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)

Prolactin responses to provocative thyrotropin-releasing factor (TRH) stimulation were evaluated in 43 chronic alcoholic men were divided into groups for analysis based on the presence or absence of gynecomastia and the histologic appearance of their livers as determined by percutaneous liver biopsy. Compared to the normal volunteers, alcoholics with reversible liver disease (fatty liver) had reduced basal prolactin levels and exaggerated TRH responses. In contrast, alcoholics with cirrhosis and gynecomastia had markedly elevated basal prolactin levels and reduced responses to TRH. The results of this study combined with previously reported findings in cirrhotic men provide a basis for a possible explanation for the signs of feminization frequently found in alcoholic men.
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PMID:Hyperprolactinemia and thyrotropin-releasing factor (TRH) responses in men with alcoholic liver disease. 10 34

A significant increase of basal plasma prolactin levels (radioimmunoassayed) in 75 patients with liver cirrhosis was found in comparison to 50 male controls (8.5+/-4.5 (SD) vs. 5.5+/-1.7 ng/ml p less than 0.001). The extent and incidence of hyperprolactinaemia in 48 patients with alcoholic cirrhosis was more pronounced than in 27 cases of cirrhosis of non-alcoholic aetiologies (mean 9.7+/-4.8 vs. 5.7+/-2.1 ng/ml). No relation to ascites formation as well as to the development of gynaecomastia was apparent. Prolactin release following thyrotropin-releasing hormone was markedly enhanced in alcoholic as compared to non-alcoholic cirrhosis. Possibly hyperprolactinaemia and increased pituitary hormone reserve reflects hyperoestrogenism but changes of the hypothalamic regulation cannot be excluded as yet.
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PMID:Plasma prolactin and prolactin release in liver cirrhosis. 40 18

Serum prolactin levels were determined following stimulation by sulpiride in 20 patients with nonalcoholic liver cirrhosis and 10 normal controls. Prolactin response was essentially the same in the two groups. Only 5 cirrhotics, all with ascites, showed a lower prolactin response after sulpiride stimulation. This was interpreted as a consequence of a rapid prolactin escape from blood into the ascitic fluid, as it was shown to be the case in 2 of these patients. It is concluded that prolactin secretion in nonalcoholic liver cirrhosis is essentially normal. The higher prolactin levels found by others in alcoholic cirrhosis could be the result of a direct effect of alcohol on hypothalamic structures involved in prolactin secretion.
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PMID:Prolactin secretion in nonalcoholic liver cirrhosis. 73 36

In addition to direct toxic effects on endocrine organs chronic alcohol intake affects regulation of endocrine systems by disturbed liver function. As a result in patients with alcohol-induced liver cirrhosis gonadal axis is characterized by low total and free testosterone, elevated estradiol. LH, FSH, and sexual hormone binding globulin and an enhanced conversion of testosterone to estradiol. Prolactin also is found to be elevated. The thyrotropic axis is characterised by low T3- und T4- as well as elevated rT3-values and normal TSH. STH is elevated, while somatomedin C is decreased. The corticotropic axis may show an abolished circadian rhythm, a negative Dexamethasone-test, low transcortin and elevated free cortisol levels. The disturbance of the calcitropic axis leads to osteoporosis and osteomalacia, due to intestinal hyperparathyroidism and vitamin D malnutrition. In 50% of chronic alcoholics there are elevated insulin and glucagon values and a pathological glucose tolerance test.
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PMID:[Alcohol and endocrinologic homeostasis]. 306 42

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

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

A reduced thyrotropin (TSH) response to TSH-releasing hormone (TRH) has been reported in a portion of abstinent alcoholic men without evidence of cirrhosis of the liver. It is not known whether this neuroendocrine change is a precursor of alcoholism or a sequelae of heavy alcohol consumption. Three of four published studies have found evidence for differences in TRH-induced TSH response in subjects at high risk for alcoholism, based on family history, compared with subjects at low risk for alcoholism. To test further the hypothesis that the TRH-induced TSH response is a vulnerability marker for alcoholism, we tested 25 young men with an alcoholic father [family history-positive (FHP)] and matched them, on alcohol consumption, to 25 young men with no identified first- or second-degree relatives with alcoholism [family history-negative (FHN)]. FHP subjects were further categorized based on whether their father had shown signs of alcohol problems before age 25 years (FHP-Early, n = 10) or after age 24 years (FHP-Late, n = 12). FHP subjects did not differ from FHN subjects in their baseline levels of thyroid hormones, glucose, cortisol, or TSH. However, the distribution of TSH responses in the FHP subjects was skewed toward lower values, compared with FHN subjects (p = 0.12). Furthermore, FHP-Late subjects had lower TSH responses than FHN subjects (p = 0.02), whereas the TSH response of FHP-Early subjects was not different from FHN subjects. Prolactin responses to TRH were similar across all groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thyrotropin and prolactin responses to thyrotropin-releasing hormone in young men at high or low risk for alcoholism. 856 Dec 81

Prolactin-secreting tumours (prolactinomas) are benign neoplasms constituting about 40 percent of all pituitary tumours. The incidence of these tumours varies with age and sex, occurring most frequently in females between 20 and 40-years-old. The clinical symptoms of prolactinomas are menstrual dysfunction and galactorrhea in women and loss of libido and potency in men. Differential diagnosis of the disease should include the intake of various drugs, hypothyroidism, renal failure, liver cirrhosis, compression of the pituitary stalk by other pathologies, idiopathic hyperprolactinemia and other types of pituitary adenomas. The aims of treatment are to restore or to achieve eugonadism through the normalisation of hyperprolactinemia and control of tumour mass. Because of the established effectiveness in the majority of cases and small number of acceptable adverse effects, dopamine agonists are considered the drugs of choice. Transsphenoidal surgery remains an option when medical therapy is neither effective nor well tolerated. The authors review the diagnosis and management of prolactinomas, including progress made in recent years.
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PMID:[Prolactinoma]. 1970 10

Hyperprolactinemia is a frequent endocrine disorder with well known harmful effects on the reproductive system and bone metabolism. Besides prolactinomas several drugs and disorders such as renal failure and hypothyroidism have been shown to cause hyperprolactinemia. Based on former studies, liver cirrhosis has also been suggested to cause hyperprolactinemia, while mechanisms have not been identified yet. In this study, we set out to investigate the prevalence and predictors of hyperprolactinemia in 178 patients with liver cirrhosis of different etio-logies. Eighteen out of 178 patients - 7 females and 11 males - displayed elevated serum pro-lactin levels. When patients were excluded who suffered from co-morbidities or took medication that are discussed to potentially interfere with prolactin metabolism, only 3 males displayed increased serum prolactin levels. Prolactin levels were similar in patients with liver cirrhosis of different etiologies. Our data suggest that hyperprolactinemia is not commonly found in patients with liver cirrhosis, but is mostly associated with intake of drugs or presence of comorbidites which are known to potentially cause hyperprolactinemia. We thus hypothesize that in contrast to former studies liver cirrhosis is not a common cause of hyperprolactinemia and that in the absence of co-morbidities or drugs that are known to potentially increase prolactin levels, marked hyperprolactinemia needs further investigation in patients with liver cirrhosis.
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PMID:Serum prolactin in advanced chronic liver disease. 2481 31