"Liver function tests" are not always tests of liver function.

A child with Wilm's tumor and a child with immune thrombocytopenic purpura (ITP) were each noted to have persistent elevations of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH). Both children underwent thorough evaluation for liver disease and, as a result, experienced delays in treatment of the Wilm's tumor and ITP. Eventually both children were found to have extremely elevated serum creatine kinase (CK). Muscle biopsy confirmed diagnoses of Duchenne's muscular dystrophy in one child, and Becker's muscular dystrophy in the second. Hematologists/oncologists should consider obtaining a serum CK to rule out muscle disease in patients with unexplained elevations of AST, ALT, and LDH.     

N-nitrosodialkylamines do not function as substrates for liver monoamine oxidase.

Since reports in the literature [Rowland, I.R., Lake, B. G. & Gangolli, S. D. (1980) Mutat. Res. 72, 63-72] have implicated hepatic monoamine oxidase (EC 1.4.3.4) in the activation of N-nitrosodialkylamines to mutagens, it is of basic pharmacological and biochemical interest to determine if these compounds could serve as substrates for this enzyme. The dialkylnitrosamines N-nitrosodiethylamine, N-nitrosodimethylamine, and N-nitrosodibenzylamine were tested and found not to be substrates, competitive inhibitors, or irreversible inhibitors of liver monoamine oxidase. Thus, any role for monoamine oxidase participation in the mutagenic activation of these compounds must be subsequent to an initial conversion of these compounds to their respective secondary amines.     

The relationship between conventional liver tests,quantitative function tests,and histopathology in cirrhosis

Thirty patients with cirrhosis were evaluated with the 2-hr [¹⁴C]aminopyrine breath test (score) and with conventional liver tests. Of the 30 patients, 24 also had current liver biopsies. There was a good correlation between necroinflammatory activity in the 24 cirrhotic liver biopsies and the 2-hr aminopyrine scores. All five patients who had at least grade 2 necroinflammatory activity on their biopsy had an abnormal prothrombin time (>3.5 sec above control) and their aminopyrine score was less than 2%. The correlation was good between the 2-hr aminopyrine score and the prothrombin time (seconds over control). No correlation was found between the 2-hr aminopyrine score and either the serum aspartate aminotransferase (SGOT) or any other liver test except for the prothrombin time. It seems that the 2-hr aminopyrine score and prothrombin time are more likely to give a quantitative estimate of total functioning parenchymal mass which is left unaffected by hepatocellular disease in cirrhosis, than the other commonly used liver tests.     

Amygdala lesions do not compromise the cortical network for false-belief reasoning

