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BACKGROUND: Patients with chronic gastrointestinal disease such as inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), celiac disease, gastroesophageal reflux disease (GERD), pancreatitis, and chronic liver disease (CLD) often suffer from obesity because of coincidence (IBD, IBS, celiac disease) or related pathophysiology (GERD, pancreatitis and CLD). It is unclear if such patients need a particular diagnostic and treatment that differs from the needs of lean gastrointestinal patients. The present guideline addresses this question according to current knowledge and evidence.OBJECTIVE: The present practical guideline is intended for clinicians and practitioners in general medicine, gastroenterology, surgery and other obesity management, including dietitians and focuses on obesity care in patients with chronic gastrointestinal diseases.METHODS: The present practical guideline is the shortened version of a previously published scientific guideline developed according to the standard operating procedure for ESPEN guidelines. The content has been re-structured and transformed into flow-charts that allow a quick navigation through the text.RESULTS: In 100 recommendations (3× A, 33× B, 24 × 0, 40× GPP, all with a consensus grade of 90% or more) care of gastrointestinal patients with obesity - including sarcopenic obesity - is addressed in a multidisciplinary way. A particular emphasis is on CLD, especially metabolic associated liver disease, since such diseases are closely related to obesity, whereas liver cirrhosis is rather associated with sarcopenic obesity. A special chapter is dedicated to obesity care in patients undergoing bariatric surgery. The guideline focuses on adults, not on children, for whom data are scarce. Whether some of the recommendations apply to children must be left to the judgment of the experienced pediatrician.CONCLUSION: The present practical guideline offers in a condensed way evidence-based advice how to care for patients with chronic gastrointestinal diseases and concomitant obesity, an increasingly frequent constellation in clinical practice.

The present guideline is an update and extension of the ESPEN scientific guideline on Clinical Nutrition in Inflammatory Bowel Disease published first in 2017. The guideline has been rearranged according to the ESPEN practical guideline on Clinical Nutrition in Inflammatory Bowel Disease published in 2020. All recommendations have been checked and, if needed, revised based on new literature, before they underwent the ESPEN consensus procedure. Moreover, a new chapter on microbiota modulation as a new option in IBD treatment has been added. The number of recommendations has been increased to 71 recommendations in the guideline update. The guideline is aimed at professionals working in clinical practice, either in hospitals or in outpatient medicine, and treating patients with IBD. General aspects of care in patients with IBD, and specific aspects during active disease and in remission are addressed. All recommendations are equipped with evidence grades, consensus rates, short commentaries and links to cited literature.

Background: Patients with chronic gastrointestinal (GI) disease such as inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), celiac disease, gastroesophageal reflux disease (GERD), pancrea-titis, and chronic liver disease (CLD) often suffer from obesity because of coincidence (IBD, IBS, celiac disease) or related pathophysiology (GERD, pancreatitis and CLD). It is unclear if such patients need a particular diagnostic and treatment that differs from the needs of lean GI patients. The present guideline addresses this question according to current knowledge and evidence.Objective: The objective of the guideline is to give advice to all professionals working in the field of gastroenterology care including physicians, surgeons, dietitians and others how to handle patients with GI disease and obesity.Methods: The present guideline was developed according to the standard operating procedure for ESPEN guidelines, following the Scottish Intercollegiate Guidelines Network (SIGN) grading system (A, B, 0, and good practice point (GPP)). The procedure included an online voting (Delphi) and a final consensus conference.Results: In 100 recommendations (3x A, 33x B, 24x 0, 40x GPP, all with a consensus grade of 90% or more) care of GI patients with obesity -including sarcopenic obesity -is addressed in a multidisciplinary way. A particular emphasis is on CLD, especially fatty liver disease, since such diseases are closely related to obesity, whereas liver cirrhosis is rather associated with sarcopenic obesity. A special chapter is dedi-cated to obesity care in patients undergoing bariatric surgery. The guideline focuses on adults, not on children, for whom data are scarce. Whether some of the recommendations apply to children must be left to the judgment of the experienced pediatrician.Conclusion: The present guideline offers for the first time evidence-based advice how to care for patients with chronic GI diseases and concomitant obesity, an increasingly frequent constellation in clinical practice.(c) 2022 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Background Patients with chronic gastrointestinal (GI) disease such as inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), celiac disease, gastroesophageal reflux disease (GERD), pancreatitis, and chronic liver disease (CLD) often suffer from obesity because of coincidence (IBD, IBS, celiac disease) or related pathophysiology (GERD, pancreatitis and CLD). It is unclear if such patients need a particular diagnostic and treatment that differs from the needs of lean GI patients. The present guideline addresses this question according to current knowledge and evidence. Objective The objective of the guideline is to give advice to all professionals working in the field of gastroenterology care including physicians, surgeons, dietitians and others how to handle patients with GI disease and obesity. Methods The present guideline was developed according to the standard operating procedure for European Society for Clinical Nutrition and Metabolism guidelines, following the Scottish Intercollegiate Guidelines Network grading system (A, B, 0, and good practice point [GPP]). The procedure included an online voting (Delphi) and a final consensus conference. Results In 100 recommendations (3x A, 33x B, 24x 0, 40x GPP, all with a consensus grade of 90% or more) care of GI patients with obesity - including sarcopenic obesity - is addressed in a multidisciplinary way. A particular emphasis is on CLD, especially fatty liver disease, since such diseases are closely related to obesity, whereas liver cirrhosis is rather associated with sarcopenic obesity. A special chapter is dedicated to obesity care in patients undergoing bariatric surgery. The guideline focuses on adults, not on children, for whom data are scarce. Whether some of the recommendations apply to children must be left to the judgment of the experienced pediatrician. Conclusion The present guideline offers for the first time evidence-based advice how to care for patients with chronic GI diseases and concomitant obesity, an increasingly frequent constellation in clinical practice.

