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1.
J Int Med Res ; 49(1): 300060520982829, 2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-33496629

RESUMO

Bullous pemphigoid (BP) is an autoimmune disease that requires immunosuppressive therapy. Systemic corticosteroids are considered the standard treatment for moderate-to-severe BP. Kaposi's sarcoma (KS) is a rare multifocal endothelial tumour that affects the skin, mucosa and viscera. As an angioproliferative disease of obscure aetiopathogenesis and histogenesis, KS is associated with human herpesvirus 8 (HHV-8). This current case report describes a rare occurrence of extensive cutaneous KS in a 60-year-old Chinese male patient after oral methylprednisolone treatment for BP with an emphasis on its pathological characterization. A total of more than 40 nodules were found on his trunk and lower limbs covering more than 20% of his body surface area. Immunohistochemical staining of biopsy samples from the lesion showed the patient was positive for HHV-8, CD31, CD34, XIIIa, ERG and Ki-67. The Epstein-Barr virus test showed the patient tested negative for immunoglobulin (Ig)A and IgM, but was positive for IgG. Immunosuppression associated with the treatment for BP may activate a latent HHV-8 infection and induce the development of KS.


Assuntos
Infecções por Vírus Epstein-Barr , Penfigoide Bolhoso , Sarcoma de Kaposi , China , Herpesvirus Humano 4 , Humanos , Doença Iatrogênica , Masculino , Metilprednisolona/uso terapêutico , Pessoa de Meia-Idade , Penfigoide Bolhoso/induzido quimicamente , Penfigoide Bolhoso/tratamento farmacológico
2.
J Craniofac Surg ; 28(6): 1462-1467, 2017 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-28708646

RESUMO

BACKGROUND: Cultured epithelial cells transplantation is a known surgical technique for vitiligo. OBJECTIVE: To evaluate the factors influencing efficacy and safety of cultured epithelial cells transplantation in 9-month follow-up. METHODS: Demographic, clinical, and repigmentation outcomes were reviewed for patients with facial segmental vitiligo who had undergone cultured epithelial cells transplantation from November 2013 to July 2015 at the clinic of the Department of Dermatology, Huashan Hospital, China. RESULTS: Twenty-eight patients who had undergone cultured epithelial cells transplantation were included. A satisfactory result (>50% repigmentation) was achieved in 79% patients with facial segmental vitiligo in 9 months. The treatment effect was significantly different in 6th month (P = 0.032), 9th month (P = 0.006) compared with 3rd month. Disease stability did significantly affect repigmentation outcome in 9th month (Z = 2.113, P = 0.035). No significant difference was observed between single segmental type versus mixed type (Z = 1.081, P = 0.280). Adverse effects were nearly absent. CONCLUSION: Cultured epithelial cells transplantation is a relatively safe and effective therapy for facial segmental stable vitiligo patients.


Assuntos
Transplante de Células/métodos , Células Cultivadas/transplante , Células Epiteliais/transplante , Face/fisiopatologia , Vitiligo , Humanos , Vitiligo/fisiopatologia , Vitiligo/terapia
3.
J Burn Care Res ; 33(6): e295-308, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-22955159

RESUMO

Toxic epidermal necrolysis (TEN) represents the most severe drug-related skin condition that is potentially life-threatening with no well-established treatments. The application of corticosteroid therapy is controversial, whereas recently intravenous immunoglobulin (IVIG) therapy is emerging as a promising new method. A severity-of-illness score for TEN (SCORTEN) has gained acceptance in some western countries. In this study, our objectives were to assess the applicability of SCORTEN in Chinese patients with TEN and to evaluate the efficacy of the combination therapy of IVIG and corticosteroid in these patients. We performed a retrospective review of data from 61 patients with TEN treated at our intensive care unit from 2000 to 2010 to assess the performance of SCORTEN. In particular, 55 patients between 2002 and 2010 were grouped as a series to compare the therapeutic effects of corticosteroid therapy and IVIG combined therapy contemporaneously. During this period, 16 patients were administered with corticosteroid therapy and 39 were treated with the combination therapy. An initial dose of 1.5 mg/kg/day of methylprednisolone was given to all TEN patients. The combination therapy was combined with a total dose of 2 g/kg IVIG within 5 days. Areas under receiver operating characteristic curves and Hosmer-Lemeshow statistic were analyzed to illustrate the performance of SCORTEN. The comparison of the efficacy of the two therapies was conducted on the basis of clinical outcomes, standardized mortality ratio (SMR), and survival analysis. The overall actual mortality of patients between 2000 and 2010 was 16% (10/61), statistically insignificantly lower than predicted (24%, SMR = 67.98). Excellent discriminatory power (the areas under the receiver operating characteristic curves: 88.9, 88.2, 90.6%) and good calibration (P = .637, .833, .530) were found in all the groups. In patients admitted between 2002 and 2010, IVIG combined therapy showed a trend toward reducing the mortality rate (13%, SMR = 52.35), whereas corticosteroid monotherapy suggested no such difference (31%, SMR = 123.92). Besides, the cumulative survival rates of the combination therapy were higher at almost all the levels of SCORTEN (P = .002), especially at the score of 5 (P = 3.10 × 10⁻7). Compared with corticosteroid alone, the combination therapy arrested progression earlier (P = .013), although it did not significantly lead to a tapering of corticosteroid or a reduction of the time of hospitalization. We concluded that SCORTEN was generally applicable to Chinese patients with TEN. The comparison of the effect indicated that the combination therapy might achieve a better therapeutic effect than the administration of corticosteroid alone, especially in severe TEN patients.


