Level Liver Disease Research Articles

Importance of thyroid-stimulating hormone levels in liver disease.

Objectives Recently, several studies have reported the association between elevation of thyroid-stimulating hormone (TSH) levels and liver disease, especially, non-alcoholic fatty liver disease (NAFLD). We aimed to evaluate the incidence and risk factors of TSH elevation in patients with liver disease. Methods We retrospectively reviewed the data of patients aged <18 years who were diagnosed with liver disease between January 2015 and March 2019. Results Among the 77 patients, 17 (22.1%) had subclinical hypothyroidism and 3 (17.6%) progressed to overt hypothyroidism. A total of 26 (33.8%) patients had NAFLD, and 6 (23.1%) had subclinical hypothyroidism. The ultrasound grade of liver steatosis was not related to the elevation of TSH levels. The median age was significantly younger in patients with TSH elevation (5 vs. 9 years, p = 0.017). Albumin levels were significantly decreased (3.9 vs. 4.3g/dL, p = 0.007), and total bilirubin levels were elevated (2.2 vs. 0.6mg/dL, p = 0.001) in patients with subclinical hypothyroidism. Conclusions TSH elevation commonly occurs in patients with liver disease, especially those with younger age. The cause of liver disease was not a risk factor for TSH elevation.

Adiponectin and interlukin-10 in patients with liver diseases before and after liver transplantation

Background/Aims: Hepatitis C virus (HCV) infection is a global blood-borne disease with the highest prevalence in Egypt. This study was carried out to evaluate the prevalence of adiponectin, Interleukin-10 levels in liver diseases and to identify the potential role of adipocyte derived adiponectin in patients with end stage before and after liver transplantation. Subject & method: The study population included 69 subjects classified as follow: Control group (G1) healthy individuals, group (G2) Anti HCV +ve & HCV RNA +ve by PCR, group (G3) Anti-HCV +ve H before liver transplantation (G4b) and after one week of liver transplantation (G4a). Result: Adiponectin levels showed highly significant decrease in G2 (P <0.002), G3 showed insignificant decrease (P<0.6), G4b showed highly significant increased (P <0.0001) and G4a showed insignificant decrease (P<0.08) compared with control group G1. IL-10 levels showed highly significant increase in patients groups (G2, G3, G4b and G4a) as compared with control group (P<0.0001). Conclusion: Adiponectin and IL-10 may be used as biomarker and/or a mediator of inflammatory states in liver diseases in patients with chronic hepatitis C. We suggest that high adiponectin and IL-10 levels in chronic liver disease before liver transplantation might reflect one of the body’s anti-inflammatory mechanisms in chronic liver diseases.

Chronic HBV Infection: Assessment and Management of Disease in a Young Adult Clinic

Introduction Chronic hepatitis B (CHB) is a dynamic disease process with patients moving between disease phases over time. The majority of young adults infected with CHB are exposed to the virus perinatally or in the early years of life. Despite this, the extent of liver disease in this group remains ill-defined, as are the indications and timing of treatment. The aim of this study was to elucidate the extent of liver disease in a cohort of patients identified for a newly established young adult viral hepatitis clinic. Methods Only young adults who underwent liver biopsy for the assessment of CHB were included in the study. 70 patients (male=49), median age 26 (range 16–30), were examined. Data on ethnicity, BMI and eAg status were collated. Longitudinal data including viral load and ALT were recorded for 6–18 months prior to each patient undergoing liver biopsy. Normal ALT levels in the group were defined as; 30 years), (male=45), median age 43 (range 32–71), undergoing liver biopsy for disease assessment. Results 38/70 of the young adults were eAg positive; median ALT over the course of follow-up was 61 (range 11–1050). 14 were Caucasian, 38 Asian and 18 Afro-Caribbean. Median BMI was 22.7 (range 17.9–35.6). By univariate analysis male gender and eAg positive disease were significant in predicting more marked disease with a higher FS (p≥0.05), but abnormal ALT and non-Caucasians in particular demonstrated marked significance (p=0.0002 and p=0.001 respectively). When evaluating the level of liver disease in young adults compared with that found in the 51 older CHB patients, there was no statistical difference between the FS reported in the two groups, presence of fibrosis (p=0.93); presence of moderate to severe fibrosis (p=0.6), demonstrating a trend towards higher FS with older age. However, normal ALT over the course of follow-up in the young adult group, was significantly associated with no fibrosis (p=.001). Conclusion These data highlight the importance of formal disease assessment in this age group, as comparable levels of liver fibrosis are present in young adults as in older patients. However, closer scrutiny with assessment of ALT according to Prati criteria may identify patients with milder disease. This study emphasises the advantages of a young adult clinic in providing greater focus on CHB in this age group, enabling the early and timely intervention with therapeutic options where indicated.

