Background: Rosacea is a chronic inflammatory disease which requires treatment to maintain remission. Objective: Recently, the effect of Demodex mites in recurrence of rosacea has been described. Although there is limited data, previous reports have suggested that oral metronidazole demonstrated efficacy in treatment of rosacea. Methods: Fifty-eight Korean patients with rosacea who received treatment with oral minocycline (50 mg twice daily) only or with two-week of oral metronidazole (250 mg thrice daily) were evaluated retrospectively. Their responses were evaluated by Investigator’s Global Assessment (IGA), Clinician’s Erythema Assessment (CEA), and patient’s Global Assessment. The recurrence rate and odds ratio of risk factors for recurrence were also estimated. Results: The combination treatment group reported earlier clinical improvement and lower mean IGA and CEA than the monotherapy group. Approximately 48% of patients with combination treatment did not show relapse within 24 weeks, which is significantly higher than that in the monotherapy group (p=0.042). Conclusion Add-on therapy of oral metronidazole appeared to be a significant protective factor for recurrence of rosacea (p<0.05). This study suggests that oral metronidazole can be added to oral minocycline to reduce relapses in rosacea patients with tolerable safety.

Background: Psoriasis is a chronic inflammatory skin disease, wherein macrophages play a key role. An imbalance in transition from the classical activation (M1) to alternative activation (M2) phenotype in macrophages contributes to development of persistent inflammation. However, the role of M2 macrophages in disease severity of psoriasis is not yet elucidated. Objective: This study was performed to investigate the expression of pan-macropahge marker cluster of differentiation (CD) 68 and M2 marker CD163 in lesional and non-lesional skin samples of patients with psoriasis and determine the relationship of their expression to the disease severity of psoriasis. Methods: A retrospective study was performed using 21 lesional and 13 non-lesional skin samples from 21 patients with psoriasis. We reviewed the clinical information and evaluated CD68 and CD163 expression in 34 skin samples via immunohistochemical staining. Results: Lesional skin showed significantly higher expression of CD68 and CD163 than non-lesional skin. Notably, CD163 expression was negatively correlated with clinical severity. Conclusion CD163-expressing M2 macrophages are associated with a low severity of psoriasis.

Pervanadate, a complex of vanadate and H2O2, has an insulin mimetic effect, and acts as an inhibitor of protein tyrosine phosphatase. Pervanadate-induced phospholipase D (PLD) activation is known to be dependent on the tyrosine phosphorylation of cellular proteins and protein kinase C (PKC) activation, and yet underlying molecular mechanisms are not clearly understood. Here, we investigated the signaling pathway of pervanadate-induced PLD activation in Rat2 fibroblasts. Pervanadate increased PLD activity in dose- and time- dependent manner. Protein tyrosine kinase inhibitor, genistein, blocked PLD activation. Interestingly, AG-1478, a specific inhibitor of the tyrosine kinase activity of epidermal growth factor receptor (EGFR) blocked not only the PLD activation completely but also phosphorylation of p38 mitogen- activated protein kinase (MAPK). However, AG-1295, an inhibitor specific for the tyrosine kinase activity of pletlet drived growth factor receptor (PDGFR) did not show any effect on the PLD activation by pervanadate. We further found that pervanadate increased phosphorylation levels of p38, extracellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK). SB203580, a p38 MAPK inhibitor, blocked the PLD activation completely. However, the inhibitions of ERK by the treatment of PD98059 or of JNK by the overexpression of JNK interacting peptide JBD did not show any effect on pervanadate-induced PLD activation. Inhibition or down-regulation of PKC did not alter the pervanadate-induced PLD activation in Rat2 cells. Thus, these results suggest that pervanadate-induced PLD activation is coupled to the transactivation of EGFR by pervanadate resulting in the activation of p38 MAP kinase.
Animals ; Cell Line ; Enzyme Activation/drug effects ; Fibroblasts ; Mitogen-Activated Protein Kinases/metabolism ; Phospholipase D/*metabolism ; Rats ; Receptor, Epidermal Growth Factor/*agonists/*metabolism ; Vanadates/*pharmacology ; src-Family Kinases/metabolism

BACKGROUND: Combination of metformin to reduce the fasting plasma glucose level and an α-glucosidase inhibitor to decrease the postprandial glucose level is expected to generate a complementary effect. We compared the efficacy and safety of a fixed-dose combination of voglibose plus metformin (vogmet) with metformin monotherapy in drug-naïve newly-diagnosed type 2 diabetes mellitus. METHODS: A total of 187 eligible patients aged 20 to 70 years, with a glycosylated hemoglobin (HbA1c) level of 7.0% to 11.0%, were randomized into either vogmet or metformin treatments for 24 weeks. A change in the HbA1c level from baseline was measured at week 24. RESULTS: The reduction in the levels of HbA1c was −1.62%±0.07% in the vogmet group and −1.31%±0.07% in the metformin group (P=0.003), and significantly more vogmet-treated patients achieved the target HbA1c levels of <6.5% (P=0.002) or <7% (P=0.039). Glycemic variability was also significantly improved with vogmet treatment, estimated by M-values (P=0.004). Gastrointestinal adverse events and hypoglycemia (%) were numerically lower in the vogmet-treated group. Moreover, a significant weight loss was observed with vogmet treatment compared with metformin (−1.63 kg vs. −0.86 kg, P=0.039). CONCLUSION: Vogmet is a safe antihyperglycemic agent that controls blood glucose level effectively, yields weight loss, and is superior to metformin in terms of various key glycemic parameters without increasing the risk of hypoglycemia.
Blood Glucose ; Diabetes Mellitus, Type 2 ; Fasting ; Glucose ; Hemoglobin A, Glycosylated ; Humans ; Hypoglycemia ; Metformin ; Weight Loss