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The Dynamax appliance is a treatment modality for the correction of the Skeletal II malocclusion characterized by a mandibular retrusion. Progressive mandibular advancement, maxillary expansion, control of maxillary growth, incisor torque and control of vertical facial development are incorporated into a two-part appliance. The design facilitates laboratory construction, clinical handling and patient acceptability. A prefabricated spring module forms the basis of the appliance, allowing both maxillary expansion and mandibular advancement. An easily adjustable progressive forward position of the lower jaw makes a construction bite unnecessary. The spring module provides most of the structure of the appliance so that minimal acrylic is required and the appliance is fully contained within the freeway space. Contact between the upper and lower parts of the appliance occurs posteriorly in the lingual sulcus. Here the depth permits an extended vertical contact, to maintain a protrusive mandibular position throughout the range of mandibular opening, including during sleep. The lower portion of the appliance may be fixed or removable and multibracket treatment can be carried out in one or both arches at the same time as the orthopaedics. [ABSTRACT FROM AUTHOR]

Background: In registration trials, zafirlukast, an asthma medication, caused asymptomatic elevated aminotransferase levels in up to 5% of participants. Until now, however, no cases of severe hepatitis attributed to zafirlukast have been reported.Objective: To report the clinical characteristics of three patients with severe hepatitis due to zafirlukast.Design: Case report.Setting: One community hospital and two university hospitals.Patients: Three middle-aged women taking zafirlukast, 20 mg twice per day.Intervention: Discontinuation of zafirlukast therapy in three patients, steroid therapy in two patients, and orthotopic liver transplantation in one patient.Measurements: Serum aminotransferase and bilirubin levels, standard blood tests for causes of hepatitis other than drug toxicity, and liver biopsy in two patients.Results: Patient 1 recovered spontaneously, had a severe relapse after inadvertent rechallenge with the medication, and ultimately made a complete recovery. Patient 2 developed subfulminant hepatic failure and required liver transplantation. Patient 3 developed severe hepatitis that improved after treatment with corticosteroids. Liver tissue was available from two patients and showed histologic changes commonly associated with drug reactions.Conclusion: Patients receiving zafirlukast may develop severe liver injury and should be observed for signs and symptoms of hepatitis. [ABSTRACT FROM AUTHOR]

The three reported cases demonstrate that troglitazone is an idiosyncratic hepatotoxin that can lead to irreversible liver injury. Thus, troglitazone should be prescribed with caution and should not be used as a first-line agent in the treatment of type II DM when potentially less toxic alternatives are available. It remains to be seen whether the hepatotoxicity associated with troglitazone is a drug-class effect or specific to troglitazone. Other thiazolidinediones currently in clinical trials may be able to provide the therapeutic benefits of troglitazone without significant hepatotoxicity. If troglitazone is used, frequent monitoring of serum aminotransferases and symptoms is mandatory. However, as illustrated by these and other cases reported to date, the onset of troglitazone-induced liver injury is insidious and temporally variable. Thus, the value of close monitoring and when, if ever, it is safe to stop such monitoring are currently unclear. [ABSTRACT FROM AUTHOR]

OBJECTIVES: Plasma endothelin-1 (ET-1) levels are increased in patients with cirrhosis and ET-1 production is increased in the liver itself during experimental injury. These data suggest a possible role for this vasoactive peptide in intrahepatic microcirculatory changes that contribute to the pathogenesis of portal hypertension in cirrhosis. Therefore the aims of this study were to determine whether ET-1 levels were abnormal in the livers of patients with cirrhosis and to investigate possible clinical correlates of altered hepatic ET-1 in cirrhosis. METHODS: Liver specimens were obtained from explants at the time of liver transplantation in 62 cirrhotic patients; 49 without pretransplantation transjugular intrahepatic portosystemic shunt (TIPS) and 13 with pretransplantation TIPS. The presence of ascites was evaluated by physical examination and ultrasonography. Control specimens consisted of livers with normal morphology obtained from patients who died from nonliver-related causes. Hepatic ET-1 was measured by enzyme immunoassay. RESULTS: Hepatic ET-1 levels in cirrhotics without (0.17 pg/mg liver tissue) or with TIPS (0.12 pg/mg) were higher than in control patients [0.04 pg/mg (p = 0.02 for ET-1 levels in cirrhotics with or without TIPS vs control)]. In cirrhotics without ascites who had not had TIPS, ET-1 levels (0.07 pg/mg [0.04-1.00]) were similar to those of the controls. In contrast, ET-1 content was increased in cirrhotics with small (0.11 pg/mg; p = 0.0002) and moderate-to-large (0.69 pg/mg; p = 0.0002) amounts of ascites compared to patients without ascites. There was a modest correlation between ET-1 levels and Child-Pugh score (correlation coefficient 0.32; p = 0.03) and ET-1 levels were significantly higher in patients with Child-Pugh score of 13 or greater (0.88 pg/mg; p = 0.02) than in those with Child-Pugh score of 12 or less (0.16 pg/mg). CONCLUSIONS: Hepatic tissue ET-1 levels are increased in the liver of patients with cirrhosis. This increase appears to be proportional to the severity of both liver disease and ascites. These data raise a possible role for ET-1 in modulation of intrahepatic resistance in cirrhotic portal hypertension. [ABSTRACT FROM AUTHOR]

Two West Indian patients with Kveim-biopsy proven sarcoidosis developed chronic cholestatic liver disease, clinically and biochemically similar to primary biliary cirrhosis. Liver histology revealed multiple granulomas with reduction in bile ducts and, in one patient, progression to biliary cirrhosis. Portal hypertension was present in both patients leading to severe variceal haemorrhage in one. Mitochondrial antibody was negative in both patients and when used in conjunction with the Kveim-Siltzbach skin test serves to differentiate chronic intrahepatic cholestasis secondary to sarcoidosis from primary biliary cirrhosis. [ABSTRACT FROM PUBLISHER]

Background: Hyperbilirubinemia after creation of transjugular intrahepatic portosystemic shunts (TIPS) has been attributed to hemolysis and portal diversion, but the causes and natural history of this condition remain unknown.Objective: To determine clinical outcomes and predictors of severe hyperbilirubinemia after TIPS creation.Design: Retrospective analysis of all patients who underwent TIPS creation from June 1990 to September 1996.Setting: Academic medical center.Patients: 19 adults who developed severe hyperbilirubinemia (bilirubin level > 171.0 micromol/L) within 1 month after TIPS creation were compared with 213 adults who did not develop hyperbilirubinemia after TIPS creation.Intervention: TIPS creation.Measurements: Laboratory measures and clinical outcomes.Results: According to laboratory indices, hemolysis was unlikely to have occurred. By 90 days, 95% of patients with hyperbilirubinemia had died or had undergone liver transplantation compared with 17% of controls (P < 0.001). Predictors of hyperbilirubinemia included nonalcoholic causes of liver disease (P = 0.01) and a pre-TIPS prothrombin time of 17 seconds or more (P = 0.016).Conclusions: Severe hyperbilirubinemia after TIPS creation heralds a high risk for death or need for liver transplantation. Reduced hepatic reserve predicts the development of hyperbilirubinemia. [ABSTRACT FROM AUTHOR]