Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The radioimmunoassay (RIA) and the competitive ligand binding assay (CLBA) are convenient routine methods for the precise and reproducible measurement of TBG in large numbers of serum samples. 2. There is an age dependent variation of the TBG-concentration in serum. There is a steady decrease of TBG with increasing age with a minimum between the 20th and 50th year. In higher age TBG increases again significantly. 3. There are significantly negative correlation between TBG-serum levels on the one hand and free T4- and T3- fractions on the other. The low TBG-level in hyperthyroid patients increases gradually to normal during treatment with thyroid blocking drugs, the elevated TBG-concentrations in hypothyroid patients decrease to normal during treatment with thyroid hormones. 4. Estrogen stimulates TBG-synthesis in the liver. During enhanced endogenous estrogen production (pregnancy) as well as during exogenous estrogen application a rise occurs in TBG-concentration in serum, which seems to be dose related. 5. Androgens induces a decrease of the TBG-concentration in serum. 6. During viral hepatitis and in compensated cirrhosis of the liver TBG-concentration is significantly elevated. In cirrhosis of the liver with poor hepatic function the TBG-concentration is decreased. 7. The T4/TBG-quotient is a good parameter to estimate free T4-concentration in serum.
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PMID:[Thyroxine-binding globulin (TBG). Clinical studies on the regulation of TBG concentration in serum and the value of TBG for the evaluation of thyroid function]. 11 50

To determine serum thyroxine-binding globulin (TBG) levels, we used radioimmunoassay, and compared the results obtained with other tests in 231 patients with chronic hepatitis B virus infection to evaluate its clinical implications. All of these patients were hepatitis B surface antigen (HBsAg)-positive. Among them, 38 patients had hepatocellular carcinoma (HCC), 18 had chronic persistent hepatitis, 70 had chronic lobular or active hepatitis (grouped as CAH), 31 had active cirrhosis (AC), 25 had inactive cirrhosis, 20 had decompensated cirrhosis, and 29 were "healthy" HBsAg carriers. Twenty-seven patients with acute hepatitis, 12 with cancer metastasis to the liver, and 81 normal adults served as disease or normal controls. The results showed that serum TBG level increased significantly in patients with CAH, AC, or HCC. Serum TBG did not correlate with albumin or bilirubin level, but correlated with alanine aminotransferase (ALT) positively in patients with CAH (p less than 0.001) and negatively in patients with HCC (p less than 0.01) (slope difference p less than 0.05). Serial determination of serum TBG and ALT also showed parallel changes in 15 patients with CAH, but not in nine patients with HCC. In contrast, the fall and rise of serum TBG levels in patients with HCC coincided with tumor resection and recurrence. The data suggest that serum TBG elevation in patients with hepatitis activity is the result of hepatocellular damage, whereas that in patients with HCC is due to increased synthesis. Whether serum TBG elevation without concomitant rise of ALT could be used as a marker of HCC awaits further study.
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PMID:Thyroxine-binding globulin in patients with chronic hepatitis B virus infection: different implications in hepatitis and hepatocellular carcinoma. 168 51

The liver plays a dominant role in the metabolism of the thyroidal hormones; it is here that the 5' deiodase acts to convert part of T4 to T3. There are eight further circulating iodothyronines: the rT3, mainly derived from T4, appears to be the major inhibitor of T4 and T3. Thus, if rT3 increases, the metabolic effects of T3 and T4 can be quite different. In the course of some chronic systemic diseases (e.g. hepatic cirrhosis) rT3 increases simultaneously with the decrease of T3 levels. Therefore we can describe particular alterations of the thyroidal pattern typical of chronic liver diseases: low T3 syndrome, low T3 and T4 syndrome, high T4 syndrome, mixed forms. T3 and T4 diminish due to inefficient hepatic deiodination and defective hepatocellular uptake. Inefficient hepatic deiodination and defective hepatocellular uptake. T4 levels decrease, most likely because of an inefficient production of thyroid binding globulin, or the action of a peripheral binding inhibitor. During acute liver diseases and primitive biliary cirrhosis, we can observe an increase of T4 and TBG together with an increase of the acute phase proteins. Such complex hormonal mechanisms are not influenced by TSH, which appears normal or inhibited, as the TRH stimulus test is normal. The explication can be found in an enhanced conversion of T4 to T3 in the pituitary gland. The biological and clinical significance of these mechanisms might be that of creating a "protective" state for an organism in a catabolic state by reducing the circulating T3. A relationship has been found between circulating thyroidal hormones levels, particularly the T3, rT3 and rT3/T3 ratio, and the state of hepatic functional insufficiency.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Liver and thyroid gland. Physiopathologic and clinical relationships]. 219 47

