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)

Because the liver is of considerable importance in metabolism of thyroid hormones, plasma levels of thyroxine (T4), triiodotyronine (T3) with their unbound fractions (FT4 and FT3), reverse T3 (rT3)--an inactive isomer of T3-tyrotropin (TSH) and TSH response to thyrotropin releasing hormone (TRH; 250 micrograms i.V.) were determined by radioimmunoassays in 50 clinically euthyroid patients with alcoholic cirrhosis. T4 mean concentration (7.3 micrograms/dl) did not differ from normal values but T3 was decreased (101 vs 154 ng/dl; p less than 0.001) and was correlated with the degree of liver damage appreciated by a clinico-biological index. FT4 was elevated in patients (17.1 vs 13.1 pg/ml; p less than 0.02) although FT3 was slightly decreased (3.4 vs 4.5 pg/ml; p less than 0.10) with an increased FT4: FT3 ratio (7.0 vs 3.0; p less than 0.02). rT3 was elevated (592 vs 206 ng/100 ml; p less than 0.001) and correlated with FT4/FT3: rT3/T3 ratio (p less than 0.01) and with the severity of the cirrhosis. Basal TSH levels (3.3 microU/ml) and TSH responsiveness to TRH was normal though very scattered, and independant from T3 and T4 values. It may be concluded that: 1. euthyroidy in cirrhosis assessed by a normal responsiveness to TRH, results from a compensatory increase in FT4. 2. The low T3 and FT3 levels may proceed from an impairment of peripheral T4 in to T3 conversion with a deviation pathway towards rT3. 3. T3 and rT3 levels provide valuable index of the severity of the cirrhosis.
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PMID:Thyroid status in fifty patients with alcoholic cirrhosis. 11 93

A study of thyroid function was undertaken in 53 patients with chronic alcoholism the following tests were performed: T3 RIA, T4 RIA, T3 test and I.V. TRH-test. The patients were divided into 3 groups according to the degree of liver injury: histologically documented fibrosteatosis (group 1), cirrhosis (group 2); group 3 consisted of severe cirrhosis with coagulation defects precluding liver biopsy. 32 healthy subjects served as controls. Free thyroxine index was normal in the 3 groups of patients; on the contrary, serum T3 RIA was significantly reduced in the 2nd and the 3rd group. The decrease of T3 correlated with the degree of hepatocellular failure. TRH test was almost always normal. If patients are separated into two groups according to their circulating T3 levels, it appears that subjects with low T3 show a TRH-induced increase in TSH lower than in the other group, but not significantly different from normal subjects, suggesting an inadequate hypothalamic reactivity.
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PMID:[TRH response in 53 patients with chronic alcoholism (author's transl)]. 11 79

The hypothalamo-pituitary gonadal function was evaluated in eleven chronically alcoholic menopausal women by measurement of basal serum oestradiol, FSH, LH and prolactin, followed by LHRH-TRH test and administration of clomiphene citrate. All patients had hepatic damage, fibrosteatosis or cirrhosis. Two subgroups have been isolated according to urinary and serum estrogen levels: seven patients with urinary estrogen output less than 14 microgram per 24 h and plasma oestradiol less than 40 pg per ml were considered as post menopausal women: basal values of FSH and LH and their response to LHRH did not differ from that observed in normal menopausal women; clomiphene citrate induced a significant suppression of FSH and LH blood levels. Four women with urinary estrogen output greater than 14 microgram per 24 h and plasma oestradiol greater than 40 pg per ml were considered in menopausal transition. Their basal and post LHRH-FSH blood levels were lower than in the control group. These results suggest a normal hypothalamo-pituitary-gonadal axis at least in the post menopausal alcoholic women.
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PMID:Effects of chronic alcoholism on the pituitary-gonadal function of women during menopausal transition and in the post menopausal period. 36 30

Serum concentrations of thyroid hormones and TSH response to TRH are studied in normal controls and in patients with liver cirrhosis. T3 levels are significantly diminished in the cirrhotic group while the mean total T4 concentration, the basal TSH and the magnitude of the peak response to TRH are similar in cirrhotic and control patients. However when the cirrhotic patients are separated in two groups according to the level of arterial ammonemia, it appears that the group with hyperammonemia (n = 10) has a significantly higher peak response than the control group. Since hyperammonemia is a wittness of hepatic encephalopathy it is suggested that TSH release or synthesis may be modified by this situation resulting from a cerebral accumulation of false neurotransmitters and a depletion of aminergic mediators.
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PMID:[Alterations in thyroid hormones and thyrotropin response to TRH in cirrhotic patients with or without hyperammonemia (author's transl)]. 41 33