The amygdala plays an integral role in human social cognition and behavior, with clear links to emotion recognition, trust judgments, anthropomorphization, and psychiatric disorders ranging from social phobia to autism. A central feature of human social cognition is a theory-of-mind (ToM) that enables the representation other people''s mental states as distinct from one''s own. Numerous neuroimaging studies of the best studied use of ToM—false-belief reasoning—suggest that it relies on a specific cortical network; moreover, the amygdala is structurally and functionally connected with many components of this cortical network. It remains unknown whether the cortical implementation of any form of ToM depends on amygdala function. Here we investigated this question directly by conducting functional MRI on two patients with rare bilateral amygdala lesions while they performed a neuroimaging protocol standardized for measuring cortical activity associated with false-belief reasoning. We compared patient responses with those of two healthy comparison groups that included 480 adults. Based on both univariate and multivariate comparisons, neither patient showed any evidence of atypical cortical activity or any evidence of atypical behavioral performance; moreover, this pattern of typical cortical and behavioral response was replicated for both patients in a follow-up session. These findings argue that the amygdala is not necessary for the cortical implementation of ToM in adulthood and suggest a reevaluation of the role of the amygdala and its cortical interactions in human social cognition.The amygdala is considered a critical node of the “social brain” that contributes to myriad social behaviors exhibited by primates (1–4). Neurons in both the monkey (5) and human amygdala (6) respond prominently to faces, and lesions of the monkey amygdala result in complex impairments in social behavior (7, 8). Rare bilateral lesions of the amygdala in human patients impair the ability to infer emotions from facial expressions (9, 10), to make more complex social judgments from faces (11), and to guide appropriate social behaviors (12).A core social ability of humans that emerges early in childhood has been long studied under the name of “theory-of-mind” (ToM), an ability to impute mental states to other people. Amygdala lesions can impair the ability to impute such mental states spontaneously to animated geometric shapes (13, 14) as well as other complex expressions of ToM (15). These impairments in social cognition following amygdala lesions also have been compared with the intensively studied impairments in mental-state understanding observed in autism spectrum disorder (16, 17). Indeed, the amygdala has been implicated in emotional and social dysfunction in a number of psychiatric disorders (18).Neuroimaging studies of ToM-related abilities, on the other hand, have focused largely on cortical networks (19, 20). One of these networks, based on using a localizer requiring subjects to infer false beliefs from written stories (the “False-Belief Localizer”) (21, 22) has become so well established that it is commonly referred to as the “ToM network” and prominently includes the temporoparietal junction as well as medial frontoparietal and anterior temporal cortices (23–28).If the amygdala plays a critical role in social cognition, why is it not regularly identified in neuroimaging studies of ToM? One answer may be that these studies have been focused more on cortical networks, and possible amygdala activations are either underreported or underdiscussed. A second answer may be that the blood oxygenation level-dependent (BOLD) response is more difficult to evoke in the amygdala than in cortex (29, 30). However, the amygdala’s vast connectivity with most of the neocortex (31), prominently including some of the key nodes of the false-belief network such as the medial prefrontal cortex (32, 33), together with its role in social cognition reviewed above, justifies a strong hypothesis. That hypothesis is that the cortical false-belief network should include or be modulated by the amygdala. The clear prediction from this hypothesis is that lesions of the amygdala should alter the functional response of cortical regions critical to ToM.To test this prediction in the most direct way, we used functional MRI (fMRI) in two rare patients with bilateral amygdala lesions and closely interrogated BOLD responses within the amygdala in a large group of neurologically healthy controls. The patients with amygdala lesions had developmental-onset calcifications of the amygdala resulting from Urbach–Wiethe disease (34) (raising interesting further questions about the possible developmental contributions of the amygdala to the false-belief reasoning network, issues we take up in Discussion). To evoke false-belief network activation, each patient performed the well-established False-Belief Localizer twice in separate MRI sessions. The False-Belief Localizer (often called simply the “ToM Localizer”) developed by Rebecca Saxe and colleagues (21, 22) uses brief verbal narratives to manipulate the demand to represent another person''s false belief about reality.At the outset, we clarify that the False-Belief Localizer does not exhaustively represent the range and complexity of the human capacity to reason about mental states (35). In fact, many different behavioral tasks have been used to manipulate mental-state reasoning in previous neuroimaging studies (23, 26), and recent evidence has demonstrated convincingly that these various tasks are not interchangeable manipulations of a single ToM capacity but rather modulate dissociable cortical networks (28, 36). Nonetheless, several reasons justify our decision to focus here on the False-Belief Localizer. First, given that false-belief representation historically has been considered the most unequivocal expression of ToM (37), theory and research on ToM has long maintained a central focus on the capacity to represent false beliefs (38, 39). Second, the focus of ToM research on false-belief reasoning has remained strong in neuroimaging studies of social cognition, in large part because of the efforts of Saxe and colleagues (21, 22) to optimize and make publicly available an efficient protocol for this purpose. Because this same basic protocol has been used in numerous neuroimaging studies of neurologically healthy adults, it is now possible to generate large empirical distributions against which new data points can be compared (40). Therefore, the present study tests the hypothesis that cortical function during false-belief reasoning would show abnormalities in the absence of the amygdala, using this same false-belief neuroimaging task.     

Superiority of the Child-Pugh classification to quantitative liver function tests for assessing prognosis of liver cirrhosis

To evaluate the prognostic value of quantitative liver function tests in comparison with established prognostic variables, the data of 47 patients with liver cirrhosis were analysed. A total of 16 variables, comprising the galactose elimination capacity and the indocyanine green clearance, the Child-Pugh classification, and several clinical and biochemical variables were subjected to Kaplan-Meier life-table analysis and Cox proportional hazards regression analysis. As independent variables, poor prognosis was associated significantly with increasing Child-Pugh score (p less than 0.00001), whereas the galactose elimination capacity (p = 0.03) and the indocyanine green clearance (p less than 0.001) were less sensitive indicators. The regression analysis showed prognostic value in decreasing sequence for Child-Pugh classification, age, sex, history of upper GI haemorrhage, and alkaline phosphatase activity. The quantitative liver function tests evaluated in the present work have less prognostic value than routinely accessible variables.     

