Malnutrition in cirrhosis.
Explore the source record for details and available documents.
Energy Metabolism↗
Biomedical subjects
M J Müller
Publications and source records attributed to M J Müller.
[Prevention of smoking from the psychological medicine perspective].
Smoking is a complex socio-psycho-biological behavior with high prevalence and high risk for several diseases. Referring to a widely accepted concept of prevention, the review presents recent psychological and pharmacological strategies to cease smoking with respect to theory, application, and evaluation. Primary prevention, which includes appropriate settings in schools, families, and social groups, seems adequate in preventing people from health problems associated with tobacco-smoke. Although evaluations are rarely found, curricula starting at childhood and intensive training programs for adolescents can be presently recommended. These programs have to take into account specific group characteristics and should focus on active and self-controlled behavior without smoking. Additionally, negative short-term effects of smoking should be emphasized more clearly instead of longterm risks of smoking. The broad diversity of secondary prevention programs for smoking cessation and relapse prevention includes well established and efficient psychological and pharmacological treatments. Flexible combinations of psychotherapeutic and pharmacological strategies (e.g. behavioral skill training programs and nicotine replacement therapy), which also consider the strength of nicotine dependence and withdrawal symptoms, are most promising. For smokers, who continue to smoke despite of health damages (e.g. cardiovascular diseases, cancer), intensive psychotherapeutic regimens (tertiary prevention) are suggested. However, evaluation on this issue is almost missing. In summary, smoking prevention programs can be considered to be cost-effective. Nevertheless, 1 year abstinence rates range only between 20-30%. Furthermore, there is a strong need for psychobiological research on the development of smoking behavior, on long-term follow-up of prevention programs, and on outcome prediction.
Combined Modality Therapy↗
The influence of nicotine on performance, mood, and physiological parameters as related to smoking habit, gender, and suggestibility.
Based on previous observations that sensory suggestibility might be related to cholinergic drug effects, and that individual susceptibility to nicotine as defined by response differences to various doses is lower in males, nonsmokers, and highly suggestible subjects, the present study investigated whether nicotine serum blood levels, cardiovascular responses, and sensory suggestibility show differences according to gender and smoking habit, and whether differences in nicotine susceptibility measured by a discrimination task by subjective ratings on activation can be reproduced in the direction predicted by the previous data. In a double-blind threefold cross-over design 48 subjects divided according to smoking habit, gender, and sensory suggestibility were tested in balanced order under the influence of an oral dose of 0, 0.014, or 0.028 mg/kg body weight of nicotine. Results revealed higher serum levels of nicotine in males and smokers, a dose-dependent increase in heart rate and systolic and diastolic blood pressure, partly interacting with gender or smoking habit (females and nonsmokers showing larger increase with the low doses), and a change in suggestibility in the expected direction (decrease with the low dose, increase with the large one only in female nonsmokers). A fourfold interaction among dose, smoking habit, gender, and suggestibility for the discrimination task partly reproduced the observations of higher nicotine susceptibility in females and non-smokers, whereas suggestibility did not seem to reveal the expected changes. Also, on a subjective level larger doses were necessary to make male smokers feel activated, while the other groups showed the biphasic response pattern to the two nicotine doses. In conclusion, the data justify further research on the concept of nicotine susceptibility defined by biphasic effects of nicotine on vigilance.
Administration, Oral↗
Metabolism of energy-yielding substrates in patients with liver cirrhosis.
Explore the source record for details and available documents.
Basal Metabolism↗
Are patients with liver cirrhosis hypermetabolic?
