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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many pathways of essential neutral amino acid metabolism in the CNS are influenced by precursor availability. Since the delivery of circulating amino acids to brain cells is primarily controlled by the rate of amino acid transport through the blood-brain barrier (BBB), pathways of brain amino acid metaboliransport system. The Km of BBB transport is in the 0.1--0.6 mM range, which approximates the physiologic plasma levels and forms the basis of the unusual sensitivity of the brain to competition effects on neutral amino acid transport. Unlike the brain, the Km of amino acid transport into other organs is in the 1--10 mM range or greater, which frees these tissues from competition effects in the physiologic range of plasma amino acids. Tryptophan circulates 80--90% bound to albumin; however, the capacity/affinity ratio of the BBB neutral amino acid transport system exceeds the capacity/affinity ratio of albumin binding of tryptophan, which enables the carrier to strip tryptophan off albumin as it traverses the brain capillary. The activity of the BBB neutral amino acid transport system is probably not modulated by insulin, but is influenced by changes in thyroid hormone status; the transport system is also induced in states of hepatic encephalopathy and this induction process is the primary cause of the increased brain tryptophan and serotonin levels in cirrhosis.
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PMID:The role of blood-brain barrier transport of tryptophan and other neutral amino acids in the regulation of substrate-limited pathways of brain amino acid metabolism. 38 9

Levels of serum triiodothyronine (T3), reverse triiodothyronine (rT3), and thyroxine (T4) were determined in 29 patients with alcoholic cirrhosis, seven patients with acute hepatitis, and 14 control patients hospitalized for chronic disease. Serum T3 levels were decreased significantly and serum rT3 levels increased significantly in the patients with alcoholic cirrhosis. Serum T3 and T4 levels were lower and rT3 levels higher in the cirrhotic patients who died within three months of the study compared with those who survived. A combination of prothrombin time, aminopyrine breath test results, and rT3 and T3 determinations gave significant predictive information about survival in patients with cirrhosis. The data suggest that assay of serum thyroid hormone levels together with prothrombin time and the aminopyrine breath test may be helpful in assessing the course and prognosis of patients with liver disease.
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PMID:Serum thyroid hormone levels in patients with liver disease. 48 43

The, in non-thyroidal illnesses, frequently occurring changes in the serum concentrations of peripheral thyroid hormones, are shown in patients with acute myocardial infarction, compensated and decompensated cirrhosis of the liver, renal insufficiency and in rheumatoid arthritis. The observed changes, (pathological) low total triiodothyronine, low or normal total thyroxine, and normal thyrotrophine), can make the diagnosis of hyperthyroidism impossible. Only in control measurements, after cessation of the simultaneous non-thyroidal illness, the peripheral thyroid hormone concentrations are found to be in the hyperthyroid range. The only way to establish the diagnosis, (or confirm the clinical suspicion), is to prove non-responsiveness of the pituitary to a TRH-stimulus. TRH-tests have, however, no diagnostic value in illnesses that affect pituitary function directly, such as terminal renal insufficiency. The diagnosis of hypothyroidism can be established by measurement of the basal thyrotrophine serum concentration (elevated) or by measurement of the serum concentrations of 3,3'5'-triiodothyronine (reverse T3), which is, according to a recent report, observed to be significantly decreased.
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PMID:[Evaluation of thyroid function in non-thyroid diseases]. 75 17

