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Summary Introduction Malnutrition is associated with a higher morbidity resulting in an increased need for medical resources and economic expenses. In order to ensure sufficient nutritional care it is mandatory to identify the effect of malnutrition and nutritional care on direct cost and reimbursement. The primary aim of this study was to evaluate the economic effect of a nutritional screening procedure on the identification and coding of malnutrition in the G-DRG system. Methods All G-DRG relevant parameters of 541 consecutive patients at a gastroenterology ward were documented. Moreover, all patients were screened for malnutrition by a dietician according to the subjective global assessment (SGA). Patients were then grouped into the appropriate G-DRG and the effective cost weight (CW) was calculated. Results Ninety-two of 541 patients (19%) were classified malnourished (SGA B or C). Recognition of malnutrition increase from 4% to 19%. Malnourished patients exhibited a significantly increased length of hospital stay (7.7±7 to 11±9, P 0.0001 ). In 26/98 (27%) patients, the coding of malnutrition was considered relevant by grouping and resulted in a rise of DRG benefit. Mean case mix value and patients’ complexity and comorbidity level (PCCL) increased after including malnutrition in the codification (CV 1.53±2.9 to 1.65±2.9, P = 0.001 and PCCL 2.69±1.4 to 3.47±0.82, P 0.0001 ). The reimbursement increase by 360 €/malnourished patient or an additional reimbursement of 35280 € (8.3% of the total reimbursement for all patients of 423186 €). Nutritional support in a subgroup of 50 randomly selected patients resulted in additional costs of 10268 €. Forty-four of these patients (86%) were classified malnourished (32 SGA B and 12 SGA C). However, the subsequent reimbursement covered only approximately 75% of the expenses (7869 €), but did not include the potential financial benefits resulting from clinical interventions. Conclusion Malnourished patients can be detected with a structured assessment and documentation of nutritional status and this is partly reflected in the G-DRG/ICD 10 system. In addition to increasing direct health care reimbursement, nutritional screening and intervention has the potential to improve health care quality.

In approximately 25% of patients with acute or chronic pancreatitis the cause remains unclear. Despite progress in understanding so-called idiopathic pancreatitis, more diagnostic criteria are needed. We report on a patient who presented with jaundice, but without pain or fever. Under the assumption of pancreatic cancer the patient underwent hemipancreatoduodenectomy. Histological examination showed chronic sclerosing inflammation of the pancreas and bile ducts without any signs of malignancy. Ten weeks later he developed bilateral parotid swelling and recurrent bouts of fever. Again liver enzymes were elevated and unsuccessfully treated with antibiotics for bacterial cholangitis. Further biopsies from submandibular gland, lymph nodes and liver again showed chronic sclerosing inflammation with lymphoplasmacytic infiltration. For sicca symptoms the diagnosis of a primary Sjogren's syndrome was proposed. However, with corticosteroid treatment the patient improved remarkably but after tapering he relapsed. On the basis of established criteria, we diagnosed autoimmune pancreatitis with (1) diffuse swelling of the pancreas, (2) irregularities of the pancreatic duct, (3) lymphoplasmacytic infiltration, (4) response to corticosteroids, (5) hypergammaglobulinaemia, and (6) disproportionately raised IgG4. In addition, the patient fulfilled the criteria for secondary Sjogren's syndrome. Autoimmune pancreatitis may present as an isolated or syndromic disease. It is an autoimmune disorder of unknown cause and should be included in the differential diagnosis of pancreatic disorders.

Background and Aims: To evaluate genotyping for two DNA variants (c.1993+327C>T and c.1438+117G>A), recently found to be associated with adult-type hypolactasia, in the diagnosis of lactose intolerance. Methods: In total, 166 consecutive patients with gastrointestinal symptoms mimicking hypolactasia admitted to the clinic between March 2002 and December 2002 were included. Genotyping for the two DNA variants (c.1993+327C>T and c.1438+117G>A) and standard H2 breath test was performed. Results: Among 116 patients with positive H2 breath test, the c.1993+327C variantwas detectablein 106 (91.4%) patients. Among 50 patients with negative H2 breath test, the c.1993+327Cvariantwas seen in 2 patients. Sensitivity, specificity, positive and negative predictive values for the c.1993+327C variant were 91.4, 96.0, 98.1 and 82.8%, respectively. Genotyping for the c.1438+117G variant did not bring any additional information. Among 4 of the 10 patients with positive H2 breath test but negative for the c.1993+327C and the c.1438+117G variant,further evaluation revealed other diseases known to cause secondary hypolactasia such as celiac disease and short bowel syndrome. Conclusion: In symptomatic patients, genotyping for the DNA variant c.1993+327C is a reliable test for adult-type hypolactasia with high sensitivity and specificity and thus provides a new tool in the diagnostic workup of hypolactasia.

