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)

Elevated plasma concentrations and abnormal secretory patterns of GH have been found in patients with cirrhosis of the liver. Displacement of brain dopaminergic monoamines by false "neurotransmitters' produced in the gut has been postulated as a cause of encephalopathy. In this study basal GH plasma levels and their response to TRH and L-DOPA were determined in thirty-nine cirrhotic patients and fifteen controls. Eleven patients had evidence of encephalopathy (Group 1), twenty-eight did not (Group 2). Both basal levels and the mean peak response to TRH were significantly higher in the cirrhotic patients that in the controls (Group 3). Peak values were moderately, but not significantly, higher in Group 1 than in Group 2. The response to L-DOPA was considerably lower in the encephalopathic patients in comparison with the subjects of both Group 2 and Group 3. This finding is consistent with depletion of active "neurotransmitters' in CNS. Our data fail to demonstrate clearly whether the paradoxical response to TRH can also be related to these abnormalities of monoamine metabolism in cirrhotics.
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PMID:Growth hormone (GH) secretion in hepatic encephalopathy. 679 Feb 2

The effects of acute TRH and cimetidine administration on the plasma prolactin (PRL) response have been studied in cirrhotic patients with impaired glucose tolerance (IGT). I v. TRH administration stimulates PRL release both in cirrhotics and controls; i.v. cimetidine did not induced a significant rise of PRL in liver cirrhosis. Present findings demonstrate that PRL is not responsible for the deterioration of glucose handling in alcoholic cirrhotic patients examined.
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PMID:Prolactin release in liver cirrhosis with impaired glucose tolerance (IGT). 679 17

The relationship between chronic hepatosplenic schistosomiaisis (CHES) and circulating thyroid hormones as well as the TSH response to TRH were investigated in 41 hospitalized CHES patients and compared to those in 11 patients with non-CHES cirrhosis with severe hepatic failure. CHES patients were subdivided into 3 groups depending on the severity of parenchymal dysfunction, based upon a composite clinical and laboratory index. Angiographic and hemodynamic studies of CHES patients revealed altered hepatic arteriograms, suggesting a decreased arterial blood flow associated with an increased venous blood flow from the portal system. A significantly reduced serum concentration of total T4 (but not free T4) was only found in the cirrhotic patients. Compared to CHES groups I and II, CHES group III patients and the non-CHES cirrhotics had significantly lower mean serum T3 levels of 80 +/- 12 and 52 +/- 8 ng/dl, respectively. The serum rT3 concentration was elevated (69 +/- 6.2 ng/dl) only in the cirrhotic patients. Both basal and peak TSH levels after TRH were within the normal range for all 4 groups of patients. The basal (40.7 +/- 8.3 ng/ml) and peak (85.5 +/- 13.7 ng/ml) serum PRL levels T4-binding globulin after TRH administration were only elevated in the cirrhotic group. Although the mean T4-binding globulin values were lower in CHES group III (17.5 +/- 3.2 micrograms/ml) and in the non-CHES cirrhotic group (18.3 +/- 2.1 micrograms/ml) compared to those in groups I (21.8 +/- 2.2 micrograms/ml) and II (20.4 +/- 2.3 micrograms/ml), the differences between groups were not statistically significant. It was concluded that hemodynamic changes without parenchymal failure have little, if any, effect on the hepatic T4 5'-monodeiodination to T3, and that the low T3 and high rT3 state does not modify the pituitary secretion of TSH, presumably by a local (at the thyrotroph level) normal conversion of T4 to T3, even at very low peripheral T3 concentrations.
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PMID:Thyroid function and chronic hepatosplenic schistosomiasis: peripheral conversion of thyroxine to 3,5,3'-triiodothyronine and pituitary-thyroid relationship. 680 3