In order to clarify the role of free fatty acid (FFA) in thyroid hormone abnormalities in patients with nonthyroidal illness, thyroid function, FFA, inhibitor of extrathyroidal conversion of T4 to T3 (IEC) and thyroid hormone binding inhibitor (THBI) were studied in 99 patients with various nonthyroidal illnesses including diabetes mellitus (DM) (n = 35), liver cirrhosis (LC) (n = 33), chronic obstructive pulmonary disease (COPD) (n = 17) and chronic heart failure (CHF) (n = 14). Patients were divided into three groups based on the level of serum T3: Group I (T3 < 50 ng/dl), Group II (50 < or = T3 < 80) and Group III (80 < or = T3). Serum T4, FT3 and the T3/T4 ratio decreased significantly in the order Group III, Group II and Group I (Group III > II > I). The plasma FFA level was 0.91 +/- 0.12 mmol/l in Group I (P < 0.05, vs. Group III), 0.65 +/- 0.06 in Group II and 0.54 +/- 0.04 in Group III, respectively. The incidence of positive IEC was 80.0% in Group I (P < 0.05, vs. Group III), 53.7% in Group II (P < 0.05, vs. Group III) and 34.2% in Group III. However, IEC was not correlated with the serum T3 concentration. The incidence of positive THBI was 80% in Group I (P < 0.05, vs. Group III), 68.3% in Group II and 47.4% in Group III, but THBI was not correlated with the serum T4 level. Positive correlations were observed among FFA, IEC and THBI (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma free fatty acids, inhibitor of extrathyroidal conversion of T4 to T3 and thyroid hormone binding inhibitor in patients with various nonthyroidal illnesses. 147 85

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.
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PMID:Energy expenditure and substrate oxidation in patients with cirrhosis: the impact of cause, clinical staging and nutritional state. 156 18

The aim of our study is to prove whether the development of the low-T3-syndrome in patients with liver cirrhosis is associated with their prognosis. For this purpose we determined the peripheral thyroid hormone levels in 28 patients with liver cirrhosis. For prognosis assessment we calculated the Prognostic Index (PI) on the basis of Cox's regression model as recently described by us. Calculating this index we used 11 parameters: liver morphology, consciousness, spider naevi, PCV, thrombocytes, gamma-GT, cholesterol, albumin, Quick's value, IgA, and potassium. It is demonstrated that there is an inverse correlation between T3-serum levels and PI (p = 0.03). An association could not be detected neither between reverse T3 and PI nor between T3 and rT3. On the other hand basal TSH was also inversely associated with PI. Thus, the low T3-serum levels did not induce a rise of basal TSH in cirrhotics. Moreover, the mean serum-T3-concentration differed significantly from that of 6 decreased patients and from that of the surviving (p = 0.00076). It seems to be true that low T3-serum levels are a very sensitive parameter for prognosis prediction in patients with liver cirrhosis.
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PMID:Development of the low-T3-syndrome and prognosis assessment in patients with liver cirrhosis. 181 59

The effect of propranolol on thyroid hormones of 7 healthy subjects and 10 patients with histologically proven alcoholic liver cirrhosis was investigated. The fractions of plasma T3 and free T4 were determined by specific radioimmunoassay before and after two weeks of propranolol administration. Under basal conditions, both T3 and FT4 levels were found significantly lower in patients with cirrhosis than in healthy subjects (1.86 +/- 0.10 vs. 1.18 +/- 0.41 nmol/l, p less than 0.001; 9.31 +/- 0.41 vs. 8.17 +/- 0.91 pg/ml, p less than 0.05, respectively). In healthy subjects propranolol administration led to a significant reduction of T3 serum levels (from 1.88 +/- 0.10 to 1.51 +/- 0.12 nmol/L, p less than 0.001), while in patients with liver cirrhosis no significant changes in T3 and FT4 were found. In patients with liver cirrhosis propranolol administration did not affect thyroid hormone levels.
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PMID:The effect of propranolol on thyroid function in patients with liver cirrhosis. 177 51