Background. Keratin 8 is a major component of intermediate filaments in single-layered epithelia of the gastrointestinal tract. Keratin 8 deficient mice display signs of colitis and diarrhoea characteristic for inflammatory bowel disease. Very recently, two keratin 8 mutations, Y54H and G62C, were identified. Aims. We investigated if these keratin 8 missense mutations were associated with inflammatory bowel disease. Patients. In total, 217 German patients with Crohn’s disease, 131 German patients with ulcerative colitis, and 560 German control subjects were enrolled in this study. Methods. Samples were analysed by PCR amplification and subsequent melting curve analysis using fluorescence resonance energy transfer probes. Results. The G62C mutation was detected in five (2.3%) patients presenting with Crohn’s disease and in three (2.3%) with ulcerative colitis. In comparison, 9 (1.6%) out of 560 controls were heterozygous for this mutation. No patient or control was homozygous for this mutation. Patients carrying one mutant allele did not show any noticeable characteristics in their corresponding phenotype. In contrast, the Y54H mutation was observed in neither any of the 348 patients with inflammatory bowel disease nor in any control subject. Conclusions. Our data indicate that both keratin 8 mutations, G62C and Y54H, do not play a relevant pathogenic role in inflammatory bowel disease.

Campath-1H, a monoclonal antibody against human CD52, is used for the therapy of refractory or relapsed chronic lymphocytic leukemia (CLL). Treatment with campath is associated with an increased incidence of infections and also fatal reactivation of viral infections. Reactivation of hepatitis B virus (HBV) in HBsAg-positive patients is a well-documented complication of cytotoxic or immunosuppressive therapy and has also been observed after treatment with rituximab. To date, there are no reports on campath treatment in HBsAg carriers. Here, we present the case of a patient with heavily pretreated CLL who was HBsAg-positive with a high virus load (2 billion copies/mL). He required treatment because of progressive CLL with massive bone marrow infiltration, severe anemia and thrombocytopenia. Campath was initiated and lamivudine, an inhibitor of reverse transcriptase, was simultaneously given to prevent HBV proliferation. During the treatment, no deterioration of liver parameters was observed, and the virus load decreased. After therapy with campath, hemoglobin and platelet counts increased markedly. This report shows that lamivudine is highly effective in inhibiting HBV proliferation and can be used to prevent HBV flare-up during campath treatment in patients tested positive for HBs antigen.

Background & aims: Chronic pancreatitis and pancreatic adenocarcinoma are associated with alcohol abuse, consumption of tobacco smoke, and environmental aromatic hydrocarbon exposure. The role of genetic factors is incompletely defined. Uridine 5′-diphosphate glucuronosyltransferases are phase II detoxifying enzymes capable of tobacco-borne toxicant inactivation and cellular protection. This study analyzes UGT1A7 gene polymorphisms in pancreatic diseases. Methods: Genomic DNA from northern German white patients with pancreatic adenocarcinoma (n = 52) and chronic pancreatitis (n = 146), as well as healthy blood donors (n = 235) was analyzed by UGT1A7-specific PCR, sequencing analysis, and temperature gradient gel electrophoresis. Pancreatic expression of UGT1A genes was identified by duplex reverse-transcription PCR. Results: Predominant expression of the UGT1A7 gene was identified in human pancreatic tissue. Pancreatic adenocarcinoma was associated with the low detoxification activity UGT1A7∗3 allele, which combines the W208R, N129K, and R131K mutations (odds ratio [OR], 1.98; 95% confidence interval [CI ], 1.24–3.14; P = 0.003). The association of UGT1A7∗3 was especially strong in smokers with pancreatic carcinoma who were younger than 55 years (OR, 4.7; 95% CI, 1.9–11.8; P = 0.0009). Chronic pancreatitis was also associated with UGT1A7∗3 (OR, 1.76; 95% CI, 1.26–2.46; P = 0.0009). UGT1A7∗3 was specifically associated with the subgroup of patients with alcoholic pancreatitis, of whom 89% were smokers (OR, 2.24; 95% CI, 1.46–3.43; P = 0.0001) but was not associated with the nonalcoholic pancreatitis subgroup. Conclusions: The UGT1A7 gene is predominantly expressed in human pancreas. The low detoxification activity UGT1A7∗3 allele is identified as a novel risk factor of pancreatic diseases defining the interaction of genetic predisposition and environmentally induced oxidative injury.

