Hormone Excretion in Liver Disease 1

Dohan, F. C.; Richardson, E.; Bluemle, Lewis W.; György, Paul

doi:10.1172/jci102633

Cited by 54 publications

(9 citation statements)

References 19 publications

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“…Rupp et al [1951] and Dohan et al [1952] found increased levels in rather more than half, and increased free oestrogens in less than half of their patients. Dohan et al [1952] also found, when the three fractions were separated approximately, that both conjugated and unconjugated 'oestriol'was increased to a greater extent and more frequently than 'oestrone' or 'oestradiol'.…”

Section: Discussionmentioning

confidence: 79%

URINARY EXCRETION OF OESTRONE, OESTRADIOL-17β AND OESTRIOL IN PATIENTS WITH CHRONIC LIVER DAMAGE

Cameron¹

1957

Journal of Endocrinology

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The urinary excretion of oestrone, oestradiol-17\g=b\ and oestriol has been estimated by a chemical technique in nine men and three women with chronic liver disease.Combined oestrone, oestradiol and oestriol excretion was above normal limits in only two patients, both men. One excreted more than normal amounts of all three oestrogens; the other excreted more oestriol only. In addition, four men and one woman excreted more oestriol than normal, but this was not sufficient to increase the combined excretion of these three oestrogens beyond levels found in healthy controls. These findings are contrary to many published conclusions based on bioassay.Oestrogen excretion has been contrasted with the clinical findings. There was no correlation between increased oestrogen excretion and gynaecomastia. There was, however, a suggestive association of increased oestriol excretion, testicular atrophy, and a history of alcoholism. No association was established between an increased excretion of any oestrogen and the presence of ascites, jaundice, spider naevi and palmar erythema. Some implications of these findings are discussed.Patients with chronic liver disease frequently show alteration in their secondary sexual characteristics and sexual function. Men experience, at an early stage of their illness, loss of libido and diminished sexual potency, and clinical examination often reveals small testes, loss of axillary hair, and sometimes enlargement of the breasts.

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Section: Discussionmentioning

confidence: 79%

URINARY EXCRETION OF OESTRONE, OESTRADIOL-17β AND OESTRIOL IN PATIENTS WITH CHRONIC LIVER DAMAGE

Cameron¹

1957

Journal of Endocrinology

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“…Glass, Edmonson, and Soll (1940), Rupp, Cantarow, Rakoff, and Paschkis (1951), Pincus, Rakoff, Cohen, and Tumen (1951), and Dohan, Richardson, Bluemle, and Gyorgy (1952), using bioassay methods, all found in approximately 48% of the patients studied values which usually were less than twice the normal maximum but occasionally were as high as seven times the normal. Later workers, using colorimetric measurements, have investigated a smaller number of patients and have found raised values in only approximately 20% of the cases, and no value has exceeded twice the normal maximum (Cameron, 1957;Lyngbye and Mogensen, 1961).…”

mentioning

confidence: 90%

“…Glass, Edmonson, and Soll (1944) administered oestrone and oestradiol to three patients with liver disease and recovered 83-86% of the biological activity of the administered dose in the urine whereas values of 10% would have been expected for normal individuals. On the other hand, Dohan et al (1952) and Cameron (1957) measured endogenous urinary oestriol, oestrone, and oestradiol separately and found that the major urinary oestrogen in liver disease is often oestriol, which is the least biologically active of the three. After the administration of oestrone, oestradiol, or their esters to patients with liver disease, St0a, Bass0e, and Emberland (1958), in a study of five cases, found a decreased recovery as the three oestrogens in two and an increased recovery in one, and Lyngbye and 'Present address: Royal Women's Hospital, Melbourne, Australia.…”

