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)

At this time, when the acquired immunodeficiency syndrome, hepatitis, and other blood-borne diseases threaten patients, with bleeding disorders, who need treatment with blood products, it is rewarding to realize that a number of them can be safely and effectively treated through the stimulation of their own VIII:C and vWF production with desmopressin. Desmopressin is clinically useful for treatment of patients with moderate and mild hemophilia. The limits of the clinical indications are the nature of the bleeding episode, the resting factor level, the level that must be achieved, and the length of time the level must be maintained to manage any given bleeding episode. Desmopressin can be used more extensively to raise VIII:C in von Willebrand's disease, than in classic hemophilia, because fewer of the patients have the severe form of the disease that is unresponsive to desmopressin. VIII:C increases to about four times the resting values that can be expected in both hemophilia and von Willebrand's disease, but it must be kept in mind that the range of individual responses is large. Even though it is not easy to correct the prolonged bleeding time, particularly in patients with dysfunctional vWF, this drawback is of clinical importance for only a minority of cases. Use of desmopressin in acquired diseases of primary hemostasis has been proposed more recently, and our experience is more limited than for congenital bleeding disorders. Uremia is probably the most firmly established indication, because the bleeding time is often dramatically shortened by desmopressin, and hemorrhages can be stopped or prevented. The indications for the compound in liver cirrhosis and congenital and acquired platelet dysfunctions are promising but much less well-established. The mechanism of action of desmopressin is not well-known, and more work must be done to fill this important gap. This problem is not only of theoretical importance, because understanding of the mechanism of action of the compound should open up new perspectives into understanding the physiological mechanisms that regulate hemostasis. Many unclarified aspects of the mechanism of desmopressin action might be elucidated by using specific antagonists and also by using appropriate animal models. (Dogs and primates respond partially to desmopressin, but rats and rabbits do not respond at all).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Vasopressin analogues. Their role in disorders of hemostasis. 312 21

The concentrations of total proteins, albumin, alpha 1-acid glycoprotein (AGP), and nonesterified fatty acids (NEFA) were measured in the serum of 21 newborn infants and 13 children, aged 1-13 months, and in the plasma of 31 volunteers, 25 patients with renal failure, 27 patients with cirrhosis, 39 uremic patients undergoing hemodialysis, and 20 elderly subjects. The concentration of albumin in the volunteers was higher than in all other groups. The concentration of AGP in the volunteers was higher than in newborn infants but lower than in elderly subjects, patients with renal failure, and those with chronic uremia. The concentration of NEFA in volunteers was higher than in newborn infants and patients with renal failure and lower than in elderly subjects and patients with cirrhosis.
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PMID:Effects of development, aging, and renal and hepatic insufficiency as well as hemodialysis on the plasma concentrations of albumin and alpha 1-acid glycoprotein: implications for binding of drugs. 375 Mar 66

Cytologic examination of 3H-thymidine-labeled mesothelial cells in the pleural fluid revealed that single and small-sized cells with slight basophilic cytoplasm scarcely stainable by PAS and colloidal iron are in the DNA-synthetic phase and that these are exfoliating cells from the pleural surface. While abnormal labeling in a few arranged and binuclear cells suggesting accelerated or disturbed mesothelial mobilization was frequently found in congestive cardiac failure, liver cirrhosis, and uremia, it never occurred in single and large-sized activated cells possessing rich PAS-positive granules, cells in large clusters or sheet-like arrangements, or multinuclear giant cells. Transmission electron microscopical observation of these labeled cells proved that a smooth cellular surface and scant intracytoplasmic organelles, by which undifferentiated cells are generally characterized, are essential for DNA-synthesizing mesothelial cells. Probably as a result of some pleural irritation, surface lining cells immediately enter the cell cycle and at once revert to an undifferentiated form capable of DNA synthesis, after which they may be released as a single form, and differentiate and transform into mature, activated cells with a bleb-like surface structure or microvilli, and finally may proliferate in the fluid.
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PMID:Cytological and ultrastructural characteristics of DNA synthesizing mesothelial cells in pleural effusion. 378 59

