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)

This study deals with 29 patients with cirrhosis, caused by alcohol in 23 cases, at a stage of edematoascitic decompensation. Calcemia was low 88 +/- 7 mg/l) as well as calciuria 87 +/- 92 mg/24 h). Phosphoremia and hydroxyprolinuria were within normal limits. A moderate diminution of 25 OH D3 (29,5 +/- 18 ng/ml) was observed in most patients but one third of them had no or very low levels of parathormone and 10 out of 27 had an elevated level of calcitonin. Bone histomorphometry which was done in 24 cases showed a discrete osteoporosis, a relative hyperosteoidosis and a hyperosteoclasis. There was a very significant relationship between hypocalcemia, and hypoalbuminemia but the other abnormalities could not be correlated significantly with either the duration or the severity of the disease. Hypocalcemia and bone histomorphometric abnormalities of cirrhosis can certainly not be explained only by a lack of liver hydroxylation of vitamin D.
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PMID:[Vitamin D, parathormone, calcitonin and bone histomorphometry in patients with cirrhosis]. 75 54

In advanced cirrhosis and hepatorenal syndrome, peripheral vasodilation is a prominent feature and may be pathophysiologically relevant. To determine whether the potent vasodilator, calcitonin gene-related peptide (CGRP), circulates at abnormal levels in patients with these disorders, we observed eight patients with alcoholic cirrhosis and hepatorenal syndrome, seven with alcoholic cirrhosis and ascites without hepatorenal syndrome, and 10 healthy controls. Plasma CGRP levels were higher in patients with alcoholic cirrhosis and hepatorenal syndrome (364 +/- 166 pg/ml) than in healthy controls (143 +/- 54 pg/ml, p less than 0.01). In patients with cirrhosis and ascites without hepatorenal syndrome, plasma CGRP levels were less elevated (291 +/- 257 pg/ml, NS). The identity of immunoreactive CGRP and synthetic hCGRP was confirmed by high performance liquid chromatography. These results suggest that CGRP may play a role in hepatorenal syndrome. However, to establish whether circulating CGRP contributes to the hemodynamic change in hepatorenal syndrome requires study of a larger number of patients and additional control groups.
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PMID:Calcitonin gene-related peptide in hepatorenal syndrome. A possible mediator of peripheral vasodilation? 153 10

The etiology of the hyperkinetic circulatory state in cirrhosis is equivocal and reduced peripheral vascular resistance is a major unsolved problem in hepatic pathophysiology. It is therefore sensible to search for vasodilators. A recently discovered neuropeptide, calcitonin gene-related peptide (CGRP), is a highly potent vasodilator. We determined the circulating concentration of immunoreactive CGRP in different vascular beds in 35 patients with cirrhosis and in eight patients with minor disorders. Plasma CGRP was significantly increased in the cirrhotic patients compared with patients with minor disorders (59 vs. 46 pmol/l, p less than 0.01), as well as with 232 healthy persons (37 pmol/l, p less than 0.0001). Moreover, circulating CGRP increased significantly with the severity of cirrhosis (Child-Turcotte group A, 56; group B, 59; group C, 71 pmol/l; p less than 0.025). No significant arterio-venous net extraction or release of CGRP was found across the hepato-intestinal system, kidney, lung or limb. In conclusion, elevated circulating CGRP may play a role in the haemodynamic derangement of cirrhosis. The lack of organ arterio-venous differences suggests a widespread release and degradation of CGRP in many tissues and gives no evidence of decreased degradation as the cause of increased plasma CGRP in patients with cirrhosis.
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PMID:Increased circulating calcitonin gene-related peptide (CGRP) in cirrhosis. 200 68

Increased levels of plasmatic calcitonin (PC) have been found in patients afflicted with liver cirrhosis (LC). Different circulating polypeptides of calcitonin with contrasting molecular weight (MW) have been observed by way of several methods of identification. The aim of our study is identify these types of PC in patients afflicted with LC, using a gel chromatography technique, comparing them with those obtained from patients with thyroid medullar carcinoma (TMC). A first PC peak with MW of 30,000 daltons (D) corresponding to macromolecular types of PC of LC was observed. Furthermore, a second peak of PC, corresponding to a synthetic human calcitonin and to monomers of PC in patients with TMC was noted. This indicates is a slight increase of monomeric PC in patients with LC, although its biological function is unknown.
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PMID:[The identification of plasma calcitonin in liver cirrhosis]. 210 8

A group of ten patients suffering cirrhosis who were treated with 100 U/l of calcitonin was studied with the aim of knowing whether in patients with cirrhosis the calcitonin is able to provoke the usual characteristic biologic modifications on the basis of the knowledge of their hormonal high levels accompanied of oesteopenia. Regarding their baseline determinations, no statistically significant modifications have been observed in calcium, phosphorous, alkaline phosphatase or its thermostable and thermolabile fractions, magnesium, uric acid and creatinine plasma concentrations respectively. This absence of a biological response to calcitonin could be due either to a numeric or functional damage of the hormone receptors or a diminished biodisponibility, although there are facts suggesting a lesser hormone biopotenciality in these patients.
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PMID:[Results of the functional tests using calcitonin in patients with chronic diffuse hepatopathy]. 239 81

