RESUMO
BACKGROUND: Hepatocellular carcinoma is the most common cause of primary liver neoplasms and is one of the main causes of death in patients with liver cirrhosis. High Alpha fetoprotein serum levels have been found in 60-70% of patients with Hepatocellular carcinoma; nevertheless, there are other causes that increase this protein. Alpha fetoprotein levels > or =200 and 400 ng/mL in patients with an identifiable liver mass by imaging techniques are diagnostic of hepatocellular carcinoma with high specificity. METHODS: We analysed the sensitivity and specificity of the progressive increase of the levels of alpha fetoprotein for the detection of hepatocellular carcinoma in patients with liver cirrhosis. Seventy-four patients with cirrhosis without hepatocellular carcinoma and 193 with hepatic lesions diagnosed by biopsy and shown by image scans were included. Sensitivity and specificity of transversal determination of alpha fetoprotein > or = 200 and 400 ng/mL and monthly progressive elevation of alpha fetoprotein were analysed. Areas under the ROC curves were compared. Positive and negative predictive values adjusted to a 5 and 10% prevalence were calculated. RESULTS: For an elevation of alpha fetoprotein > or= 200 and 400 ng/mL the specificity is of 100% in both cases, with a sensitivity of 36.3 and 20.2%, respectively. For an alpha fetoprotein elevation rate > or =7 ng/mL/month, sensitivity was of 71.4% and specificity of 100%. The area under the ROC curve of the progressive elevation was significantly greater than that of the transversal determination of alpha fetoprotein. The positive and negative predictive values modified to a 10% prevalence are of: 98.8% and 96.92%, respectively; while for a prevalence of 5% they were of 97.4% and 98.52%, respectively. CONCLUSION: The progressive elevation of alpha fetoprotein > or =7 ng/mL/month in patients with liver cirrhosis is useful for the diagnosis of hepatocellular carcinoma in patients that do not reach alphaFP levels > or =200 ng/mL. Prospective studies are required to confirm this observation.
Assuntos
Carcinoma Hepatocelular/diagnóstico , Cirrose Hepática/sangue , Neoplasias Hepáticas/diagnóstico , alfa-Fetoproteínas/análise , Carcinoma Hepatocelular/sangue , Feminino , Humanos , Neoplasias Hepáticas/sangue , Masculino , Pessoa de Meia-Idade , Sensibilidade e EspecificidadeRESUMO
Hepatocellular carcinoma is the fifth most common malignant neoplasm worldwide. Most patients are not candidates to surgical treatment. The prognosis of this neoplasm is poor, with an overall survival rate of 8 weeks in unresectable tumors. Estrogen receptors have been found in up to 33% of this tumors, reason why treatment with tamoxifen or progesterone compounds have been tried to diminish this neoplasm's progression but its use remains controversial. In our institution, thirteen patients were treated with tamoxifen (20- 40 mg/day) and 26 received supportive measures only. The clinical and tumoral characteristics were similar in both groups. Survival in the Tamoxifen group was of 5.5 +/- 1.7 months while in the supportive measures group was of 2.1 +/- 0.5 months (p = 0.018). Other factors related to an increased survival were: female gender and the Okuda score; age, TNM and alphaFP were not related to survival. The multivariate analysis showed that treatment with tamoxifen duplicates survival independently of the tumoral stage and functional hepatic reserve. It seems that the benefit of treatment with tamoxifen is limited and is not associated to the presence of estrogen receptors. In our study a 69 year-old man with diagnosis of non-resectable hepatocellular carcinoma and negative estrogen receptors, was treated with tamoxifen with a partial response and an overall survival of 4 years until November 2005. Despite some case reports that have shown tumoral regression, while other studies do not report any survival benefits. It is important to identify patients that would benefit from treatment with tamoxifen.
Assuntos
Antineoplásicos Hormonais/uso terapêutico , Carcinoma Hepatocelular/tratamento farmacológico , Neoplasias Hepáticas/tratamento farmacológico , Receptores de Estrogênio/antagonistas & inibidores , Tamoxifeno/uso terapêutico , Carcinoma Hepatocelular/diagnóstico por imagem , Feminino , Humanos , Neoplasias Hepáticas/diagnóstico por imagem , Masculino , Pessoa de Meia-Idade , Estadiamento de Neoplasias , Cuidados Paliativos , Estudos Retrospectivos , Fatores Sexuais , Análise de Sobrevida , Tomografia Computadorizada por Raios XRESUMO
BACKGROUND: Hepatocellular carcinoma (HCC) is a malignant neoplasm associated with liver cirrhosis, with an annual incidence of 3% to 9%, which is one of the main causes of death in patients with cirrhosis. Viral hepatitis is associated with an increased risk of HCC, probably due to an inflammatory reaction. Colchicine is an antiinflammatory agent that inhibits the formation of intracellular microtubules, affecting mitosis and fibrogenesis. Diverse clinical studies have failed to demonstrate the benefit of colchicine over the progression of fibrosis in patients with liver cirrhosis; nevertheless, to the authors' knowledge there are no studies that evaluate its effect in the development of HCC. METHODS: The effect of the administration of colchicine on the development of HCC was evaluated in 186 patients with hepatitis virus-related liver cirrhosis in a retrospective cohort study. The minimum follow-up time was 3 years (median, 84 months +/- 2.8 months). One hundred sixteen patients received treatment with colchicine. The characteristics of both groups were similar. RESULTS: The percentage of patients who developed HCC was significantly smaller in the colchicine group when compared with the noncolchicine group (9% vs. 29%; P = .001). On multivariate analysis, an alpha-fetoprotein level > or = 5 ng/dL (P = .03), a platelet count < 100,000 at diagnosis (P = .05), alanine aminotransferase > or = 52 IU (P = .006), and a lack of treatment with colchicine (P = .0001) were found to be associated with an earlier development of HCC. The average time for the development of HCC was 222 months +/- 15 months and 150 months +/- 12 months in the patients who received and who did not receive colchicine, respectively. CONCLUSIONS: The results suggest that treatment with colchicine prevents and delays the development of HCC in patients with hepatitis virus-related cirrhosis. The protective mechanisms of colchicine over the development of HCC could be related to antiinflammatory properties and inhibition of mitosis. Prospective studies to confirm this observation with a greater number of patients and long-term follow-up may be indicated.
