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)

In the present paper the following non-endocrine internal diseases are discussed: liver cirrhosis, diabetes, chronic renal failure and morbus Crohn. In alcoholic liver patients under fifty, hypospermia and oligozoospermia can be observed. The hormone assays showed moderately increased FSH- and LH-values in the serum; prolactin, testosterone and estradiol remained normal. An increased binding of testosterone to SHBG is supposed, and the androgen deficiency symptoms are considered to be due to the elevated binding of testosterone to SHBG. The other non-endocrine internal diseases and drug-groups (cytostatics, steroids, neuroleptics, antihypertensives, antiarrhythmics, nitrofurans, levamisole, fungicides and salazosulfapyridine) are reviewed on the basis of literature. After the administration of 1 g per day of cimetidine for four weeks in patients under fifty with duodenal ulcer, notable andrological side effects were not revealed by neither clinical nor hormone examinations.
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PMID:[Andrological abnormalities in internal diseases and following drug therapy]. 311 48

1. The responses of plasma aldosterone and plasma prolactin concentrations to metoclopramide (10 mg intravenously) were evaluated over 2 h in eight healthy controls and in 23 patients with cirrhosis (10 without and 13 with ascites). Plasma renin activity, glomerular filtration rate and renal sodium excretion were also determined. 2. Metoclopramide did not significantly influence plasma renin activity, whereas both plasma aldosterone and plasma prolactin rose significantly. The incremental areas under the curves did not differ among controls and cirrhotic patients without and with ascites. No significant correlations between plasma prolactin and aldosterone, either under basal conditions or after metoclopramide administration, were found in either controls or patients. 3. Glomerular filtration rate did not change after metoclopramide. Renal sodium excretion in controls and cirrhotic patients without ascites was also unaffected, whereas it decreased significantly in cirrhotic patients with ascites. In the latter, renal sodium excretion was inversely correlated with plasma aldosterone both under basal conditions and after metoclopramide administration. 4. The dopaminergic control of aldosterone secretion does not appear to be significantly altered in cirrhosis. Metoclopramide administration to cirrhotic patients with ascites leads to an increase in plasma aldosterone that may enhance renal sodium retention.
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PMID:Unaltered dopaminergic modulation of aldosterone secretion in cirrhosis. 333 58

The Authors, after having examined the factors responsible for the hyperprolactinemia in the cirrhotic, confirm the lack of a relationship between the increase in the prolactinic reserve and gynecomastia and between the amount of the prolactinic reserve and the degree of liver disorder. While hyperestrinism and the false transmitters lost most of their pathogenetic importance, other factors such as GABA, the Serotonin and the VIP, offered a new pathogenetic prospective. The prolactin reserve was studied in 63 patients affected by cirrhosis and in 25 affected by fibrosis and hepatic fibrosteatosis, pointing out an increase in the prolactin reserve in 61% of cirrhotic patients and an absence of pathological reports in patients affected by fibrotic hepatopathies. These data confirm the low pathogenetic responsability to be strictly ascribed to ethanol and the preminent role of liver cirrhosis and portal hypertension in the prolactin turnover.
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PMID:[Prolactin in chronic alcoholic liver diseases with and without gynecomastia]. 388 40

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

Seven males with liver cirrhosis associated with hepatitis and one with schistosomal liver fibrosis were studied for hypophyseal gonadal dysfunction and compared to six age matched controls. Cirrhotics as a group had higher serum 17 beta estradiol levels (22.1 +/- 6.3 vs 7.8 +/- 0.8 pg/ml, p less than 0.05) which did not rise after four days of human chorionic gonadotropin (hCG) stimulation. Conversely, there was an adequate rise in serum testosterone level after hCG stimulation (332.8 +/- 99.7 ng/dl baseline to 887.6 +/- 67.1 ng/dl, p less than 0.01). Compared to the controls, cirrhotics had lower baseline serum follicle stimulating hormone (FSH) (3.6 +/- 1.7 vs. 10.2 +/- 1.5 mIu/ml, p less than 0.02) and higher serum prolactin (13.5 +/- 2.5 vs. 6.8 +/- 1.0 ng/ml, p less than 0.05). Pituitary dynamic function testing in cirrhotics revealed blunted response of luteinizing hormone (LH) and FSH, to luteinizing hormone releasing hormone (LHRH) in four out of eight subjects tested. We conclude that the mechanism of hypogonadism in non-alcoholic cirrhosis is mostly hypogonadotropic in origin rather than primary gonadal injury which is common in alcoholic cirrhosis.
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PMID:Hypophyseal-gonadal dysfunction in men with non-alcoholic liver cirrhosis. 392 49