Hypermetabolism is not a constant feature of liver cirrhosis. It may occur in up to 18% of cirrhotics. Most of the deviations are due to increases in resting energy expenditure (REE). Dietary induced thermogenesis (DIT) is normal or slightly increased whilst the thermic effect of exercise TEE is of minor importance in cirrhosis. The increase in REE which reflects a systemic manifestation of liver disease cannot be identified by the clinical and biochemical measures of liver function. An increased REE is frequently seen in malnourished patients and this is mainly due to disproportional loss in muscle mass. Some cirrhotic patients cannot reduce REE in response to weight loss. This problem is not specific for liver cirrhosis but is also seen in other cachectic groups of patients. Adjustment of REE per kg fat free mass (FFM) may lead to erroneous conclusions (i) because of the non linearity of REE over the range of FFM and (ii) the different contributions of muscle mass and non-muscle body cell mass (BCM) to FFM over the range of FFM. There is circumstantial evidence that the metabolic rate per kg BCM is increased in malnourished cirrhotics. More specifically, cirrhosis increases in REE are associated with a deterioration in hepatic circulation. Increased sympathetic nervous system activity is frequently seen in cirrhosis and may provide a link between between reduced nutritive portal flow and increased whole body oxygen consumption. Increased REE is also associated with weight loss, a poorer liver function and a higher mortality after liver transplantation and thus may have prognostic value. Taken together, REE is variable in patients with cirrhosis. Hypermetabolism is seen in malnourished patients and those with impaired splanchnic hemodynamics. Hypermetabolism is associated with a poorer outcome after liver transplantation.
Journal Article↗
Resting energy expenditure and nutritional state in patients with liver cirrhosis before and after liver transplantation.
Resting energy expenditure (REE), body composition, and the biochemical parameters of liver function were measured in 26 patients before and 432 days (range: 103-1022 days) after liver transplantation (LTX). PreLTX REE was variable (mean: 1638 +/- 308 kcal/day, range: 1220-2190 kcal/day or +10 +/- 11% of Harris Benedict = HB prediction, range: -19 - +33%) and was closely related to body cell mass (r = 0.66, p < 0.0003). PostLTX REE was variable (mean: 1612 +/- 358 kcal/day, range: 1010-2490 kcal/day or +5 +/- 15% of HB prediction, range: -20 - +37%) and was closely related to body cell mass (r = 0.65, p < 0.0006). When compared with preLTX values only small changes in mean REE (-71 +/- 43 kcal/day) and a close correlation between pre and postLTX REE (r = 0.82, p < 0.001) were observed. In contrast to REE, changes in body weight were highly variable (-16.5 - +32.7 kg/year). This variance was not explained by the number of postoperative complications, pre and postLTX liver function, possible graft rejection and/or hepatitis reinfection. Pre-operative hypermetabolism (i.e. REE >+20% of HB prediction) was associated with postoperative hypermetabolism and a reduced liver function before and after LTX. Hypermetabolic patients had a poorer nutritional outcome after LTX (weight change: 0 +/- 8.4 kg/year) when compared with normometabolic controls (weight change: +5.7 +/- 7.4 kg/year; p < 0.05). There was no significant association between deviations in pre and postLTX REE and changes in body weight. When corrected for changes in the nutritional state our data provide evidence for the persistence of resting energy expenditure in liver transplant patients.
Journal Article↗
Skeletal muscle glycogen content in patients with cirrhosis.
We investigated stable cirrhotic patients for muscle glycogen content. Muscle biopsy samples were taken of 14 patients after overnight fasting. Electron microscopy showed normal intracellular distribution of glycogen (n = 8). Muscle glycogen concentration was 16.5 +/- 7.1 gm/kg wet muscle weight (normal range, 10 to 20 gm/kg). Basal, early postabsorptive, exercise-induced and insulin-induced respiratory quotients as well as insulin sensitivity (euglycemic clamp technique, 7.2 pmol insulin/kg body weight/min) and glucose tolerance were assessed. The glucose disposal rate was 23.0 +/- 10.1 mumol/kg/min (mean +/- S.D.), indicating moderate insulin resistance in these patients. We found no association between basal muscle glycogen content and basal or postprandial respiratory quotient, insulin sensitivity, nutritional status or glucose tolerance. However, there was a positive correlation between muscle glycogen content and exercise, as well as insulin-induced respiratory quotient (r = 0.651, p < 0.03 and r = 0.587, p < 0.03, respectively). We conclude that postabsorptive muscle glycogen stores, which are effectively maintained in patients with cirrhosis, are one determinant of exercise-induced and insulin-induced whole body fuel metabolism in these patients.
Adult↗
Tumour necrosis factor receptor levels are linked to the acute-phase response and malnutrition in human-immunodeficiency-virus-infected patients.
