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)

Anterior pituitary functions and sex steroid levels were measured in 12 patients with idiopathic haemochromatosis (eight males, four postmenopausal females) and age-matched controls, 12 with diabetes mellitus and five with hepatic cirrhosis. In idiopathic haemochromatosis gonadotrophin deficiency was present in seven of 12 patients including six of seven patients who had clinical evidence of hypogonadism. Basal prolactin levels were significantly lower in the patients with idiopathic haemochromatosis compared with either of the control groups (p less than 0.02). Nine patients with idiopathic haemochromatosis exhibited subnormal prolactin responses to thyrotrophin releasing hormone. Thyroid and adrenocortical functions were normal in all patients with idiopathic haemochromatosis. Testosterone values were subnormal in five of eight males with idiopathic haemochromatosis; females with idiopathic haemochromatosis had significantly lower testosterone values compared with the diabetic females (p less than 0.05). Oestradiol values in both sexes and sex hormone binding globulin values in the males were not significantly different in patients with idiopathic haemochromatosis compared with the controls. Sex hormone binding globulin levels were significantly higher in females with idiopathic haemochromatosis compared with either diabetic or cirrhotic females (p less than 0.05). Impairment of anterior pituitary function occurs in idiopathic haemochromatosis but is selective; gonadotrophin and prolactin deficiencies are common. Clinical hypogonadism is usually hypogonadotrophic in origin.
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PMID:Endocrine abnormalities in idiopathic haemochromatosis. 668 54

Portocaval anastomosis (PCA) in the normal male rat causes profound alterations in testicular morphology and function and in plasma levels of sex steroids as well as of gonadotropins. Testicular atrophy is accompanied by a significant decrease of plasma testosterone (0.03 ng/ml versus 0.99 ng/ml) and an increase of estradiol (76.2 pg/ml versus 39.7 pg/ml) and estrone (68. pg/ml versus 45.5 pg/ml). Plasma levels of gonadotropins (LH, FSH) and prolactin are lowered too (LH: 15 ng/ml versus 28.5 ng/ml, FSH:119 versus 182 ng/ml, prolactin:53 versus 109 ng/ml). The altered sex hormone metabolism is reflected in marked changes of the morphology and nucleic acid content of the metabolizing organs i.e. liver, gonades and kidney. The results of this study are consistent with the hypothesis that portosystemic shunt per se plays an important role in the pathogenesis of the disturbed metabolism of sex hormones observed in patients with liver cirrhosis and portal hypertension.
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PMID:[Sex hormones and fertility following portacaval anastomosis in rats]. 670 37

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

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

Plasma prolactin levels are often raised in patients with liver cirrhosis and portal hypertension. To obtain more insight into the underlying mechanisms we examined the synthesis and release of prolactin in male rats with partially ligated portal veins. Portal hypertension led to an increase in pituitary prolactin, plasma prolactin, and plasma 17 beta-estradiol, and a decrease in hypophyseal stalk dopamine levels. Castration decreased plasma prolactin levels and prevented the induction of hyperprolactinemia by portal hypertension. Administration of dihydrotestosterone to castrated animals did not affect prolactin levels in the pituitary gland or in the plasma. Plasma tryptophan and tyrosine concentrations did not change in portal hypertension. A low protein diet caused a decrease in plasma tryptophan and an increase in plasma tyrosine levels without affecting prolactin levels in either controls or portal hypertensive rats. The hyperprolactinemia of portal hypertension is probably caused by elevated estrogen levels which interfere with hypothalamic dopamine release. Changes in plasma amino acid levels are of little importance in the regulation of prolactin release in portal hypertensive rats.U
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PMID:hyperprolactinemia of portal hypertension in rats. 705 21

We investigated a group of 111 amenorrhoeic females with associated liver disease. These comprised alcoholic cirrhotics (N = 38), non-alcoholic cirrhotics (N = 12), non-cirrhotic alcoholics (N = 21) and those suffering from other chronic liver diseases (N = 40) admitted to our medical department from 1986 to 1991. The serum levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), oestradiol, testosterone, sex hormone binding globulin (SHBG) and prolactin were measured. Serum LH was decreased below the normal range in 50% of patients with alcoholic cirrhosis and in 42% of patients with non-alcoholic cirrhosis. One third of non-cirrhotic alcoholics also had decreased LH, in contrast to only 8% of patients with other chronic liver diseases (p < 0.01). A close correlation was found between LH and FSH when all patients were pooled (r = 0.91, p < 0.001). A gonadotrophin-releasing hormone (GnRH) injection elicited a clear LH and FSH response in 11 out of 14 patients with cirrhosis, indicating that the hypothalamus rather than the pituitary is the site of disturbance in gonadotrophin secretion. Serum SHBG was within normal limits and similar in all four groups. In nine females with alcoholic cirrhosis who abstained for 3 months, serum SHBG increased significantly from 39 +/- 18 to 70 +/- 25 nmol/l (p < 0.001), while LH increased in five of nine females and was unchanged in four. In conclusion, half of the amenorrhoeic females with alcoholic as well as non-alcoholic cirrhosis had inappropriately low serum LH and FSH levels, indicating dysfunction of the hypothalamo-pituitary axis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inappropriately low levels of gonadotrophins in amenorrhoeic women with alcoholic and non-alcoholic cirrhosis. 771 82

