/genetics ; Retinoid X Receptors/genetics ; Tretinoin/administration & dosage/*analogs & derivatives