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)

The enzyme gamma-glutamyl transpeptidase is widely distributed throughout the body, notably kidney, seminal vesicles, pancreas, liver, spleen and brain. Being one of the enzymes of the gamma-glutamyl cycle, it is involved in aminoacid transport, catalysing a transpeptidation reaction between gamma-glutamyl peptides and most common amino acids. Methods of assay of the enzyme are based on its ability also to act on synthetic amides of glutamic acid; kinetic methods monitoring the release of p-nitroaniline from the substrate L-gamma-glutamyl p-nitroanilide are the most satisfactory. In diseases of the liver, the highest levels occur in association with cirrhosis, alcoholism, hepatic secondaries and cholestasis. As the enzyme is present in the endoplasmic reticulum of the hepatocyte, its activity is increased in situations leading to microsomal enzyme induction. Raised levels can also occur in pancreatitis, diabetes, myocardial infarction, congestive cardiac failure, chronic renal failure, cerebrovascular accidents, cerebral tumours and chronic obstructive pulmonary disease. Although the lack of specificity must be recognised, the estimation can be useful in the elucidation of some clearly defined problems arising during investigation of patients with suspected hepatic disease, especially where performed as part of a biochemical profile.
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PMID:Role of gamma-glutamyl transpeptidase activity in the diagnosis of hepatobiliary disease. 24 76

Our patient, with cirrhosis and chronic renal failure, represents an example of the susceptibility of a compromised host to Aeromonas infections. This patient, however, differs from previously reported cases in at least two important aspects. First, it is possible that her portal of entry was a fresh A-V fistula puncture site rather than an intestinal site. The temporal relationship of exposure to flood water prior to the onset of sepsis lends support to this possibility. Epidemiologic investigation of the dialysis center failed to reveal Aeromonas isolates from cultures of the water supply, machinery, or other patients. Second, this case is unique in that our patient developed a destructive aortic valve endocarditis resulting in valvular perforations and acute aortic insufficiency. Furthermore, this infection was initiated on what appears to have been a previously normal valve. Based on a review of the literature and the virulence demonstrated by A. hydrophila in our patient, we conclude that organisms of the genus Aeromonas are capable of inducing serious human infection. Such infections are more likely to occur in compromised hosts. A. hydrophila has accounted for the majority of reported infections.
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PMID:Human aeromonas infections: a review of the literature and a case report of endocarditis. 34 23

A 38-year-old man suffering from chronic recurrent hepatic enchephalopathy due to liver cirrhosis complicated with chronic renal failure had been maintained well by regular hemodialysis treatment for 14 months. Only four episodes of hepatic encephalopathy occurred in that period. Each of four episodes of disturbed consciousness was accompanied by slightly elevated blood ammonia levels. Energetic serial dialysis for 5-7 days was necessary for its recovery. The factors causing hepatic encephalopathy did not appear to be easily dialysable as compared with those of uremic coma. It is concluded that the hemodialysis is quite an effective treatment for the recurrent type of hepatic encephalopathy.
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PMID:A patient with recurrent hepatic encephalopathy and chronic renal failure treated successfully with long-term hemodialysis. 60 71

Pathologically low serum total triiodothyronine (T3) concentrations are a characteristic finding in patients with severe non-thyroidal illnesses. No adequate explanation has yet been offered for this phenomenon. We have, therefore, investigated the serum concentrations of total thyroxine (T4), total T3 and total 3,3',5'-triiodothyronine (reverse T3)--the metabolically-inactive metabolite of thyroxine--and of TSH in 13 patients with acute myocardial infarction, in 12 patients with compensated liver cirrhosis, in 9 patients with decompensated liver cirrhosis and in 15 patients with chronic renal failure on chronic intermittent haemodialysis by radioimmunoassay. The values obtained were compared to corresponding values of a normal control group (n - 23). According to our results the decrease in serum T3 combined with normal T4 concentrations in severe non-thyroidal illnesses seems to be a consequence of an alteration in thyroxine degradation. Two different possibilities of alteration can be considered: 1. inhibition of the overall deiodinationof T4, leading to low total T3 serum concentrations with concomitant normal to low reverse T3 serum concentrations (chronic uraemia), 2. a shift in the monodeiodination of T4 towards enhanced reverse T3 production, leading also to low total T3 concentrations, but with a concomitant increase in reverse T3 serum concentrations (myocardial infarction, liver cirrhosis). The results obtained in our patients with liver cirrhosis show, moreover, that this alteration of T4 metabolism depends on the severity of the illness.
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PMID:[Serum concentrations of thyroid hormones in severe non-thyroidal illnesses (author's transl)]. 63 38