Elevated serum calcitonin (SC) levels have been observed in cirrhotic patients although the biological activity of this hormone in such patients is not known. Twenty one patients diagnosed histologically of alcoholic hepatic cirrhosis (AC) and 12 healthy controls were studied evaluating the degree of hepatocellular failure by means of clinical and biological criteria. Serum calcitonin was determined by means of a radioimmuno assay (RIA) and a radioimmunometric assay (IRMA) in which by combining two monoclonal antibodies, mature calcitonin is determined. These levels almost correspond to levels of biologically active calcitonin. The results obtained show a significant increase in SC in patients with AC when compared to controls, both by RIA (280 +/- 197 pg/ml, p less than 0.001) and IRMA (18 +/- 6 pg/ml, p less than 0.01). Control values were 57 +/- 23 pg/ml and 12 +/- 7 pg/ml respectively. Mean SC values in cirrhotic patients obtained by RIA were 4.9 times greater than their controls while the increase in SC in cirrhotics determined by IRMA was 1.5 times the control, thus obtaining a significant direct correlation between SC and severity of hepatic failure. According to our results, the elevated SC found in cirrhotics is mainly due to immature or non active forms directly related with the degree of severity of the hepatic failure and probably to high Molecular Weight molecules. The slight increase in mature SC in this type of patients is probably due to hormonal mechanism of bone regulation, defendants of hepatic osteodystrophy.
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PMID:[Heterogeneity of calcitonin in liver cirrhosis]. 260 81

Immunoreactive serum levels of human chorionic gonadotrophin (HCG), its alpha- and beta- subunits (alpha-HCG and beta-HCG), calcitonin (CT), parathyroid hormone (PTH), prolactin (PRL), adrenocorticotropic hormone (ACTH), and growth hormone (GH) were increased in 8 to 68% of 44 patients with hepatocellular carcinoma. With the exception of two patients, ACTH and PRL levels were only moderately increased, while alpha-HCG, GH, ACTH and PRL levels were not significantly different from the levels found in cirrhosis suggesting that metabolic effects due to impaired liver function may be responsible for their increase in liver cirrhosis and primary liver cell carcinoma. In contrast, HCG, beta-HCG, CT and PTH were associated with a higher incidence of elevated immunoreactive hormone levels than the other peptide hormones; higher concentrations were noted in tumor patients than with liver cirrhosis alone. Therefore, we suggest that metabolic effects due to cirrhosis may influence the serum levels and be more important than ectopic secretion by hepatocellular carcinoma.
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PMID:Peptide hormones in liver cirrhosis and hepatocellular carcinoma. 627 36

Plasma immunoreactive calcitonin (iCT) is elevated in primary liver cancer and its measurement has been proposed as a tumour marker. Since iCT is also frequently raised in alcoholic liver cirrhosis, it would be of practical relevance to distinguish this condition from primary hepatoma by measuring the plasma level of iCT. We measured plasma iCT levels in 23 subjects with primary liver cancer, in 27 with hepatic cirrhosis and in 42 healthy subjects who served as normal controls. A gel-chromatography analysis was carried out on the plasma of two cases of hepatoma, two of cancer and cirrhosis, and two of alcoholic liver cirrhosis. The subjects with primary liver cancer had values of plasma iCT (pg/ml; mean +/- SE) of 342 +/- 41; those with liver cirrhosis 159 +/- 22, and normal controls 73 +/- 3. The increase in primary liver cancer was significant in comparison both healthy subjects (P less than 0.001) and with cirrhotic patients (P less than 0.001). Twenty-two out of 23 patients with primary liver cancer and 13 out of 27 with liver cirrhosis had elevated iCT values (upper normal limit 113 pg/ml). There was no significant difference between plasma iCT values of patients with cancer and those with cirrhosis. However, we measured iCT values higher than 400 pg/ml only in patients with primary liver cancer. The gel-filtration analysis showed 3 or 4 peaks of iCT with a molecular weight higher than synthetic human calcitonin. The results suggest that plasma iCT levels can be considered a reliable marker of liver cancer, whereas its discriminating power between liver cancer and cirrhosis was not entirely satisfactory.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcitonin in hepatoma and cirrhosis. 632 18

Liver cirrhosis impairs gastric mucosal resistance to luminal acid in humans and in animal models. Because we have previously shown that pentagastrin enhances defensive as well as aggressive factors implicated in mucosal injury, we examined the hypothesis that the pentagastrin-mediated enhancement of mucosal defense mechanisms may be impaired in cirrhotic rats. Increased acid backdiffusion and susceptibility to gross mucosal injury, associated with an elimination of the hyperemic response to gastric barrier disruption, was observed in cirrhotic rats. In in vivo microscopic studies in anesthetized rats, cirrhosis had no effect on pentagastrin-associated enhancement of mucus gel thickness or baseline gastric mucosal blood flow, although baseline mucus gel thickness was decreased. Cirrhosis did, however, abolish the luminal acid-related hyperemic response to pentagastrin, which was associated with impaired intracellular pH homeostasis during acid superfusion. Cirrhosis did not alter submucosal calcitonin gene-related peptide immunoreactive nerves. We conclude that acid backdiffusion and pentagastrin-associated hyperemic responses are important mucosal defensive factors that are specifically impaired by cirrhosis.
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PMID:Impairment of the gastric hyperemic response to luminal acid in cirrhotic rats. 877 3

According to cirrhotic patient's hyperkinetic circulatory state and to different pathophysiologic moments of kidney and liver failure, it is suggested that in cirrhosis a vasoactive balance is changed to more active vasodilatation. Also calcitonin gene-related peptide (CGRP) is likely involved in this change.
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PMID:[Vasodilation in cirrhosis: is CGRP (calcitonin gene-related peptide) also among the possible mediators?]. 926 3


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