The, in non-thyroidal illnesses, frequently occurring changes in the serum concentrations of peripheral thyroid hormones, are shown in patients with acute myocardial infarction, compensated and decompensated cirrhosis of the liver, renal insufficiency and in rheumatoid arthritis. The observed changes, (pathological) low total triiodothyronine, low or normal total thyroxine, and normal thyrotrophine), can make the diagnosis of hyperthyroidism impossible. Only in control measurements, after cessation of the simultaneous non-thyroidal illness, the peripheral thyroid hormone concentrations are found to be in the hyperthyroid range. The only way to establish the diagnosis, (or confirm the clinical suspicion), is to prove non-responsiveness of the pituitary to a TRH-stimulus. TRH-tests have, however, no diagnostic value in illnesses that affect pituitary function directly, such as terminal renal insufficiency. The diagnosis of hypothyroidism can be established by measurement of the basal thyrotrophine serum concentration (elevated) or by measurement of the serum concentrations of 3,3'5'-triiodothyronine (reverse T3), which is, according to a recent report, observed to be significantly decreased.
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PMID:[Evaluation of thyroid function in non-thyroid diseases]. 75 17

We studied endocrine functions at baseline and after TRH and LHRH stimulation in a group of 7 young male patients with genetic hemochromatosis (HE) without liver damage (i.e. fibrosis and cirrhosis). In five patients endocrine re-evaluations after complete iron depletion was also performed. Mean basal testosterone (T), FSH, LH and PRL were significantly lower than in controls. Serum T increased normally after HCG stimulation. The normal or high increments of LH after LHRH stimulation suggest that secretion capacity of LH was intact and that hypothalamic dysfunction could be responsible for the preclinical gonadal deficiency found in our patients. The response of PRL to TRH indicates that secretion capacity of lactotrophs although present, was decreased and did not improve after phlebotomy therapy. After iron depletion the two patients with the lowest basal T levels showed the highest increments indicating that in the early stages of hypothalamic-pituitary damage gonadal dysfunction is still reversible in HE patients.
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PMID:Preclinical hypogonadism in genetic hemochromatosis in the early stage of the disease: evidence of hypothalamic dysfunction. 140 47

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

The liver plays a dominant role in the metabolism of the thyroidal hormones; it is here that the 5' deiodase acts to convert part of T4 to T3. There are eight further circulating iodothyronines: the rT3, mainly derived from T4, appears to be the major inhibitor of T4 and T3. Thus, if rT3 increases, the metabolic effects of T3 and T4 can be quite different. In the course of some chronic systemic diseases (e.g. hepatic cirrhosis) rT3 increases simultaneously with the decrease of T3 levels. Therefore we can describe particular alterations of the thyroidal pattern typical of chronic liver diseases: low T3 syndrome, low T3 and T4 syndrome, high T4 syndrome, mixed forms. T3 and T4 diminish due to inefficient hepatic deiodination and defective hepatocellular uptake. Inefficient hepatic deiodination and defective hepatocellular uptake. T4 levels decrease, most likely because of an inefficient production of thyroid binding globulin, or the action of a peripheral binding inhibitor. During acute liver diseases and primitive biliary cirrhosis, we can observe an increase of T4 and TBG together with an increase of the acute phase proteins. Such complex hormonal mechanisms are not influenced by TSH, which appears normal or inhibited, as the TRH stimulus test is normal. The explication can be found in an enhanced conversion of T4 to T3 in the pituitary gland. The biological and clinical significance of these mechanisms might be that of creating a "protective" state for an organism in a catabolic state by reducing the circulating T3. A relationship has been found between circulating thyroidal hormones levels, particularly the T3, rT3 and rT3/T3 ratio, and the state of hepatic functional insufficiency.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Liver and thyroid gland. Physiopathologic and clinical relationships]. 219 47