ZusammenfassungDieses zweite Positionspapier der Sektion Metabolismus und Ernährung der Deutschen Interdisziplinären Vereinigung für Intensiv- und Notfallmedizin (DIVI) gibt Empfehlungen zum laborchemischen Monitoring der Makro- und Mikronährstoffzufuhr sowie zum Einsatz der indirekten Kalorimetrie im Rahmen der medizinischen Ernährungstherapie erwachsener Intensivpatient:innen. Zusätzlich werden Empfehlungen zur krankheitsbezogenen bzw. individuellen (Spiegelbestimmung) Substitution und (Hochdosis‑)Pharmakotherapie von Vitaminen und Spurenelementen vorgenommen.

Background Cytokine treatment with Interferon-alpha (IFN-α) represents a clinical model of immune associated depression, but it remains unclear if it is of the same entity as major depressive disorder (MDD). The study focuses on possible gender differences in IFN-α induced depression and effects of a pre-emptive antidepressant treatment. Methods Data from 181 patients with chronic hepatitis C infection (cHC) without history of mental illnesses undergoing treatment with IFN-α 2a and ribavirin were re-analyzed for gender effects. Patients with a pre-emptive antidepressant therapy with Escitalopram (n = 90, verum group) to prevent IFN-induced depression were compared to patients who received placebo (n = 91). Depressive symptoms before and during HCV-treatment were assessed using the Montgomery–Asberg Depression Rating Scale (MADRS), Beck's Depression Inventory (BDI) and the Hamilton Anxiety Rating Scale. Results We found significant differences regarding the incidence and severity of depressive symptoms between men and women for patients without antidepressant pre-treatment (placebo group). Significantly more women without pre-emptive antidepressant therapy suffered from clinically relevant depression (MADRS values ≥ 13, p = 0.041) and self-rated depressive symptoms (BDI ≥ 17, p = 0.024). Antidepressant pre-treatment showed comparable effects regarding the reduction of incidence and severity of depression in both women and men. Conclusions Compared to MDD, IFN-alpha-induced depression in patients with cHC is also characterized by gender differences with an increased risk for women but no gender difference regarding the effects of an antidepressant pre-treatment is found. Our data strengthens the hypothesis that Interferon-induced depression serves as a clinical model for immune related depressive disorders.

At the time of admission to an intensive or intermediate care unit, assessment of the patients' nutritional status may have both prognostic and therapeutic relevance with regard to the planning of individualized medical nutrition therapy (MNT). MNT has definitely no priority in the initial treatment of a critically ill patient, but is often also neglected during the course of the disease. Especially with prolonged length of stay, there is an increasing risk of malnutrition with considerable prognostic macro- and/or micronutrient deficit. So far, there are no structured, evidence-based recommendations for assessing nutritional status in intensive or intermediate care patients. This position paper of the Section Metabolism and Nutrition of the German Interdisciplinary Association for Intensive and Emergency Medicine (DIVI) presents consensus-based recommendations for the assessment and technical monitoring of nutritional status of patients in intensive and intermediate care units. These recommendations supplement the current S2k guideline "Clinical Nutrition in Intensive Care Medicine" of the German Society for Nutritional Medicine (DGEM) and the DIVI.Die Erhebung des Ernährungsstatus zum Zeitpunkt der Aufnahme im Intensiv- oder Intermediate Care Bereich hat sowohl prognostische als auch therapeutische Relevanz im Hinblick auf die Planung einer individualisierten medizinischen Ernährungstherapie (engl. „medical nutrition therapy“, MNT). Diese Planung wird im Rahmen der Erstversorgung eines vital bedrohlichen Krankheitsbilds nachvollziehbar nicht priorisiert, jedoch im weiteren Verlauf häufig auch oft nicht mehr angemessen durchgeführt. Vor allem bei längerer Verweildauer besteht das Risiko einer Mangelernährung mit Aufbau eines kumulativen, prognoserelevanten Makro- und/oder Mikronährstoffdefizits. Bisher gibt es für Patient*innen auf Intensiv- und Intermediate Care Einheiten keine strukturierten Empfehlungen zur Erhebung des Ernährungsstatus. Das vorliegende Positionspapier der Sektion Metabolismus und Ernährung der Deutschen Interdisziplinären Vereinigung für Intensiv- und Notfallmedizin (DIVI) beinhaltet konsensbasierte Empfehlungen zur Erfassung und zum apparativen Monitoring des Ernährungsstatus von Patient*innen auf Intensiv- und Intermediate Care Stationen. Diese Empfehlungen ergänzen die aktuelle S2k-Leitlinie „Klinische Ernährung in der Intensivmedizin“ der Deutschen Gesellschaft für Ernährungsmedizin (DGEM) und der DIVI.

With prolonged pandemic conditions, and emerging evidence but persisting low awareness of the importance of nutritional derangements, ESPEN has promoted in close collaboration with World Health Organization-Europe a call for papers on all aspects relating COVID-19 and nutrition as well as nutritional care, in the Society Journals Clinical Nutrition and Clinical Nutrition ESPEN. Although more COVID-related papers are being submitted and continue to be evaluated, ESPEN and WHO present the current editorial to summarize the many published findings supporting major interactions between nutritional status and COVID-19. These include 1) high risk of developing the disease and high risk of severe disease in the presence of pre-existing undernutrition (malnutrition) including micronutrient deficiencies; 2) high risk of developing malnutrition during the course of COVID-19, with substantial impact on long-term sequelae and risk of long COVID; 3) persons with obesity are also prone to develop or worsen malnutrition and its negative consequences during the course of COVID-19; 4) malnutrition screening and implementation of nutritional care may improve disease outcomes; 5) social and public health determinants contribute to the interaction between nutritional status and COVID-19, including negative impact of lockdown and social limitations on nutrition quality and nutritional status. We believe the evidence supports the need to consider COVID-19 as (also) a case of malnutrition-enhanced disease and disease-related malnutrition, with added risk for persons both with and without obesity. Similarities with many other disease conditions further support recommendations to implement standard nutritional screening and care in COVID-19 patients, and they underscore the relevance of appropriate nutritional and lifestyle prevention policies to limit infection risk and mitigate the negative health impact of acute pandemic bouts.