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

To evaluate the level of serum thyroxine-binding globulin (TBG) in various liver diseases, TBG and T4, T3, FT4 were measured by radioimmunoassay in 29 HBsAg carriers (C), 27 patients with acute hepatitis (AH), 18 patients with inactive chronic hepatitis, 70 patients with chronic active hepatitis (CAH), 31 patients with active cirrhosis (AC), 20 patients with inactive cirrhosis (IC), 38 patients with hepatocellular carcinoma (HCC), 12 patients with metastatic Ca to the liver (Met.) and in 81 normal controls. All the patients were clinically euthyroid. The TBG as well as T4 in patients with AH, CAH, AC HCC and, Met. were significantly higher than those in controls. The T3 level was significantly elevated in CAH and AC patients. The TBG level did not correlate with serum albumin or bilirubin levels, but did correlate significantly with alanine transaminase (ALT) (r = 0.54, p less than 0.01). However, the correlation was positive in chronic active hepatitis (r = 0.40, p less than 0.01) but negative in hepatocellular carcinoma (r = -0.32, p less than 0.05). The data suggested: (1) Significant TBG and T4 elevation was found in all active liver diseases and HCC. (2) In the presence of high T4 in patients with liver disease, normal FT4 excluded the diagnosis of hyperthyroidism. (3) The elevation of TBG levels in chronic hepatitis appeared to parallel the severity of hepatocytolysis, and therefore might be the result of hepatocytolysis; while the elevation of TBG in HCC might be due to increased synthesis by the malignant cells.
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PMID:[Changes in thyroid hormone concentration in liver disease]. 250 36

Serum thyroxine was significantly higher in 59 patients with hepatocellular carcinoma than in normal subjects, patients with uncomplicated cirrhosis (48), or other primary tumours with or without hepatic metastases (50). Elevated thyroxine levels appeared attributable to high levels of thyroxine binding globulin which showed a positive linear correlation with serum thyroxine in all groups studied. Despite this hyperthyroxinaemia all patients appeared clinically euthyroid and, consistent with this, T3 was elevated in only one patient and the free thyroxine index was normal in all. Amongst a group of 25 cirrhotic patients who were followed-up for between 12 and 72 months, there was a striking dissociation between the TBG values of those destined to develop HCC and those who did not. In the former group TBG rose steadily with time whereas in the latter group levels remained stable, or, more often, fell. The rises in TBG occurred prior to any clinical signs of tumour development and may be one of the earliest serological changes to occur during carcinogenesis in the cirrhotic liver.
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PMID:Hyperthyroxinaemia in hepatocellular carcinoma: relation to thyroid binding globulin in the clinical and preclinical stages of the disease. 283 1

Basal plasma concentrations of thyroxine (T4), 3,3',5-triiodothyronine (T3), free T4 index (TF4I), free T3 index (FT3I) reverse T3, 3,3',5-triiodothyronine (rT3), resin T3 uptake (TR3U), thyroxine-binding globulin (TBG), thyrotropin (TSH), prolactin (PRL) and growth hormone (GH) as well as thyrotropin releasing hormone (TRH) stimulated TSH, PRL and GH were investigated in 31 consecutive male patients (mean age 41 years) with chronic alcoholism. According to the histology of their liver biopsies the patients were divided into three groups: patients with normal livers, steatosis and cirrhosis. The control group consisted of 30 healthy males. The patients had abstained from alcohol for at least one week when studied, and they were on a nutritionally adequate diet. All had consumed a daily minimum of 52 g ethanol for at least 5 years. None of the patients had severe or decompensated liver disease. The patients had significantly reduced T3 and rT3 plasma levels compared to normals. Patients with cirrhosis of the liver had increased TBG and normal RT3U levels, while those without cirrhosis had increased RT3U and normal TBG levels. Plasma concentrations of basal as well as TRH-stimulated TSH and PRL were unchanged in alcoholic patients, whereas basal as well as stimulated GH levels were increased in cirrhotic alcoholics. It is concluded that alcohol per se influences T3 levels, but not the part of the hypothalamic-pituitary axis studied, and that the binding proteins are mostly determined by the degree of liver disease.
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PMID:Pituitary-thyroid function and thyrotropin, prolactin and growth hormone responses to TRH in patients with chronic alcoholism. 309 23

