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)

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

Unlike other pituitary hormones, PRL is under tonic inhibition by the hypothalamus by way of the PRL inhibitory factor, dopamine. GAP and GABA may also be inhibitory. PRL-releasing factors include TRH and VIP and possibly others. Circulating PRL is predominantly monomeric, although some patients with hyperprolactinemia appear to have increased quantities of the less biologically active polymeric forms. PRL is secreted episodically, with an increase in the amplitude of the secretory pulses with sleep. A transitory increase also occurs in response to the protein component of meals. Basal PRL levels increase in response to the hormonal milieu of pregnancy, and suckling postpartum triggers PRL release. Pathologic increases of PRL owing to hypothalamic dysregulation occur with a variety of medications, including the neuroleptics, metoclopramide, antidepressants, methyldopa, reserpine and verapamil, abuse of opiates and cocaine, renal insufficiency, cirrhosis, hypothyroidism, adrenal insufficiency, neurogenic stimulation, and idiopathically. Hyperprolactinemia also may occur from structural lesions of the stalk and hypothalamus, which cause disinhibition with or without maintenance of PRF activity, ectopic neoplasm production, and, most commonly, from prolactinomas. Diagnostic testing consists of routine chemistry and thyroid testing and imaging with MRI or CT. Dopamine agonists are the treatment of choice of prolactinomas of all sizes. Transsphenoidal surgery is an alternative for the patient who does not respond to medical therapy or who wishes definitive tumor removal, realizing that long-term cure is achieved in only 50% to 60% of patients with microadenomas and a much lower number in those with macroadenomas. Radiotherapy is reserved for patients who do respond to either medical or surgical treatment. Patients wishing to become pregnant usually are treated with bromocriptine, although prepregnancy surgical debulking may be advisable for those with large macroadenomas to reduce problems with tumor enlargement.
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PMID:Pathologic hyperprolactinemia. 148 80

Men suffering from liver cirrhosis were examined. They demonstrated a decrease in the blood content of gonadotropic hormones and testosterone and a rise of estradiol and prolactin. The changes indicated were more pronounced in decompensated liver cirrhosis and were associated with lipid peroxidation activation and a reduction of the count of T suppressor lymphocytes. As a result, the treatment of men suffering from decompensated liver cirrhosis and hyperprolactinemia by parlodel lowered blood prolactin and activity of lipid peroxidation. The use of chorionic gonadotropin for the treatment of men with decompensated liver cirrhosis and a low content of blood lutropin produces an immunomodulatory effect. Parlodel and chorionic gonadotropin favour a decrease of the cytolytic syndrome.
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PMID:[The immunomodulating and hepatotropic effect of correcting hyperprolactinemia and hypophyseal gonadotropic dysfunction in liver cirrhosis patients]. 150 76

The clinical signs and symptoms of sexual dysfunction with amenorrhoea, loss of libido and infertility, are frequently found in chronic alcoholic women. But few investigations have been made concerning hormonal changes in fertile aged women experiencing sexual dysfunction. In order to assess prolactin levels of fertile-aged women with alcoholism under 40 years of age-excluding those with liver cirrhosis were surveyed. We found that many of them (82.6%) had moderate elevations of plasma prolactin. Hyperprolactinemia is commonly associated with amenorrhoea and hypogonadism. An acute alcohol loading experiment was conducted on 6 healthy female volunteers in luteal phases of their menstrual cycles in order to evaluate the effects of alcohol on the hypothalamo-pituitary-ovarian axis. Evidence was obtained that alcohol intake caused transient hyperprolactinemia. The present results indicated that hyperprolactinemia can occur with high frequency among alcoholic women and this causes sexual dysfunction and ovarian dysfunction. The etiology of hyperprolactinemia could not be explained solely by the direct action of alcohol, rather, liver dysfunction must be implicated.
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PMID:[A study on hyperprolactinemia in female patients with alcoholics]. 206 37

Sex hormone binding globulin (SHBG) is a glycoprotein possessing high affinity binding for 17 beta-hydroxysteriod hormones such as testosterone and oestradiol. It is probably synthesized in the liver, plasma concentrations being regulated by, amongst other things, androgen/oestrogen balance, thyroid hormones, insulin and dietary factors, it is involved in transport of sex steroids in plasma and its concentration is a major factor regulating their distribution between the protein-bound and free states. Its detailed role in the delivery of hormones to target tissues is not yet clear. Plasma SHBG concentrations are affected by a number of different diseases, high values being found in hyperthyroidism, hypogonadism, androgen insensitivity and hepatic cirrhosis in men. Low concentrations are found in myxoedema, hyperprolactinaemia and syndromes of excessive androgen activity. Concentrations are also affected by drugs such as androgens, oestrogens, thyroid hormones and anti-convulsants. Measurement of SHBG is useful in the evaluation of mild disorders of androgen metabolism and enables identification of those women with hirsutism who are more likely to respond to oestrogen therapy. Testosterone:SHBG ratios correlate well with both measured and calculated values of free testosterone and help to discriminate subjects with excessive androgen activity from normal individuals.
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PMID:Sex hormone binding globulin: origin, function and clinical significance. 208 Aug 56

Various breast abnormalities have been described in patients treated chronically with cimetidine, but galactorrhea has been reported only twice in the medical literature. In both cases, there appeared to be an associated hyperprolactinemia. These problems could well represent a consequence of histamine2-receptor blockade. We report here a female patient with hepatic cirrhosis and portal hypertension who developed hyperprolactinemia and galactorrhea while on long-term cimetidine therapy. Both the hyperprolactinemia and the galactorrhea disappeared when the patient was switched to ranitidine, an alternative H2-receptor blocker. A review of the previous case reports and relevant literature is included.
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PMID:Cimetidine-induced galactorrhea. 271 15

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

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

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


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