Cytokine treatment with Interferon-alpha (IFN-α) represents a clinical model of immune associated depression, but it remains unclear if it is of the same entity as major depressive disorder (MDD). The study focuses on possible gender differences in IFN-α induced depression and effects of a pre-emptive antidepressant treatment.Data from 181 patients with chronic hepatitis C infection (cHC) without history of mental illnesses undergoing treatment with IFN-α 2a and ribavirin were re-analyzed for gender effects. Patients with a pre-emptive antidepressant therapy with Escitalopram (n = 90, verum group) to prevent IFN-induced depression were compared to patients who received placebo (n = 91). Depressive symptoms before and during HCV-treatment were assessed using the Montgomery-Asberg Depression Rating Scale (MADRS), Beck's Depression Inventory (BDI) and the Hamilton Anxiety Rating Scale.We found significant differences regarding the incidence and severity of depressive symptoms between men and women for patients without antidepressant pre-treatment (placebo group). Significantly more women without pre-emptive antidepressant therapy suffered from clinically relevant depression (MADRS values ≥ 13, p = 0.041) and self-rated depressive symptoms (BDI ≥ 17, p = 0.024). Antidepressant pre-treatment showed comparable effects regarding the reduction of incidence and severity of depression in both women and men.Compared to MDD, IFN-alpha-induced depression in patients with cHC is also characterized by gender differences with an increased risk for women but no gender difference regarding the effects of an antidepressant pre-treatment is found. Our data strengthens the hypothesis that Interferon-induced depression serves as a clinical model for immune related depressive disorders.

ZusammenfassungIn den letzten Jahren häuft sich die Nennung der Nicht-Zöliakie-Gluten-/Weizen-Sensitivität (NCGS, „non celiac gluten sensitivity“) sowohl in den Medien, aber auch in Fachkreisen. Die Existenz und die möglichen verantwortlichen Trigger werden kontrovers diskutiert. Drei internationale Expertentreffen mit Empfehlungen zur NCGS waren nicht unabhängig organisiert und wenig transparent bezüglich potenzieller Interessenkonflikte der Teilnehmer.Die vorliegende Stellungnahme enthält wichtige Überlegungen aus allergologischer und ernährungsphysiologischer Sicht: (1) Aufgrund häufiger Selbstdiagnosen, unklarer Prävalenz und unbestätigter Ätiologie der NCGS sind validierte Diagnosekriterien und/oder verlässliche Biomarker notwendig. (2) Infolge hoher Nocebo- und häufiger Placebo-Effekte konnte Gluten bislang nicht sicher als Auslöser einer NCGS identifiziert werden. Doppelblinde, placebokontrollierte Provokationen (DBPCFC: double-blind, placebo-controlled food challenge) sind bei Verdacht auf NCGS nur in modifizierter Form (verändertes Verhältnis von Placebo zu Verum) geeignet. (3) Zahlreiche Störgrößen (Confounder) erschweren die Bewertung subjektiver Symptome unter glutenarmer/-freier Kost. Letztere kann je nach Lebensmittelauswahl (z. B. vermehrt Gemüse mit löslichen Ballaststoffen) physiologische Verdauungseffekte bewirken und gastrointestinale Transitzeiten unabhängig vom Glutenverzicht verändern. (4) Streng glutenfreie Kost ist bei einer gesicherten Zöliakie wissenschaftlich begründet und unerlässlich. Bei einem medizinisch unbegründeten Glutenverzicht überwiegen jedoch potenzielle Nachteile und Risiken. (5) Aktuell kann wegen fehlender überzeugender Diagnosekriterien bei Verdacht einer NCGS ausschließlich eine sorgfältige Differenzialdiagnostik empfohlen werden. Hierzu gehören eine sorgfältige Anamnese, einschließlich eines Ernährungs- und Symptomtagebuchs, eine allergologische Diagnostik und ein sicherer Ausschluss einer Zöliakie.Wir befürworten ein derartiges strukturiertes Vorgehen, da ohne eine medizinisch gesicherte Diagnose die Durchführung einer längeren Glutenkarenz nicht zu empfehlen ist. Englische Fassung http://link.springer.com/journal/40629

Within the last decade, non-celiac gluten/wheat sensitivity (NCGS) has been increasingly discussed not only in the media but also among medical specialties. The existence and the possible triggers of NCGS are controversial. Three international expert meetings which proposed recommendations for NCGS were not independently organized and only partially transparent regarding potential conflicts of interest of the participants. The present position statement reflects the following aspects about NCGS from an allergist’s and nutritionist’s point of view: (A) Validated diagnostic criteria and/or reliable biomarkers are still required. Currently, this condition is frequently self-diagnosed, of unknown prevalence and non-validated etiology. (B) Gluten has not been reliably identified as an elicitor of NCGS because of high nocebo and placebo effects. Double-blind, placebo-controlled provocation tests are of limited value for the diagnosis of NCGS and should be performed in a modified manner (changed relation of placebo and active substance). (C) Several confounders hamper the assessment of subjective symptoms during gluten-reduced or gluten-free diets. Depending on the selection of food items, e.g., an increased vegetable intake with soluble fibers, diets may induce physiological digestive effects and can modify gastrointestinal transit times independent from the avoidance of gluten. (D) A gluten-free diet is mandatory in celiac disease based on scientific evidence. However, a medically unjustified avoidance of gluten may bear potential disadvantages and risks. (E) Due to a lack of diagnostic criteria, a thorough differential diagnostic work-up is recommended when NCGS is suspected. This includes a careful patient history together with a food-intake and symptom diary, if necessary an allergy diagnostic workup and a reliable exclusion of celiac disease. We recommend such a structured procedure since a medically proven diagnosis is required before considering the avoidance of gluten.

