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)

Three cortisol fractions, protein-unbound (U-F), transcortin-bound (Tr-F) and albumin-bound cortisol (Al-F) were measured in patients with dysproteinemia by a newly devised isocolloidosmolar equilibrium dialysis method. Total cortisol (Total-F) concentrations in patients with liver cirrhosis (LC), anorexia nervosa (AN) and cachexia due to cancer (CA) were higher than in normal subjects, and those in patients with nephrotic syndrome (NS) and multiple myeloma (MM) remained within the normal range. In all groups of patients, the U-F concentration, which is believed to be the sole active fraction of cortisol, showed significantly higher values than in the normal subjects. We, therefore attempted to find which of the two binding proteins contributes to the elevated U-F concentrations. Concentrations of each cortisol fraction are greatly changed by alterations in the Total-F concentration. We therefore compared the Tr-F against Total-F and Al-F, and U-F against Total-E of patients with those of normal subjects. It was found that decreased transcortin-binding and not albumin-binding in the patients with cirrhosis, nephrotic syndrome and myeloma contributed to an increase in the U-F concentration. Although decreased binding of albumin due to hypoalbuminemia was found in LC, NS, MM, CA and AN, it had relatively little effect on cortisol distribution in the serum.
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PMID:The serum concentrations of unbound, transcortin bound and albumin bound cortisol in patients with dysproteinemia. 718 82

A possible role of HBsAg in hepatic glomerulonephritis was evaluated in kidney specimens from 104 patients with various diseases. Huang's method using formalin-fixed and paraffin-embedded sections was applied to the kidney from 65 cases. Only 4 (3.8%) with liver cirrhosis had glomerular HBsAg deposition; 3 on frozen and one on paraffin sections. In one case of crescentic glomerulonephritis, HBsAg appeared to have had a pathogenetic role with glomerular immunofluorescence dominant for IgM, less intense IgG and negative IgA. The glomerular HBsAg in the remaining 3 patients with hepatic IgA glomerulonephritis was likely to be concomitant or superimposed. One of them had a nephrotic syndrome for which corticosteroid treatment was given, resulting in a near-complete remission and disappearance of HBsAg in the glomeruli, but the glomerular immunohistology was unaffected by the treatment. The present findings suggest that HBsAg has only a minor role.
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PMID:Hepatic glomerulonephritis. Role of hepatitis B surface antigen (HBsAg). 728 2

High-risk patients who should receive the pneumococcal vaccine include asplenic patients, those with sickle cell anemia, nephrotic syndrome, congestive heart failure, pulmonary or renal disease, insulin-dependent diabetics, alcoholics with cirrhosis and immunocompromised patients. The vaccine should not be used in children under two years of age. It is safe, relatively inexpensive and effective when antibody response can be generated.
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PMID:Use of the pneumococcal vaccine. 729 14

We tested serum samples from four categories of patients with nephrological problems (nephrotic syndrome, stable chronic renal failure, haemodialysis patients and renal transplant recipients), patients with chronic liver disease and volunteer blood donors for the presence of antibody to hepatitis C virus (HCV). Screening was done by second-generation enzyme linked immunosorbent assay (ELISA) and confirmation with second-generation recombinant immunoblot assay (RIBA). Of all the renal patients, only 6.3% of the transplant patients tested positive for anti-HCV, while in patients with chronic liver disease anti-HCV was detected in 2.6% of the patients with chronic hepatitis and in none with liver cirrhosis or hepatocellular carcinoma. This finding of low prevalence in these patient groups was not in keeping with findings in studies done elsewhere. Our anti-HCV prevalence of 0.9% in blood donors was comparable to that found in Europe, USA and Taiwan. We recommend that the low prevalence of anti-HCV in some of our high risk groups should not lead to complacence and hence further studies are necessary to evaluate the infectivity of anti-HCV positive patients and the potential for cross infection.
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PMID:The prevalence of hepatitis C virus antibodies in renal patients, blood donors and patients with chronic liver disease in Kenya. 749 4

