RESUMO
We present a case report indicating that the administration of phentermine, an appetite suppressant with sympathomimetic activity, can provoke an intracerebral hemorrhage. A 48-year-old woman with no previously established cerebrovascular risk fa ctors and who had taken phentermine for 30 days developed sudden-onset left hemiparesis. Brain magnetic resonance imaging revealed an acute intracerebral hemorrhage involving the right thalamus. This case indicates that physicians should be aware of the relevant cause of medication history including appetite suppressants in young patients with an acute intracerebral hemorrhage.
Assuntos
Feminino , Humanos , Pessoa de Meia-Idade , Depressores do Apetite , Apetite , Encéfalo , Hemorragia Cerebral , Imageamento por Ressonância Magnética , Paresia , Fentermina , TálamoRESUMO
BACKGROUND/AIMS: Although transcatheter arterial chemoembolization (TACE) is a major treatment modality for unresectable hepatocellular carcinoma (HCC), acute hepatic failure after TACE is not rare. However, reports dealing with this important complication are not good enough and results are often variable. The purpose of this study was to evaluate the incidence and associated risk factors of acute hepatic failure after TACE. METHODS: From January 2001 to November 2004, six hundred and thirtytwo TACE sessions were performed in 377 patients (294 men and 83 women). Adriamycin mixed lipiodol solution and gelfoam were used for TACE. Various clinical and radiological factors before and after the procedure were reviewed retrospectively. Univariate and multivariate analyses were performed to evaluate the risk factors associated with the development of acute hepatic failure after TACE. RESULTS: Acute hepatic failure occurred in 76 (12.0%) of the 632 TACE sessions within 14 days. Univariate analysis revealed that Child-Pugh class, 1st TACE, total bilirubin level, number of involved segments, total size of tumor, presence of right portal vein thrombosis (PVT) or main PVT, involvement of segment 1, 5, 6, 7, modified UICC stage, and doses of chemotherapeutic agent were significantly different between the patients with or without hepatic failure after TACE. Among them, elevated total bilirubin (p=0.001, E (beta)=1.449), presence of right (p=0.035, E (beta)=2.109) or main (p=0.011, E (beta)=4.067) PVT were independently associated factors in multivariate analysis. CONCLUSIONS: The incidence of acute hepatic failure after TACE was 12.0%. Elevated bilirubin level and portal vein thrombosis could be considered as the predictive factors for acute hepatic failure after TACE in HCC patients.