Alterations in carbohydrate metabolism are frequently observed in cirrhosis, and approximately 15% to 30% of patients have overt diabetes. In a retrospective and prospective study in cirrhosis, we analyzed the prognostic significance of diabetes, which was defined as the presence of hyperglycemia and overt glycosuria that in most cases required dietary restrictions or active treatment. The clinical records of all patients with cirrhosis admitted to our department for the period 1980 to 1985 were reviewed in 1985 and 1986, and surviving patients were prospectively followed up until December 1991. Final status could be obtained in 354 (98 with diabetes) of 382 eligible patients; 110 were alive at the end of follow-up. Prognostic factors were identified by Kaplan-Meier analysis, followed by Cox's stepwise regression. The model identified, in sequence, albumin, ascites, age, encephalopathy, bilirubin, diabetes, and platelets as prognostic factors. The larger mortality rate in patients with diabetes was not due to complications of diabetes but to an increased risk of hepatocellular failure. Diabetes was no longer a risk factor as a covariate in a subgroup of 271 patients when varices were added but was again significant when patients who died of gastrointestinal bleeding were excluded. The presence of diabetes, clinically detectable and often requiring adequate treatment, is a risk factor for long-term survival in cirrhosis. (HEPATOLOGY 1994;20:119-125.) Alterations in carbohydrate metabolism are frequent in cirrhosis, the prevalence being dependent of the stage of the disease (1, 2) and on the diagnostic criteria used (3). In 15% to 30% of patients the clinical and laboratory picture is that of overt diabetes (4, 5) with fasting hyperglycemia and frank glycosuria. Diabetes follows cirrhosis in approximately 50% of patients with associated diseases, but the two conditions may be simultaneously diagnosed, or cirrhosis may even follow diabetes (4). The association is clinically relevant and may need specific pharmacological treatment, dietary restrictions,

No abstract

No abstract

No abstract

The optimal management of mild traumatic brain injury (TBI) patients with injuries identified by computed tomography (CT) brain scan is unclear. Some guidelines recommend hospital admission for an observation period of at least 24 h. Others argue that selected lower-risk patients can be discharged from the Emergency Department (ED). The objective of our review and meta-analysis was to estimate the risk of death, neurosurgical intervention, and clinical deterioration in mild TBI patients with injuries identified by CT brain scan, and assess which patient factors affect the risk of these outcomes. A systematic review and meta-analysis adhering to PRISMA standards of protocol and reporting were conducted. Study selection was performed by two independent reviewers. Meta-analysis using a random effects model was undertaken to estimate pooled risks for: clinical deterioration, neurosurgical intervention, and death. Meta-regression was used to explore between-study variation in outcome estimates using study population characteristics. Forty-nine primary studies and five reviews were identified that met the inclusion criteria. The estimated pooled risk for the outcomes of interest were: clinical deterioration 11.7% (95% confidence interval [CI]: 11.7%–15.8%), neurosurgical intervention 3.5% (95% CI: 2.2%–4.9%), and death 1.4% (95% CI: 0.8%–2.2%). Twenty-one studies presented within-study estimates of the effect of patient factors. Meta-regression of study characteristics and pooling of within-study estimates of risk factor effect found the following factors significantly affected the risk for adverse outcomes: age, initial Glasgow Coma Scale (GCS), type of injury, and anti-coagulation. The generalizability of many studies was limited due to population selection. Mild TBI patients with injuries identified by CT brain scan have a small but clinically important risk for serious adverse outcomes. This review has identified several prognostic factors; research is needed to derive and validate a usable clinical decision rule so that low-risk patients can be safely discharged from the ED.

