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)

Basal T4, T3, TSH, prolactin and growth hormone levels were determined in several groups: patients with postnecrotic cirrhosis with hepatocellular carcinoma (n = 14); patients with postnecrotic cirrhosis but without hepatocellular carcinoma (n = 26); cholangiolar carcinoma (n = 9); and normal controls age-matched to within 5 yr of the liver disease subjects studied. In addition, TRH stimulation (400 micrograms TRH) was performed; TSH, prolactin and growth hormone responses over a 180-min time interval were evaluated for each subject. The responses observed varied between liver disease groups. The presence or absence of hepatocellular carcinoma was found to determine, at least in part, the type of response observed. Similarly, the presence or absence of hepatic encephalopathy determined, and/or reflected, at least in part, the type of response observed. Finally, for purposes of continuity, basal and TRH-stimulated levels of TSH, prolactin, growth hormone, T4 and T3 are compared in 3 settings of cirrhosis: alcoholic, nonalcoholic postnecrotic cirrhosis, and postnecrotic cirrhosis with hepatocellular carcinoma.
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PMID:Thyroid and pituitary hormone responses to TRH in advanced nonalcoholic liver disease. 303 51

The change in the levels of free thyroid hormones and the pathophysiology of the hypothalamo-pituitary-thyroid axis of patients with nonthyroidal illness (NTI) have not been clearly elucidated so far. Therefore, it was thought of interest to investigate this problem by determining free thyroid hormones and TSH in serum and the response of TSH to TRH in these patients. The subjects employed in this study were 71 cases with hemodialysis, 40 cases with diabetes mellitus, 24 cases with liver cirrhosis, 12 cases with various cancers, 10 cases with anorexia nervosa and 110 normal subjects as controls. The serum total protein, albumin, free T4, free T3, TSH and other parameters of thyroid function were determined, and the TRH test was performed on about 10 patients of each group. Serum TSH was not only determined by a conventional assay system, but with a highly sensitive method, and the data were compared with one another. It was found that the serum free T3 levels were significantly low in all the groups investigated, but the serum free T4 levels were significantly low only in the groups with hemodialysis, decompensated liver cirrhosis, cancers and anorexia nervosa. No significant lowering of serum free T4 was observed in the patients with diabetes mellitus, acute hepatitis and compensated liver cirrhosis. However, serum TSH levels tended to be higher in all the groups studied, though they were not significant. The response of TSH to TRH was low or delayed in about 20-50% of patients with hemodialysis, diabetes mellitus, liver cirrhosis, cancers and anorexia nervosa. It was observed that the serum rT3 concentration was significantly high in the patients with diabetes mellitus and anorexia nervosa but significantly low in the patients on hemodialysis. In the rest of the groups, there were found many cases who showed high levels of serum rT3 although they were not statistically significant. These results indicate that low concentrations of serum free T3 observed in the majority of the patients with severe NTI were, at least in part, due to the decrease in the peripheral conversion of T4 to T3 and the lowered sensitivity of the anterior pituitary to thyroid hormones and TRH.
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PMID:[Serum free thyroid hormones and response of TSH to TRH in nonthyroidal illnesses]. 310 Mar 46

In order to evaluate the possible involvement of muscarinic cholinergic receptors in the GH response to TRH in patients with liver cirrhosis, 8 males with post-hepatitic cirrhosis and 11 males with post-alcoholic cirrhosis were primed with the anticholinergic agent pirenzepine and tested with TRH. In addition, 10 male patients affected by piecemeal necrosis were tested in a similar manner. High basal concentrations of GH were found in all groups. None of the patients with piecemeal necrosis responded to TRH, whereas in patients with post-hepatitic and in post-alcoholic cirrhosis, TRH induced a significant rise in GH levels. The priming with pirenzepine (40 mg given iv 10 min before TRH) completely blocked the TRH-induced GH increase, but did not affect the TRH-induced TSH release. These data suggest that a muscarinic cholinergic pathway is involved in the anomalous response of GH to TRH in patients with liver cirrhosis. The lack of effect of pirenzepine on the TRH-stimulated TSH release suggests that the muscarinic cholinergic mediation is peculiar for the effect of TRH on GH secretion.
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PMID:Cholinergic mediation of growth hormone secretion induced by thyrotropin-releasing hormone in cirrhotic patients. 310