肝功能试验的评价

近年来，肝功能试验的品种和数量并无增加，相反，有些试验己被废弃，有些则限于研究或特殊情况下应用，但对一些常用试验的认识和解释有发展。现对常用肝功能试验作一评价。     

Prognostic value of quantitative liver function tests in viral cirrhosis: a prospective study

BACKGROUND AND AIMS: Widespread application of quantitative liver function tests as a prognostic tool is controversial. In this study we assessed the predictivity of serial evaluations of galactose elimination capacity (GEC) and the monoethylglycinexylidide (MEGX) test on survival in viral cirrhosis, and secondarily we compared these tests with Child-Turcotte-Pugh (CTP) and Model for End Stage Liver Disease (MELD) scores. METHODS: In a cohort of 35 patients with viral cirrhosis, GEC and MEGX were evaluated every 6 months for 24 months and compared with CTP and MELD scores at the same time intervals. The end points were patient death or liver transplantation. RESULTS: Statistically significant differences between dead/transplanted patients and survivors were found for basal values of GEC, MEGX, CTP and MELD. Receiver-operating characteristics curves of CTP and MELD scores showed a higher prognostic accuracy than GEC and MEGX. On multivariate analysis, neither GEC nor MEGX were independent predictors of survival. Repeated-measures analysis of GEC and MEGX did not increase the prognostic accuracy of these tests and did not add useful prognostic information on patient outcome during the following 6 months. CONCLUSIONS: Our data suggest that neither single nor repeated determinations of GEC and MEGX are superior to CTP and MELD scores in predicting prognosis of patients with viral cirrhosis.     

Ketone bodies do not give falsely positive alcohol tests

Ketosis, as observed in diabetic ketoacidosis or secondary to hypoglycaemia, may be associated with symptoms resembling those of acute alcoholism. It is thus essential to rule out the possibility that ketone bodies cross-react with any method of ethanol determination. Two currently used methods for detecting ethanol in the expired air (Alcotest and a fuel cell electrode), and three methods for blood determination (the nitrochromic method, gas liquid chromatography, and the TDX-REA method) were examined. No cross-reaction was found in nine grossly ketotic diabetic subjects. In vitro 3-hydroxybutyrate, acetoacetate or acetone, alone (30 mmol l-1) or in association, did not cross-react in the assays studied.     

Interpretation of liver function tests]

Liver function tests (LFT) are helpful screening tools to detect hepatic dysfunction. LFT are further used to categorize hepatic dysfunctions, to estimate the severity of hepatic disease, and for the follow-up of liver diseases. Since liver performs a variety of functions, no single test is sufficient alone to provide complete estimate of function of liver. Effective interpretation of the hepatic function panel requires knowledge of underlying pathophysiology and the characteristics of panel tests. This review includes a classification of liver diseases, which are commonly detected by routine LFT, a list of liver functions with appropriate tests for each function, and a guide to panel interpretation and further laboratory investigation.     

Comparison of quantitative liver function tests to clinical, laboratory chemical and biopsy findings in patients with liver diseases

Quantitative liver function tests (QLFT), e.g. 1) galactose elimination capacity (GEK) and 2) fractional indocyanine-green elimination constant k (ICG) were performed in patients with various liver diseases. Retrospectively the results of QLFT were compared to clinical, histological and laboratory findings which are known to reflect severity of liver disease. Patients showing clinical symptoms like ascites and/or encephalopathy demonstrated lower values for GEK and ICG. In addition similar data were obtained for those patients who showed histological evidence of cirrhosis. When dividing up the group of cirrhotics according to PUGH's classification, correspondingly lower results of QLFT were observed between different PUGH classes, however, due to a substantial overlap an individual classification could not be achieved by QLFT. Compared to routine laboratory tests which might estimate hepatic functional impairment the following correlations were found: GEK to albumin: r = 0.47, p < 0.01, to Quick: r = 0.44, p < 0.001, to bilirubin: r = -0.23, p < 0.05, ICG to albumin: r = 0.45, p < 0.01, to Quick: r = 0.53, p < 0.001, to bilirubin: r = -0.42, p < 0.001. No correlation could be demonstrated to transaminase activity. The results obtained support the view that QLFT are capable of estimating hepatic function, however, compared to conventional characteristics of advanced liver disease only moderate correlations were detected. A superiority of quantitative liver function tests could not be detected.