1. Increased release of tumour necrosis factor is thought to contribute to human-immunodeficiency-virus-associated wasting syndrome. Elevated serum concentrations of tumour necrosis factor have, however, mainly been found during acute opportunistic infections and were not correlated with the degree of wasting. This finding may be explained by the paracrine release and the rapid inactivation of tumour necrosis factor. Serum levels of the two recently detected soluble tumour necrosis factor receptor proteins (p55 and p75) are assumed to reflect tumour necrosis factor release. 2. Serum levels of soluble tumour necrosis factor receptors 55 and 75 were measured by an enzyme-linked immunological and biological binding assay in 45 human-immunodeficiency-virus-infected patients and seven healthy control subjects. Patients were followed up for survival. Serum albumin, prealbumin, total iron-binding capacity (transferrin) and C-reactive protein concentrations were measured using standard laboratory methods. Body composition was determined by bioelectrical impedance analysis. 3. Serum concentrations of soluble tumour necrosis factor receptor 55 and 75 were both significantly increased in human-immunodeficiency-virus-infected patients as compared with the health control subjects (P < 0.05); soluble tumour necrosis factor receptor concentrations were even more increased in patients with elevated C-reactive protein levels (> or = 5mg/l) as compared with those with normal C-reactive protein levels (< 5mg/l; P < 0.0001 and P < 0.01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
Acute-Phase Reaction↗
Salivary testosterone and simple reaction time parameters.
A study on 64 healthy young men was carried out to investigate the relationships between salivary testosterone (TS) levels and simple reaction time (RT) parameters under baseline and experimental stress conditions. Two similar simple RT tasks during an anticipation period (test 1, without feedback) and a stress period (test 2, feedback) were used. Electric skin shocks (test 2) were either given contingently to previous performance or noncontingently using a yoked design. Saliva samples obtained during the baseline period were used to split the sample into groups of low and high TS levels according to the median. As expected, lower TS baseline levels were associated with higher mean RT and intraindividual standard deviations. Furthermore, lower TS levels combined with noncontingent feedback resulted in larger numbers of passive avoidance reactions.
Adult↗
Glucose intolerance in liver cirrhosis: role of hepatic and non-hepatic influences.
Oral glucose tolerance was tested in a heterogeneous group of 108 patients with liver cirrhosis. Data were compared with those from 181 subjects without liver disease (44% normal, 35% impaired glucose tolerance and 21% type 2 diabetes mellitus). In cirrhosis, 27% of the patients had normal, 36% had impaired glucose tolerance, and 37% were diabetic. There was no association between glucose intolerance or diabetes and the aetiology of cirrhosis, the duration of the disease, the biochemical indicators of hepatocyte damage, cholestasis and/or liver function. Only weak associations were found between the results of quantitative liver functions tests (caffeine, xylocaine, indocyanine green) and basal and post load glucose and insulin concentrations. Cirrhotics with 1st degree relatives with type 2 diabetes mellitus (n = 16) did not show an increased prevalence of diabetes. Older and/or malnourished patients were more frequently glucose intolerant. Using the plasma glucose concentration 120 minutes after glucose load as the dependent variable, multivariate regression analysis showed that 54% of its variance is associated with the following variables: basal plasma glucose (36%) and free fatty acid concentration (5%), age (3%), basal glucose oxidation rate (3%), muscle mass (3%) and plasma free glycerol at 120 minutes after glucose load (3%). By contrast, the clinical state of the patients (i.e. the CHILD-Pugh score) accounted for only 2% of the variance. We conclude that glucose tolerance is variable in cirrhosis. After manifestation of liver disease, glucose intolerance or diabetes cannot be explained by the clinical, histological or biochemical signs of liver disease.
Adult↗
Markers of bone metabolism during short-term administration of thyroxine in healthy volunteers.