In order to investigate whether the variations in prolactin (PRL) secretion found in patients with liver cirrhosis are related to the derangement of neurotransmitter metabolism, serum PRL levels were measured in 8 patients with hepatic encephalopathy (a condition where neurotransmission is severely deranged), in 10 patients with liver cirrhosis but without encephalopathy and in 10 control subjects under control conditions and in response to nomifensine, levodopa and synthetic TRH administration. Inhibition of endogenous catecholamine reuptake by nomifensine was able to significantly reduce PRL levels in normal subjects and in patients with liver cirrhosis, whereas only one out of 8 patients with hepatic encephalopathy showed a reduction in PRL levels. On the contrary, levodopa administration was able to reduce PRL secretion in all the subjects studied. PRL release by TRH was greater in patients with liver disease than in controls. The results seem to indicate that the derangement in neurotransmitter metabolism which occurs in liver cirrhosis is one, but not the sole cause of alterations of PRL secretion in liver cirrhosis. The failure of nomifensine to depress PRL is an early finding in the course of encephalopathy and may be of diagnostic value.
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PMID:Failure of nomifensine to reduce serum prolactin levels in patients with hepatic encephalopathy. 392 93

Basal thyroid hormone levels were measured in 68 women with liver cirrhosis (LC) of different etiology (alcoholic n = 34, posthepatitic B n = 9, PBC n = 5, cryptogenetic n = 18, M. Wilson n = 2). In addition the rise of TSH after 400 micrograms TRH was measured in 23 women with LC and compared with the data obtained from 17 women of a control group. There was no difference of the median T4-concentrations (LC 8.0 micrograms/dl versus 7.2 micrograms/dl) but a significant correlation of T4 to the grade of decompensation of LC. In contrast of T4 there was a marked decrease of T3 in LC-patients (109 ng/dl versus 143 ng/dl) and a rise of reverse T3 (0.21 ng/ml versus 0.13 ng/ml). The decrease of T3 and rise of reverse T3 equally correlated to the severeness of LC. TBG concentrations fell according to the grade of decompensation of LC and T4/TBG-quotient exhibited no difference to the control data (0.51 both). Though basal thyroid hormones and TSH show euthyroidism the significant augmented TSH release after TRH (delta-TSH 7.0 versus 3.2 microU/ml) indicate a status of latent hypothyroidism. In alcoholic cirrhosis the degree of TSH release was much higher than in non alcoholic cirrhosis. Estradiol and estrone levels correlated significantly negatively to T4, T3, estrone negatively to TBG and positively to reverse T3 but not to TSH and TSH release. Otherwise TSH release correlated positively to estradiol. The thyroid status in women with liver cirrhosis does not differ from the thyroid hormone profile found in men with cirrhosis.
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PMID:[Thyroid hormones in women with liver cirrhosis]. 393 Aug 34

The median plasma level of prolactin in 94 women with cirrhosis of the liver did not differ significantly when compared with a control group (8,0 versus 7,2 ng/ml). Nevertheless 22% of the investigated women exhibited a plasma prolactin level higher than 15 ng/ml. The prolactin concentrations correlated to the severeness of cirrhosis and in the subgroup with decompensated cirrhosis the prolactin concentrations were found to be significantly elevated (12 ng/ml). Like basal prolactin the TRH-induced prolactin release showed no significant difference between cirrhotic women and controls (36,1 versus 38,5 ng/ml). No difference could be observed between the prolactin concentrations of alcoholic or non alcoholic cirrhotic women, and prolactin did not correlate with estradiol or estrone plasma levels. Other factors than cirrhosis itself (i.e. medical treatment, renal insufficiency, stress) must be discussed as causing hyperprolactinemia in cirrhosis.
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PMID:[Prolactin in females with liver cirrhosis]. 393