Patients with cancer are at particularly high risk for malnutrition because both the disease and its treatments threaten their nutritional status. Yet cancer-related nutritional risk is sometimes overlooked or under-treated by clinicians, patients, and their families. The European Society for Clinical Nutrition and Metabolism (ESPEN) recently published evidence-based guidelines for nutritional care in patients with cancer. In further support of these guidelines, an ESPEN oncology expert group met for a Cancer and Nutrition Workshop in Berlin on October 24 and 25, 2016. The group examined the causes and consequences of cancer-related malnutrition, reviewed treatment approaches currently available, and built the rationale and impetus for clinicians involved with care of patients with cancer to take actions that facilitate nutrition support in practice. The content of this position paper is based on presentations and discussions at the Berlin meeting. The expert group emphasized 3 key steps to update nutritional care for people with cancer: (1) screen all patients with cancer for nutritional risk early in the course of their care, regardless of body mass index and weight history; (2) expand nutrition-related assessment practices to include measures of anorexia, body composition, inflammatory biomarkers, resting energy expenditure, and physical function; (3) use multimodal nutritional interventions with individualized plans, including care focused on increasing nutritional intake, lessening inflammation and hypermetabolic stress, and increasing physical activity.

ZusammenfassungDie vorliegende Erklärung fasst die von DGEM, BDEM und VDOE gemeinsam getragenen Überzeugungen und Kernforderungen in Bezug auf die Verbesserung der ernährungsmedizinischen Versorgung, Ernährungsberatung und Ernährungsbildung in Deutschland zusammen.

Both acute and chronic pancreatitis are frequent diseases of the pancreas, which, despite being of benign nature, are related to a significant risk of malnutrition and may require nutritional support. Acute necrotizing pancreatitis is encountered in 20% of patients with acute pancreatitis, is associated with increased morbidity and mortality, and may require artificial nutrition by enteral or parenteral route, as well as additional endoscopic, radiological or surgical interventions. Chronic pancreatitis represents a chronic inflammation of the pancreatic gland with development of fibrosis. Abdominal pain leading to decreased oral intake, as well as exocrine and endocrine failure are frequent complications of the disease. All of the above represent risk factors related to malnutrition. Therefore, patients with chronic pancreatitis should be considered at risk, screened and supplemented accordingly. Moreover, osteoporosis and increased facture risk should be acknowledged in patients with chronic pancreatitis, and preventive measures should be considered.

Infektionen des Dickdarms durch Clostridium difficile nehmen seit der letzten Jahrtausendwende in Deutschland und den USA kontinuierlich zu. Nach dem Absetzen des auslosenden Antibiotikums fuhrt die Therapie mit einem indizierten Antibiotikum in etwa 80% der Falle zur Ausheilung. Die restlichen Falle, die rezidivierend verlaufen, sprechen zu etwa 60% auf erneute Antibiose an. Die ubrigen Rezidive sind deutlich schlechter zu behandeln. Die Stuhltransplantation (fecal microbiota transplantation, FMT) stellt fur diese Patienten eine neue therapeutische Option dar. 16 Patienten mit Rezidiv einer Clostridium-difficile-Kolitis wurden mittels FMT behandelt. Retrospektiv wurden die Ergebnisse ausgewertet und mit denen der einzigen beiden randomisierten Studien verglichen. Durch den ersten Eingriff konnten 11 von 16 (68,75%) Patienten geheilt werden. Die funf nicht ansprechenden Patienten erhielten eine zweite FMT mit dem Ergebnis, dass schlieslich 14 von 16 (87,5%) Patienten kuriert werden konnten. Im Vergleich zu den Ergebnissen der Universitat von Amsterdam (81,3% nach erster FMT und 93,8% nach zweiter FMT) und des Massachusetts General Hospitals in Boston (70% nach erster FMT und 90% nach zweiter FMT) erzielte unsere Form der Transplantation etwas schlechtere Ergebnisse. Das zum Teil deutlich hohere Alter und die Behandlung von intensivpflichtigen Patienten in unserer Gruppe erklaren diesen Befund aber gut. Daher pladieren wir fur eine breitere Anwendung des Verfahrens in nicht universitaren Kliniken zur Therapie des Rezidivs der Clostridium-difficile-Kolitis.

Summary Purpose The nomenclature in clinical nutrition differs locally, among (para)medical disciplines, and both nationally and internationally. The inconsistencies hamper public, professional and scientific discussions. A working group of the German Society of Nutritional Medicine (DGEM) was established to work out definitions for the relevant terms used in nutritional support within Germany. Methods Terms were searched in (inter)national hard print technical literature (medical dictionaries, text books, (inter)national guidelines and online (PubMed, Embase, CINAHL, Google Scholar, general internet). (Inter)nationally agreed definitions published by Clinical Nutrition Societies were preferred to other reports. Results The terms were organised into four categories totaling 53 definitions: 1. Fields and structure: medical nutrition, clinical nutrition, nutrition steering committee, nutritional care, care catering, dietetics (dietary advice), obesity as part of clinical nutrition (obesity team), nutritional support (nutrition support team, malnutrition screening, nutritional support therapy), functional nutrition, nutritional assessment, nutrition therapy plan, nutritional therapy, 2. Nutritional conditions: disease-related malnutrition (starvation induced malnutrition, chronic disease-related malnutrition, acute disease-related malnutrition), cachexia, sarcopenia, specific nutrient deficiencies, refeeding syndrome, 3. Forms of nutrition: diet (regular diet, therapeutic diet, fortified food), artificial nutritional support (oral nutritional supplementation, enteral nutrition, parenteral nutrition) 4. Products: oral nutritional supplements and enteral formulas (whole protein formula, peptide-based formula, free amino acid formula, standard formula), parenteral solutions (total nutrient admixtures, multi-chamber systems, multiple bottle systems). Conclusion A comprehensive list of definitions for terms in nutritional support has been established for the first time and is made available to the international community for further development and discussions.