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confidence: 99%

Oestrogen metabolism and excretion in liver disease

Brown¹,

Crean²,

Ginsburg³

1964

Gut

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EDITORIAL SYNOPSIS Raised urinary oestrogen excretion was noted in 16 men and women with liver disease. The study suggests that the increased output of urinary oestrogens was usually due to increased secretion rates of the primary oestrogenic hormones rather than to impaired oestrogen metabolism by the liver.Numerous workers have reported a raised output of urinary oestrogens in men and women with various types of liver disease. Glass, Edmonson, and Soll (1940), Rupp, Cantarow, Rakoff, and Paschkis (1951), Pincus, Rakoff, Cohen, and Tumen (1951), and Dohan, Richardson, Bluemle, and Gyorgy (1952), using bioassay methods, all found in approximately 48% of the patients studied values which usually were less than twice the normal maximum but occasionally were as high as seven times the normal. Later workers, using colorimetric measurements, have investigated a smaller number of patients and have found raised values in only approximately 20% of the cases, and no value has exceeded twice the normal maximum (Cameron, 1957;Lyngbye and Mogensen, 1961). This raised output has been attributed to impaired metabolism by the diseased liver but evidence for this concept has been conflicting. Glass, Edmonson, and Soll (1944) administered oestrone and oestradiol to three patients with liver disease and recovered 83-86% of the biological activity of the administered dose in the urine whereas values of 10% would have been expected for normal individuals. On the other hand, Dohan et al. (1952) and Cameron (1957) measured endogenous urinary oestriol, oestrone, and oestradiol separately and found that the major urinary oestrogen in liver disease is often oestriol, which is the least biologically active of the three. After the administration of oestrone, oestradiol, or their esters to patients with liver disease, St0a, Bass0e, and Emberland (1958), in a study of five cases, found a decreased recovery as the three oestrogens in two and an increased recovery in one, and Lyngbye and 'Present address: Royal Women's Hospital, Melbourne, Australia. 2Present address:

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“…Until recently studies of adrenal cortical function in both acute and chronic liver disease were based on measurements of urinary steroids. There has been general agreement that the urinary 17-ketosteroids are low in various forms of liver disease -acute viral hepatitis (18)(19)(20)(21), toxic hepatitis (20), portal cirrhosis (18)(19)(20)(21)(22), biliary cirrhosis (23,24), and also in obstructive jaundice (18)(19)(20)(21)25). Urinary androgen excretion, as measured by bioassay, has also been found to be low in cirrhosis of the liver (26,27).…”

mentioning

confidence: 99%

Adrenocortical Steroid Metabolism and Adrenal Cortical Function in Liver Disease

Peterson¹

1960

J. Clin. Invest.

134

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Zondek (1) as early as 1934 demonstrated that enzymes of the liver destroyed the biological activity of the estrogens. Since then both in tivo and in vitro studies have provided much evidence to show that the liver is the organ primarily responsible for the catabolism of the steroid hormones: estrogens, androgens, progesterone, and the corticosteroids (2). However, not until the development of improved methods for measurement of certain of the adrenocortical steroids and their metabolites, and the availability of labeled radioactive cortisol, corticosterone, and aldosterone has it been possible accurately to evaluate the influence of liver disease on the rate of degradation and synthesis of the steroids in man. The studies here reported are based on the use of certain of these newer techniques.On incubation with rat liver tissue, cortisol and cortisone are rapidly metabolized, but only very slowly with other tissues (3-5). Perfusion studies have demonstrated a very rapid metabolism of the steroids by the liver but not by other organs (6-8). Hechter, Frank, Caspi and Frank (9) found that the major portion of the cortisone and cortisol administered into the portal vein in dogs was not recovered as unaltered steroid from the hepatic venous blood. Bradlow, Dobriner and Gallagher (10) found that 70 per cent of a dose of tritium-labeled cortisone administered to mice was found in the liver within five minutes after intravenous administration. Administered cortisol also disappears rapidly from the circulation in rats (11), and this rapid metabolism can be prevented by hepatectomy but not by nephrectomy (12).The liver in man has a high capacity for metabolizing the circulating blood cortisol, as demonstrated by the fact that the level of 17-hydroxycorticosteroids in the hepatic vein blood is lower than the level in the arterial blood (13,14). Adrenocortical steroids administered intravenously

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Hormone Excretion in Liver Disease 1

Cited by 54 publications

References 19 publications

URINARY EXCRETION OF OESTRONE, OESTRADIOL-17β AND OESTRIOL IN PATIENTS WITH CHRONIC LIVER DAMAGE

URINARY EXCRETION OF OESTRONE, OESTRADIOL-17β AND OESTRIOL IN PATIENTS WITH CHRONIC LIVER DAMAGE

Oestrogen metabolism and excretion in liver disease

Adrenocortical Steroid Metabolism and Adrenal Cortical Function in Liver Disease

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