The increase in plasma cyclic adenosine-3':5'-monophosphate (cAMP) was measured after intravenous injection of 1 mg of glucagon in 26 normal subjects, 36 patients with hyperthyroidism, 35 patients with hypothyroidism and 24 patients with euthyroid goitre. While patients with euthyroid goitre responded normally, the plasma cyclic AMP response in patients with hyperthyroidism was considerably increased and in those with hypothyroidism decreased. 4 patients with cirrhosis of the liver had reduced responses and 1 patient with extrahepatic obstructive jaundice an enhanced response. This test seems to be a valuable additional parameter for the description of the thyroid-dependent metabolic situation. However, because of its unspecificity it cannot replace the measurement of serum T3, T4 and thyrotropin (TSH) response to thyroliberin (TRH).
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PMID:[The effect of thyroid function on the increase of plasma cyclic AMP following glucagon injection (author's transl)]. 625 72

Prolactin levels are elevated in patients with liver cirrhosis and hepatic encephalopathy. Patients with hepatic encephalopathy also have an abnormal plasma amino acid composition, with a relative excess of aromatic amino acids, and a relative decrease in branched chain amino acid levels. In order to study the effect of the plasma amino acid composition on prolactin release, we measured plasma PRL at 0, 10, 20, 30, 40, 50 and 60 minutes after 400 micrograms TRH, both after infusion of a conventional amino acid mixture and after a branched chain amino acid enriched mixture (BCAA) in 5 patients with cirrhosis of the liver and hepatic encephalopathy. After conventional amino acid infusion, a depressed branched chain/aromatic amino acid ratio was found in all patients, together with an increased PRL response to TRH. After BCAA infusion the branched chain/aromatic amino acid ratio normalized. At the same time the excessive PRL response to TRH stimulation was significantly lower in all patients. This suggests that the elevated PRL levels in hepatic encephalopathy are caused by a disturbance of hypothalamic neurotransmitter systems, due to altered amino acid-neurotransmitter precursor levels.
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PMID:Hyperprolactinemia in hepatic encephalopathy: the effect of infusion of an amino acid mixture with excess branched chain amino acids. 641 78

Urinary excretion of estrogens and plasma concentrations of estrone, estradiol, LH, FSH, PRL, progesterone, testosterone, and sex hormone binding globulin were measured in nine chronic alcoholic women with cirrhosis or alcoholic fatty liver. They were aged 24-40 yr and all had secondary amenorrhea which had lasted for at least 3 months. The response of pituitary gonadotropin secretion to administration of LHRH and estradiol benzoate and of PRL secretion to TRH were also investigated. Urinary excretion of estrogens in the alcoholic women with liver disease was similar to that in normal postmenopausal women and less than half that in normal women of the same age in the midfollicular phase of the menstrual cycle. Plasma estradiol levels in the alcoholic women were lower than in the menstruating women but higher than in the postmenopausal women, whereas their plasma estrone levels were higher than in the menstruating women. Plasma concentrations of progesterone and testosterone in the alcoholic women did not differ from those in the postmenopausal women but were lower than in the menstruating women. In spite of the relative estrogen deficiency plasma LH and FSH levels were not elevated in the alcoholic women. The responses of LH and FSH to LHRH were similar in the patients and in the menstruating women. Intramuscular administration of estradiol benzoate did not increase plasma LH and FSH concentrations in the alcoholic women. Hyperprolactinemia was not found and there were no differences in the PRL responses to TRH between the patients and the control groups. In conclusion, disturbed regulation of gonadotropin secretion is an important factor in the genesis of estrogen deficiency and amenorrhea in alcoholic women with liver disease, although ovarian function may also be directly impaired.
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PMID:Sex hormones in amenorrheic women with alcoholic liver disease. 642 68

Basal plasma thyroid hormone, testosterone and cortisol levels, TSH and PRL responses to TRH, and LH and FSH responses to LRH were assessed in six young subjects with normal liver function and anatomy before and after portacaval anastomosis. All tests were normal and unchanged by the operations. It is concluded that in patients with normal liver function, portal systemic shunting does not produce alterations in the pituitary-gonadal and pituitary-thyroid axes. The abnormalities of these endocrine functions in patients with cirrhosis are probably related to the severity of hepatocellular dysfunction rather than to the effects of portal systemic shunting.
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PMID:Pituitary and thyroid function before and after portacaval anastomosis in patients with normal livers. 677 96


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