Hepatic parenchymal tissue is known to be one of the major sites of thyroid hormone metabolism as well as glucagon action. Alterations in circulating thyroid hormone concentrations, as well as hyperglucagonemia, are well documented in subjects with hepatic cirrhosis and advanced liver dysfunction. Also, we have documented recently that hyperglucagonemia induced in normal subjects alters thyroid hormone metabolism, with lowering of serum T3 and a rise in serum reverse T3 (rT3) levels. Thus, it is conceivable that rising glucagon concentrations are responsible for altered thyroid hormone levels in hepatic cirrhosis. To examine this hypothesis, this study determined relationships between plasma glucose, glucagon, insulin, and insulin:glucagon ratio on one hand, and thyroid hormone concentrations on the other, in 51 subjects with hepatic cirrhosis. Significant negative correlations were noted between plasma glucagon and serum T3 (r = -0.418, p less than 0.001) as well as T3:T4 ratio (r = -0.627, p less than 0.0001), whereas significant positive correlations were observed between plasma glucagon and serum rT3 (r = 0.504, p less than 0.001) as well as rT3:T4 ratio (r = 0.644, p less than 0.0001). No such significant relationships were noted between either insulin, glucose and insulin:glucagon ratio on one hand and any of thyroid hormone indices on the other. Therefore, this study indicates that, in hepatic cirrhosis, circulating glucagon concentrations may play a major contributing role in induction of altered serum thyroid hormone concentration by influencing thyroid hormone metabolism.
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PMID:Low serum T3 and raised reverse T3 levels in hepatic cirrhosis: role of glucagon. 192 46

Nuclear tri-iodothyronine (T3) maximal binding capacity (MBC) and thyroxine- and T3-stimulated cellular oxygen consumption and glucose consumption were examined in mononuclear blood cells from six patients with liver cirrhosis (LC), in six patients with alcoholic hepatitis (AH), and in six healthy control subjects. Serum T3 was decreased in patients with LC. The MBC of T3 was increased significantly (P less than 0.05) in cells from patients with LC compared with patients with AH and controls, whereas the equilibrium association constants did not differ. Unstimulated glucose consumption was slightly increased (P less than 0.05) in cells from patients with AH and LC compared with controls. Thyroid hormone-stimulated glucose consumption was significantly (P less than 0.05) increased in cells from patients with LC compared with controls and patients with AH. Unstimulated oxygen consumption did not differ between the groups, but thyroid hormone-stimulated oxygen consumption was depressed in cells from patients with AC (P less than 0.05) compared with patients with LC and with controls. We conclude that both thyroid hormone-stimulated glucose consumption and T3 nuclear receptor binding in cells from patients with LC are increased, and suggest that the observed changes are responsible for maintenance of euthyroidism in the face of reduced circulating T3.
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PMID:Increased nuclear tri-iodothyronine binding and thyroid hormone-stimulated glucose consumption in mononuclear blood cells from patients with liver cirrhosis. 200 22

This work was performed in order to analyze thyroid hormone picture of alcoholic patients with reference to hepatic damage. Forty consecutive patients of male sex, aged 28-64 years, were investigated. They consumed more of 50 g ethanol/day for at least 2 years. According to investigations on hepatic condition, 2 cases had normal liver, 22 cases had steatosis and 16 had cirrhosis. None of patients disclosed a clinical and/or hormonal behaviour pointing to alterations of thyroid function. In alcoholics serum T3 levels resulted significantly lower compared to a control group of 40 healthy males (P less than 0.001), independently of degree of hepatic damage. Instead, serum T4 levels did not result significantly different in the comparison between alcoholics and controls. Serum FT3 and FT4 levels resulted significantly higher (P less than 0.001) only in alcoholics with liver cirrhosis. In comparison with normals, serum rT3 was significantly lower in alcoholics without liver cirrhosis (P less than 0.001), but significantly higher in alcoholics with liver cirrhosis (P less than 0.005). Serum TBG behaved in the same manner. According to euthyroidism in our alcoholic patients basal and TRH-stimulated TSH were normal, however significantly lower when compared to controls (P less than 0.005). On the whole these results suggest the existence of an autonomous ethanol-dependent mechanism that determine decreased serum T3 levels in the alcoholics, in absence of serum T4 variations. In the alcoholic with liver cirrhosis, an increased conversion of T4 in rT3, correlated to hepatic damage, joins to previous mechanism. The tendency to low secretion of pituitary TSH might be dependent of action of alcohol on neuromodulation of TRH secretion.
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PMID:[The thyroid hormone picture of alcoholics in connection with their liver status]. 238 53


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