Prediction of liver fibrosis according to serum collagen VI level in children with cystic fibrosis.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to B Gerling.
Explore the source record for details and available documents.
BACKGROUND/AIMS: The aminoterminal procollagen type-III-peptide, which can be released during collagen type III deposition, has been suggested as a serum marker of fibrogenesis in patients with chronic liver disease. However, longitudinal studies correlating procollagen type-III-peptide concentrations in serum with the evolution of liver fibrosis are still needed. The purpose of the present study was to prove the significance of procollagen type-III-peptide concentrations in serum as a non-invasive marker of liver fibrogenesis in an animal model that best resembles progressive human liver fibrosis. METHODS: In 88 female Wistar rats the biliary system was occluded by double ligation of the choledochal duct followed by retrograde injection of a mixture of prolamine/ethanole (Ethibloc). Sixteen rats served as controls. Groups of 8-10 rats were sacrificed at days 2, 7, 14, 21, 30, 32, 35, 60 and 90 after bile duct occlusion. In the groups histological staging (fibrosis score), determination of total liver hydroxyproline, measurement of serum procollagen type-III-peptide and routine liver function tests were performed. RESULTS: First histological signs of liver fibrosis were seen as early as 7 days after bile duct occlusion. Progressive fibrosis was paralleled by an increase of serum procollagen type-III-peptide. There was a significant correlation between serum procollagen type-III-peptide and histological stages of fibrosis (r = 0.80; p < 0.0001) as well as between serum procollagen type-III-peptide and hydroxyproline in total liver tissue (r = 0.85; p < 0.0001) CONCLUSIONS: These results indicate that: (1) complete bile duct occlusion in rats produces progressive hepatic fibrosis resembling human secondary biliary fibrosis, and (2) procollagen type-III-peptide concentrations in serum reflect ongoing collagen formation in the liver unrelated to serum markers of cholestasis and inflammation.
On one occasion during a busy ICD follow-up clinic, the preceding patient's parameters for rate, PDF, and delay were inadvertently programmed into the subsequent patient's generator using the CPI Programmer Model 2035. This occurred after capacitor reformation, without pressing the "Program" button. The source of this reprogramming error was failure to clear the programmer memory of the previous patient's data, usually achieved by turning the programmer off between patients (or selecting "New Patient" from the menu). At our next ICD follow-up clinic, we purposely did not turn off the programmer between two sets of patients. On both occasions the above finding was repeated and confirmed. These observations indicate the potential for serious reprogramming errors that can occur simply by not clearing the programmer's memory between clinic patients.
We describe a patient in whom multiple episodes of pulmonary and systemic embolization occurred in the setting of right ventricular infarction. The mechanism of paradoxical embolization was determined based on transesophageal echocardiographic findings that included right atrial spontaneous contrast, appendage thrombosis, patent foramen ovale with right-to-left atrial shunting, and absence of left ventricular thrombosis. Recurrent thromboembolization was prevented by percutaneous placement of a "clam-shell" occluder across the patent foramen. This clinical scenario may be more common than previously believed and is best detected with transesophageal echocardiography. Early identification of this condition can lead to prompt treatment and prevention of subsequent thromboembolic morbidity.
Radionuclide-based procedures have achieved frequent application in acute myocardial infarction (MI). While these methods can be employed in diagnosis and assessment of therapy, diagnosis usually can be made more easily and with less expense when other methods are employed. Assessment of therapy, while potentially of value, has not been evaluated in a manner which can provide practical guidelines for clinical application. Practical utility has been associated with the use of radionuclide-based techniques in prognostication after infarction; this application is crucial to the formulation and optimization of management decisions. While myocardial perfusion scintigraphy and infarct-avid-agent imaging have been employed in prognostication after infarction, the largest body of prognostic data are available in association with radionuclide cineangiography. When determined in the early hours after infarction, a left ventricular ejection fraction (LVEF) less than 30% indicates a high likelihood of in-hospital mortality, irrespective of the site of infarction. When determined shortly prior to hospital discharge, LVEF less than 30% indicates a high likelihood of posthospital mortality, perhaps as high as 25% during the first year, and reaching 30% by the end of 2 years after infarction. Conversely, LVEF greater than or equal to 30% indicates an 8% 2-year postinfarction mortality risk. While LVEF is a highly potent risk descriptor, considerable evidence suggests the LVEF determined during exercise prior to hospital discharge also provides risk stratification, and may be superior to, or at least additive to, LVEF at rest as a prognostic index.(ABSTRACT TRUNCATED AT 250 WORDS)
Explore the source record for details and available documents.