The purpose of this article is to present detailed data on the nutritional assessment in cirrhotic patients. The exact frequency and types of malnutrition, its associations with the aetiology of liver disease, liver dysfunction and clinical staging in liver cirrhosis are unknown. A new classification system is presented which may help to suggest some interventional guidelines. Physical (anthropometry, 24-h urinary creatinine excretion, bioelectrical impedance analysis (BIA), total body potassium counting, ultrasound examination) and metabolic (indirect calorimetry) assessment of nutritional status was therefore performed in 123 patients with liver cirrhosis, who were considered as potential candidates for liver transplantation. Data were related to the clinical, biochemical, histological and prognostic data of liver disease. Of our patients 65% showed some signs of protein-calorie malnutrition as indicated by low body cell mass, reduced serum albumin concentrations or abnormal skinfold thickness. Of these 34% were considered as "kwashiorkor-like" (normal body composition, serum albumin less than 35 g/l), and 18% were "marastic" (reduced body weight, body cell mass, and fat mass). However, 49% of the malnourished group had reduced body cell mass in association with increased fat mass and frequently presented with a normal body weight ("mixed" or "obese" type). Protein-calorie malnutrition did not correlate with the aetiology of the disease and biochemical parameters of liver function. Malnutrition was observed at all clinical stages but was more frequently seen at advanced stages. We conclude that malnutrition associated with liver cirrhosis is not a clear phenomenon. Its clinical presentation is heterogenous and not reflected by the histological or biochemical parameters of liver disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Many clinicians subjectively feel that cirrhotic patients frequently have clinical signs of hypermetabolism. However, it is unknown whether hypermetabolism is a constant feature of chronic liver disease, corresponds to liver destruction and repair or is of prognostic value. This article is about resting energy expenditure and substrate oxidation rates in 123 patients with biopsy-proven cirrhosis differing with respect to cause, duration of the disease, biochemical parameters of parenchymal cell damage, cholestasis, liver function, number of complications, clinical staging and nutritional state. Resting energy expenditure varied between 1,090 and 2,300 kcal/day and differed from the predicted values in 70% of the patients. Resting energy expenditure was closely related to fat-free mass, and 52% of the variability could be explained by fat-free mass, age and sex. Of all the patients, 18% were hypermetabolic and 31% were hypometabolic. Hypermetabolism showed no strict association with the cause of cirrhosis, the duration of the disease, liver function, cholestasis, cell damage, clinical staging, blood hemoglobin, plasma thyroid hormone levels or human leukocyte antigens. An increased resting energy expenditure was associated with significant losses of muscle, body cell mass and extracellular mass at unchanged body fat, whereas fat and fat-free mass were increased in hypometabolic patients when compared with normometabolic patients. Lipid oxidation was increased, but glucose oxidation was reduced in nearly all patients with cirrhosis. This was most pronounced at advanced stages of liver disease. Although similar with respect to liver function and clinical staging, 76.2% of hypermetabolic patients had transplants within the observation period, compared with only 16.7% and 8.1% in the normometabolic group and hypometabolic group, respectively. Posttransplantation mortality was independent of pretransplantation resting energy expenditure, but it increased significantly in patients with losses in body cell mass. In conclusion, hypermetabolism is not a constant feature of cirrhosis and results more from extrahepatic than from hepatic factors. It may cause malnutrition and contributes to the clinical outcome of patients with chronic liver disease.

Imbalances in epithelium-matrix interactions have been discussed as a pathomechanism in ulcerative colitis, causing a colonic mucosal barrier dysfunction. Laminin, the major noncollagenous component of the basement membrane, plays a role in epithelial basal lamina formation and promotes differentiation of human enterocytes. We therefore investigated the distribution of laminin in ulcerative colitis affected colonic tissues. Tissue specimens from both affected and nonaffected colonic regions were obtained from ten patients with ulcerative colitis during colonoscopies or operations. Healthy tissue from five patients with colorectal cancer was used as control. After histological classification, the localization and distribution of the basement membrane associated extracellular matrix proteins were determined by immunohistochemistry. Paraffin-embedded sections were incubated with antibodies against laminin and type IV and V collagen. No positive immunoreactivity against laminin was found in most of the epithelial basement membranes surrounding the crypts in affected colonic tissues, without involvement of the subendothelial structures. In contrast, a type IV and V collagen accumulation occurred in all these tissue samples. The lack of laminin in combination with an overexpression of type IV and V collagen, as reported for the first time in this paper, leads to changes in basement membrane structure. These findings indicate that the three-dimensional network of the colonic epithelial basement membrane and its function are seriously disturbed in exacerbating ulcerative colitis. This provides new insights into the importance of cell-matrix interactions for physiological and pathological mechanisms in the etiology of ulcerative colitis.