Vol. 3 Issue 1
On the cover: Official Journal of the Mexican Association of Hepatology
The treatment of chronic hepatitis C virus (HCV) has improved greatly over the past decade. Over half of all patients treated with the combination of peginterferon and ribavirin have the opportunity to achieve sustained virologic response. The major factors which interfere with this goal are the side effects of therapy which require that the doses of peginterferon or ribavirin be reduced or that these medications be discontinued. While some of these side effects can be overcome and treatment continued, some side effects are severe and potentially life threatening. Appropriate recognition and management of these side effects will both improve response to therapy and avoid unnecessary morbidity and mortality.
Treatment of experimental animals with prototypical enzyme inducers represents a useful tool to characterize the role of different isozymes in drug metabolism and to improve our knowledge on factors regulating their synthesis at the transcriptional level. The effect of model enzyme inducers on phase II (conjugating) enzyme families, including UDP-glucuronosyltransferase’s and glutathione-S-transferase’s, has been well characterized in rodent liver. More recently, the effect of inducers on the expression of canalicular multidrug resistance-associated protein 2 (Mrp2) has been focused upon. The identification of a number of conjugated drugs as Mrp2 substrates suggests that both the conjugation and transport systems act coordinately to improve drug elimination from the body. We provide evidence about circumstances resulting in the simultaneous upregulation of phase II enzymes and Mrp2 in hepatic and extrahepatic tissues, most likely involving activation of common nuclear receptors (e.g. FXR, PXR). Additionally, we provide an analysis of examples of drug-induced toxicity leading to the simultaneous downregulation of both systems. Potential therapeutic strategies based on the modulation of expression of these systems are also briefly commented upon.
Background: In the last decades it has been suggested that the main cause of liver cirrhosis in Mexico is alcohol. Currently in Western countries hepatitis C virus (HCV) infection is one of the leading causes of endstage liver disease and liver transplantation. In Mexico, we have no data relative to the etiology of liver cirrhosis. The aim of this study was to investigate the main causes of liver cirrhosis in Mexico. Methods: Eight hospitals located in different areas of the country were invited to participate in this study. Those hospitals provide health care to different social classes of the country. The inclusion criteria were the presence of either an histological or a clinical and biochemical diagnosis of liver cirrhosis. Results: A total of 1,486 cases were included in this study. The etiology of liver cirrhosis was alcohol in 587 (39.5%), HCV 544 (36.6%), cryptogenic 154 (10.4%), PBC 84 (5.7), HBV 75 (5.0%) and other 42 (2.8). There was not statistical difference between alcohol and HCV. Conclusions: We conclude that the main causes of liver cirrhosis in Mexico are alcohol and HCV.
Introduction: The hemostatic system in newborn is a dynamic evolving process health-status dependent. Objective. To explore the changes in coagulation inhibitors and fibrinolytic system in newborn with neonatal cholestasis, according liver damage intensity. Methods: In a cross-sectional design, we studied fibrinolysis and coagulation inhibitor proteins, and serum ferritin (SF) in patients with neonatal cholestasis. We stratified the cases according the results of ALT or AST < 100 UI (group I) and ≥100 U/L (group II). Results: We included 24 newborn, 8 for Group I and 16 cases for group II. We documented statistical differences in ATIII values (43.4 vs 27.4%, p < 0,01), plasmin inhibitor (93.5 vs 63.6%, p < 0.01), SF (649 vs 1410 ug/L, p 0.01). The group II cases showed association with SF values (f 20.6, p < 0.01) and plasmin inhibitor (f 40.4, p < 0.01). AST and ALT were related significantly to ATIII concentrations and SF. Discussion: We documented tendency to prothrombotic state (lower ATIII and greater plasmin inhibitor activity), with low plasminogen related to the intensity of liver dysfunction in neonatal cholestasis. We need to determine the role of iron overload in physiopathology of the disease.
A 30-year-old woman presented with hepatomegaly and an audible hepatic bruit at 24 weeks gestation. Non-contrast MRI demonstrated an exophytic 12.6 x 7.8 x 12.8 cm mass arising from the right lobe of the liver with a central scar, suggestive of focal nodular hyperplasia (FNH). Conservative management included monthly abdominal ultrasound examinations until the time of delivery, to assess growth of the mass and monitor for risk of rupture. Seven weeks post partum the patient experienced severe right upper quadrant pain. A CT angiogram of the liver demonstrated a stable mass with no evidence of bleed or rupture and multiple hypervascular masses throughout the liver. Surgical resection of the dominant lesion was performed. Histological examination of the lesion confirmed FNH. The patient is now 22 months post surgery with radiographic evidence of stable multifocal FNH.