Kurt Grüngreiff

University Hospital Magdeburg

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Dirk Reinhold

Otto-von-Guericke University Magdeburg

Heiner Wedemeyer

Medizinische Hochschule Hannover

Annegret Reinhold

Otto-von-Guericke University Magdeburg

Karina Guttek

Otto-von-Guericke University Magdeburg

Karin Weißenborn

Medizinische Hochschule Hannover

G. Kircheis

Klinikum Brandenburg

Manfred Wiese

University Hospital Leipzig

Claudia Schubert

University Medical Center Hamburg-Eppendorf

H Tenckhoff

University Hospital Leipzig

U. Kullig

Krankenhaus Dresden-Friedrichstadt

Cooperative Institutions

Medizinische Hochschule Hannover

Otto-von-Guericke University Magdeburg

University Hospital Magdeburg

Goethe University Frankfurt

German Center for Infection Research

University College London

University Hospital Frankfurt

Klinikum Magdeburg

Charité - Universitätsmedizin Berlin

Leipzig University

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HepNet-Register zur sekundären Prävention der hepatischen Enzephalopathie (HE-Register)

Zeitschrift für Gastroenterologie (2018)

MM Gabriel G. Kircheis Svenja Hardtke Daniel Markwardt Peter Buggisch

Die hepatische Enzephalopathie (HE) ist eine häufige Komplikation der Leberzirrhose und hat wesentlichen Einfluss auf die Lebensqualität. Zudem steigt mit jeder manifesten HE-Episode das Risiko, kurzfristig eine weitere Episode zu erleiden oder zu versterben. Entsprechende Daten sind jedoch überwiegend älteren Datums und nicht unter den aktuellen Behandlungsmöglichkeiten erhoben.

10.1055/s-0038-1668846

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A Polymorphism Near IL28B Is Associated With Spontaneous Clearance of Acute Hepatitis C Virus and Jaundice

Gastroenterology (2010)

Hans L. Tillmann A. Thompson Keyur Patel Manfred Wiese H Tenckhoff

Pegylated interferon

10.1053/j.gastro.2010.07.005

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Citations (322)

[Behavior of plasma amino acids in alcohol-induced chronic liver diseases].

PubMed (1983)

Kurt Grüngreiff Kleine Fd B Lössner

In chronic liver diseases of alcoholic and non-alcoholic origin there are strikine differences of aspartate, glutamate and prolin. Where as plasma levels of aspartate and prolin are in most cases higher than in non-alcoholics, glutamate shows a contrary behaviour except in hepatic coma. The plasma ratio of alpha-amino-butyric acid to leucin allows no distinction of alcoholic from non-alcoholic liver lesion.

Chronic alcoholic

Coma (optics)

Chronic alcoholism

Hepatic coma

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P: 47 Risk of Recurrent Hepatic Encephalopathy (HE) in Patients With Liver Cirrhosis: A German Registry Study

The American Journal of Gastroenterology (2019)

