Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bumetanide is a recently introduced diuretic that inhibits sodium transport in the thick ascending limb of the loop of Henle. It is structurally and pharmacologically similar to furosemide, but is approximately 40 times as potent on a milligram-for-milligram basis. After oral administration, it is rapidly absorbed, with peak serum concentrations attained at approximately 30 minutes. Its pharmacokinetic parameters are similar to those of furosemide. Bumetanide has demonstrated efficacy in the management of edema associated with congestive heart failure, hepatic cirrhosis, and renal insufficiency. Bumetanide has demonstrated an adverse-reaction profile similar to that of furosemide, although the incidence of hypochloremia and hypokalemia is greater with bumetanide. The incidence of hyperglycemia and ototoxicity is greater with furosemide. The principal indication for bumetanide may be in patients with increased risk of ototoxicity. Cost considerations should relegate bumetanide to a secondary role for the treatment of sodium and fluid retention in most clinical settings.
 ...
PMID:Bumetanide: a new loop diuretic (Bumex, Roche Laboratories). 635 86

Piretanide is a high-ceiling, loop-active diuretic that has been developed for treatment of congestive heart failure, hypertension and edematous states caused by renal and hepatic diseases. Piretanide is structurally related to furosemide and bumetanide; when administered orally, 6 mg of piretanide is as effective as 40 mg of furosemide, and when administered intravenously, 12 mg of piretanide is as effective as 40 mg of furosemide. Piretanide enhances water and sodium excretion in patients with congestive heart failure, with nephrotic syndrome and with cirrhosis and ascites. Adverse effects reported to date are limited to those attributable to excess loss of fluid and electrolytes. Under some conditions, piretanide appears to be less potassium wasting than thiazide diuretics or other loop-active diuretics.
 ...
PMID:Piretanide: a loop-active diuretic. Pharmacology, therapeutic efficacy and adverse effects. 638 44

Severe congestive cardiac failure developed in a few weeks in a 44 year old man who had undergone porto-caval anastamosis for post-hepatitis cirrhosis one year previously and then treated for anaemia by repeated blood transfusion and chronic daily oral iron therapy. Infiltrative, congestive and restrictive cardiomyopathy was diagnosed in the presence of global cardiomegaly, electrocardiographic changes (microvoltage, diffuse ST-T wave changes), echocardiographic appearances (dilatation of the left ventricle, with hypertrophic and hypokinetic walls), and hemodynamic signs of adiastole with equalisation of filling pressures at 15 mmHg and a cardiac index of 1,88 l/min/m2. Cardiac haemochromatosis was confirmed by the laboratory (serum iron: 35 mumol/l; siderophilin saturation: 100 p. 100; serum ferritin: 1854 ng/ml; induced siderouria: 51 mg/24 hours) and histological findings (endomyocardial biopsy showing pigment overload). The absence of a family history, of homozygote A3 antigen, of diabetes, of iron overload on hepatic biopsy one year previously, excluded the diagnosis of familial idiopathic haemochromatosis. A secondary form of the disease was diagnosed on a possible genetic predisposition (heterozygote A3 antigen) and on environmental factors (blood transfusions, iron therapy, cirrhosis, alcoholism and perhaps the porto-caval anastamosis. Cardiac haemochromatosis was cured in this case by iron chelating therapy comprising daily subcutaneous infusions of 2 g of desferrioxamine for 2 months. The cure was confirmed by regression of the signs of clinical cardiac failure and of cardiomegaly, the increase in QRS voltages and the near normalisation of the hemodynamic and laboratory findings.
 ...
PMID:[Adiastole caused by a secondary cardiac hemochromatosis. Successful treatment with an iron chelating agent]. 641 3

