The clinical course of generalized pustular psoriasis (GPP) is variable and unpredictable. Sufficient data on the clinical course of the disease has not been reported due to its rarity. To investigate the clinical features and course of GPP according to its subtypes, medical records of patients diagnosed with GPP from 2002 to 2012 at two tertiary hospitals were reviewed. The data included patient demographics, associated symptoms, aggravating factors, patterns of relapse and prognosis. Thirty-three patients with GPP were included in our study, with a mean age of 45.6 years and a male : female ratio of 1:1.2. Patients were categorized based on the following subtypes: acute GPP, 21 (63.6%); GPP of pregnancy, two (6.1%); juvenile GPP, three (9.1%); and annular GPP, seven (21.2%). In the acute GPP population, skin lesions cleared within 2 months in 11 (73.3%) patients, and six (40.0%) of these had no relapse. Severe complications, abortion or death, were observed in two patients (100.0%) with GPP of pregnancy. Nineteen (76.0%) of the GPP patients experienced persistence or relapse of skin lesions. The patterns of skin lesions upon relapse included plaques in six patients (31.6%), pustules in eight patients (42.1%), and plaques and pustules in five patients (26.3%). Among acute GPP patients, 16.7% of patients with no relapse had a history of plaque psoriasis. However, 77.8% of patients with persistence and relapse in their clinical course had a history of plaque psoriasis. In conclusion, our study presents the detailed clinical course of GPP by subtype in Korean patients.
Simvastatin, a 3-hydroxy-3-methylglutaryl coenzyme-A reductase inhibitor, is used to reduce cholesterol levels. Accumulating evidence has revealed the immunomodulatory and anti-inflammatory effects of simvastatin that prevent cardiovascular diseases. In addition, the beneficial effects of statins on fibrosis of various organs have been reported. However, the functional effect of statins on dermal fibrosis of keloids has not yet been explored. The objective of this study was to determine whether simvastatin could affect dermal fibrosis associated with keloids. We examined the effect of simvastatin on transforming growth factor (TGF)-β1-induced production of type I collagen, connective tissue growth factor (CTGF or CCN2), and α-smooth muscle actin (α-SMA). Keloid fibroblasts were cultured and exposed to different concentrations of simvastatin in the presence of TGF-β1, and the effects of simvastatin on TGF-β1-induced collagen and CTGF production in keloid fibroblasts were determined. The type I collagen, CTGF, and α-SMA expression levels and the Smad2 and Smad3 phosphorylation levels were assessed by Western blotting. The effect of simvastatin on cell viability was evaluated by assessing the colorimetric conversion of 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide. Simvastatin suppressed TGF-β1-induced type I collagen, CTGF, and α-SMA production in a concentration-dependent manner. The TGF-β1-induced Smad2 and Smad3 phosphorylation levels were abrogated by simvastatin pretreatment. The inhibition of type I collagen, CTGF, and α-SMA expression by simvastatin was reversed by geranylgeranyl pyrophosphate, suggesting that the simvastatin-induced cellular responses were due to inhibition of small GTPase Rho involvement. A RhoA activation assay showed that preincubation with simvastatin significantly blocked TGF-β1-induced RhoA activation. The Rho-associated coiled kinase inhibitor Y27632 abrogated TGF-β1-induced production of type I collagen, CTGF, and α-SMA. However, Y27632 had no significant effect on TGF-β1-induced phosphorylation of Smad2 and Smad3. In conclusion, the present study suggests that simvastatin is an effective inhibitor of TGF-β1-induced type I collagen, CTGF, and α-SMA production in keloid fibroblasts.
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