RESUMO
BACKGROUND: Hepatic recurrence is seen in approximately 40â% of patients undergoing hepatectomy for colorectal metastases. The authors assessed the benefit and the main prognostic factors for a second liver resection of recurrent colorectal metastases. METHODS: This study reports the experience with second liver resections for recurrent liver metastases at a German University Hospital. A total of 39 parameters from 60 patients were identified from a prospective database and analysed as to their influence on recurrence-free survival and overall survival. RESULTS: At a median follow-up of 26 months (range: 2-173 months) after second hepatic resection, recurrence-free survival at 3 and 5 years were 50â% and 37â%, respectively. The overall survival at three and five years were 61â% and 52â%, respectively. Recurrence was identified in 58.3â% of the patients. Recurrences involved exclusively the liver in 19 patients (31.6â%). By multivariate analysis (Cox proportional hazard model), a time interval between diagnosis of the liver metastases of less than 24 months after operation for colorectal primary carcinoma (HR: 6.47, p = 0.002), a CEA level of 4.0 ng/mL or more (HR: 3.48, p = 0.004) at the time of first liver metastases and a size of second liver metastases of 80 mm or more (HR: 4.73, p = 0.007) were independent prognostic factors for a reduced recurrence-free survival. A repeat recurrence of liver metastases without the option of curative resection was the only risk factor for overall survival after second hepatic resection (p = 0.009). In these cases, mortality risk was 4.51-fold, however, when the second liver recurrence was resectable, the mortality risk increased only 1.4-fold. CONCLUSIONS: Technically resectable recurrent colorectal hepatic metastases should be resected the same as the first metastases. Characteristics of the primary metastasis as well as parameters of the hepatic recurrence are shown to influence the prognosis of patients after resection of recurrent liver metastases. Repeat resection of colorectal liver metastases allows for improved survival in patients even after two previous liver operations.
Assuntos
Neoplasias Colorretais/cirurgia , Hepatectomia , Neoplasias Hepáticas/secundário , Neoplasias Hepáticas/cirurgia , Recidiva Local de Neoplasia/cirurgia , Adulto , Idoso , Neoplasias Colorretais/mortalidade , Neoplasias Colorretais/patologia , Comportamento Cooperativo , Intervalo Livre de Doença , Feminino , Alemanha , Hospitais Universitários , Humanos , Comunicação Interdisciplinar , Fígado/patologia , Neoplasias Hepáticas/mortalidade , Neoplasias Hepáticas/patologia , Masculino , Pessoa de Meia-Idade , Recidiva Local de Neoplasia/mortalidade , Recidiva Local de Neoplasia/patologia , Prognóstico , Modelos de Riscos Proporcionais , Reoperação , Carga TumoralRESUMO
Diabetes mellitus is a common disease among patients with pancreatic cancer and chronic pancreatitis, disorders of the exocrine pancreas. Different clinical features of diabetes are associated with these two conditions: hyperinsulinemia and peripheral insulin resistance are the prevailing diabetic traits in pancreatic cancer, whereas reduced islet cell mass and impaired insulin secretion are typically observed in chronic pancreatitis. Whether or not a causal relationship exists between diabetes and pancreatic carcinoma is an intriguing but unanswered question. Diabetes often precedes pancreatic cancer and is thus regarded as a potential risk factor for malignancy. Conversely, pancreatic cancer may secrete diabetogenic factors. Given these findings, there is increasing interest in whether close monitoring of the glycemic profile may aid early detection of pancreatic tumor lesions.
Assuntos
Complicações do Diabetes , Pancreatopatias/etiologia , Animais , Carcinoma Ductal Pancreático/complicações , Carcinoma Ductal Pancreático/metabolismo , Complicações do Diabetes/epidemiologia , Diabetes Mellitus/etiologia , Humanos , Pancreatopatias/complicações , Pancreatopatias/epidemiologia , Neoplasias Pancreáticas/complicações , Neoplasias Pancreáticas/metabolismo , Fatores de RiscoRESUMO
Less than 10% of pancreatic ductal adenocarcinomas are based on a hereditary syndrome. In contrast a positive family history for pancreatic cancer raises the individual risk for the development of pancreatic and extrapancreatic malignancies.While 70% of hereditary pancreatic carcinomas can be attributed to the familiar pancreatic cancer syndrome 30% are caused by other hereditary syndromes, e.g., Peutz-Jeghers syndrome or familial adenomatous polyposis. Furthermore, genetically determined pancreatitis (e.g., hereditary pancreatitis or cystic fibrosis) can lead to pancreatic cancer.Up to now conclusive data for routine screening of high risk patients are not available which is due in part to the difficult identification of high risk patients and the problematic classification of detected pancreatic lesions. Therefore, high risk patients should be included in controlled clinical trials for screening. Small pancreatic lesions are not clear indications for surgical resection as false positive results can hamper a clear diagnosis and prophylactic pancreatectomy is not recommended. In the case of a histologically proven carcinoma a prophylactic extension of resection might be reasonable. Prevention of familial pancreatic cancer can be achieved through nicotine abstinence.
Assuntos
Carcinoma Ductal Pancreático/genética , Carcinoma/genética , Neoplasias Pancreáticas/genética , Algoritmos , Carcinoma/patologia , Carcinoma/prevenção & controle , Carcinoma/cirurgia , Carcinoma Ductal Pancreático/patologia , Carcinoma Ductal Pancreático/prevenção & controle , Carcinoma Ductal Pancreático/cirurgia , Análise Mutacional de DNA , Diagnóstico Precoce , Humanos , Programas de Rastreamento , Neoplasias Primárias Múltiplas/diagnóstico , Neoplasias Primárias Múltiplas/genética , Pâncreas/patologia , Pancreatectomia , Neoplasias Pancreáticas/patologia , Neoplasias Pancreáticas/prevenção & controle , Neoplasias Pancreáticas/cirurgia , Linhagem , Fatores de Risco , Abandono do Hábito de Fumar , SíndromeRESUMO
The scapula is subdivided into head, collum, and blade. Due to the expression pattern of Emx2 and the absence of the scapula blade in Emx2 knockout mice, it has been suggested that Emx2 is involved in the formation of the scapula. Micromanipulation experiments revealed that ectoderm ablation over the somites does not affect Emx2 expression but inhibits the formation of the scapula blade indicating that Emx2 is not sufficient to induce scapula blade formation. Furthermore, we show that the formation of the scapula head is dependent, scapula blade formation independent of FGFR-1-mediated signaling. Overexpression of Emx2 does not influence scapula blade formation but leads to the development of an additional posterior digit in the anterior border of the limb. Taken together, the data presented implicate that Emx2 expression is necessary but not sufficient for the development of the scapula blade. It is not a marker for scapula development but rather provides positional information along the proximodistal and anterior-posterior limb axes, whereas the specificity of the developing skeletal elements is determined by the concerted interaction of Emx2 with other factors.