Protein binding of disopyramide, binding capacities, affinity constants and serum concentrations of alpha 1-acid glycoprotein (AAG) were studied in five groups of patients. A: young healthy volunteers (n = 8); B: elderly patients with minor symptoms of ischaemic heart disease (n = 9); C: patients with cirrhosis of the liver and normal values of coagulation factors (II, VII and X), albumin and immunoglobulin G (n = 8); D: patients with cirrhosis and at least two abnormal of the previously mentioned values (n = 9) and E: eleven patients with severely impaired renal function. Subfractions of AAG (Fr1, Fr2 and Fr3) were determined by affinoimmunoelectrophoresis. AAG concentration was significantly (P less than 0.005) elevated in group E patients and decreased (P less than 0.025) in group D patients. Fr2 is probably associated with the high affinity, first binding site of disopyramide to AAG. Earlier observations of a reduced qualitative binding of disopyramide in patients with cirrhosis can be explained by a significant decrease in Fr2 (P less than 0.001) in group D patients. The protein binding of disopyramide in patients with uraemia was significantly increased due to a significant (P less than 0.005) increase in AAG concentration in spite of a smaller (P less than 0.025) affinity constant. Suggestions for therapeutic drug monitoring based on total serum concentrations are given.
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PMID:Quantitative and qualitative binding characteristics of disopyramide in serum from patients with decreased renal and hepatic function. 381 61

Inter-alpha-trypsin inhibitor (I alpha I) and the immunologically related prealbumin-like-migrating proteinase inhibitor (pA-PI) were investigated by crossed immunoelectrophoresis in sera from 68 persons with myocardial infarction, neoplastic diseases, inflammatory diseases, collagenosis, cirrhosis of the liver or uremia. The concentration of pA-PI in serum increased during each of these diseases (p less than 0.01). The concentration of I alpha I was significantly decreased in patients with cirrhosis (p less than 0.01). In day to day studies of a patient with myocardial infarction, a patient with erysipelas and a postoperative patient the concentration of I alpha I was low normal to decreased in the first days of the conditions and increased thereafter to high normal values. A comparison of the concentration of pA-PI with the excretion of the immunologically identical urinary proteinase inhibitor (UPI) showed that the excretion could not be caused by simple overflow of pA-PI in the kidney. The excretion of UPI followed closely the acute-phase-response, as measured by serum C-reactive protein.
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PMID:Human inter-alpha-trypsin inhibitor and immunologically related inhibitors investigated by quantitative immunoelectrophoresis. II. Pathological conditions. 382 22

Desmopressin acetate 0.3 microgram/kg was given intravenously to nine patients with chronic liver disease and to a further six such patients in a double blind controlled study versus placebo. Desmopressin acetate significantly shortened the bleeding time compared with basal values in both groups and compared with placebo. There was also a significant decrease in partial thromboplastin time (but not prothrombin time) and significant increases in factor VIII and its components, von Willebrand factor and ristocetin cofactor activity, but not in factors VII, IX, X, XI, or XII. Increased fibrinolysis could be blocked by concomitant administration of tranexamic acid. No important side effects were seen. The multimer pattern of von Willebrand factor was studied for the first time in chronic liver disease. It was normal, but after administration of desmopressin acetate the percentage of multimers of higher molecular weight increased significantly. This may be an important mechanism in the shortening of the bleeding time in cirrhosis, as has been shown in uraemia and other conditions after administration of desmopressin acetate. Desmopressin acetate may be useful in correcting defects in primary haemostasis in chronic liver disease.
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PMID:Desmopressin and bleeding time in patients with cirrhosis. 393 77

Of 48 patients with fulminant hepatic failure who progressed to grade III or IV encephalopathy 38 showed evidence of renal impairment. In 32 of these patients the underlying cause could be placed initially into one of three categories-prerenal uraemia (4 patients), acute tubular necrosis (16), and "functional renal failure" (12). The latter differed in several respects from that seen with liver failure secondary to cirrhosis. The frequency and type of renal impairment was the same in those patients in whom the fulminant hepatic failure had resulted from an overdose of paracetamol as in the other aetiological groups.Abnormalities in plasma electrolytes were common-in particular hypernatraemia occurred in 11 patients from an osmotic diuresis precipitated by hypertonic dextrose or fructose given intravenously, and from the sodium in the fresh frozen plasma used to correct the coagulation disturbance when renal excretion of this ion was inappropriately low.
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PMID:Frequency and type of renal and electrolyte disorders in fulminant hepatic failure. 481 48