Die Ernahrung von kritisch kranken Patienten erfordert Fingerspitzengefuhl. Eine zu niedrige wie auch eine zu hohe Energiezufuhr konnen gleichermasen zu Schadigungen fuhren. Wichtig also zu wissen, wie der Ernahrungsstatus des Patienten bei der Aufnahme auf die Intensivstation aussieht und wie der individuelle Energiebedarf errechnet wird.

Fragestellung: Die akute und chronische Pankreatitis sind haufige Erkrankungen. Wahrend ca. 80 % der Patienten mit akuter Pankreatitis eine eher geringe Morbiditat aufweisen, verlauft die Erkrankung bei 20 % der Patienten schwer mit z. T. signifikanter Letalitat. Die chronische Pankreatitis hat aufgrund der oftmals schmerzbedingten reduzierten Nahrungsaufnahme und einer Maldigestion ein hohes Risiko fur Ernahrungsdefizite. Die vorliegende S3-Leitlinie gibt Empfehlungen zum ernahrungsmedizinischen Management dieser Erkrankungen. Methodik: Es wurde eine systematische Literaturrecherche zur Ernahrung bei den genannten Krankheitsbildern durchgefuhrt. Die Ergebnisse wurden in einer interdisziplinaren Arbeitsgruppe diskutiert. Auf dieser Basis wurden von der Arbeitsgruppe 32 Empfehlungen erarbeitet und bewertet, die im Rahmen der vorliegenden S3-Leitlinie in einem Delphi-Verfahren und einer Konsensuskonferenz vorgestellt, diskutiert und verabschiedet wurden. Ergebnisse: In der ernahrungsmedizinischen Betreuung von Patienten mit akuter Pankreatitis hat es in den letzten 15 Jahren einen wesentlichen Paradigmenwechsel gegeben. Gestutzt auf entsprechende Studien konnen mit signifikanter Evidenz Empfehlungen fur die Ernahrung von Patienten mit akuter Pankreatitis gegeben werden. Wahrend bei der leichten bis moderaten akuten Pankreatitis eine liberale und fruhzeitige orale Nahrungsaufnahme moglich ist, ist bei der schweren akuten Pankreatitis eine fruhzeitige enterale kunstliche Ernahrung indiziert. Durch diese Masnahme kann nicht nur die Morbiditat, sondern auch die Letalitat gesenkt werden. Patienten mit chronischer Pankreatitis profitieren von einem ernahrungsmedizinischen Assessment und gezielten diatetischen Interventionen. Schlussfolgerung: Eine individuelle, der klinischen Situation angepasste Ernahrungstherapie ist ein wesentlicher Baustein in der multimodalen Therapie der akuten und chronischen Pankreatitis.

Since the turn of the millennium there has been an alarming increase in the incidence and severity of clostridium difficile infections. Stopping medication with the triggering antibiotic and switching to a recommended antibiotic leads to healing up in 80%. However, patients who relapse have a 40% risk of an additional relapse and those with 2 or more episodes face a 60% risk. Fecal microbiota transplantation (FMT) is a new therapeutic option. Up to now there only exist two randomized studies (University of Amsterdam and the Massachusetts General Hospital in Boston).Data from 16 patients with recurrent clostridium difficile infection who had undergone FMT at a local hospital in the city of Bremen, Germany, were reviewed and compared to the results of the 2 randomized studies.11 out of 16 patients got cured after the first FMT (68.75%). The remaining 5 patients received a second FMT, with cure in 3 patients. The overall response rate was 14 from 16 patients (87.5%).In comparison to the response rates of the University of Amsterdam (81.3% after the first and 93.8% after the second FMT) and of the Massachusetts General Hospital in Boston (70% after the first and 90% after the second FMT) we received slightly worse results. But, treatment of notably older patients and intensive care patients in our group explain these findings well. Therefore, we advocate a wide use of FMT for the treatment of recurrent clostridium difficile colitis in non-university hospitals.

Hintergrund. Tumorpatienten sind haufig von einer Mangelernahrung betroffen. Die Folgen sind eine Verschlechterung von Lebensqualitat und Leistungsfahigkeit, geringere Toleranz gegenuber einer Tumortherapie sowie eine geringere Uberlebenszeit.

The aim of this study was to compare 2 protocols regarding the initiation of oral nutrition in patients with mild acute pancreatitis.We randomized 143 patients to the Lipase directed (LIP) (n = 74) and the self selected PAT (n = 69) group. In the (PAT) group, the patients restarted eating through self-selection. In the LIP group, serum lipase had to normalize before eating.The mean time between admission and oral nutrition was 2 days (interquartile range [IQR], 1-3) in the PAT group and 3 days (IQR, 2-4) in the LIP group (P0.005). Before and after the first meal, the mean Δ visual analogue scale (VAS) was +3.14 mm (±11.5 mm) in the PAT group and +2.85 mm (±16.4) in the LIP group (P = 0.597). The length of hospital stay was 7 days (median; IQR, 5-10.5) in the PAT group and 8 days (median; IQR, 5.75-12) in the LIP group (P = 0.315).We were not able to demonstrate a difference in postprandial abdominal pain or in the length of hospital stay. Patients with self-selected eating, however, were able to restart eating 1 day earlier, and this difference was found to be significant. Our data suggest that normalization of serum lipase is not obligatory for enteral nutrition in mild acute pancreatitis.