We investigated the influence of L-thyroxine (L-T4) treatment over 3 weeks on biochemical markers of bone turnover in 12 healthy young men (age 25.6 +/- 1.4 years, BMI: 22.6 +/- 2.5 kg/m2). Serum parameters indicating bone formation [bone Gla protein (BGP), carboxyterminal propeptide of type I procollagen (PICP), and bone-specific alkaline phosphatase (BAP)] and bone resorption [cross-linked carboxyterminal telopeptide of type I collagen (ICTP) and the urinary excretion of pyridinoline (Pyr) and deoxypyridinoline (D-Pyr)] were measured before and after three weeks of treatment with 300 micrograms L-T4/d. T3 and T4 significantly increased and TSH decreased to almost undetectable levels even when measured with a third generation TSH assay. Markers of bone formation showed variable responses with a small but significant increase in BGP but not in PICP or BAP. In contrast, all parameters of bone resorption increased significantly with a good correlation between D-Pyr excretion and the serum parameter ICTP (r = 0.78, p < 0.0001). These changes in bone-turnover markers were not necessarily paralleled by comparable increments of other markers of tissue thyrotoxicosis (SHBG, pulse rate, VO2), suggesting a variability in tissue sensitivity. These rapid responding parameters, especially in the easily obtainable serum parameter ICTP, might be valuable tools in the evaluation of several states of thyroxine excess.
Adult↗
Determination of anatomical skeletal muscle mass by whole body nuclear magnetic resonance.
Explore the source record for details and available documents.
Adult↗
Who should undergo a very low energy diet?
Explore the source record for details and available documents.
Diet, Reducing↗
Reduced metabolic efficiency in patients with Crohn's disease.
Malnutrition is frequently seen in patients with inflammatory bowel disease, and parenteral or enteral nutrition is considered essential in this patient group. However, many patients with Crohn's disease have difficulties in gaining weight in response to overfeeding, suggesting reduced energy retention. Substrate utilization and nutrient balances as well as changes in body composition were followed in 10 patients with Crohn's disease immediately in the course of remission on low-dose steroid treatment, during an eight-day period of continuous enteral nutrition at constant (protocol 1:1.5-fold basal energy expenditure) and increasing (protocol 2:0.5- to 2.0-fold basal energy expenditure) nutrient supply. Energy, substrate, and nitrogen balances all became positive in response to overfeeding. However, fat was predominantly oxidized at an infusion rate of 1.2 g/kg body wt/day, whereas carbohydrates and proteins were effectively stored. A positive energy balance was reached at an energy infusion rate exceeding 31 kcal/kg body wt/day and corresponding substrate supplies of 1.6, 1.7, and 1.1 g/kg body wt/day for carbohydrates, fat, and protein, respectively. Nitrogen balance normalized at a supply of 0.14 g/kg body wt/day, which also reduced myofibrillar protein breakdown. Considering the relative contributions made by these nutrients in the diets, an accumulation of carbohydrates and protein but a depletion in fat became evident from nutrient balances. In fact, body weight increased by 0.12 kg/day, which was explained by an increased extracellular (+0.18 kg/day) and body cell mass (+0.04 kg/day) at reduced fat mass (-0.10 kg/day). Concomitantly, plasma T3 and insulin secretion both increased, whereas sympathetic nervous system activity decreased with overfeeding. This is contrary to data observed in healthy subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Resting energy expenditure and weight loss in human immunodeficiency virus-infected patients.
Resting energy expenditure (REE) and body composition were investigated in 60 clinically stable patients with human immunodeficiency virus (HIV) infection varying with respect to immune impairment. REEs differed significantly from predicted values (> or < 10% of the Harris-Benedict [HB] equation) in 40% of patients. Seven percent of patients showed markedly increased REE (> +20% of HB prediction), whereas REE was decreased in 13% (< -10%). Increased REE was found during all clinical stages of the disease (Walter Reed [WR] 2 through 6) and was not strictly associated with the degree of immune impairment, presence of diarrhea or Kaposi's sarcoma, nutritional state, or anamnestic wasting. Twenty-seven patients were evaluated for a mean period of 319 days; 11 lost more than 5% of their initial body weight during the observation period. Weight-losing patients were normometabolic before but showed a significantly increased REE (+7% of predicted values or +8% when compared with previous measurements) during weight loss. The degree of deviation from estimated REE was strongly associated with the degree of weight loss. We summarize that increased REE is not a constant feature of HIV infection. It is not associated with clinical and laboratory parameters of immune deficiency, but may occur during weight loss. Thus increased REE represents an inadequate adaptation to malnutrition and contributes to wasting.
