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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is a recent hypothesis that thyroxine (T4), secreted by the thyroid gland under physiological conditions, is mono-deiodinated in extrathyroidal sites to form the more active 3, 3', 5-tri-iodothyronine (T3) before exerting biological activity at target tissue level. Futhermore, circumstantial evidence suggests that the liver is an important site for the extra-thyroidal conversion of T4 to T3. Thyoid hormone pathophysiology in liver disease is therefore of interest. Patients with hepatic cirrhosis have normal or raised plasma T4 concentration and markedly reduced plasma T3 concentration. Free hormone measurement reflect this pattern and three is kinetic and other evidence to support the concept that extra-thyroidal conversion of T4 to T3 is reduced in patients with liver dysfunction. Comparable finding have however been reported in patients with other non-hepatic chronic systemic diseases but, unlike in hepatic cirrhosis, serum thyrotropin (TSH) is not increased. Increased serum TSH is found in hepatic cirrhois and is often accompanied by an abnormal TSH response to thyrotropin-releasing hormone (TRH) suggesting, in addition, disordered hypothalamic-pituitary control of thyroid function in these patients. Thyroid physiology is clearly markedly disturbed in hepatic cirrhosis but no single hypothesis adequately accounts for all the observed abnormalities. The recent finding of increased plasma 3, 3', 5-tri-iodothyronine (reverse t3; rT3) concentration in hepatic cirrhosis may ulimately clarify our understanding.
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PMID:Thyroid function in chronic liver disease. 11 92

Thyroid explorations were made in 57 patients complaining of serious illnesses in order to identify "low T3 syndrome". All these patients were clinically euthyroid as assessed by normal values of T4 concentration, RT3U ratio and FT4I. However, all the patients included in this study had significantly low serum T3 (42 +/- 29 ng/100 ml) and FT3I (0,44 +/- 0,30). Low T3 syndrome was particularly frequently seen in patients with cancer (8/10), hepatic cirrhosis (5/6), renal failure (6/7), old age (5/8) and in serious systemic diseases (6/12). Nevertheless, at adverse with other authors, we have observed less frequently the low T3 syndrome in anorexia nervosa (4/6) as well as during fasting (1/8). In 31 out of 35 patients with low or normal low T3 concentrations, the serum TSH values observed were within the normal limits in 28 cases. The etiologies of isolated decreased T3, mainly the deviation of peripheral conversion of T4 to reverse T3, are discussed. Normal metabolic state and normal TSH concentration encountered in the low T3 syndrome are equally commented.
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PMID:[Low triiodothyronine syndrome in non thyroidal diseases. Distribution and serum TSH concentration studies (author's transl)]. 73 16

We report herein a case with myxedema (primary hypothyroidism) associated with marked ascites that was found during the course of examination for a suspected decompensated state of liver cirrhosis or malignant disease. Aspirated ascitic fluid was found to have the characteristics of the exudate. Thyroid hormone replacement resulted in rapid clinical improvement with resolution of the ascites. This case is an unusual association of hypothyroidism as a cause of ascites. In all the cases with ascites of unknown etiology, the differential diagnosis requires consideration of myxedema.
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PMID:Gross ascites as a first manifestation of primary hypothyroidism due to post-treatment of radioiodine therapy for Graves' disease. 160 Feb 76