Chronic liver disease is associated with raised basal and TRH-stimulated PRL and GH levels. In a recent study we found the kidney to be the main site of prolactin elimination in patients with liver disease. In order to determine whether this is specific for PRL or a more general mechanism for polypeptide removal, we studied the elimination of GH, which resembles PRL in molecular weight and primary amino acid sequence, in 5 patients with portal hypertension and hepatic cirrhosis and 5 patients with noncirrhotic portal hypertension. Plasma GH levels were measured before and after TRH in peripheral, hepatic and renal vein samples, taken during diagnostic hepatic vein catheterization. An excessive paradoxical increase of GH after THR stimulation was found in 4 out of 5 cirrhotic patients but in none of the noncirrhotic individuals (p less than 0.025). After TRH the mean hepatic venous levels were significantly lower than the peripheral venous levels in 4 out of 5 noncirrhotic patients but in only 1 of the 5 cirrhotic patients (p less than 0.05). The mean renal vein GH levels were significantly lower than the peripheral levels in 3 out of 5 noncirrhotic patients and in none of the cirrhotic patients. In 2 patients in whom renal and hepatic plasma flow was measured, renal extraction of GH was found to be 0 to 6.4 micrograms, while liver extraction amounted to 22.1 and 34.7 micrograms of GH during the same 60-min period. Despite the similarity in molecular weight and primary amino acid sequence between PRL and GH, GH appears to be mainly taken up by the liver while PRL is mainly eliminated by the kidney in this group of patients with portal hypertension. This suggests that the renal elimination of prolactin is not solely dependent on glomerular filtration. The selective hepatic removal of growth hormone is probably related to a specific action of growth hormone on liver metabolism.
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PMID:Peripheral elimination of growth hormone in chronic liver disease. 680 53

Total serum thyroxine (T4), total serum triidothyronine (T3), thyrotropin (TSH) and TRH induced TSH release have been measured in 50 clinically euthyroid men with alcoolic cirrhosis and compared to 20 age matched control men in order to determine the thyroid status in cirrhosis. Free serum thyroxin (FT4), free triiodothyronine (FT3) and reverse T3 (rT3), were measured in 34 patients. In these patients, a clinical and biological index was devised to score the severity of the disease. Finally, thyroxine-binding-globulin (TBG) levels were measured in 20 patients. In cirrhotics, the mean total T4 level is normal but the mean T3 level is markedly reduced: FT4 is slightly raised and FT3 is decreased. Serum rT3 levels are often very high and correlated in T3. Basal TSH concentration were slightly significantly higher than normal; the mean magnitude of TSH responses to TRH is comparable to controls but the individual responses are very variable, insufficient or exaggerated, and non correlated with other thyroid function tests. The mean TBG level is also normal and non correlated with total free thyroid hormones. Correlation of thyroid function tests with liver function showed significant correlations between T3, FT3, rT3 or TSH and serum albumin concentration and particularly between T3, rT3 and the clinical and biological index. So the ratio rT3/T3 may be proposed as a valuable index of prognosis and severity of the disease. In conclusion, in alcoholic cirrhosis, thyroid function and regulation are characterized by normal T4 and low T3 levels related to reduced extrathyroidal T4 and T3 conversion levels - and thus maintain the euthyroid state - and by a hypothalamo-pituitary dysfunction. These alterations are related to the degree of liver dysfunction.
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PMID:[Thyroid function in patients with alcoholic cirrhosis (author's transl)]. 746 82

Variations in PRL secretion were observed during chronic hepatic disorders. The aim of our study was to evaluate the behaviour of PRL in patients affected by hepatic cirrhosis. 6 patients (4 males and 2 females) were studied and matched with a group of healthy controls. In all subjects PRL values were evaluated in basal conditions and after TRH stimulation. The results obtained showed higher basal levels of PRL, together with higher and more prolonged TRH responses in patients with hepatopathies than in controls (p < 0.01). These abnormalities in PRL secretion during hepatic cirrhosis could be due to alterations of neurotransmitters at central level.
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PMID:[Blood prolactin patterns in hepatic cirrhosis]. 780 Jan 92

The causes of hyperprolactinemia, the correlation between serum levels of PRL and thyroid function and magnetic resonance imaging (MRI) of the pituitary were studied in patients with chronic thyroiditis. Seventy-four female patients and 15 normal control women participated in this clinical survey. Fourteen of 74 patients with various thyroid conditions had increased serum PRL. The incidence of hyperprolactinemia in the overt primary hypothyroid group was 42.4% and was significantly higher than in any other group with normal serum thyroxine. There was a close association between the increment in serum PRL and of free triiodothyronine above the basal level after TRH administration. There were 14 patients with hyperprolactinemia in three of which serum PRL was over 60 micrograms/L. PRL producing tumor, severe primary hypothyroidism and liver cirrhosis were detected in these three patients, respectively. These results indicate that the pathogenesis of increased serum PRL was not uniform in patients with Hashimoto's thyroiditis, although there was a correlation between hyperprolactinemia and impaired thyroid function. It is proposed, therefore, to measure and follow serum levels of PRL and MRI of the pituitary in patients with chronic thyroiditis, especially with impaired thyroid function.
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PMID:Incidence of hyperprolactinemia in patients with Hashimoto's thyroiditis. 915 19