Assuntos
Carcinoma Hepatocelular/prevenção & controle , Colchicina/uso terapêutico , Hepatite Viral Humana/complicações , Cirrose Hepática/complicações , Cirrose Hepática/tratamento farmacológico , Neoplasias Hepáticas/prevenção & controle , Adulto , Anti-Inflamatórios/uso terapêutico , Estudos de Coortes , Feminino , Seguimentos , Humanos , Incidência , Cirrose Hepática/virologia , Masculino , Pessoa de Meia-Idade , Estudos RetrospectivosRESUMO
BACKGROUND: Craniopharyngioma is a rare, benign epithelial brain tumor of the suprasellar region with a high rate of recurrence. Clinical and histopathological features that might be predictors of recurrence/regrowth have not been clearly delineated. METHODS: We compared recurrence/regrowth of the tumors with the clinico-pathological characteristics, vascular density, cell proliferation index, and immunohistochemical profile (cytokeratins, epithelial membrane antigen [EMA], carcinoembrionary antigen [CEA], and laminin) of 47 patients with craniopharyngioma followed for more than 5 years. RESULTS: Tumors were adamantinomatous in 42 cases (89%) and papillary squamous in 5 cases (11%). Immunoreactivity for cytokeratin 8/18/19 was positive in 64%; cytokeratin 5 in 42%; laminin 8 in 62%; and CEA in 21%. The cell proliferation index and vascular density were greater in adamantinomatous than in papillary tumors (22+/-6 versus 17+/-3, p=0.05; and 21+/-3 versus 17+/-3, p=0.037, respectively); they were neither related to recurrence nor to regrowth. No significant differences were found between adamantinomatous and papillary tumors regarding the presence of cytokeratin, laminin, CEA or glial fibrillary acidic protein (GFAP). Recurrence rate at 5 years was 59%. No relation was found between recurrence and adjuvant radiotherapy (AR). Residual tumor after surgery, whorl-like arrays (p=0.04) and immunoreactivity for p53 (p=0.022) were significantly related to recurrence/regrowth. CONCLUSIONS: Residual tumor after surgery, immunoreactivity to p53 and presence of whorl-like arrays are associated to recurrence/regrowth of craniopharyngioma.
Assuntos
Neoplasias Encefálicas/diagnóstico , Neoplasias Encefálicas/fisiopatologia , Craniofaringioma/diagnóstico , Craniofaringioma/fisiopatologia , Recidiva Local de Neoplasia/epidemiologia , Adulto , Biomarcadores Tumorais/metabolismo , Neoplasias Encefálicas/metabolismo , Antígeno Carcinoembrionário/metabolismo , Proliferação de Células , Craniofaringioma/metabolismo , Células Epiteliais/metabolismo , Células Epiteliais/patologia , Feminino , Humanos , Imuno-Histoquímica , Queratinas/metabolismo , Laminina/metabolismo , Masculino , Mucina-1/metabolismo , Recidiva Local de Neoplasia/radioterapia , Recidiva Local de Neoplasia/cirurgia , Neovascularização Patológica/diagnóstico , Neovascularização Patológica/epidemiologia , Neovascularização Patológica/fisiopatologia , Valor Preditivo dos Testes , Prognóstico , Radioterapia/estatística & dados numéricos , Proteína Supressora de Tumor p53/metabolismoRESUMO
PURPOSE: The aim of this work was to study the effects of prolonged exposure to lead on the threshold of experimental seizures induced by pentylenetetrazole (PTZ). METHODS: The 120 Wistar male rats were allocated randomly into four groups; (A) controls, and lead-treatment groups (B, C, and D) that received lead acetate in the drinking water for a period of 30 days at concentrations of 250, 500, and 1,000 ppm, respectively. After exposure, a trial of PTZ-induced seizures was conducted in all groups, and blood contents of lead were determined by atomic absorption spectrophotometry. RESULTS: Blood lead contents increased in a dose-dependent manner. Time elapsed to develop the first myoclonic jerk and the tonic-clonic seizure was less in all lead-exposed groups than in controls. This effect was greater in the groups administered 500 and 1,000 ppm of lead. The required doses of PTZ to induce myoclonic jerks and tonic-clonic seizures were lower in lead-exposed rats than in controls. CONCLUSIONS: We found a reduction in the threshold for seizures in rats whose blood contents of lead were similar to those of humans from some areas of urban centers with high levels of air pollution.