In defining host resistance factors in uremia, experiments were designed to assess the effect of renal failure serum upon the reactivity of normal human lymphocytes to phytohemagglutinin in vitro. Normal buffy coat cells were resuspended in sera obtained from normal subjects and from 14 patients with renal failure, then stimulated with phytohemagglutinin M and the cellular response measured by the increase in thymidine or uridine uptake. The mean thymidine uptake by stimulated cells in normal sera was 14,389 +/-1695 (SEM) cpm per 2 x 10(6) lymphocytes. Uridine uptake under the same conditions was 12,540 +/-1887 cpm. Compared to these are a mean thymidine uptake of 2740 +/-457 cpm and uridine uptake of 3928 +/-667 cpm in renal failure sera. Both differences are significant at P<0.01 level. For controls representing "chronic illnesses," sera from patients with pneumococcal meningitis, cirrhosis of the liver without jaundice, rheumatoid arthritis, and paraplegia with urinary tract infection did not cause suppression. No single drug had been taken by all the renal failure patients; three patients were taking no drugs. The serum from one patient with acute renal failure suppressed thymidine uptake while her serum obtained after recovery from her illness supported a normal lymphocyte response. Improvement of lymphocyte response was also noted in 9 of 10 sera obtained from patients immediately after hemodialysis. These observations plus the inhibition of stimulated cells by normal serum mixed with renal failure serum indicate the presence of a dialyzable inhibitory factor rather than the absence of a supporting factor in the renal failure sera. Lymphocytes preincubated for 24 hr in renal failure serum responded normally when transferred to normal serum and stimulated. Cells stimulated in normal serum and transferred to renal failure serum within the initial 24 hr of incubation demonstrated depressed thymidine uptake. Also, cell survival for 72 hr incubation as judged by trypan blue exclusion and chromium-51 release was similar in normal and renal failure sera. Thus, the suppressive effect of renal failure serum does not depend upon the initial phytohemagglutinin-cell interaction nor upon a significant cytotoxic effect. These studies demonstrate that a dialyzable factor(s) in the serum of patients with renal failure can greatly suppress one parameter by which an immune function of circulating lymphocytes is assessed and provides at least, a partial explanation for delayed homograft rejections in renal failure as well as the susceptibility of such patients to various infections.
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PMID:Defective cellular immunity in renal failure: depression of reactivity of lymphocytes to phytohemagglutinin by renal failure serum. 557 33

During a period of two years pericarditis was observed in five patients with decompensated cirrhosis who had only slightly raised blood-urea-nitrogen and serum-creatinine. Although this association has not been previously described, some patients with hepatic failure seem to have pericarditis in the absence of severe uraemia.
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PMID:Fibrinous pericarditis in hepatorenal failure. 610 54

In order to assess the thyroid function of patients with nonthyroidal illness, 292 patients with nonthyroidal illness were employed in the present study. These patients were then subdivided into 6 groups according to their original illness. The groups consisted of patients with malignant illnesses (19 males and 10 females; mean age of 59.7 yr.), with chronic hepatitis (14 males and 8 females; mean age of 55.2 yr.), with liver cirrhosis (5 males and 6 females, mean age of 60.4 yr.), with uremia who had been receiving constant hemodialysis 2 approximately 3 times per week (52 males and 38 females; mean age of 48.1 yr.), with diabetes mellitus (50 males and 43 females; mean age of 52.3 yr.) and with cerebrovascular accident (21 males and 26 females; mean age of 74.9 yr.). In addition, 34 healthy persons (15 males and 19 females; mean age of 41.6 yr.) were also employed as controls. Because the differences between mean ages in these groups were significant, the relationship between age and thyroid function was examined. Significant positive correlations between age and total thyroxine (TT4) (r = 0.19; p less than 0.01), and reverse triiodothyronine (rT3) (r = 0.175; p less than 0.01) were found. A negative correlation was also found between age and total triiodothyronine (TT3) (r = 0.231; p less than 0.01). The serum levels of rT3 were elevated in patients with neoplasma and liver cirrhosis but significantly low in patients with uremia. These characteristic findings were correlated with the severity of each original disease such as % motarity, serum levels of cholinesterase, blood urea nitrogens and the blood sugar control in the diabetics. In these circumstances, multiple correlation analyses were performed in order to assess whether there might exist a negative feedback mechanism between thyrotropin and FT4/FT3. The highest partial correlation coefficient was obtained between thyrotropin and FT4. It might, therefore, be concluded that in patients with a nonthyroidal illness, decreased levels of serum thyroid hormones indicate not only the severity of the illness but also the supposed presence of a hypothyroid state.
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PMID:[Thyroid functions in nonthyroidal illness: specific changes in serum levels of thyroid hormones related in illness and the correlation between thyrotropin and free thyroid hormones in patients with nonthyroidal illnesses]. 647 79


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