Acquired Immunodeficiency Syndrome↗
Home enteral nutrition in patients with Acquired Immunodeficiency Syndrome.
UNLABELLED: 14 patients in advanced stages of HIV infection (1 ARC, 13 AIDS; sex: 1 female, 13 male; age 37.8 +/- 6.3 years; body mass index (BMI): 17.4 +/- 2.4 kg/m(2)) were followed prospectively while receiving home enteral nutrition (observation period: 62 +/- 75 days). Artificial nutrition was indicated because of severe weight loss (9-38 kg within 6-48 months, n = 7) or cerebral toxoplasmosis with eating and swallowing disorders (n = 7). In all patients a defined formula diet (175 +/- 17.7 kJ/kg body weight) was administered through an endoscopically placed gastrostomy tube (PEG). Home enteral nutrition was well tolerated by all patients and no significant PEG-related complications occurred. Enteral nutrition resulted in significant increases in body weight (p < 0.005), body cell mass (BCM, p < 0.05), total body fat (TBF, p < 0.005), serum albumin concentration (p < 0.05), and serum total iron-binding capacity (transferrin, p < 0.01). CONCLUSION: Home enteral nutrition via PEG is safe and well tolerated in patients with advanced HIV-related immunodeficiency and is capable of improving nutritional state including BCM.
Journal Article↗
Insulin resistance in liver cirrhosis. Positron-emission tomography scan analysis of skeletal muscle glucose metabolism.
BACKGROUND: Insulin resistance and glucose intolerance are a major feature of patients with liver cirrhosis. However, site and mechanism of insulin resistance in cirrhosis are unknown. We investigated insulin-induced glucose metabolism of skeletal muscle by positron-emission tomography to identify possible defects of muscle glucose metabolism in these patients. METHODS: Whole body glucose disposal and oxidation were determined by the combined use of the euglycemic-hyperinsulinemic clamp technique (insulin infusion rate: 1 mU/kg body wt per min) and indirect calorimetry in seven patients with biopsy-proven liver cirrhosis (Child: 1A, 5B, and 1C) and five healthy volunteers. Muscle glucose uptake of the thighs was measured simultaneously by dynamic [18F]fluorodeoxyglucose positron-emission tomography scan. RESULTS: Both whole body and nonoxidative glucose disposal were significantly reduced in patients with liver cirrhosis (by 48%, P < 0.001, and 79%, P < 0.0001, respectively), whereas glucose oxidation and the increase in plasma lactate were normal. Concomitantly, skeletal muscle glucose uptake was reduced by 69% in liver cirrhosis (P < 0.003) and explained 55 or 92% of whole body glucose disposal in cirrhotics and controls, respectively. Analysis of kinetic constants using a three-compartment model further indicated reduced glucose transport (P < 0.05) but unchanged phosphorylation of glucose in patients with liver cirrhosis. CONCLUSIONS: Patients with liver cirrhosis show significant insulin resistance that is characterized by both decreased glucose transport and decreased nonoxidative glucose metabolism in skeletal muscle.
Adult↗
Energy expenditure and substrate metabolism in liver cirrhosis.
Increased energy needs, a reduced synthesis of endogenous substrates and a limited energy yield from exogenous substrates characterize the metabolic dilemma in patients with liver cirrhosis. The metabolic features observed in cirrhosis are highly variable and cannot be considered as clear-cut phenomena. They obviously differ in certain aspects from the metabolic situations known from starvation or type 2 diabetes mellitus. This is not contrary to the idea that cirrhosis may resemble certain aspects of these 'standard' situations. Cirrhosis-induced disturbances in fuel homeostasis cannot be predicted from clinical and biochemical parameters of the disease. Most of the metabolic picture is present at a very early stage of liver disease. Many metabolic features are independent of the clinical course of liver disease, suggesting that they are an early and extra-hepatic manifestation. A better understanding of the variance of cirrhosis-induced alterations in metabolism may come from characterization of the metabolic 'genotype' which adds to disease-related factors in the individual patient.
Body Temperature Regulation↗