Cancer of the proximal digestive tract is associated with tobacco smoke and ethanol exposure. The UDP-glucuronosyltransferase (UGT) 1A7 is a detoxifying enzyme capable of tobacco-borne carcinogen detoxification and cellular protection and has been implicated as a cancer risk gene. In this study, UGT1A7 expression is demonstrated in oral, esophageal, and gastric tissue, which are the principle sites of proximal digestive tract cancer. Genomic DNA from the blood of 76 patients with esophageal, orolaryngeal and gastric cancer as well as from 210 healthy blood donors was analysed for the presence of UGT1A7 polymorphisms by sequencing and temperature gradient gel electrophoresis. Wild type UGT1A7 alleles were equally distributed between controls (19 %) and cancer patients (22 %). However, the UGT1A7*3 allele combining W208R, N129K and R131K missense mutations and exhibiting substantially reduced carcinogen detoxification activity was significantly associated with proximal gastrointestinal cancer and identified as a risk allele present in 32 % of cancer patients and 19 % of controls (P = 0.0008, OR 2,02 (95 %-CI 1.33-3.07)). We identify the significant association of the UGT1A7*3 allele encoding a low catalytic activity protein as a risk gene in proximal digestive tract cancer and as a potential marker for cancer susceptibility.

Editor—Chronic idiopathic pancreatitis is a genetically heterogeneous disease.1-3 Mutations of the cationic trypsinogen ( CT ) gene underlie some cases of juvenile pancreatitis,3-5 and mutations of the cystic fibrosis transmembrane conductance regulator ( CFTR ) gene have been associated with chronic pancreatitis in adults.6-8 However, these genes account for only a relatively small proportion of cases. More recently, the serine proteinase inhibitor Kazal type 1 ( SPINK1 ) gene, also called PSTI , has attracted attention as a possible cause for chronic pancreatitis.9 10 One study by Chen et al 9 did not find disease causing mutations of SPINK1 among 14 families with hereditary and 30 patients with sporadic pancreatitis, apart from two rare amino acid substitutions which were observed at a comparable frequency to the general population. By contrast, another study by Witt et al 10 reported 23 out of 68 children and adolescents with chronic pancreatitis whose disease was associated with the occurrence of SPINK1 mutations in the heterozygous or homozygous state. In particular, one founder mutation, N34S, was identified in 18/68 German patients …

During a 9-day period we investigated body composition, resting energy expenditure (REE), IL-6, TNF, and sTNFR-55 and sTNFR-75 plasma concentrations during infectious complications in 12 patients with HIV disease. At study entry, IL-6 was detectable in 5 and TNF in 10 patients. TNF was closely correlated with sTNFR-75 concentration (r = 0.84, p < 0.001) whereas sTNFR/sTNFR-55 ratio increased throughout the study. TNF concentrations were significantly correlated with the 24-hour excretion of epinephrine and norepinephrine (r = 0.64 and 0.69; each p < 0.01). Compared to expected values REE was increased by 34%. Body cell mass was the single best predictor of REE and explained 72% of its variance. In contrast, the deviation of measured from predicted REE was correlated with TNF and IL-6 concentrations (r = 0.9). We conclude that increased plasma concentrations of cytokines in complicated HIV disease display little biologic variability and relate to hypermetabolism in these patients.