To evaluate thyroid function in 19 patients with fulminant hepatitis (FH), we have measured total and free 3,5,3'-triiodothyronine (T3) and thyroxine (T4), 3,3',5'-triiodothyronine (reverse T3, rT3), thyroid-stimulating hormone (TSH) and thyroxin-binding globulin (TBG) in patients with FH, compared with those of 80 patients with other various liver diseases and of 10 healthy controls. Patients with FH showed the lowest values of serum T3 and the highest levels of rT3 among all patients with liver diseases studied. Furthermore, patients with FH showed a significant increase of rT3 in comparison with subacute hepatitis (SAH), "acute-on-chronic" (AOC) type of hepatic failure, ordinary and severe forms of acute hepatitis (AHo and AHs) and decompensated liver cirrhosis (LC-D). In addition, serum T3 and rT3 and the rT3/T3 ratio significantly correlated with prothrombin time (PT) and plasma methionine level. We also found that serum T3 and rT3 concentrations and the rT3/T3 ratio showed early and rapid normalization in cases of FH that survived, but they did not improve in patients with fatal outcome. These results suggest that serum T3, particularly rT3 concentrations and the rT3/T3 ratio may be useful indicators for assessing the severity and prognosis of patients with FH and can be considered to the sensitive indices for functioning hepatic microsomal reserve as well.
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PMID:Serum thyroid hormone levels in patients with fulminant hepatitis: usefulness of rT3 and the rT3/T3 ratio as prognostic indices. 311 36

We describe a case of liver cirrhosis lacking the expected increase in serum thyroxin (T4)-binding globulin (TBG) despite abrupt, severe increases in aspartate and alanine aminotransferases (ASAT and ALAT) in serum. Sequential change in serum T4, triiodothyronine (T3), and TBG concentrations were also measured retrospectively in serum of 10 hospitalized patients with acute viral hepatitis. Although their mean T4 and TBG concentrations significantly exceeded those in 40 normal subjects (P less than 0.002 and P less than 0.001, respectively), these values were within the normal reference intervals in five patients. ASAT and ALAT concentrations were not significantly different in patients with increased TBG and patients with normal TBG, whereas mean concentrations of serum albumin and cholinesterase and mean prothrombin times (in percent) in the former group were significantly higher than those in the latter group (P less than 0.05, P less than 0.05, and P less than 0.001, respectively). For 60 samples with increased ASAT and ALAT, TBG and albumin or cholinesterase correlated significantly (r = 0.49, P less than 0.001 and r = 0.50, P less than 0.001, respectively), but not TBG and ASAT or ALAT. Collectively, these results suggest that the increase in serum TBG in acute hepatitis may reflect its synthesis in regenerating hepatocytes rather than a simple leakage from damaged hepatocytes.
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PMID:Are increases in thyroxin-binding globulin in patients with acute hepatitis ascribable to synthesis by regenerating hepatocytes? 312 18

In order to clarify an alteration in thyroid functions in patients with chronic liver diseases, serum total and free thyroxine (T4, FT4), total and free triiodothyronine (T3, FT3), total reverse T3 (rT3), thyrotropin (TSH), thyroxine-binding globulin (TBG) concentrations, and T3 uptake (T3U) were measured by radioimmunoassays in 53 patients with chronic hepatitis (CH), 24 patients with compensated liver cirrhosis (LC), 17 patients with hepatocellular carcinoma associated with LC (HCC), and 40 normal subjects. Serum T4, T3, and rT3 in CH, and serum rT3 in HCC were significantly increased, while serum T4 in LC and serum T3 in HCC were significantly decreased. Serum TBG was increased and T3U was decreased in these patients. Serum TBG in CH and LC correlated positively with transaminase, and inversely with prothrombin time. FT4 and T4/TBG ratios in CH and LC and FT3 and T3/TBG ratios in LC and HCC were significantly decreased. Although T4/TBG ratios in HCC and T3/TBG ratios in CH were significantly decreased, FT4 in HCC and FT3 in CH were not decreased. The ratio of rT3/T3 in CH and LC correlated with various liver function tests. FT3 in LC and HCC correlated inversely with BSP (45') and positively with KICG. No differences in serum TSH values were found between chronic liver diseases and normal subjects. From these results, it was concluded that the thyroid functions in patients with chronic liver diseases were affected by the decrease in serum thyroxine, elevated serum TBG, the degree of which is in proportion to that of the liver cell damage, and impaired peripheral conversion of T4 to T3, the degree of which is in proportion to that of the hepatic dysfunction.
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PMID:Thyroid functions in patients with various chronic liver diseases. 314 45


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