Tissue factor and thrombomodulin levels are correlated with stage of cirrhosis in patients with liver disease.

Liver cirrhosis is associated with alterations of the coagulation system commonly causing bleeding as well as thromboembolic complications. The potential pathophysiological roles of tissue factor (TF) (the initiator of the extrinsic coagulation pathway) and thrombomodulin (TM) (an initiator of the anticoagulatory protein C pathway) are unknown. We therefore measured plasma concentrations of TF and TM in 111 patients with liver diseases who were evaluated for liver transplantation. We could demonstrate that the levels of both molecules increased with the Child's class of liver cirrhosis, independently of aetiology. TM was significantly elevated in Child A, B and C patients compared with patients without cirrhosis; TF only in Child C patients. The plasma TM and TF concentrations correlated with prothrombin time, activated partial thromboplastin time, and inversely with factor VII activity, cholinesterase serum activity, and serum albumin concentration. TM was elevated in patients with a bleeding tendency, but TM and TF did not differ between patients with or without prior thrombotic events. Further studies are warranted to clarify the underlying mechanisms that raise TM and TF plasma levels in liver disease with possible clinical consequences.

The pathophysiology of circulating corticotropin-releasing hormone-binding protein levels in the human.

To establish the factors that modulate circulating CRH-binding protein (CRH-BP) levels, we measured plasma CRH-BP in patients with a variety of endocrine and systemic disorders. CRH-BP was measured by RIA. Young women have higher plasma levels of CRH-BP than young men [females (n = 18), mean +/- SEM, 145 +/- 7; males (n = 20), 99 +/- 6 ng/mL; P < 0.0001], but levels do not fall with the menopause or vary during the menstrual cycle and are unaffected by estrogen replacement therapy. Levels were lower in patients with liver disease than in healthy men (26 +/- 3 vs. 99 +/- 6; P < 0.0001) and were elevated in chronic renal failure compared to those in healthy women (211 +/- 11.2 vs. 145 +/- 7; P < 0.01). Levels were unaffected by fasting in men or women (male fasted, 97 +/- 11; male fed, 97 +/- 8; female fasted, 136 +/- 9; female fed, 152 +/- 10). Dexamethasone treatment lowered CRH-BP in all subjects (129 +/- 8 vs. 111 +/- 9; P < 0.003). Similarly, CRH-BP levels were lower in patients with Cushing's syndrome (all female) than in healthy female controls (median, 82; range, 53-106; vs. median, 142; range, 101-190; P < 0.0001). In Cushing's patients, an i.v. bolus of 100 micrograms human CRH further lowered plasma CRH-BP at 15 min (81 +/- 5 vs. 50 +/- 4; P < 0.0003). Plasma levels of CRH-BP are higher in women than men, but this is unrelated to circulating estrogen levels. The low levels in liver disease and the high levels in renal failure support its hepatic origin and the kidneys as the route of clearance from plasma. The ability of glucocorticoids and exogenous CRH to lower plasma CRH-BP levels and of CRH-BP to modulate the bioactivity of circulating CRH suggest that the protein may be an important regulator of circulating CRH or related ligands.