Maria M. Gabriel G. Kircheis Svenja Hardtke Daniel Markwardt Peter Buggisch

BACKGROUND: Patients with Hepatic Encephalopathy (HE) show a low quality of life, recurrent hospitalizations and an increased mortality. We aimed to assess the natural course of patients after a recent HE-episode under the conditions of the German health system, as respective data were not available. METHODS: Fifteen sites from Germany - 8 of them liver transplant (LT) centers - took part in an observational prospective study including cirrhotic patients who had been hospitalized due to an acute episode of HE within 3 months before recruitment. Age < 18 years, no liver cirrhosis, malignancies and current hospitalization were exclusion criteria. Demographic and clinical data, health related quality of life (HRQoL) score SF-36, psychometric hepatic encephalopathy score (PHES) and critical flicker frequency (CFF) were assessed and monitored quarterly for one year. Primary endpoint was a novel clinical manifestation of HE necessitating hospital admission. Secondary endpoints were the combined endpoint of hospital admission for a novel HE episode and/or death, the dynamics of the West Haven Criteria (WHC) as well as changes in CFF, PHES and SF-36. RESULTS: A total of 115 patients were recruited. Fourteen patients (12.4 %) died during the study period due to complications of liver cirrhosis other than HE. For 67 subjects follow-up data were available in accordance with the protocol. After a median of 113 days half of the per protocol cohort (N = 34) was re-admitted due to a recurrent manifestation of HE. The patient groups with and without re-hospitalization differed significantly regarding recruitment sites (LT centers vs no LT centers) ( P = 0.005), interval from discharge to recruitment ( P = 0.007), history of more than 4 HE relapses prior to recruitment ( P = 0.029), SF-36 mental score ( P = 0.046) and PHES ≤ −3 ( P = 0.004), whereas CFF, clinical (e.g. MELD score, WHC grade) and laboratory data did not differ. Of note, CFF performance was correct only in about half of both, the total and the per protocol group. Patients with incorrect CFF performance had worse PHES results than those with valid CFF measurement. Multiple logistic regression analysis revealed a PHES test result of ≤−3 as an independent risk factor for re-hospitalization ( P = 0.046). CONCLUSIONS: Mortality in our cohort is comparatively low. Despite advanced treatment strategies, patients with a history of HE are still sincerely jeopardized to develop recurrent clinical HE. The PHES test appears useful for detection, monitoring and stratification of recurrent HE. Patients with PHES ≤−3 at baseline had an increased risk of deterioration.

Hepatic Encephalopathy

10.14309/01.ajg.0000582164.18169.ac

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Why a pinch of zinc in liver disease matters

Annals of Hepatology (2023)

Kurt Grüngreiff Dirk Reinhold Wolfgang Maret

Liver disease

10.1016/j.aohep.2023.101152

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[Pneumoperitoneum without obvious perforation--a case history].

PubMed (1978)

T Höfs Kurt Grüngreiff Kleine Fd Stephanie A. Kleine

Perforation

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Evaluation of liver disease progression in the German hepatitis C virus (1b)-contaminated anti-D cohort at 35 years after infection

Hepatology (2013)

Manfred Wiese Janett Fischer Micha Löbermann Uwe Göbel Kurt Grüngreiff

The natural course of HCV infection remains controversial. The German HCV (1b)-contaminated anti-D cohort provides an ideal population to investigate the natural course of HCV infection in a large, homogenous cohort of young women from the date of HCV inoculation. Our previous follow-up studies at 20 and 25 years after infection suggested slow fibrosis progression rates in this unique cohort. The aim of our prospective, community-based, multicenter study was to reevaluate the liver disease progression in 718 patients of the original anti-D cohort at 35 years after infection. Patients with self-limited HCV infection (n = 189) were compared to those who failed to eliminate the virus spontaneously (n = 529), comprising patients who were treatment naïve (n = 197) or achieved a sustained virological response (SVR; n = 149), respectively, failed to clear the virus (non-SVR; n = 183) after antiviral therapy. In the overall cohort, 9.3% of patients showed clinical signs of liver cirrhosis at 35 years after infection. Liver disease progression largely depended on HCV infection status. The highest proportion of patients with clinical signs of end-stage liver disease was observed in the non-SVR group (15.3%), whereas decreased cirrhosis rates were detected in the SVR group (6%) and in patients with self-limited HCV infection (1.1%; P = 6.2 × 10(-6)). Overall survival was significantly enhanced after SVR, compared to treatment-naïve patients or non-SVR (P = 0.027).The present study provides further evidence for a mild, but significant, disease progression at 35 years after infection in the German HCV (1b)-contaminated anti-D cohort. Patients with self-limited HCV infection or SVR after antiviral treatment were protected from progressive liver disease and showed the best clinical long-term outcome.

Liver disease

10.1002/hep.26644

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Citations (89)

Combined Treatment with Zinc Aspartate and Intravenous Immunoglobulins (IVIGs) Ameliorates Experimental Autoimmune Encephalomyelitis (EAE)

Journal of Immunology Research (2018)