This work was performed in order to analyze thyroid hormone picture of alcoholic patients with reference to hepatic damage. Forty consecutive patients of male sex, aged 28-64 years, were investigated. They consumed more of 50 g ethanol/day for at least 2 years. According to investigations on hepatic condition, 2 cases had normal liver, 22 cases had steatosis and 16 had cirrhosis. None of patients disclosed a clinical and/or hormonal behaviour pointing to alterations of thyroid function. In alcoholics serum T3 levels resulted significantly lower compared to a control group of 40 healthy males (P less than 0.001), independently of degree of hepatic damage. Instead, serum T4 levels did not result significantly different in the comparison between alcoholics and controls. Serum FT3 and FT4 levels resulted significantly higher (P less than 0.001) only in alcoholics with liver cirrhosis. In comparison with normals, serum rT3 was significantly lower in alcoholics without liver cirrhosis (P less than 0.001), but significantly higher in alcoholics with liver cirrhosis (P less than 0.005). Serum TBG behaved in the same manner. According to euthyroidism in our alcoholic patients basal and TRH-stimulated TSH were normal, however significantly lower when compared to controls (P less than 0.005). On the whole these results suggest the existence of an autonomous ethanol-dependent mechanism that determine decreased serum T3 levels in the alcoholics, in absence of serum T4 variations. In the alcoholic with liver cirrhosis, an increased conversion of T4 in rT3, correlated to hepatic damage, joins to previous mechanism. The tendency to low secretion of pituitary TSH might be dependent of action of alcohol on neuromodulation of TRH secretion.
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PMID:[The thyroid hormone picture of alcoholics in connection with their liver status]. 238 53

The peptide, 7B2, originally isolated from pituitary, has been shown to be present in endocrine tumors of high concentrations in pancreatic islet tumors. Plasma from most of these patients showed very high 7B2 immunoreactivity (IR-7B2) though there is a lack of knowledge concerning physiological and pathological changes in plasma IR-7B2 levels in other conditions. To assess whether or not there is any alteration in circulating IR-7B2 levels due to age, sex or any specific condition, plasma levels of IR-7B2 were measured in the fasting state in 106 healthy subjects aged 3 months to 91 years, 101 diabetics, 28 patients with hyperthyroidism. 7 patients with primary hypothyroidism, 13 patients with liver cirrhosis, 43 patients with chronic renal failure, 35 patients with cerebral vascular accident, and 26 pregnant subjects. Twenty-four cord bloods were also included. The responses of circulating IR-7B2 to oral glucose, intravenous arginine infusion, volus thyrotropin (TRH) or volus luteinizing hormone-releasing hormone (LH-RH) injection were also evaluated. Particularly high IR-7B2 levels were found to exist in cord blood. Postnatally the concentrations decreased gradually with age to adult values (15.6 +/- 2.9pmol/liter (mean +/- SE) in 20's-60's), though plasma IR-7B2 levels again increased significantly in over 70's (37.1 +/- 3.2pmol/liter; P less than 0.01). There was no significant difference in plasma 7B2 levels in either sex. Among the pathological conditions studied, significantly high IR-7B2 levels were observed in patients with chronic renal failure (175.1 +/- 35.9pmol/liter). Some of the pregnant patients in their third trimester also showed high plasma IR-7B2 levels. A small but significant rise in plasma IR-7B2 was observed after a glucose load in control subjects and diabetics. Intravenous LH-RH exerted a rise in plasma 7B2 concentrations though arginine and TRH showed no significant effect on plasma IR-7B2 concentrations. Compared with the plasma concentrations, ten to fifty-fold high levels of IR-7B2 were observed in cerebrospinal fluid (CSF) from patients with cerebrovascular accidents or multiple sclerosis. These results suggested that the kidney plays a major role in 7B2 degradation and that LH-RH simulates IR-7B2 release from the pituitary gland. Whether reduced clearance or increased production was responsible for the IR-7B2 elevation in subjects under 10 years or over 70 years requires investigation. Furthermore, high levels of IR-7B2 in CSF might indicate its specific role for the central nervous system.
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PMID:[Immunoreactive 7B2 concentrations in plasma and cerebrospinal fluid in pathophysiological conditions and the responses to oral glucose load, intravenous LH-RH, TRH and arginine infusion]. 251 84


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