Urinary and Serum Pteridines in Liver Diseases

Summary The aim of this mini-review is to show the usefulness of pteridines as clinical markers. We assayed urinary neopterin and xanthopterin levels in liver disease. Total pterins were oxidized by active carbon to yield xanthopterin. Urinary neopterin levels were elevated in patients with chronic active hepatitis and in those with chronic persistent hepatitis but not in patients with alcohol-induced liver disease or in those with non-alcoholic fatty liver. Urinary xanthopterin levels were elevated in chronic active hepatitis and alcohol- induced liver disease, but not in chronic persistent hepatitis and non-alcoholic fatty liver. Urinary neopterin levels were high in infectious diseases involving activated cell-mediated immunity, and increased urinary xanthopterin reflects liver-cell damage. We also compared plasma neopterin values in anti-hepatits C virus antibody (anti-HCV) -positive or - negative donors with elevated alanine aminotransferase (ALT). Plasma neopterin values of anti-HCV-negative donors with elevated ALT were the same as those of healthy groups. These results show that the ALT elevation in anti-HCV-negative donors is attributable mainly to steatosis due to excess body weight and/or alcohol consumption, rather than viral infection. During the course of these studies, we were also able to identify esophageal carcinoma in the very early stage by measuring urinary pteridine levels. Our results indicate that pteridines are clinically useful indicators. In particular, neopterin may be used as a means of screening for unknown viral infection.

Direct assessment of the mechanism for a raised serum bile acid level in chronic liver disease.

Impaired hepatic uptake is the major cause of raised serum bile acid levels in liver disease, but confirmation in humans by direct measurement is lacking. The synthetic gamma-labelled bile acid 75Se-homocholic acid taurine (75SeHCAT) provides a tool for the direct measurement of hepatic bile acid handling. To determine the interrelationships among hepatic handling of 75SeHCAT, the kinetics of its disappearance from plasma and serum bile acid levels in patients with chronic liver disease. We studied 12 patients with primary biliary cirrhosis and 14 with cirrhosis arising from other causes. Fasting serum bile acid levels were measured enzymatically. After intravenous administration of 75SeHCAT, we determined plasma disappearance rates (initial K1, late K2) from serial blood samples and hepatic uptake and excretory rates directly from dynamic abdominal gamma-camera scanning. Both scanning and sampling were carried out over a period of 90 min. Serum bile acid concentrations correlated with K1 and with hepatic uptake (Rs = -0.53, P < 0.01; Rs = -0.47, P < 0.02, respectively) but neither with K2 nor with the excretory rate. K1 and uptake were reduced (P < 0.05) in patients with high serum bile acid levels and in those with varices. Serum bile acid levels were higher in patients with varices (P < 0.05), which might suggest that portosystemic shunting occurred. However, this is unlikely because the varices were not independent of liver function. Hepatic bile acid uptake and excretion are independent processes. Hepatic uptake is related to initial, whereas hepatic excretion is related to late, plasma disappearance. Impaired hepatic uptake is a major determinant of the rise in serum bile acid levels in chronic liver disease.

The fibrinogen degradation products (FgDP) levels in liver disease.

We measured plasma levels of fibrinogen degradation products (FgDP) with newly developed enzyme-linked immunosorbent assay based on monoclonal antibody to assess the fibrinogenolytic state in 52 patients with various liver diseases (27 patients with liver cirrhosis, 10 with chronic hepatitis, 7 with acute hepatitis, 6 with hepatocellular carcinoma, 2 with intrahepatic cholestasis). As compared with 20 healthy subjects (upper limit: 580 ng/ml), elevated plasma levels (660-32000 ng/ml) of FgDP were found in 19 (36.5%) patients. When analyzed according to the underlying disease categories, the magnitude of elevations of FgDP were most prominent in patients with chronic hepatitis. No correlation was found between plasma FgDP levels and serum AST or ALT activity. These findings indicate that increased primary fibrinogenolysis is not rare in liver disease, but poorly correlates with liver function.