Diana Straubel Anja Thielitz Annegret Reinhold Kurt Grüngreiff Dirk Reinhold

Intravenous immunoglobulins (IVIGs) are widely used in replacement therapy of primary and secondary immunodeficiency disorders and in approved autoimmune indications. In addition, IVIG application is used off-label for treatment of other autoimmune diseases, e.g., multiple sclerosis (MS), an inflammatory autoimmune disorder with a clear T cell-mediated immune pathogenesis. The trace element zinc is shown to play a regulatory role in the maintenance of immune functions. Changes of zinc homeostasis affect both the innate and the adaptive immune system. On one hand, therapeutic zinc supplementation can normalize impaired immune functions due to zinc deficiency. On the other hand, therapeutic zinc supplementation is under consideration as a possible option to treat T cell-mediated autoimmune diseases. The aim of the present study was to investigate the influence of IVIG (Octagam®), zinc aspartate (Unizink®), and the combined application of both preparations in the experimental autoimmune encephalomyelitis (EAE), the animal model of MS. Therapeutic intraperitoneal application of zinc aspartate significantly diminished clinical signs during the relapsing-remitting phase of EAE in SJL/J mice. In contrast, IVIG given in a therapeutic manner did not influence the course of EAE. Interestingly, the combined application of both, IVIG and zinc aspartate, significantly reduced the severity of the disease during the acute and the relapsing-remitting phase of the EAE. Our data suggest that the combination of IVIG and zinc aspartate may have beneficial effects in autoimmune diseases, like MS. Further studies should verify the benefit of a controlled immunosuppressive therapy with IVIG and zinc for such diseases.

Encephalomyelitis

Therapeutic effect

Autoimmune encephalitis

10.1155/2018/5982169

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Citations (6)

The role of zinc in liver cirrhosis

Annals of Hepatology (2015)

Kurt Grüngreiff Dirk Reinhold Heiner Wedemeyer

Zinc is an essential trace element playing fundamental roles in cellular metabolism. It acts mostly by binding a wide range of proteins, thus affecting a broad spectrum of biological processes, which include cell division, growth and differentiation. Zinc is critical to a large number of structural proteins, enzymatic processes, and transcription factors. Zinc deficiency can result in a spectrum of clinical manifestations, such as poor of appetite, loss of body hair, altered taste and smell, testicular atrophy, cerebral and immune dysfunction, and diminished drug elimination capacity. These are common symptoms in patients with chronic liver diseases, especially liver cirrhosis. The liver is the main organ responsible for the zinc metabolism which can be affected by liver diseases. On the other hand, zinc deficiency may alter hepatocyte functions and also immune responses in inflammatory liver diseases. Liver cirrhosis represents the most advanced stage of chronic liver diseases and is the common outcome of chronic liver injury. It is associated with energy malnutrition, with numerous metabolic disorders, such as hypoalbuminemia, with imbalance between branched-chain amino acids and aromatic amino acids, and with reduced zinc serum concentrations. All these processes can influence the clinical outcome of patients, such ascites, hepatic encephalopathy and hepatocellular carcinoma. In the present review, we summarize the emerging evidence on the pitoval role of zinc in the pathogenesis of liver cirrhosis.

Hypoalbuminemia

Hepatic Encephalopathy

10.5604/16652681.1184191

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Citations (176)

Gilbert’s syndrome and antiviral therapy of hepatitis C

Annals of Hepatology (2009)

Katja Deterding Kurt Grüngreiff Tim O. Lankisch Andrej Potthoff Mathias Bähr

Treatment of chronic hepatitis C with type I interferons and ribavirin can be associated with exacerbation of hepatitis and sometimes liver decompensation. We report two patients with chronic hepatitis C virus infection who experienced a severe increase of bilirubin levels of up to 17 times upper the limit of normal value in the absence of deterioration of hepatic function during therapy with pegylated-interferon and ribavirin. A genetic disposition for Gilbert's syndrome explained the adverse events and permitted a continuation of therapy leading to a sustained clearance of chronic hepatitis C infection. Since one patient jaundiced already during a lead-in treatment period with ribavirin monotherapy we suggest that hyperbilirubinaemia during combination therapy is primarily caused by ribavirin rather than by effects of interferon alpha on UDP-glucuronosyltransferase activities. Of note, both patients recovered from their initial unconjugated hyperbilirubinemia despite continuation of ribavirin therapy, which indicates that compensatory mechanisms leading to a normalization of UGT1A1 activity are likely.

Liver function

Decompensation

Pegylated interferon

Hepatitis C

10.1016/s1665-2681(19)31774-0

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Citations (15)