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1.
Minerva Gastroenterol Dietol ; 65(2): 85-90, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30488680

RESUMO

BACKGROUND: Ampullary cancer accounts for only 0.2% of gastrointestinal cancers. The objective of this study was to investigate the incidence, demographics, tumor characteristics, treatment, and survival of patients with ampullary tumors. METHODS: Data on ampullary cancer between 2004 and 2013 was extracted from the Surveillance, Epidemiology and End Results (SEER) Registry. The clinical epidemiology of these tumors was analyzed using SEER*Stat. RESULTS: A total of 6803 patients with ampullary cancer were identified. Median age at diagnosis was 71±13 years. The overall age-adjusted incidence of ampullary cancer was 0.59 per 100,000 per year. A higher incidence of ampullary cancer was observed in males compared to females (0.74 vs. 0.48 per 100,000 per year). Most tumors were moderately differentiated (39.5%). The most common stage at presentation was Stage I (21%), followed by Stage II (20%). The majority (63%) of these tumors were surgically resected while 20% of patients received radiotherapy. One and 5-year cause-specific survival for ampullary cancer was 71.7% and 38.8% respectively, with a median survival of 31 months. On Cox regression analysis, black race, increasing cancer stage and grade, N1 stage, and non-surgical treatment were associated with poorer prognosis. Those who were not treated with surgical intervention were at 4.5 times increased risk for death (hazard ratio 4.5, 95% CI: 3.93-5.09, P=0.000). CONCLUSIONS: The annual incidence of ampullary cancer has been fairly constant, though males are more likely to be affected. While its incidence increases with age, patients who are treated by surgical intervention have significantly better outcomes. Additionally, through the use of endoscopic techniques, ampullary cancer can be detected and treated much earlier.


Assuntos
Ampola Hepatopancreática , Neoplasias do Ducto Colédoco , Idoso , Idoso de 80 Anos ou mais , Estudos de Coortes , Neoplasias do Ducto Colédoco/diagnóstico , Neoplasias do Ducto Colédoco/epidemiologia , Neoplasias do Ducto Colédoco/mortalidade , Neoplasias do Ducto Colédoco/terapia , Demografia , Feminino , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Programa de SEER , Taxa de Sobrevida
2.
Hypertension ; 58(4): 716-24, 2011 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-21859968

RESUMO

Preeclampsia (PE) is a life-threatening, pregnancy-induced disease and a leading cause of maternal and fetal morbidity and mortality. Despite considerable research, the causes of PE remain unclear, and there is no effective treatment. Studies in animal models that resemble this complex pregnancy-related disorder may help to identify possible therapies for PE. Complement component C1q has an important role in trophoblast migration, spiral arteries remodeling, and normal placentation. Here we show that pregnant C1q-deficient (C1q(-/-)) mice recapitulate the key features of human PE: hypertension, albuminuria, endotheliosis, decreased placental vascular endothelial growth factor (VEGF) and elevated levels of soluble VEGF receptor 1 (sFlt-1) that correlate with increased fetal death. In addition, decreased blood flow and increased oxidative stress are observed in placentas from C1q(-/-) mice. Treatment of C1q(-/-) mice with pravastatin restored trophoblast invasiveness, placental blood flow, and angiogenic balance and, thus, prevented the onset of PE. Serum-soluble receptors for VEGF-1 levels were reduced and placental VEGF levels were significantly increased in C1q(-/-) mice treated with pravastatin compared with untreated C1q(-/-) mice (VEGF: 1067±171 versus 419±194 pg/mL; P<0.01). Pravastatin treatment reduced hypertension (change in mean arterial pressure: 1±1 versus 18±3 mm Hg in C1q(-/-) untreated mice), and albuminuria (of creatinine) was reduced from 820±175 to 117±45 µg/mg (both P<0.01). Renal damage and endothelial dysfunction were significantly attenuated with pravastatin. This model that highlights the causative role of impaired trophoblast invasion in the pathogenesis of PE allowed us to identify pravastatin as a good therapeutic option to prevent PE.


Assuntos
Complemento C1q/fisiologia , Modelos Animais de Doenças , Pré-Eclâmpsia/fisiopatologia , Animais , Pressão Sanguínea/fisiologia , Movimento Celular/efeitos dos fármacos , Colagenases/metabolismo , Complemento C1q/deficiência , Complemento C1q/genética , Feminino , Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia , Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico , Camundongos , Camundongos Knockout , Placenta/irrigação sanguínea , Placenta/metabolismo , Pravastatina/farmacologia , Pravastatina/uso terapêutico , Pré-Eclâmpsia/metabolismo , Pré-Eclâmpsia/prevenção & controle , Gravidez , Fluxo Sanguíneo Regional/efeitos dos fármacos , Fluxo Sanguíneo Regional/fisiologia , Trofoblastos/citologia , Fator A de Crescimento do Endotélio Vascular/metabolismo , Receptor 1 de Fatores de Crescimento do Endotélio Vascular/metabolismo
3.
PLoS One ; 5(10): e13663, 2010 Oct 27.
Artigo em Inglês | MEDLINE | ID: mdl-21048973

RESUMO

BACKGROUND: Pre-eclampsia, a pregnancy-specific multisystemic disorder is a leading cause of maternal and perinatal mortality and morbidity. This syndrome has been known to medical science since ancient times. However, despite considerable research, the cause/s of preeclampsia remain unclear, and there is no effective treatment. Development of an animal model that recapitulates this complex pregnancy-related disorder may help to expand our understanding and may hold great potential for the design and implementation of effective treatment. METHODOLOGY/PRINCIPAL FINDINGS: Here we show that the CBA/J x DBA/2 mouse model of recurrent miscarriage is also a model of immunologically-mediated preeclampsia (PE). DBA/J mated CBA/J females spontaneously develop many features of human PE (primigravidity, albuminuria, endotheliosis, increased sensitivity to angiotensin II and increased plasma leptin levels) that correlates with bad pregnancy outcomes. We previously reported that antagonism of vascular endothelial growth factor (VEGF) signaling by soluble VEGF receptor 1 (sFlt-1) is involved in placental and fetal injury in CBA/J x DBA/2 mice. Using this animal model that recapitulates many of the features of preeclampsia in women, we found that pravastatin restores angiogenic balance, ameliorates glomerular injury, diminishes hypersensitivity to angiotensin II and protects pregnancies. CONCLUSIONS/SIGNIFICANCE: We described a new mouse model of PE, were the relevant key features of human preeclampsia develop spontaneously. The CBA/J x DBA/2 model, that recapitulates this complex disorder, helped us identify pravastatin as a candidate therapy to prevent preeclampsia and its related complications. We recognize that these studies were conducted in mice and that clinical trials are needed to confirm its application to humans.


Assuntos
Modelos Animais de Doenças , Pré-Eclâmpsia/terapia , Animais , Pressão Sanguínea , Feminino , Leptina/sangue , Camundongos , Camundongos Endogâmicos CBA , Camundongos Endogâmicos DBA , Pravastatina/administração & dosagem , Pré-Eclâmpsia/fisiopatologia , Gravidez , Resultado da Gravidez , Fator A de Crescimento do Endotélio Vascular/antagonistas & inibidores , Fator A de Crescimento do Endotélio Vascular/sangue
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