Interferon-alpha therapy has a beneficial effect in 30-40% of selected patients with chronic hepatitis B who respond by clearing hepatitis B e antigen (HBeAg) and hepatitis B viral (HBV) DNA from serum. This is usually associated with normalization of serum aminotransferase activities. On long-term follow-up of treated patients, it is apparent that many go on to clear hepatitis B surface antigen (HBsAg) from serum with considerable improvement in liver histopathology. Among patients with clinically apparent chronic HBV infection such as those with decompensated cirrhosis or the nephrotic syndrome, a serologic response is usually followed by slow but steady clinical and biochemical improvement. However, even among patients who have cleared HBsAg from serum, HBV-DNA remains detectable within the liver and may provide a source of reactivation in rare patients in association with immunosuppression.
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PMID:Long-term outcome of interferon-alpha therapy for chronic hepatitis B. 760 80

We report a case of nephrotic syndrome which mimicked membranoproliferative glomerulonephritis (MPGN) and was associated with hemophagocytic syndrome after renal death. A 41-year-old Japanese man was referred to our hospital because of nephrotic syndrome in February 1979. He had no signs, symptoms nor laboratory data suggestive of liver damage. He was diagnosed as idiopathic MPGN and administered prednisolone and cyclophosphamide (total dose of about 50,000mg). He developed end-stage renal disease, and dialysis therapy was initiated in February 1992. Simultaneously, he was diagnosed as hepatitis C virus (HCV)-positive liver cirrhosis. In August 1994, he died because of reactive homophagocytic syndrome, which occurred in the setting of immunosuppression due to chronic renal failure, liver cirrhosis, and sesecondary diabetes. In this case, we can not deny the possibility that radical therapeutic intervention against "idiopathic MPGN" had a negative effect on the clinical course of chronic HCV infection.
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PMID:[A case of nephrotic syndrome mimicking membranoproliferative glomerulonephritis (MPGN) and associated with reactive hemophagocytic syndrome after renal death]. 760 13

The pharmacokinetics of furosemide (frusemide) in patients with oedema have been relatively well studied, but in many studies it is unclear whether the disease or the oedema per se has the major effect. The rate of absorption of oral furosemide in patients with oedema was decreased, but total bioavailability was almost unchanged. The peak serum concentration (Cmax) and time taken to achieve Cmax were either decreased or unchanged. Binding of furosemide to plasma proteins is lower in patients with congestive heart failure (CHF), decompensated liver cirrhosis (DLC) and nephrotic syndrome, probably as a result of hypoalbuminaemia. The elimination half-life (t1/2) can be unchanged (CHF, DLC) or prolonged (chronic renal failure: CRF). Plasma and renal clearance are reduced in patients with CRF and nephrotic syndrome, but are almost unchanged in CHF and DLC. Disease-induced disorders are mainly responsible for the alterations of furosemide pharmacokinetics in oedematous conditions, while the influence of oedema per se is probably not clinically relevant. The pharmacokinetics of digoxin have been studied in a small number of studies only. In patients with CHF, considerable interindividual differences have been found. Because digoxin has a narrow therapeutic window, this drug should be administered cautiously to oedematous patients. Theophylline has higher bioavailability in patients with oedema, with a significantly higher Cmax in patients with hepatic cirrhosis and CHF than in healthy volunteers (29 and 22%, respectively). Furthermore, clearance decreases and t1/2 increases in these patients. Angiotensin converting enzyme (ACE) inhibitors are often administered as prodrugs, and their pharmacokinetic profile could be influenced by the diseases that accompany oedematous states. However, the effect of oedema is difficult to discriminate from that of the disease. Individual ACE inhibitors are affected differently, but importantly the dosage of perindopril should be reduced in patients with CHF, while for most other ACE inhibitors the changes in pharmacokinetic parameters are clinically irrelevant. In conclusion, studies on pharmacokinetic changes in oedema are limited. Besides affecting absorption (after oral administration) and conversion of the prodrug to the active form, probably as a result of the associated disease, oedema has not been proven to cause any clinically relevant changes in pharmacokinetic parameters for individual drugs. However, further studies of this aspect of pharmacokinetics are needed.
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PMID:Pharmacokinetic changes in patients with oedema. 761 78