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

Hyperprolactinemia is frequent in clinical endocrinology. Its commonest causes are, besides pregnancy and lactation, drugs, mainly involving the generally used psychopharmaca and the equally ubiquitously prescribed estrogens. The single most important cause is a pituitary tumor, the prolactinoma, but lesions of the hypothalamus or pituitary stalk, primary hypothyroidism, liver cirrhosis and chronic renal failure, among others, may also provoke hyperprolactinemia. The clinical features of hyperprolactinemia in women are mainly amenorrhea, or irregular menses, galactorrhea, hirsutism, infertility and loss of libido. In men loss of libido and/or impotence are the most important symptoms, accompanied by infertility. Macroadenoma, more frequently seen in men than in women, may cause tumor symptoms such as headache and ophthalmologic disorders (visual field loss). The main biochemical finding is hyperprolactinemia, which should be repeatedly checked. In general, high concentrations are mainly found in large adenomas, while microadenomas usually involve only mild hyperprolactinemia, though there are numerous exceptions. While dynamic tests of prolactin secretion have provided useful information about the pathophysiology of prolactin secretion, their use in routine clinical work is controversial and of limited value. As a routine neuroradiological examination, high resolution CT of the pituitary area is to be recommended. In all hyperprolactinemic patients with suspicion of macroadenoma, ophthalmologic evaluation of fundus and visual fields should be performed. Dopaminergic drugs such as bromocriptine rapidly reduce serum prolactin levels in hyperprolactinemic women and men with micro- or macroadenoma. With these drugs considerable tumor shrinkage is possible.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hyperprolactinemia]. 395 83

Patients with chronic liver diseases were evaluated for: 1) the ability of somatostatin to affect the thyrotropin-releasing hormone (TRH) induced growth hormone (GH) rise; 2) the competence of luteinizing-hormone releasing hormone (LH-RH) to release GH; 3) the non-specific releasing effect of TRH and LH-RH on other anterior pituitary (AP) hormones. In 6 patients, infusion of somatostatin (100 micrograms iv bolus + 375 micrograms i.v. infusion) completely abolished the TRH (400 micrograms i.v.)-induced GH rise; in none of 12 patients, of whom 7 were GH-responders to TRH, did LH-RH (100 micrograms i.v.) cause release of GH; 4) finally, LH-RH (12 patients) did not increase plasma prolactin (PRL) and TRH (7 patients) did not evoke a non-specific release of gonadotropins. It is concluded that: 1) abnormal GH-responsiveness to TRH is the unique alteration in AP responsiveness to hypothalamic hormones present in liver cirrhosis; 2) the mechanism(s) subserving the altered GH response to TRH is different from that underlying the TRH-induced GH rise present in another pathologic state i.e. acromegaly, a condition in which the effect of TRH escapes somatostatin suppression and LH-RH evokes GH and PRL release.
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PMID:Growth hormone response to thyrotropin-releasing hormone in liver cirrhosis: unique alteration in anterior pituitary responsiveness to hypothalamic hormones. 612 95

Immunoreactive serum levels of human chorionic gonadotrophin (HCG), its alpha- and beta- subunits (alpha-HCG and beta-HCG), calcitonin (CT), parathyroid hormone (PTH), prolactin (PRL), adrenocorticotropic hormone (ACTH), and growth hormone (GH) were increased in 8 to 68% of 44 patients with hepatocellular carcinoma. With the exception of two patients, ACTH and PRL levels were only moderately increased, while alpha-HCG, GH, ACTH and PRL levels were not significantly different from the levels found in cirrhosis suggesting that metabolic effects due to impaired liver function may be responsible for their increase in liver cirrhosis and primary liver cell carcinoma. In contrast, HCG, beta-HCG, CT and PTH were associated with a higher incidence of elevated immunoreactive hormone levels than the other peptide hormones; higher concentrations were noted in tumor patients than with liver cirrhosis alone. Therefore, we suggest that metabolic effects due to cirrhosis may influence the serum levels and be more important than ectopic secretion by hepatocellular carcinoma.
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PMID:Peptide hormones in liver cirrhosis and hepatocellular carcinoma. 627 36

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


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