Nuclear tri-iodothyronine (T3) maximal binding capacity (MBC) and thyroxine- and T3-stimulated cellular oxygen consumption and glucose consumption were examined in mononuclear blood cells from six patients with liver cirrhosis (LC), in six patients with alcoholic hepatitis (AH), and in six healthy control subjects. Serum T3 was decreased in patients with LC. The MBC of T3 was increased significantly (P less than 0.05) in cells from patients with LC compared with patients with AH and controls, whereas the equilibrium association constants did not differ. Unstimulated glucose consumption was slightly increased (P less than 0.05) in cells from patients with AH and LC compared with controls. Thyroid hormone-stimulated glucose consumption was significantly (P less than 0.05) increased in cells from patients with LC compared with controls and patients with AH. Unstimulated oxygen consumption did not differ between the groups, but thyroid hormone-stimulated oxygen consumption was depressed in cells from patients with AC (P less than 0.05) compared with patients with LC and with controls. We conclude that both thyroid hormone-stimulated glucose consumption and T3 nuclear receptor binding in cells from patients with LC are increased, and suggest that the observed changes are responsible for maintenance of euthyroidism in the face of reduced circulating T3.
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PMID:Increased nuclear tri-iodothyronine binding and thyroid hormone-stimulated glucose consumption in mononuclear blood cells from patients with liver cirrhosis. 200 22

Thyroid dysfunction has long been reported in patients with liver disease, but limited information is available on thyroid gland size in cirrhosis. Most studies were carried out on small, selected series of patients, and no study has measured thyroid volume in relation to the etiology of liver disease. Thyroid volume was measured at ultrasound in 118 consecutive patients with cirrhosis of different etiology and 48 healthy subjects matched for age and sex. No subjects had evidence of overt thyroid disease. The mean volume was increased by 17% (from 16.0 [SD 5.2] ml in controls to 18.8 [7.6] in cirrhosis; P less than 0.025), and thyroid enlargement (antero-posterior diameter greater than 20 mm) was present in 38% of cases, in the presence of hormone values indicative of low-T3 syndrome. No significant differences in thyroid gland size were observed in relation to the extent of liver dysfunction or to the etiology of liver disease. The prevalence of thyroid nodules was similar in controls and in patients with cirrhosis. In only 8% of cases were laboratory values indicative of hypothyroidism, with low free triiodothyronine and raised thyroid-stimulating hormone levels; in these patients thyroid volume was decreased on average by 26%. This was mainly the case with patients with primary biliary and alcoholic cirrhosis. The largest mean thyroid volume was observed in patients with HBsAg + ve postnecrotic cirrhosis, whose thyroid volume was increased on average by 37%, and 53% of subjects had thyroid enlargement. This finding raises the question of a possible direct involvement of the thyroid in hepatitis B virus infection.
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PMID:Thyroid gland size and function in patients with cirrhosis of the liver. 205 4

Grading of goitre size according to WHO or the palpatory estimation of thyroid volume does not allow a quantitative estimation of thyroid size or an objective follow-up during treatment with e.g. radioiodine. The present and other studies have demonstrated that the ultrasonic evaluation of thyroid volume is both accurate and precise. In addition, it is non-invasive, rapid, inexpensive and without discomfort to the patient. Using this technique it was demonstrated that thyroid volume increases with increasing age and body weight in both sexes, with weight having the most pronounced influence. The relationship between thyroid volume, body weight and age in non-goitrous healthy subjects can be described using a formula that allows the calculation of normal thyroid size for a population: Thyroid volume (ml) = 1.97 + 0.21 x bodyweight (kg) + 0.06 x age (years). Cigarette smoking is associated with an approximately 10-fold increase in goitre frequency probably due to a combination of an increased sympathetic stimulation of the thyroid and an iodine deficiency state caused by inhalation of thiocyanate. Although no seasonal alteration in serum TSH level could be demonstrated thyroid volume is 23% higher in the winter than in the summer. Cyclic alterations of thyroid volume possibly related to TSH alterations have been found with a 50% difference between minimum values in the first half and maximum values in the second half of the menstrual cycle. Nonthyroidal illnesses are associated with marked alterations in thyroid volume. Thus, chronic renal disease and acute hepatic disease demonstrate significant increases in thyroid volume although the precise mechanisms have not been clarified. Chronic hepatic disease per se and chronic nonrenal nonhepatic disease does not seem to influence thyroid volume. Chronic alcoholism, however, with or without liver cirrhosis is associated with a marked decrease in thyroid volume and an increase in the amount of fibrosis probably related to a direct toxic effect of alcohol on the thyroid. All these factors should be kept in mind when goitre frequency, goitrogenic action of drugs and goitre treatment effects are evaluated.
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PMID:Thyroid size determined by ultrasound. Influence of physiological factors and non-thyroidal disease. 219 37