The physiology of the release of antidiuretic hormone (ADH) from the posterior pituitary is briefly reviewed. The importance of both osmolar and non-osmolar stimuli is emphasised. Osmolar and non-osmolar factors usually reinforce each other; for example, hydropenia leads to hyperosmolality and hypovolaemia, both promoting ADH release, while hydration has the opposite effect. In disease, osmolar and non-osmolar factors may become dissociated leading to baroreceptor-mediated ADH release in the presence of hyponatraemia and hypo-osmolality. Examples include heart failure, glucocorticoid or thyroxine deficiency, hepatic cirrhosis and nephrotic syndrome with or without the superimposed effect of diuretics, i.e. conditions in which circulatory, and in particular effective arterial, volume is reduced. It is dangerous to label such conditions as 'inappropriate' secretion of ADH since the maintenance of circulating volume is at least as important a physiological requirement as the defence of tonicity. The syndrome of inappropriate secretion of ADH (SIADH) is uncommon in childhood and should only be diagnosed when physiological release of ADH in response to non-osmolar as well as osmolar factors has been excluded. Criteria for the correct identification of SIADH are discussed; the presence of continuing urinary sodium excretion in the presence of hyponatraemia and hypo-osmolality is essential to the diagnosis. SIADH in children is usually due to intracranial disease or injury. The mainstay of treatment is water restriction which reverses all the physiological abnormalities of the condition. Hypertonic saline is rarely indicated for the short-term control of neurological manifestations such as seizures. Drugs have little or no place in the treatment of SIADH in children.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The syndrome of inappropriate secretion of antidiuretic hormone. 861 39

In this work we analyze the renal and systemic factors involved in the sodium retention in two conditions: in extracellular volume depletion and in edema forming states, particularly liver cirrhosis with ascitis. In this paper we accept that the volume loss of body fluids stimulates the "effective arterial blood volume" (VAE). This term results from a decrease in the arterial blood volume secondary to a fall in cardiac output or a peripheral arterial vasodilatation. The reduction in the VAE stimulates: the high pressure baroreceptors (carotid sinus and aortic arch); the intrarrenal mechanisms, such as the yuxtaglomerular apparatus and the renin angiotensin aldosterone system; the sympathetic adrenergic system; the non osmotic release of antidiuretic hormone; prostaglandins (PGE1, Tromboxane) and endothelin; and inhibits the atrial natriuretic peptide. We also describe the sodium transport mechanisms along the nephron during physiological conditions and after volume depletion, and in edema formation states, specially hepatic cirrhosis with ascitis. We speculate that the intrarenal mechanisms are more important and persistent than the systemic mechanisms. It is possible that the sodium retention of these states might be the result of direct stimuli of the tubular sodium transport mechanisms in the different segments of the nephron, mediated by the co and counter transports, ATPase activity or by the second messengers cyclic AMP and cyclic GMP. The clonation and structural characterization of the different sodium transports may help us to establish, more precisely, the intracellular tubular mechanisms responsible for the tendency of the body to retain sodium. The amount of information generated in the future may help us to demonstrate, with more precision, the mechanisms responsible for the sodium retention and excretion in normal and pathological conditions, particularly the edema forming states such as cardiac failure, nephrotic syndrome and hepatic cirrhosis with ascitis.
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PMID:[Renal and extra-renal mechanisms of sodium and water retention in cirrhosis with ascites]. 777 18

We present a case of multiple symmetric lipomatosis Type I (Madelung's disease) with severe organic affection, hepatic cirrhosis, sever sensitive polyneuropathy and neuropathic ulceration at the left lower limb. A nephrotic syndrome developed in a larval form due to proliferative glomerulonephritis as the result of a metainfectious complications of the infection at the lower limb. We discuss the etiopathogenicity of the organic affection and we highlight the pathogenic links between the disease and its complications.
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PMID:[Nephrotic syndrome associated with symmetrical multiple lipomatosis (Madelung's disease)]. 779 19


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