The galactose elimination capacity, a measure of the functional liver cell mass, and liver volume were measured in 50 normal subjects of five different age groups (less than 50, 51 to 60, 61 to 70, 71 to 80 and greater than 81 years). The volume of the liver was evaluated by ultrasonography. All subjects had normal routine liver function tests and no history of liver disease. Galactose elimination progressively decreased from 3.05 +/- 0.58 (S.D.) mmoles per min in younger subjects to 1.83 +/- 0.24 mmoles per min in subjects over 81 (p less than 0.00003), without any change in the apparent volume of distribution of the sugar. Similarly, the estimated volume of the liver decreased from 110 +/- 14 units to 75 +/- 13 units with increasing age (p less than 0.0002). Both galactose elimination capacity and the estimated liver volume inversely correlated with age (r = -0.728 and r = -0.579, respectively) whereas a positive correlation was observed between galactose elimination and the estimated liver volume (r = 0.520). Part correlation analysis confirmed that age, when entered in a multiple regression already containing body weight and estimated liver volume as independent variables, had a significant effect on liver function, whereas no significant independent effect of liver volume was present. Both age and body weight had a significant independent effect on the estimated liver volume. The maximum functional capacity of the liver, measured by galactose elimination, is reduced in the elderly. Although several factors may play a role, our data suggest that aging is associated with a slight decline in the intrinsic metabolic activity of the hepatic parenchyma.

No abstract

Zinc deficiency is common in cirrhosis and has been tent is common in patients with advanced cirrhosis, involved in the altered nitrogen metabolism. In this particularly of alcohol origin, 2 but the biochemical basis study, we measured the effects of zinc supplementation for zinc deficiency is still unknown. Several factors, on the dynamics of amino acid-derived urea synthesis such as poor dietary intake, impaired intestinal absorp-in cirrhosis with mild or latent encephalopathy. The he-tion, and excessive urinary losses may be responsible patic conversion of amino acids into urea was studied in for reduced whole-body zinc content. 3 eight patients with advanced cirrhosis under controled The importance of zinc deficiency in precipitating ep-conditions of substrate availability (continuous alanine isodes of hepatic encephalopathy is a matter of discus-infusion), before and after 3-month oral zinc sulfate sup-sion. In a single patient with cirrhosis and severe recur-plementation (600 mg/d). Eight more patients, matched rent hepatic encephalopathy, zinc levels after zinc for hepatocellular failure and encephalopathy, served as controls. Plasma zinc levels were reduced in all pa-supplementation and artificially induced zinc defi-tients and returned to normal after oral zinc. The ala-ciency correlated closely with mental state and electro-nine-stimulated urea nitrogen synthesis rate in relation encephalography tracings. 4 In a randomized double-to a-amino-N concentration-the functional hepatic ni-blind trial, zinc sulfate oral supplements increased to trogen clearance-increased by 25% after zinc supple-normal plasma zinc levels of cirrhotic patients and sig-mentation, i.e., more urea was produced at any a-amino-nificantly improved mild encephalopathy of the chronic N concentration. Basal and alanine-induced glucagon type. 5 During treatment, ammonia levels decreased, decreased by 50%, and the ammonia response to alanine and plasma urea concentration increased. The results decreased by 30%. Psychometric tests improved, as did routine and dynamic liver function tests and the Child-were not confirmed in a short-term crossover study Pugh score. Also, the plasma concentration of lipid per-with zinc acetate supplements, which failed to normal-oxides was reduced by zinc. No significant changes were ize plasma zinc levels. 6 Also episodes of acute encepha-observed in the control group. Our data indicate that lopathy after gastrointestinal hemorrhage have been long-term oral zinc speeds up the kinetics of urea forma-successfully treated with zinc. 7 In cirrhotic rats, zinc tion from amino acids and ammonia. Changes in the hor-supplementation was shown to increase the hepatic ac-monal drive and/or the antioxidant activity of zinc might tivity of ornithine transcarbamoylase, a key-enzyme of be involved in the general improvement in liver func-urea cycle. 8 This was accompanied by increased urea tion, whereas the beneficial effects on encephalopathy might stem from decreased ammonia. (HEPATOLOGY formation and decreased ammonia l...