RESUMO
Cachexia, a paraneoplastic syndrome markedly associated with worsened prognosis in cancer patients, provokes profound wasting of both lean and adipose mass in an association with a state of metabolic "chaos". The white adipose tissue responds to cachexia with marked local inflammation and may be thus a relevant contributor to systemic inflammation. To address this hypothesis we examined the correlation between tissue expression of adipokines and plasma concentration in cachectic and stable weight patients with or without cancer. Adiponectin and liver-derived CRP concentration were significantly higher in the cachectic groups when compared with stable weight patients (P<0.01). The concentration of plasma IL-6 was higher (11.4-fold) in the cancer cachectic group when compared with weight-stable controls, and presented a significant correlation with the presence of cancer (P<0.001). A marked increase (5-fold) in IL-6 as a result of the interaction between the presence of cachexia and the presence of tumour was observed in the subcutaneous tissue of the patients, yet not in the visceral depot. Plasma adiponectin levels were higher in cachectic cancer patients, compared with stable weight cancer patients individually matched by age, sex, and BMI, and the subcutaneous depot was found to be the main contributing tissue, rather than the visceral pad. Based on the results we concluded that the subcutaneous adipose tissue is associated with plasma changes that may function as markers of cachexia.
Assuntos
Tecido Adiposo/metabolismo , Biomarcadores Tumorais/sangue , Caquexia/sangue , Neoplasias/sangue , Adiponectina/sangue , Adiponectina/genética , Tecido Adiposo/patologia , Idoso , Caquexia/complicações , Caquexia/patologia , Feminino , Regulação da Expressão Gênica , Humanos , Mediadores da Inflamação/metabolismo , Interleucina-10/genética , Interleucina-10/metabolismo , Interleucina-6/sangue , Interleucina-6/genética , Leptina/genética , Leptina/metabolismo , Masculino , Pessoa de Meia-Idade , Estadiamento de Neoplasias , Neoplasias/complicações , Neoplasias/patologia , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismoRESUMO
Cancer cachexia is a multifaceted syndrome whose aetiology is extremely complex and is directly related to poor patient prognosis and survival. Changes in lipid metabolism in cancer cachexia result in marked reduction of total fat mass, increased lipolysis, total oxidation of fatty acids, hyperlipidaemia, hypertriglyceridaemia, and hypercholesterolaemia. These changes are believed to be induced by inflammatory mediators, such as tumour necrosis factor-α (TNF-α) and other factors. Attention has recently been drawn to the current theory that cachexia is a chronic inflammatory state, mainly caused by the host's reaction to the tumour. Changes in expression of numerous inflammatory mediators, notably in white adipose tissue (WAT), may trigger several changes in WAT homeostasis. The inhibition of adipocyte differentiation by PPARγ is paralleled by the appearance of smaller adipocytes, which may partially account for the inhibitory effect of PPARγ on inflammatory gene expression. Furthermore, inflammatory modulation and/or inhibition seems to be dependent on the IKK/NF-κB pathway, suggesting that a possible interaction between NF-κB and PPARγ is required to modulate WAT inflammation induced by cancer cachexia. In this article, current literature on the possible mechanisms of NF-κB and PPARγ regulation of WAT cells during cancer cachexia are discussed. This review aims to assess the role of a possible interaction between NF-κB and PPARγ in the setting of cancer cachexia as well as its significant role as a potential modulator of chronic inflammation that could be explored therapeutically.
Assuntos
Tecido Adiposo/metabolismo , Tecido Adiposo/patologia , Caquexia/complicações , Núcleo Celular/metabolismo , Inflamação/complicações , Neoplasias/complicações , Fatores de Transcrição/metabolismo , Animais , Caquexia/patologia , Humanos , Inflamação/patologia , Neoplasias/patologiaRESUMO
Nonpulmonary metastases from osteogenic sarcoma are rare. A patient had a localized osteogenic sarcoma of the left femur which recurred in the abdomen, a previously unreported metastatic site. An 18-year-old boy was treated for osteosarcoma. He had abdominal pain, vomiting, weight loss, and symptoms of intestinal obstruction at the time of relapse. The patient had diffuse widespread intraabdominal osteogenic sarcoma as the only site of initial recurrence. Abdominal computerized tomography revealed ascites and calcified masses on the hepatic and peritoneal surfaces. Laparoscopic visualization of the abdomen showed hemorrhagic ascites and multiple calcified tumor on the peritoneum, diaphragm, and liver. A biopsy of a representative lesion confirmed the diagnosis of osteogenic sarcoma. The patient died from progressive disease. As the initial treatment for patients with osteogenic sarcoma is intensified, the pattern of metastases may change. Unusual sites of recurrence such as in this patient may become more prevalent. A clinical presentation of an acute abdomen in a patient previously treated for osteogenic sarcoma should prompt suspicion of intraabdominal recurrence.
Assuntos
Humanos , Dor Abdominal , OsteossarcomaRESUMO
METHODS: The authors retrospectively review 22 patients with irresectable esophageal cancer in whom an isoperistaltic substernal gastric esophagogastric bypass was performed. RESULTS: After the operation eighteen patients (82%) regained normal swallowing. Seven patients developed anastomotic stenosis that was successfully treated in six by surgery or endoscopic dilatation. Two patients evolved with cervical fistulae until their death. As a whole, there was a statistically significant improvement in swallowing capability (p = 0.0352). Seventeen patients (77%) had postoperative complications, the most common being cervical fistulae (in 13.59%), pneumonia (in 10.45%) and anastomotic stenosis (in 7.32%). Postoperative morbidity was significantly associated with preoperative diseases and ASA class III (p < 0.05). There were three postoperative deaths (14%). Postoperative mortality was significantly related to severe malnutrition and preoperative associated disease (p < 0.05). CONCLUSIONS: The conclusion is that the procedure has acceptable morbidity and mortality for the population under consideration, permitting palliation of dysphagia in the majority of cases.
Assuntos
Carcinoma de Células Escamosas/cirurgia , Neoplasias Esofágicas/cirurgia , Esôfago/cirurgia , Cuidados Paliativos , Estômago/cirurgia , Adulto , Idoso , Carcinoma de Células Escamosas/complicações , Transtornos de Deglutição/etiologia , Transtornos de Deglutição/cirurgia , Neoplasias Esofágicas/complicações , Feminino , Humanos , Masculino , Métodos , Pessoa de Meia-Idade , Complicações Pós-Operatórias , Estudos Retrospectivos , Resultado do TratamentoRESUMO
BACKGROUND: Several studies in the literature have shown that older patients have a poor prognosis after the treatment of cancer. They are frequently considered to have a high surgical risk and undergo substandard treatment. PATIENTS AND METHODS: This case-control study analyzes complications, mortality, and survival in 115 patients 70 years of age or older and 115 controls matched by site and clinical stage. Most tumors were located at the oral cavity, salivary glands, pharynx, or larynx. RESULTS: The frequency of postoperative complications, mortality, and recurrences were similar in both groups. Twenty elderly patients and 9 controls died due to causes not related to cancer. The 5-year survival rates were 43% for the elderly patients and 55.6% for the control patients (P = 0.1038). CONCLUSION: The main causes of death in the elderly patients were not related to cancer or treatment complications. This emphasizes the need for the use of standard treatment for all patients who remain in good medical status.