Exocrine pancreatic insufficiency (EPI) resulting from conditions such as chronic pancreatitis (CP), acute pancreatitis (AP) and upper gastrointestinal (GI) surgery increases risk for malnutrition and metabolic problems. Poor nutrition is associated with more complications and higher mortality. Therefore, effective nutritional management should be a high priority in these patients. In CP, poor nutrition has been shown to significantly affect quality of life and functional status. Clinical study data show that dietary counselling combined with pancreatic enzyme replacement therapy is effective in improving nutritional status and is therefore recommended in these patients. In AP, early enteral nutrition reduces complications and mortality. However, EPI persists in many cases after the resolution of AP; these patients remain at increased risk for malnutrition and require further nutritional support. In patients undergoing surgery, preoperative weight loss is a risk factor for postoperative morbidity and mortality; outcomes can be improved considerably by preoperative screening to identify high-risk patients and by providing appropriate perioperative nutritional support. Pre- and perioperative enteral nutrition are cost-effective interventions that can improve outcomes in patients undergoing GI surgery. In all of these patient populations, nutritional management, including risk assessment and individualized nutritional support, is a key component of an effective multimodal therapeutic approach.

Adipokines are fat-derived hormones and cytokines with immune-modulating and metabolic properties. Most of them are associated with insulin resistance. The aim of the present investigation was to evaluate circulating levels of adipokines and glucose homeostasis in patients with inflammatory bowel disease (IBD) and to evaluate possible associations with the course and characteristics of the disease.Serum leptin, resistin, visfatin, retinol-binding protein-4, adiponectin, glucose, insulin, and inflammatory parameters were analyzed in 93 patients with inactive IBD (49 with Crohn's disease [CD], 44 with ulcerative colitis [UC]), 35 patients with active IBD (18 with CD, 17 with UC), and 37 age- and body mass index-matched healthy controls. Ninety-two patients were followed for 6 mo.Leptin was similar in patients with IBD and controls, whereas resistin and visfatin were increased in patients with active disease but not in those in remission. In active and inactive disease, adiponectin was decreased (P0.001) and retinol-binding protein-4 was increased (P0.001) compared with controls. About 60% of patients with IBD showed increased levels of insulin, whereas serum glucose remained normal, resulting in increased homeostasis model assessment values in most patients. Hyperinsulinemia was associated with the decrease in adiponectin (r = -0.572, P0.001) and proved to be an independent protective factor for 6-mo maintenance of remission (P = 0.016).IBD led to largely similar alterations in circulating adipokines and hyperinsulinemia in patients with CD and those with UC. The unexpected protective effect of hyperinsulinemia on relapse rate denotes the role of the metabolic-inflammatory response as a modulator in IBD.

Assessment of the severity of acute pancreatitis (AP), together with the patient's nutritional status is crucial in the decision making process that determines the need for artificial nutrition. Both should be done on admission and at frequent intervals thereafter. The indication for nutritional support in AP is actual or anticipated inadequate oral intake for 5-7 days. This period may be shorter in those with pre-existing malnutrition. Substrate metabolism in severe AP is similar to that in severe sepsis or trauma. Parenteral amino acids, glucose and lipid infusion do not affect pancreatic secretion and function. If lipids are administered, serum triglycerides must be monitored regularly. The use of intravenous lipids as part of parenteral nutrition (PN) is safe and feasible when hypertriglyceridemia is avoided. PN is indicated only in those patients who are unable to tolerate targeted requirements by the enteral route. As rates of EN tolerance increase then volumes of PN should be decreased. When PN is administered, particular attention should be given to avoid overfeeding. When PN is indicated, a parenteral glutamine supplementation should be considered. In chronic pancreatitis PN may, on rare occasions, be indicated in patients with gastric outlet obstruction secondary to duodenal stenosis or those with complex fistulation, and in occasional malnourished patients prior to surgery. © 2009 European Society for Clinical Nutrition and Metabolism.

Purpose: The homozygous p.C282Y variant of the HFE gene is a major risk factor for hereditary hemochromatosis, a disorder of iron metabolism resulting in progressive iron accumulation in a variety of organs including the pancreas. Heterozygosity of p.C282Y and p.H63D may increase susceptibility to chronic liver and pancreatic disease. This study determines the frequencies of p.C282Y and p.H63D alterations in patients with chronic pancreatitis and pancreatic adenocarcinoma. Methods: In total, 958 patients (349 with alcoholic pancreatitis, 343 with idiopathic pancreatitis, 64 with familial chronic pancreatitis, 34 with acute pancreatitis, and 168 with pancreatic adenocarcinoma) were enrolled and compared with 681 healthy and 100 alcoholic controls. Furthermore, 45 parent–offspring trios were included for segregation analysis. Genotyping of p.C282Y and p.H63D was performed by restriction fragment length polymorphism or melting curve analyses. Results: No significant differences were found in heterozygosity for p.C282Y and p.H63D when patients with alcoholic (8.0/21.5%), idiopathic (7.3/24.5%), or familial (9.8/23.0%) pancreatitis, or pancreatic adenocarcinoma (5.4/28.6%) were compared with healthy (6.2/24.8%) and alcoholic (7.0/25.0%) controls. Neither genotype was associated with the presence of secondary diabetes mellitus in patients with chronic pancreatitis. Conclusion: Although hemochromatosis is associated with pancreatic pathology, the p.C282Y and p.H63D variants do not play a significant role in the pathogenesis of chronic pancreatitis or pancreatic adenocarcinoma.

Summary Background Alteration of the leptin system appears to play a role in the inflammatory–metabolic response in catabolic diseases such as chronic liver diseases. Aim To investigate the association between leptin components, inflammatory markers and hepatic energy and substrate metabolism. Methods We investigated in vivo hepatic substrate and leptin metabolism in 40 patients employing a combination of arterial and hepatic vein catheterization techniques and hepatic blood flow measurements. In addition to metabolic, inflammatory and neuroendocrine parameters, circulating levels of free leptin, bound leptin and soluble leptin receptor were determined. Results Compared with controls, bound leptin and soluble leptin receptor levels were significantly elevated in cirrhosis, while free leptin did not increase. In cirrhosis bound leptin was correlated with soluble leptin receptor (r = 0.70, P

Summary Secondary sclerosing cholangitis is a rare complication of acute bacterial cholangitis. The natural course of the disease is a slow progression over years. Here we report about a patient in whom sclerosing cholangitis evolved much faster as a consequence of a persistent biliary infection with vancomycin-resistant enterococci. The infection could be treated successfully with prolonged therapy with linezolid and teicoplanin. This is the first report of sclerosing cholangitis caused by vancomycin-resistant enterococci. It illustrates the rapidity with which this disease can evolve as a fulminant and ultimately fatal complication of acute bacterial cholangitis.

