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)

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

The present work investigates the sex hormone profiles in 50 male patients with liver cirrhosis of different etiology according to the degree of liver dysfunction. The only hormonal impairment in well-compensated cirrhotics (group A) was an increase in mean serum concentrations of estrone, androstenedione, and sex hormone binding globulin. In decompensated cirrhotic patients with ascites (group B), low mean levels of total and free testosterone were found along with normal gonadotropins mean levels. Estrone and androstenedione levels were still elevated, whereas sex hormone binding globulin levels were not different from controls. In decompensated cirrhotics patients with encephalopathy (group C), total and free testosterone mean levels were lower than in group B, and LH mean levels were elevated; estrone levels were markedly high, but androstenedione levels were subnormal; sex hormone binding globulin concentrations were again not different from controls. The few patients with high prolactin levels belonged primarily to this group. Estradiol mean levels were not significantly elevated in any of the groups. It is concluded that the various hormonal patterns of gonadal failure and of the impairment of steroid metabolism and transport, observed in cirrhosis, can be attributed to the degree of liver dysfunction.
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PMID:Sex hormones and sex hormone binding globulin in males with compensated and decompensated cirrhosis of the liver. 249 23

Gonadal function in idiopathic hemochromatosis (IHC) was evaluated by comparing clinical features and levels of sex hormones in 10 male patients with IHC (cirrhosis, 4; fibrosis, 6), 6 male patients with alcoholic cirrhosis (AC) and 10 healthy, age-matched controls. Impotence was present in 9 IHC and all AC patients and was associated with decreased plasma testosterone levels. However, gynecomastia, a feature in all patients with AC, was not present in IHC, and plasma sex hormone binding globulin was normal. Patients with IHC showed significantly lower basal estradiol levels (17.7 +/- 6.3 pg per ml) than did controls (28.5 +/- 8.5 pg per ml), and low LH levels (p less than 0.01), which were insufficiently stimulated by luteinizing hormone releasing hormone (n = 8) as well as a decrease in prolactin concentration (2.9 +/- 1.4 vs. 5.9 +/- 1.9 ng per ml in the controls) suggesting pituitary failure. Synthesizing capacity of sex hormones was determined by adrenocorticotropic hormone and human chorionic gonadotropin administration. Basal and stimulated levels of androstenedione and cortisol indicated normal function of the adrenals in IHC. However after adrenocorticotropic hormone, estrone levels increased to only 16.2 +/- 8.4 pg per ml (controls, 27.3 +/- 4.7 pg per ml; p less than 0.01). Increments of estrone (12.5 +/- 9.2 pg per ml) and estradiol (17.9 +/- 11.6 pg per ml) were also lower in IHC following human chorionic gonadotropin administration than in controls (26.0 +/- 7.2 and 37.5 +/- 11.4 pg per ml, respectively). In contrast, plasma human chorionic gonadotropin raised testosterone levels 3.3-fold in IHC and 2.2-fold in controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Androgen and estrogen response to adrenal and gonadal stimulation in idiopathic hemochromatosis: evidence for decreased estrogen formation. 298 1

Eighteen women with hepatic cirrhosis were examined for plasma levels of testosterone, estrone, estradiol, progesterone and sex hormone binding globulin. For eight who were amenorrheic, with advanced liver cirrhosis and ascites, the reduction of testosterone and rise in estrone and sex hormone binding globulin concentrations were significant. Plasma extradiol and progesterone were lower than normal levels, but the differences were not statistically significant. The other ten patients were menstruating (mostly irregularly), and their hormonal levels were assessed in different states of their cycles. All of them did not ovulate, had low levels of plasma progesterone and also showed consistent estrone concentration excess relative to estradiol and significant lowering of testosterone and elevation of sex hormone binding globulin. These findings are compared with previous reports on males with liver cirrhosis.
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PMID:Sex steroids in women with liver cirrhosis. 610 50

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

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

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

Human sex hormone binding globulin (SHBG) is encoded by a normal and a variant allele. The resulting SHBG phenotypes (the homozygous normal SHBG, the heterozygous SHBG and the homozygous variant SHBG phenotype) can be distinguished by their electrophoretic patterns. We developed a novel detection system allowing us to distinguish between the different electrophoretic patterns in small amounts of plasma or serum (10 microliters). Small aliquots of Blue Sepharose were added to diluted sera or plasma samples for removal of albumin and the supernatants were subsequently applied to Western blotting. This method of detection was used to determine the distribution of SHBG phenotypes in healthy controls of both sexes and in five different pathological conditions characterized by changes in the SHBG level or endocrine disturbances (malignant and benign ovarian neoplasms, hirsutism, liver cirrhosis and alcoholism). The distribution of SHBG phenotypes was independent of such conditions and in agreement with the expected phenotype distribution of a bi-allelic gene in both healthy controls and patients (Hardy Weinberg law). An allele frequency of 0.13 was found for the SHBG variant allele based on the experimental values. Differences in SHBG phenotypes do not appear to have any clinical significance and no sex difference was found in the SHBG phenotype distribution.
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PMID:Sex hormone binding globulin phenotypes: their detection and distribution in healthy adults and in different clinical conditions. 808 1

Testicular atrophy, loss of libido and feminization are observed in patients with nonalcoholic liver cirrhosis, Serum total and free testosterone levels are decreased in patients with advanced liver cirrhosis and is normal in compensated cirrhotic patients. In compensated liver cirrhosis, sex hormone binding globulin is increased, and is related with increasing serum total testosterone. Serum total and free estradiol levels and ratio of estradiol to testosterone are increased in cirrhotic patients. Hyperestrogenization is related with female physical characteristics. Gonadal dysfunctions observed in cirrhotic patients are primary in the gonadal failure, then a concomitant with pituitary defect occurs. These abnormalities in liver cirrhosis are reversible.
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PMID:[Gonadal dysfunctions in liver cirrhosis]. 811 82

The reason for the large male predominance in the occurrence of hepatocellular carcinoma (HCC) remains unknown, and sex hormones may contribute to this phenomenon. We examined possible associations of serum levels of testosterone, free testosterone, estradiol, sex hormone binding globulin, and testosterone:estradiol ratio (T:E2 ratio) with HCC development in a follow-up study of 46 Japanese male patients with liver cirrhosis predominantly of hepatitis C virus origin (76%). Serum samples were collected between December 1985 and December 1987, and the patients were completely followed until the end of 1995 for an average of 5.1 years. During the follow-up period, 20 patients (43%) developed HCC. Univariate analysis demonstrated that serum T:E2 ratio and testosterone were significant predictors of HCC; the hazard ratios (and 95% confidence intervals) in the middle and upper tertiles relative to the lower tertile were 2.0 (0.5-7.6) and 4.0 (1.1-14.6; P trend = 0.03) for T:E2 ratio and 0.8 (0.2-3.1) and 2.9 (1.0-8.5; P trend = 0.05) for testosterone. Adjustment for age, serum albumin, hepatitis virus markers, and other clinicobiological variables substantially increased the corresponding hazard ratios. In multivariate analysis, serum free testosterone appeared to be associated with increased risk, yet independent associations with estradiol and sex hormone binding globulin were not evident. These results indicate that elevated serum testosterone, together with decreased serum estrogens, may promote the development of HCC in cirrhosis.
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PMID:Serum testosterone:estradiol ratio and the development of hepatocellular carcinoma among male cirrhotic patients. 1101 36


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