Human plasma prekallikrein (Fletcher factor) clotting activity and antigen levels have been examined in various clinical conditions. Prekallikrein antigen was measured by a newly developed, specific, and sensitive radioimmunoassay. The assay had no demonstrable cross-reactivity with human urinary kallikrein nor, in the species tested, animal plasma prekallikrein. This assay was able to measure plasma kallikrein after its biological functions had been inactivated by plasma inhibitors. Normal human pooled plasma contained approximately 50 microgram/ml prekallikrein. Quantitative measurement of plasma prekallikrein was possible for concentrations as low as 0.3% of that of normal pooled plasma. A good correlation (correlation coefficient = 0.71) existed between titers of plasma prekallikrein measured by Fletcher factor clotting assays and radioimmunoassays among 40 normal subjects. Both prekallikrein clotting activity and antigen were significantly reduced in plasmas of patients with advanced hepatic cirrhosis or DIC. Prekallikrein activity and antigen were mildly decreased in plasmas or serums of patients with chronic renal failure and nephrotic syndrome but were normal in those of patients under treatment with warfarin or suffering from SLE, rheumatoid arthritis, sarcoidosis, or HANE. Human cord serum contained a lower titer of prekallikrein antigen than adult serum. Strenuous physical exercise did not significantly change plasma prekallikrein levels.
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PMID:Human plasma prekallikrein (Fletcher factor) clotting activity and antigen in health and disease. 65 66

The consequences of chronic renal insufficiency relevant to hepatic failure are not well appreciated. We describe a patient with chronic cirrhosis and marked porto-systemic shunting who, after the onset of chronic renal failure, developed intractable encephalopathy which improved markedly during an eight month period of maintenance hemodialysis.
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PMID:Exacerbation of hepatic encephalopathy by chronic renal failure: response to maintenance hemodialysis. 66 27

Evidence of chronic hepatitis was found on histological examination in nine out of 15 patients positive for hepatitis-B surface antigen (HBsAg) who had either chronic renal failure or a functioning renal transplant. Cirrhosis had already developed in three of the patients, who deteriorated rapidly and died. Liver biopsies from the remaining 12 patients showed the features of chronic aggressive hepatitis in two, chronic persistent hepatitis in four, and minor histological lesions in six. The persistence of HBsAg in patients with renal failure or in those receiving immunosuppressive drugs after a transplant must indicate some impairment of the normal immune response to hepatitis-B viral antigens. Nevertheless, cellular or humoral immunity to HBsAg was detected in all eight patients with chronic hepatitis tested compared with only one out of five with minimal liver lesions, which suggests that the severity of the liver damage may be directly related to the degree of immunocompetence.
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PMID:Immune response to HBsAg and the spectrum of liver lesions in HBsAg-positive patients with chronic renal disease. 77 35

Literature on the role of estrogens in men is reviewed. The primary active estrogens in males and females are estradiol-17beta (E2), estrone (E1), and estriol (E3). The active constituents of serum E2 and testosterone (T) are those which are not bound by testosterone-estrogen binding globulin (TEBG). The concentration of TEBG is stimulated by estrogen and suppressed by androgens. Both E1 and E2 appear to be derived from the peripheral metabolism of T and androstenedione. The metabolism and physiological roles of estrogens in men are briefly discussed. The association of gynecomastia with puberty, cirrhosis of the liver, hyperthyroidism, chronic renal failure, refeeding gynecomastia, administration of digitalis and diuretics, neoplasms, and hypergonadotropic hypogonadism is reviewed. In older men, the ratio of free E2:T is increased. The relationship of andorgens, estrogens, and male sex behavior is briefly reviewed. Areas for future research include the mechanisms by which estrogens and androgens exert antagonistic effects on similar tissues, variations in the fractional conversionr ate of androgens to estrogens, the etiology of pubertal gynecomastia, the role of the free E2:T ratio in male social and sexual behavior, and the interrelation between behavior, nutrition, hormone secretion, and degenerative changes such as benign prostatic hyperplasia.
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PMID:Estrogens and the human male. 77 4