Summary Background & aims Circulating leptin and insulin concentrations are physiologically representing energy homeostasis. However, the artificial situation of long-term total parenteral nutrition (TPN) and its effects on serum leptin and insulin is not fully understood. Methods We studied 42 gastroenterological patients who received TPN for 19±11 days. Serum leptin and insulin levels as well as body composition assessed by bioelectrical impedance analysis were evaluated on days 0, 7 and 14. Insulin sensitivity was estimated by calculating the QUICKI. Results Before the start of TPN, leptin correlated positively with female gender ( P 0.03 ), BMI ( P 0.02 ), fat mass ( P 0.02 ), insulin levels ( P 0.001 ) and QUICKI ( P 0.001 ). Within the first week of TPN, an increase of leptin levels was found only in patients with a body fat mass of >30% ( P 0.02 ). As these were predominantly women, their leptin levels increased likewise ( P 0.003 ). In regression analysis, fat mass ( P 0.001 ), female gender ( P 0.04 ), insulin levels ( P 0.03 ), and i.v. glucose supply rates ( P 0.05 ) were independently associated to leptin levels. Conclusions TPN—especially glucose—induces a neurohumoral response as shown here for leptin and insulin that is mainly depending on the fat mass. Better understanding of this regulatory mechanism during artificial nutrition could offer a new approach to improve its therapeutic effects.

The adipokine resistin has been implicated in obesity and insulin resistance. Liver cirrhosis is associated with decreased body fat mass and insulin resistance. We determined plasma resistin levels in 57 patients with cirrhosis, 13 after liver transplantation, and 30 controls and correlated these with hemodynamic as well as hepatic and systemic metabolic parameters. Patients with cirrhosis had, dependent on the clinical stage, an overall 86% increase in resistin levels ( P < 0.001) with hepatic venous resistin being higher than arterial levels ( P < 0.001). Circulating resistin was significantly correlated with plasma TNF-α levels ( r = 0.62, P < 0.001). No correlation was observed between resistin and hepatic hemodynamics, body fat mass, systemic energy metabolism, and the degree of insulin resistance. However, plasma resistin in cirrhosis was negatively associated with hepatic glucose production ( r = −0.47, P < 0.01) and positively with circulating free fatty acids (FFA; r = 0.40, P < 0.01) and ketone bodies ( r = 0.48, P < 0.001) as well as hepatic ketone body production ( r = 0.40, P < 0.01). After liver transplantation, plasma resistin levels remained unchanged, whereas insulin resistance was significantly improved ( P < 0.01). These data provide novel insights into the role of resistin in the pathophysiological background of a catabolic disease in humans and also indicate that resistin inhibition may not represent a suitable therapeutic strategy for the treatment of insulin resistance and diabetes in patients with liver cirrhosis.

Chronic pancreatitis is a common inflammatory disease of the pancreas. Mutations in the genes encoding cationic trypsinogen (PRSS1) and the pancreatic secretory trypsin inhibitor (SPINK1) are associated with chronic pancreatitis. Because increased proteolytic activity owing to mutated PRSS1 enhances the risk for chronic pancreatitis, mutations in the gene encoding anionic trypsinogen (PRSS2) may also predispose to disease. Here we analyzed PRSS2 in individuals with chronic pancreatitis and controls and found, to our surprise, that a variant of codon 191 (G191R) is overrepresented in control subjects: G191R was present in 220/6,459 (3.4%) controls but in only 32/2,466 (1.3%) affected individuals (odds ratio 0.37; P = 1.1 x 10(-8)). Upon activation by enterokinase or trypsin, purified recombinant G191R protein showed a complete loss of trypsin activity owing to the introduction of a new tryptic cleavage site that renders the enzyme hypersensitive to autocatalytic proteolysis. In conclusion, the G191R variant of PRSS2 mitigates intrapancreatic trypsin activity and thereby protects against chronic pancreatitis. The initial experiments were supported by the DFG (Wi 2036/1-1). This work was supported by the Sonnenfeld-Stiftung, Berlin, Germany (to H.W.), the US National Institutes of Health (NIH) (grant DK058088 to M.S.-T.), INSERM (Institut National de la Santé et de la Recherche Médicale) and the Programme Hospitalier de Recherche Clinique (grant PHRC R 08-04 to C.F.)

Background Until now, hydrophilic and lipophilic vitamin preparations had to be administered separately during total parenteral nutrition. By addition of glycocholic acid, a vitamin supplement (Cernevit, Baxter, Heidelberg, Germany) was developed that combines all vitamins into one vial. However, little information exists about possible consequences of bile acid administration such as glycocholic acid, especially if liver disease is pre-existing. Aim To evaluate the effects of total parenteral nutrition with a vitamin preparation containing high doses of glycocholic acid in patients with and without liver disease. Methods In a prospective, randomized-controlled trial, 74 patients, 36 of them with hepatobiliary disease, received total parenteral nutrition for 16 +/- 11 days, either with Cernevit or control vitamin supplements. Patients were closely monitored for clinical and biochemical parameters including serum bile acid profiles measured by high-performance liquid chromatography. Results Serum glycocholic acid increased in patients with liver disease treated with Cernevit, whereas total bile acids did not significantly change. Other liver function tests remained stable during treatment. No adverse events during Cernevit administration were noted except for a reversible slight increase of transaminases in one patient. Conclusions Cernevit was well tolerated after repeated dosing, even in patients with severe liver disease. Apart from standard controls of liver biochemistry, no specific surveillance is necessary during treatment with Cernevit.