Background: An abnormal immune response may play a pathogenetic role in chronic pancreatitis. However, to date characterization of the systemic immunological changes in patients with chronic pancreatitis has not been undertaken. Methods: Lymphocyte phenotypes and proliferation (3H-thymidine) after stimulation with mitogens and interleukin-2 were studied in peripheral mononuclear cells from 11 patients with chronic pancreatitis (alcohol-induced n = 6; idiopathic pancreatitis n = 5). The natural killer cell activity was investigated in a 51Cr release cytotoxicity assay. In vitro cytokine release of stimulated mononuclear cells was measured. Results: Flow cytometric studies showed a significant decrease in the percentage of circulating CD8+, CD56+ and CD25+ cells in patients with chronic pancreatitis independent of the etiology. Comparing all patients with chronic pancreatitis to controls, the proliferation rate was not significantly increased, but patients with pain (n = 5) showed increased proliferation in comparison to patients without pain (n = 6). No significant difference in natural killer cytotoxicity was observed. The in vitro release of tumor necrosis factor-α and interleukin-10 by stimulated mononuclear cells was increased. Conclusions: Chronic pancreatitis is accompanied by systemic immune dysregulation. The observed changes in peripheral mononuclear cells reveal additional evidence that the cell-mediated immune response may contribute to the development of pain and tissue destruction in chronic pancreatitis.

To determine whether certain nutrients and dietary factors act as modulators of the immune system and improve the nutritional status of immunocompromised patients.Controlled, double-blind, crossover phase trials of the effects of a fortified formula in patients infected with the human immunodeficiency virus (HIV). Patients consumed a control formula for 4 months and a study formula for 4 months.Ten men with symptomatic HIV infection who were following stable medication regimens and had no malignancies, mycobacteriosis, or additional virus infection requiring systemic treatment.Formula fortified with alpha-linolenic acid (1.8 g/day), arginine (7.8 g/day), and RNA (0.75 g/day) and a standard formula.Nutritional status determined by anthropometric, bioelectrical, biochemical, and dietary assessment; energy expenditure determined by indirect calorimetry; disease progression; CD4 lymphocyte counts; HIV p24 antigen plasma concentrations; tumor necrosis factor (TNF) receptor proteins; and compliance control parameters.Student's t tests for paired and unpaired data.Fortified nutrition resulted in a weight gain (+ 2.9 kg/4 months vs -0.5 kg/4 months with the control formula, P.05), an incorporation of eicosaenoic acid into erythrocyte cell membranes (+ 47% of baseline values, P.05), and increased plasma arginine concentrations (96.8 +/- 45.1 vs 51.8 +/- 20.9 mumol/L, P.01). The serum concentrations of the soluble tumor necrosis factor receptor (sTNFR) proteins increased during the study period (sTNFR 55 = + 0.23 vs -0.40 ng/mL, P.001; sTNFR 75 = + 0.90 vs -0.36 ng/mL, P.01), whereas no changes in CD4+ lymphocyte counts were observed.Increasing dietary intakes of n-3 polyunsaturated fatty acids, L-arginine, and RNA increased body weight, possibly by modulating the negative effects of TNF.

Although malnutrition and wasting are known features of human immunodeficiency virus (HIV) infection, their incidence and possible association with immunologic impairment are largely unknown, as is the prognostic value of the nutritional state. Nutritional, clinical, and immunologic parameters were measured in 100 outpatients in different stages of HIV infection. In addition, 39 patients with AIDS were prospectively followed for a mean period of 343 (range, 53-650) days. Sixty-three percent of the patients showed evidence of malnutrition, 21% suffered from wasting. A reduced body cell mass and decreased serum albumin levels were observed in 32 and 14%, respectively, predominantly in more advanced disease stages. Fourteen of 39 AIDS patients died after a mean survival of 212 days. Survivors showed significantly larger initial body cell mass values and higher initial serum albumin levels compared with nonsurvivors, whereas CD4+ lymphocyte counts, disease complications, and medication were all similar in both groups. Kaplan-Meier analyses revealed a significantly prolonged survival in patients with a body cell mass > 30% of body weight or serum albumin levels exceeding 30 g/L. Factor analyses indicated that the parameters of nutritional state were independent from each other and from CD4+ lymphocyte counts. Malnutrition occurs frequently during HIV infection and increases with disease progress. It strongly predicts patient survival independent of CD4+ lymphocyte counts.