The liver plays an important role in the intermediate metabolism of numerous substances involved in hormonal action. Starting from the presupposition that the pineal has an inhibitory effect on the reproduction system through melatonin (aMT) and that hepatic cirrhosis can be included among the pathologies characterised by sexual disorders, the authors felt that it was interesting to evaluate the light/darkness rhythm of aMT in some patients suffering from hepatic cirrhosis in order to highlight the possible pathogenetic role of aMT in causing the altered sexual activity observed in this pathology. A total of 4 subjects (3 males and 1 female), with a mean age of 60.5 years, suffering from hepatic cirrhosis and a matched group of healthy controls were included in the study. Circadian changes in aMT plasma levels and plasma levels before and after TRH stimulus (200 micrograms) of aMT and PRL were studied in all subjects. The results revealed the presence of a circadian rhythm of aMT with a nocturnal peak secretion in both groups; in patients with cirrhosis, however, the rhythm appeared to be "out of phase" and presented a late and prolonged increase in aMT compared to controls. Responses to TRH did not show any differences in aMT between the two groups, but the response to PRL was higher and longer than in hepatopathic patients. These findings showed an alteration in the secretory pattern of aMT in cirrhotic patients which can be attributed to reduced hormone metabolism at an hepatic level. The altered response to PRL is attributable to an altered neurotransmitter function at the central level.
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PMID:[Circadian rhythm of melatonin in liver cirrhosis]. 956 Oct 18

The aim of this study was to estimate thyroid function and the prevalence of thyroid antibodies among HCV seropositive patients. We undertook a screening for thyroid dysfunction, and antithyroperoxidase (ATPO) and antithyroglobulin (ATG) antibodies, in 215 HCV seropositive patients referred for hepatologic consultation, 118 males and 97 females, mean age 44 +/- 14 years, range 16-80 years. No patient was treated with interferon and all were seronegative for HIV. Eighteen patients (8%) had antithyroid antibodies, 12 with ATPO antibodies (5.6%) and 10 with ATG antibodies (4.7%). Four patients had both ATPO and ATG antibodies (1.8%), one case of Graves' disease and 3 cases of autoimmune hypothyroidism found during this study. Five patients (2.3%) had hyperthyroidism, three cases of Graves' disease, one case of iodine load and a case of Grave's disease incidentally diagnosed during medical examination. Eleven patients (5.1%) had hypothyroidism, one case already known and treated without antithyroid antibodies, 4 cases of autoimmune etiology (3 diagnosed in consultation and one already known and compensated hypothyroidism), one case of amiodarone-induced hypothyroidism discovered during this study, 5 cases of hypothyroidism without antibodies (two cases of compensated hypothyroidism with normal TRH stimulating test, two cases with severe liver cirrhosis and one case with chronic hepatitis). Twelve patients had antithyroid antibodies with normal TSH levels. The prevalence of ATPO and ATG antibodies in our study is similar to the prevalence usually observed in general population and does not suggest a pathogenic role of HCV in autoimmune thyroid disorders.
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PMID:[Thyroid function and autoimmunity in 215 patients seropositive for the hepatitis C virus]. 975 92

Information on GH in relation to epilepsy is sparse, and to our knowledge there is no information on GH levels during status epilepticus in man. We studied GH in serum in six patients during status epilepticus, and in a control group of six seizure-free patients with epilepsy, before and after injection of TRH. The baseline GH values before TRH administration were within the normal range in all patients. After injection of TRH all patients with status epilepticus showed a paradoxical peak-shaped increase of GH to at least twice their baseline levels within 45 min after the injection (median basal GH value 1.5 mU/l and median peak GH value 6. 5 mU/l, mean increase 330%). No uniform reaction to TRH was observed in the control group (median basal GH value 2.7 U/l and median of the highest value within 45 min 5.2mU/l). A paradoxical peak reaction of GH to TRH was significantly more frequent in the status epilepticus group compared with the control group (P=0.008, Fisher exact probability test). TRH is not considered a GH-releasing hormone in humans during normal conditions, but a paradoxical response of GH to TRH, similar to that observed during status epilepticus, has been reported in various other pathological conditions, such as acromegaly, liver cirrhosis, mental depression and hypothyroidism. Our results of GH release after TRH administration in patients with status epilepticus suggest an altered regulation of GH as a result of the long-standing epileptic activity.
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PMID:Paradoxical GH response to TRH during status epilepticus in man. 1009 49


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