Thyroid hormone serum concentrations were measured in clinically apparently euthyroid patients suffering from diseases that have symptoms in common with thyroid dysfunction. The diseases investigated were: anorexia nervosa (n = 13), myocardial infarction (n = 13) cirrhosis of the liver (n = 19), terminal renal insufficiency (n = 30) and rheumatoid arthritis (n = 14). In each group, the patients were divided into groups according to the degree of their disease. A relative decrease in 3,5,3'-triiodothyronine (TT3) serum levels is the most pronounced effect of all the non-thyroidal ailments investigated. Individual observations show that total and free thyroxine levels can also be lowered by some acute illnesses. Moreover, the extent of the decrease in TT3 serum levels depends significantly on the severity of the non-thyroidal illness. This phenomenon was observed in all ailments investigated. Based on our findings it is concluded that the diagnosis of thyroid dysfunction may be extremely difficult in many non-thyroidal illnesses. This study should help the clinician to evaluate laboratory hormone data correctly in respect to the diagnosis of thyroid dysfunction in patients with non-thyroidal illnesses.
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PMID:[The effect of nonthyroidal diseases on the serum hormone level of the thyroid gland function regulation cycle]. 661 91

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

Thyroid function and thyroid gland volume were studied in 40 consecutive alcoholic patients with histologically proven cirrhosis of the liver, and compared with data obtained from 40 sex-, age-, and weight-matched normal subjects. Thyroid volume, measured ultrasonically, was significantly decreased in the patients with cirrhosis: median, 11 ml (range, 6-16 ml); compared to normal subjects: median, 20 ml (range, 10-31 ml) (P less than 0.001). Serum T3 concentrations were significantly reduced: median, 1.5 nmol/liter (range, 0.1-2.5 nmol/liter); compared to normal subjects: median, 2.2 nmol/liter (range, 1.5-2.8 nmol/liter) (P less than 0.001). The free T3 index was reduced accordingly. Serum TSH levels were significantly increased in cirrhosis: median, 2.1 microU/ml (range, 0.4-5.3 microU/ml); compared to normal subjects: median, 1.1 microU/ml (range, 0.3-3.8 microU/ml) (P less than 0.05). No significant differences were found in T3 resin uptake, free T4 index, or serum T4 levels between the two groups. No significant correlations could be demonstrated between thyroid gland volume and biochemical indices of liver function or thyroid function tests. It is suggested that alcohol might have a direct effect on the thyroid gland.
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PMID:Decreased thyroid gland volume in alcoholic cirrhosis of the liver. 670 93

Thyroid function was investigated in patients with liver cirrhosis. 123I uptake after four hours was significantly reduced in the liver cirrhosis group (n = 19) compared with the control group (n = 16) (2.6 +/- 0.3% vs. 5.0 +/- 0.6%, mean +/- SE, p < 0.01). There was no significant difference in the blood inorganic iodine level between the two groups, and the blood 123I count after ingestion of 123I capsules was not significantly different between the two groups. The area of the thyroid was slightly smaller in the cirrhosis group. A thyroid stimulating hormone (TSH) loading test showed no significant difference in the TSH value at any time point. The serum albumin level and prothrombin time were significantly associated with the 4-hour thyroidal 123I uptake (p < 0.01, p < 0.05, respectively). We show that the thyroidal inorganic iodine uptake was reduced in patients with liver cirrhosis and this reduction correlates with the severity of liver cirrhosis. Possible mechanisms include abnormal thyroid iodine transport capacity or reduced turnover of thyroid hormones resulting in a reduction in iodine uptake in liver cirrhosis.
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PMID:Reduced thyroidal uptake of inorganic iodine in liver cirrhosis. 898 67


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