Assuntos
Corticosteroides/uso terapêutico , Imunização Passiva/métodos , Imunoglobulinas Intravenosas/uso terapêutico , Metilprednisolona/uso terapêutico , Índice de Gravidade de Doença , Síndrome de Stevens-Johnson/tratamento farmacológico , Adulto , Área Sob a Curva , Biópsia , Distribuição de Qui-Quadrado , China , Feminino , Humanos , Unidades de Terapia Intensiva , Masculino , Curva ROC , Estudos Retrospectivos , Síndrome de Stevens-Johnson/mortalidade , Análise de Sobrevida , Resultado do Tratamento
4.
Pharmacogenomics ; 13(10): 1193-201, 2012 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-22909208

RESUMO

AIM: Allopurinol is widely used as an effective urate-lowering drug and is one of the most frequent causes of cutaneous adverse drug reactions (cADRs). Recently, a strong association of HLA-B*58:01 with allopurinol-induced severe cADRs was identified. This study investigated the predisposition to different types of allopurinol-cADRs conferred by HLA-B*5801 in a Han population from mainland China. PATIENTS & METHODS: HLA-B genotyping was performed on 38 Chinese patients with different types of allopurinol-cADRs from 2008 to 2011. RESULTS: All the allopurinol-cADR patients carried HLA-B*58:01, in contrast with only 11.11% (7/63) in the allopurinol-tolerant patients (odds ratio [OR] = 580.07; p < 0.0001) and 13.99% (80/572) in a Han Chinese population from the human MHC database (dbMHC; OR: 471.09; p < 0.0001) carried the genotype. Each type of allopurinol cADRs revealed a statistically significant association with HLA-B*58:01. In particular, the risk of allopurinol-induced maculopapular eruption was significantly higher in patients with HLA-B*58:01 (OR: 339.00; p < 0.0001). CONCLUSION: The strong association of both the mild and severe types of allopurinol cADRs with the HLA-B*58:01 allele were observed. The results indicated that the prospective use of a genetic test of HLA-B*58:01 might reduce the prevalence of allopurinol-induced cADRs. Original submitted 7 March 2012; Revision submitted 21 May 2012.


Assuntos
Alopurinol , Antígenos HLA-B/genética , Síndrome de Stevens-Johnson/genética , Adulto , Idoso , Idoso de 80 Anos ou mais , Alelos , Alopurinol/administração & dosagem , Alopurinol/toxicidade , China , Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/genética , Exantema/induzido quimicamente , Exantema/genética , Feminino , Predisposição Genética para Doença , Genótipo , Humanos , Masculino , Pessoa de Meia-Idade , Risco , Síndrome de Stevens-Johnson/induzido quimicamente
5.
Brain Res ; 1360: 159-67, 2010 Nov 11.
Artigo em Inglês | MEDLINE | ID: mdl-20828541

RESUMO

Astaxanthin (ATX), the most abundant flavonoids in propolis, has been proven to exert neuroprotective property against glutamate-induced neurotoxicity and ischemia-reperfusion-induced apoptosis. Previous study have revealed that ATX can rescue PC12 cells from Aß(25-35)-induced apoptotic death. However, the mechanisms by which ATX mediates its therapeutic effects in vitro are unclear. In the present study, we explored the underlying mechanisms involved in the protective effects of ATX on the Aß(25-35)-induced cytotoxicity in SH-SY5Y cells. Pre-treatment with ATX for 4h significantly reduced the Aß(25-35)-induced viability loss, apoptotic rate and attenuated Aß-mediated ROS production. In addition, ATX inhibited Aß(25-35)-induced lowered membrane potential, decreased Bcl-2/Bax ratio. We also demonstrated that ATX could prevent the activation of p38MAPK kinase pathways induced by Aß. Moreover, we for the first time have revealed the ATX increased antioxidant enzyme heme oxygenase-1 (HO-1) expression in concentration-dependent and time-dependent manners, which were correlated with its protective effect against Aß(25-35)-induced injury. Because the inhibitor of HO-1 activity, ZnPP reversed the protective effect of ATX against Aß(25-35)-induced cell death. We also demonstrated that the specific ERK inhibitor, PD98059, concentration-dependently blocked on ATX-induced HO-1 expression, and meanwhile PD98059 reversed the protective effect of ATX against Aß25-35-induced cell death. Taken together, these findings suggest that astaxanthin can induce HO-1 expression through activation of ERK signal pathways, thereby protecting the SH-SY5Y cells from Aß(25-35)-induced oxidative cell death.


Assuntos
Peptídeos beta-Amiloides/antagonistas & inibidores , Peptídeos beta-Amiloides/toxicidade , Heme Oxigenase-1/biossíntese , Proteína Quinase 1 Ativada por Mitógeno/fisiologia , Proteína Quinase 3 Ativada por Mitógeno/fisiologia , Fármacos Neuroprotetores , Fragmentos de Peptídeos/antagonistas & inibidores , Fragmentos de Peptídeos/toxicidade , Proteínas Reguladoras de Apoptose/biossíntese , Western Blotting , Morte Celular/efeitos dos fármacos , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Flavonoides/farmacologia , Heme Oxigenase-1/antagonistas & inibidores , Humanos , Metaloproteinases da Matriz/metabolismo , Proteína Quinase 1 Ativada por Mitógeno/antagonistas & inibidores , Proteína Quinase 3 Ativada por Mitógeno/antagonistas & inibidores , Estresse Oxidativo/efeitos dos fármacos , Inibidores de Proteínas Quinases/farmacologia , Espécies Reativas de Oxigênio/metabolismo , Regulação para Cima/efeitos dos fármacos , Xantofilas/antagonistas & inibidores , Xantofilas/farmacologia , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
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