Changes of the fibrinolytic system in liver dysfunction: role of portal hypertension

The contribution of hemodynamic changes to the pathogenesis of accelerated fibrinolysis in liver disease was investigated in rats. In animals with hepatic lesions induced by a 7-week inhalation of carbon tetrachloride there was a significant increase in blood t-PA activity and PAI activity, with no significant change in portal pressure. Following a 10-min portal vein occlusion there was a marked increase in portal pressure and t-PA activity and a significant decrease in PAI activity. Following ligation of both portal vein and hepatic artery, t-PA activity increased to a higher extent and PAI activity was reduced to a lesser extent than changes found in portalstenosed rats. Our data suggest that high t-PA circulating levels in liver disease could be related not only to the reduced t-PA clearance as a consequence of liver injury but also to hemodynamic changes.

A clinical evaluation of serum alpha-1-antichymotrypsin levels in liver disease and cancers.

The serum levels of alpha-1-antichymotrypsin (ACT) were studied in 168 patients with various liver diseases and cancers in conjunction with other liver function tests, serum sialic acid, AFP and CEA. The ACT levels in acute viral hepatitis and chronic hepatitis were not significantly altered compared with the normal level (220 +/- 40 microgram/ml), although the level was slightly increased or decreased temporarily during the acute phase of the former. In liver cirrhosis, the mean level was significantly lower than the normal in spite of the absence of signs of hepatic decompensation (168 +/- 51 microgram/ml, p less than 0.001). In contrast to cirrhosis, the levels were increased to various extents in 65% of cases with hepatoma, in spite of the association of liver cirrhosis in the majority of them. Much higher levels were observed in all cases of metastatic liver cancers and cancers of the pancreas and the biliary tract. The elevations were observed even in cases without the increase of AFP or CEA. Both in cirrhosis and cancers, ACT levels were not correlated with any of serum bilirubin and serum enzyme activities, but were positively correlated with the levels of plasma fibrinogen and serum sialic acid. The measurement of serum ACT level can be taken advantage of for the diagnosis and monitoring of liver cirrhosis and liver cancers, particularly of hepatoma without AFP elevation.

Low blood urea levels in liver disease.

Low blood urea levels in liver disease.

An assessment of the diagnostic and prognostic value of serum vitamin B12 levels in liver disease

<b>1007</b> <h3><b>Learning Objectives</b></h3> 1.To present the imaging features of F18-FDG PET/CT of chloromas. 2. To illustrate the use of F18 FDG PET/CT as a complementary tool to anatomical imaging in...

SERUM-BILE-ACID LEVELS IN LIVER DISEASE

SERUM-BILE-ACID LEVELS IN LIVER DISEASE

EFFECT OF AN AMINE-OXIDASE INHIBITOR ON ARTERIAL AMMONIUM LEVELS IN LIVER DISEASE

EFFECT OF AN AMINE-OXIDASE INHIBITOR ON ARTERIAL AMMONIUM LEVELS IN LIVER DISEASE

BLOOD PYRUVIC-ACID AND ALPHA-KETOGLUTARIC-ACID LEVELS IN LIVER DISEASE AND HEPATIC COMA

BLOOD PYRUVIC-ACID AND ALPHA-KETOGLUTARIC-ACID LEVELS IN LIVER DISEASE AND HEPATIC COMA

An evaluation of the serum iron in liver disease.

Excerpt The internal redistribution of iron in the body occurs through the serum iron compartment, with the liver playing an important role. Yet determinations of serum iron levels in liver disease...

BLOOD-AMMONIUM LEVELS IN LIVER DISEASE AND "HEPATIC COMA"

BLOOD-AMMONIUM LEVELS IN LIVER DISEASE AND "HEPATIC COMA"