ABSTRACT
The various forms of Percutaneous Endoscopic Gastrostomy (PEG) are highly relevant in neurology, as pump-administered intrajejunal levodopa application is one of the indispensable forms of therapy in advanced Parkinson's disease. Optimal PEG placement and follow-up are therefore significant for the success of the therapy. However, the standard intrajejunal administration of levodopa gel via a JET-PEG, i. e. a PEG with an internal catheter inserted into the jejunum, is not without problems for various reasons. In particular, the considerable cumulative complication rates demand a reconsideration of the situation. The very limited absorption area of the drug in the region of the flexura duodenojejunalis must also be taken into account. Causes of complications are predominantly a non-optimal application technique of PEG and internal catheter as well as the frequent lack of an adequate follow-up. In this paper, the details of a modified and optimized application technique compared to the conventional techniques are presented. These new methods have proved their usefulness in clinical applications for years, and additionally a new application form, the Hybrid-PEG, is presented. However, many of the details derived from anatomical/physiological, surgical and endoscopic aspects must be strictly observed during the application in order to reduce or avoid minor and major complications. In particular, problems are caused by local infections in the area of the insertion point of the PEG including peritonitis, leaks and buried bumper syndrome (BBS). The relatively frequent dislocations of the internal catheter also prove to be particularly troublesome. These can ultimately be avoided by clip fixation of the catheter tip down in the jejunum. In particular, the use of the newly developed Hybrid-PEG, a combination of endoscopically controlled gastropexy with three sutures and subsequent central thread-pull-through of the PEG tube, can significantly reduce the complication rate and thus achieve a decisive improvement for patients. The aspects discussed here are highly relevant for all those involved in the therapy of advanced Parkinson's disease. Trustful interdisciplinary collaboration between neurology and endoscopy/surgery/gastroenterology is a prerequisite for good clinical outcomes.
ABSTRACT
The human serine/threonine kinase hSGK1 is expressed ubiquitously with highest transcript levels in pancreas and liver. This study has been performed to determine the hSGK1 distribution in normal liver and its putative role in fibrosing liver disease. HSGK1-localization was determined by in situ hybridization, regulation of hSGK1-transcription by Northern blotting, fibronectin synthesis and hSGK1 phosphorylation by Western blotting. In normal liver hSGK1 was mainly transcribed by Kupffer cells. In liver tissue from patients with chronic viral hepatitis, hSGK1 transcript levels were excessively high in numerous activated Kupffer cells and inflammatory cells localized within fibrous septum formations. HSGK1 transcripts were also detected in activated hepatic stellate cells. Accordingly, Western blotting revealed that tissue from fibrotic liver expresses excessive hSGK1 protein as compared to normal liver. TGF-beta1 (2 ng/ml) increases hSGK1 transcription in both human U937 macro-phages and HepG2 hepatoma cells. H(2)O(2) (0.3 mM) activated hSGK1 and increased fibronectin formation in HepG2 cells overexpressing hSGK1 but not in HepG2 cells expressing the inactive mutant hSGK1(K127R). In conclusion hSGK1 is upregulated by TGF-beta1 during hepatitis and may contribute to enhanced matrix formation during fibrosing liver disease.