Die enterale Ernahrung ist eine Form der sog. „kunstlichen Ernahrung“ und integraler Bestandteil der Therapie zahlreicher Erkrankungen. Sie dient der Verbesserung des Krankheitsverlaufs und der Prognose durch Deckung des Nahrstoffbedarfs sowie Verbesserung bzw. Erhalt des Ernahrungszustands bei Patienten mit unzureichender oraler Nahrungszufuhr. Verwendet werden industriell hergestellte Trink- und Sondennahrungen mit definierter Zusammensetzung sowie besondere Zugangswege (nasogastrale/intestinale Sonden, perkutane Gastro-/Enterostomien). Voraussetzung ist ein funktionierender Gastrointestinaltrakt. Haufig wird die enterale Ernahrung nur erganzend zur oralen oder parenteralen Ernahrung eingesetzt. Die meisten Patienten konnen mit Standardnahrungen versorgt werden. Modifikationen der Nahrungen betreffen die Energiedichte, die Nahrstoffrelation und den Gehalt an Ballaststoffen oder spezifischen Nahrstoffen, die z. B. einen Einfluss auf das Immunsystem haben. Diese modifizierten Diaten sind spezifischen Indikationsstellungen vorbehalten.

The purpose of this study was to evaluate the patency, functional and haemodynamic results of expanded-polytetrafluoroethylene (ePTFE)-covered transjugular intrahepatic portosystemic shunts in patients with liver cirrhosis.Thirteen patients with an ePTFE-covered transjugular intrahepatic portosystemic shunt stent (TIPSS) were prospectively evaluated at 6 and 12 months and compared with matched controls with mesh-wire uncovered TIPSS.At 6 months, ePTFE-TIPSS showed a significantly lower porto-caval pressure gradient (PCPG) (9 (3-21) mmHg, P = 0.006), a lower rate of dysfunction (8% versus 54%, P = 0.03) and required fewer reinterventions (2 versus 13, P = 0.02); similar results were obtained after 12 months. This resulted in a reduction in the median cost for angiographic surveillance in the covered TIPSS group at 6 and 12 months (36% and 56% compared to the uncovered TIPSS group, P = 0.002), but total procedure-related costs were higher with the ePTFE-TIPSS (6 months: 3730 (3245-6759) versus 1850 (1466-5479) euro/patient; 12 months: 3945 (3460-6759) versus 2295 (1728-5694) euro/patient) due to the higher initial cost of the ePTFE-covered TIPSS.The insertion of ePTFE-covered TIPSS results in better maintenance of lowered portal pressure and fewer reinterventions in patients with liver cirrhosis. There is strong evidence that the use of ePTFE-TIPSS does not require regular surveillance to maintain primary patency, which may then improve cost-effectiveness.

Lactose intolerance with adult-onset is due to the inadequate enzymatic activity of lactasephlorizin hydrolase (LPH). It is frequently seen in patients with Crohn disease, but the mechanism remains to be elucidated. Two DNA genotypes, C/C(-13910) and G/G(-22018), located upstream from the LCT locus, the gene encoding for LPH, were recently identified as representing genetic markers for lactose intolerance. We utilized these two DNA genotypes to study their role in inflammatory bowel disease.We investigated the prevalence of these two DNA variants using specific restriction enzyme digest assays in 166 patients with Crohn disease, in 120 healthy first-degree relatives of Crohn disease patients, in 63 patients with ulcerative colitis and in 187 healthy individuals.The analysis revealed a frequency of 21.4% of the 2 genotypes for adult-type hypolactasia in our studied German cohort of healthy individuals, which is higher than previously reported (15%) based on the hydrogen (H2) breath test. This might indicate a higher sensitivity of genotyping, but it has to be confirmed in larger cohorts. No significant difference was detectable in the frequency of the C/C(-13910) and G/G(-22018) genotypes in patients with Crohn disease (C/C(-13910): 21.7%; G/G(-22018): 22.3%) compared to first-degree relatives (C/C(-13910): 21.7%; G/G(-22018): 20.8%), patients with ulcerative colitis (C/C(-13910): 20.3%; G/G(-22018): 20.3%) and healthy individuals (C/C(-13910): 21.4%; G/G(-22018): 21.4%).The C/C(-13910) and G/G(-22018) genotype of adult-type hypolactasia is not associated with susceptibility to the pathogenesis of Crohn disease and ulcerative colitis.

The management of acute pancreatitis (AP) frequently includes parenteral nutrition, but conditionally essential amino acids such as glutamine are not included in conventional total parenteral nutrition (TPN).This study was conducted to determine whether the inclusion of glutamine has a beneficial effect in patients with AP receiving TPN.In a randomized, controlled study 28 patients with AP received either a standard TPN with 1.5 g/kg body weight protein or an isonitrogen, isocaloric TPN which contains 0.3 g/kg L -alanine- L -glutamine. Patients were assessed for nutritional and inflammatory parameters, infectious complications, length of TPN, length of hospital stay (LOS) and cost of TPN.There were no side-effects related to glutamine substitution observed. Glutamine was associated with a significant increase of cholinesterase, albumin and lymphocyte count in AP as well a decrease of C-reactive protein compared to standard TPN at day 14. There was a reduced length of TPN (10 [6-16] vs 16 [10-18] days, P0.05) and a trend of reduced LOS (21 [14-32] vs 25 [19-40] days) in AP patients receiving glutamine. The overall cost per patient for TPN did not differ (gln+: 929+/-586 vs gln-: 981+/-507 euro/patient).Our results suggest that glutamine substitution is beneficial and does not increase the overall cost of parenteral feeding in patients with acute pancreatitis.