Prolactin is known to have renal sodium retention properties in animals. In man, only two studies have suggested a similar effect in healthy volunteers or in patients with microprolactinoma. Since hyperprolactinemia is frequently observed in liver disease, this prospective study of 19 patients evaluated the influence of prolactin on urinary electrolytes excretion in cirrhosis. Basal hyperprolactinemia was found in 14 out of 19 cases. The effect of serum prolactin elevation on renal sodium and potassium excretion was studied in all patients after thyrotropin-releasing hormone stimulation (200 micrograms), with seven consecutive hourly urinary samples. Patients were separated into two groups according to amount of prolactin discharge after thyrotropin-releasing hormone injection. Group I included patients with "low prolactin release", defined as the difference between basal and peak prolactin values (delta prolactin) < 1000 mu u/ml (n = 8), and no change in natriuresis could be observed. In contrast, in group II with a "high PRL release" (delta prolactin > 1000 mu u/ml, n = 11), significant reductions in urinary sodium (p < 0.01) and potassium (p < 0.02) excretion were observed, which lasted until the third hour after thyrotropin-releasing hormone injection. A significant correlation was found between peak prolactin values and the decrements of natriuresis (r = 0.70, p < 0.02). The pattern of urinary electrolyte changes and the stability of the ratio UK/UK+Na suggest a possible sodium-retaining effect of prolactin localized proximally to the distal tubule.
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PMID:Indirect evidence to suggest that prolactin induces salt retention in cirrhosis. 783 3

High serum concentrations of growth hormone (GH) were found in five patients with chronic liver diseases, including auto-immune chronic active hepatitis (two cases), Budd-Chiari syndrome, primary biliary cirrhosis and hepatitis B virus associated cirrhosis. Mean levels of GH were 27.8 units (normal up to 5). In three patients elevated prolactin levels were also found (mean 37.3 units for two females, normal up to 20), and 36 units in one male (normal up to 9). No other endocrine disorders were found. Although the association of raised GH levels in patients with alcoholic cirrhosis is well known, its occurrence in patients with non-alcoholic chronic liver disease is not fully established. We describe the effect of the disease course, and steroid treatment on GH levels in one patient with auto-immune chronic active hepatitis, and propose possible mechanisms for this elevation.
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PMID:Elevated growth hormone levels in patients with non-alcoholic chronic liver disease. 821 92

Hyperprolactinaemia is the most common result of pituitary dysfunction and is characterized by alteration on the reproductive function. After a review of the hypothalamic control mechanisms and of the local paracrine and autocrine factors regulating prolactin secretion, the most common physiological, pharmacological and pathological causes of hyperprolactinaemia are described. The clinical pictures of hyperprolactinaemia in man and woman are then summarized. The diagnostic protocol used in this Institute is then described: confirmation of the existence and entity of hyperprolactinaemia by means of a prolactin profile; exclusion of pharmacological or extra pituitary causes (cirrhosis, primitive hypothyroidism, chronic renal failure, etc.); neuro-radiological evaluation of the sella region, by means of standard X-ray, computer tomography scan, nuclear magnetic resonance. The drugs commonly used in medical treatment of hyperprolactinaemia such as a bromocriptine, other-derived compounds and then recent CV 205-502, and the surgical approaches (trans-sphenoidal and transcranial routes) are reported. The indication of medical or surgical treatment and the relevance of radiotherapy are finally considered.
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PMID:[The diagnosis and therapy of hyperprolactinemia]. 848 35

Because increased prolactin levels and hyperprolactinemia in the presence of encephalopathy in males with cirrhosis (alcohol-induced cirrhosis in particular) are associated with statistically increased mortality, we have examined pre-surgical levels of prolactin and other hormones, as well as the presence of encephalopathy, in 12 postmenopausal women with end-stage alcohol-induced cirrhosis in relation to liver transplant survival. Levels of estradiol were significantly lower, while luteinizing hormone (LH) and 17-hydroxyprogesterone as well as the ratio of estradiol to testosterone were significantly higher prior to transplantation among the women who survived, compared with non-survivors. A similar pattern was seen for transplant candidates who died before transplantation as compared with still-living candidates. These findings suggest that pre-operative levels of sex steroids and pituitary hormones may have prognostic value in alcoholic cirrhotic postmenopausal women undergoing liver transplantation.
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PMID:Surgical risk in alcoholic cirrhotic postmenopausal women: prognostic value of levels of hormones. 850 84


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