Serum concentrations of 3,3',5'-triiodothyronine (reverse T3, rT3) were measured in adult patients with several systemic illnesses whose serum total and/or free T3 were low, serum total T4 was low or normal, and free T4 was either normal or elevated. The mean serum rT3 was 76, 46, and 77 ng per 100 ml in patients with hepatic cirrhosis, chronic renal failure, and acute febrile illnesses, respectively; the values in patients with hepatic cirrhosis and acute febrile illness were significantly higher than, and values in patients with renal failure did not differ significantly from, the mean serum rT3 (41 ng per 100 ml) in normal subjects. The mean serum rT3 in another group of patients from Calcutta, India, who had severe protein calorie malnutrition (PCM), was 53 ng per 100 ml; it was significantly higher than the corresponding value, 22 ng per 100 ml, in the same patients after feeding treatment. Mean serum rT3 in patients with systemic illnesses was not so high as that (151 ng per 100 ml) in the normal newborn, who also has low serum T3 and normal or high T4. High serum rT3 in patients with systemic illness could not be attributed to increased serum protein binding of rT3; whenever studied, the dialyzable fraction of rT3 was not decreased but actually increased. The mean serum-free rT3 was 450,207, and 366 pg per 100 per 100 ml in patients with hepatic cirrhosis, chronic renal failure, and acute febrile illnesses, respectively; each of these values was significantly higher than the corresponding value, 98 pg per 100 ml, in normal subjects. The mean serum free rT3, 516 pg per 100 ml, in newborn cord sera was similar to that in patients with hepatic cirrhosis but was higher than that observed in patients with chronic renal failure and acute febrile illnesses. High serum rT3 and low serum T3 in patients with PCM improved to normal or towards normal after feeding treatment. Since the peripheral metabolism of T4 is normally the predominant source of T3 as well as rT3 in man, our data, demonstrating reciprocal changes in serum rT3 and T3 and no consistent change in serum T4, suggest that body metabolism of T4 may be so altered in systemic illness that the conversion of T4 to rT3 may be increased while that to T3 is decreased. The mechanism or the biological significance of such a diversion of T4, from the normally occurring conversion to highly potent T3, to the generation of poorly calorigenic rT3 in systemic illness, is not clear at this time. The data in patients with PCM demonstrate, however, that such a change in the metabolism of T4 can be reversible.
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PMID:Reciprocal changes in serum concentrations of 3,3',5-triiodothyronine (T3) in systemic illnesses. 81 82

A secific, sensitive, and reproducible radioimmunoassay for human Hageman factor (HF, factory XII) has been developed with purified human HF and monospecific rabbit antibody. Precise measurements of HF antigen were possible for concentrations as low as 0.1% of that in normal pooled plasma. A good correlation (correlation co-efficient = 0.82) existed between the titers of HF measured by clot-promoting assays and radioimmunoassays among 42 normal adults. Confirming earlier studies, HF antigen was absent in Hageman trait plasma, but other congenital deficient plasmas, including those of individuals with Fletcher trait and Fitzgerald trait, contained normal amounts of HF antigen. HF antigen was reduced in the plasmas of patients with disseminated intravascular coagulation or advanced liver cirrhosis, but it was normal in those of patients with chronic renal failure or patients under treatment with warfarin. HF antigen was detected by this assay in plasmas of primates, but not detectable in plasmas of 11 nonprimate mammalian and one avian species.
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PMID:Radioimmunoassay of human Hageman factor (factor XII). 95 1


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