Ziel: Erarbeitung eines Algorithmus fur den Einsatz von Trinknahrungen beim ambulanten erwachsenen Patienten als Beitrag zur Diskussion um die Verordnungsfahigkeit im deutschen Gesundheitssystem. Methoden und Ergebnis: Angekoppelt an die Aktualisierung der S3-Leitlinien der Deutschen Gesellschaft fur Ernahrungsmedizin e. V. (DGEM) und dem Prozess der Leitlinienentwicklung mit Delphirunden und Konsensuskonferenz folgend wurde ein Algorithmus zum Einsatz von Trinknahrungen aus Evidenz und Expertenmeinung erarbeitet. Diskussion: In einer prospektiven Evaluation muss die Praxistauglichkeit besonders der auf Expertenkonsens basierenden Zielparameter fur den Erfolg der ernahrungsmedizinischen Intervention gezeigt werden.

298 ESCITALOPRAM FOR THE PREVENTION OF PEG-IFN-a AND RIBAVIRIN ASSOCIATED DEPRESSION IN HCV-INFECTED PATIENTS: FINAL RESULTS FROM THE CIPPAD-TRIAL M. Schaefer, R. Sarkar, V. Weich, S. Effenberger, L. Heinze, U. Spengler, T. Schlaepfer, J. Ockenga, P. Buggisch, J. Reimer, R. Link, O. Kummer, K. Lieb, H. Weidenbach, M. Rentrop, T. Discher, G. Fromm, S. Zeuzem, T. Berg. Klinik fur Psychiatrie, Psychotherapie und Suchtmedizin, Kliniken Essen-Mitte, Essen, Klinik fur Psychiatrie, Campus Mitte, Charite, Universitatsmedizin Berlin, Klinik fur Gastroenterologie und Hepatologie, Charite Universitatsmedizin, Campus Virchow-Klinikum, Berlin, Medizinische Klinik II, Klinik fur Psychiatrie, Universitatsklinik Bonn, Bonn, Medizinische Klinik II, Klinikum Bremen-Mitte, Bremen, Medizinische Klinik I, Klinik fur Psychiatrie, UKE Hamburg, Hamburg, Medizinische Klinik, St. Josefs Klinik Offenburg, Offenburg, Abteilung Innere Medizin II, Universitat Freiburg, Freiburg, Klinik fur Psychiatrie, Universitatsklinikum Mainz, Mainz, II. Medizinische Klinik und Poliklinik, Klinik fur Psychiatrie, Technische Universitat Munchen, Munchen, Medizinische Klinik und Poliklinik II, Klinik fur Psychiatrie, Universitatsklinik Giessen, Giessen, Medizinische Klinik I, Goethe Universitatsklinik, Frankfurt/Main, Germany E-mail: m.schaefer@kliniken-essen-mitte.de

Despite intensive antiretroviral therapies including protease inhibitors AIDS wasting syndrome is still a clinical problem. In 1997 it was the second most frequent AIDS indicator condition (18%) in the United States and probably the most frequent clinical feature of AIDS in developing countries. Malnutrition is associated with decreased quality of life psychosocial function muscle function and leads to increased morbidity and mortality. HIV-associated malnutrition may have many causes including anorexia fatigue depression gastrointestinal disease or metabolic disturbance all of which cause a negative energy balance. Cachexia can also be observed in cancer tuberculosis and other chronic and infectious disease and for a long time it has been considered to be inevitable consequences of these conditions. Therapeutic nihilism is common. (excerpt)

with both CC and LC, and if there was associated entempathy. Methods: 32 patients with microscopic colitis (17 CC, 15 LC) diagnosed using objective histological criteria were included. Serum IgA-antiendomysial (AEA) and lgA-human tissue antitransglutaminase (AtTG) antibodies (IIF and ELISA assays, respectively) were investigated, after ruling-out lgA deficiency. The DQ2 hapforype (DQAI*0501 + DQBI*0201) was deterrmned by PCRSSP. This method detects the presence or absence of at least one copy of the haplotype. HLA-DQ2 was also assayed in 50 healthy controls from the general population. Endoscopic biopsies from 2"d-3rd portions of duodenum were obtained in DQ2 + patients. The number of intraepithefial lymphocytes (IEL) (N