We describe a three-generation family in which five individuals have arteriohepatic dysplasia (Alagille syndrome) with striking differences in the degree of severity. Two sisters presented with neonatal jaundice, peripheral pulmonic stenosis, and characteristic facial appearance including a broad forehead, deep-set eyes, prominent nose, and pointed chin. One died at 5 years of cirrhosis with portal hypertension and the other at 18 months of congestive heart failure. Their asymptomatic 32-year-old mother and 35-year-old maternal aunt have a similar facial appearance, pulmonic stenosis, skeletal anomalies, and bilateral posterior embryotoxon. Neither has evidence of clinical liver disease. The maternal grandfather, who refused evaluation, has a similar appearance, a history of liver disease, and a heart murmur. Extreme intrafamilial variability has not been reported previously and most affected individuals described in the past have followed a benign course. The pattern of severity in this family suggests the possibility of a maternal factor augmenting the clinical expression in affected offspring. The skeletal anomalies and posterior embryotoxon are valuable signs in detecting asymptomatic but affected individuals who are at risk for having offspring with this potentially lethal condition.
 ...
PMID:Arteriohepatic dysplasia (Alagille syndrome): extreme variability among affected family members. 643 40

The administration of nonsteroidal antiinflammatory drugs (NSAID) may induce marked side effects, especially on renal function. Some of these side effects are the consequence of inhibition of prostaglandin (PG) synthesis. Patients who need an increase in PG synthesis to maintain renal function (congestive heart failure, cirrhosis of the liver, preexisting renal disease) appear to be particularly at risk. Regular checks on renal function are mandatory when prescribing NSAID to such patients.
 ...
PMID:[Secondary effects of non-steroid anti-inflammatory agents on kidney function]. 661 81

Fibrous thickening of the splenic capsule is often seen in patients with hepatic cirrhosis or portal hypertension from other causes. However, most cases of capsular thickening have been considered idiopathic, with no obvious abnormality of the portal circulation. The possibility that these "idiopathic" cases also have evidence of portal hypertension was examined in a retrospective study. The splenic capsule thickness was measured in 434 consecutive autopsy specimens. Various clinical and autopsy parameters relevant to vascular disease were recorded and correlated with splenic capsular thickness. Thickened capsules were significantly more frequent in patients with advanced age, clinical history of severe congestive heart failure, cirrhosis, and hepatic portal sclerosis. It is suggested that most cases of splenic capsular thickening are caused by splenic congestion with organization of capsular and subcapsular hemorrhages.
 ...
PMID:Fibrous thickening of the splenic capsule. A response to chronic splenic congestion. 668 17

The microscopical features in specimens of liver tissue from 14 patients considered to be suffering from Diffuse Nodular Hyperplasia (DNH) were compared with the changes found in livers from five other groups of patients. The diagnoses in these groups were macronodular cirrhosis, hepatic venous occlusion, congestive cardiac failure, compensatory hyperplasia after destruction of part of the liver and chronic biliary disease respectively. In all these groups the formation of thick hepatocyte plates, thought to represent cell proliferation, was a constant and striking feature. Such plate thickening in the periportal regions was associated with congestive cardiac failure and with hepatic venous occlusion. The diffuse involvement of almost all plates formed part of the changes in DNH, cirrhosis, compensatory hyperplasia and chronic biliary disease. Normal vascular relations were retained in the patients with compensatory hyperplasia and chronic biliary disease and lost in cirrhosis and, in some parts, in DNH. The nodules were small in DNH and larger in cirrhosis, where they were surrounded by fibrous tissue. DNH appeared to be recognizable in needle biopsy specimens.
 ...
PMID:Pathological aspects of diffuse nodular hyperplasia of the liver. 673 20

Forty-three patients with ascites were evaluated with computed tomography (CT). Neoplasm accounted for 72% of the cases; the remainder included inflammatory processes (10%), cirrhosis (8%), trauma (2%), renal transplant (2%), congestive heart failure (2%), and unknown (4%). An accuracy of 93% was achieved in correctly predicting the presence of ascites alone or together with a mass. The potential for diagnostic error when mass lesions coexist with ascites is discussed and parameters are described to help avoid such errors. These include: (1) knowledge of the normal anatomy of the fluid-filled intraperitoneal space and fluid flow patterns; (2) inspection of the intra-/extraperitoneal interface; and (3) evaluation of the bowel-mesentery pattern.
 ...
PMID:CT of ascites: differential diagnosis. 677 34

We report the incidence of normal (50.4%), increased (46.7%), and decreased (2.9%) anion gap among hospitalized patients in a retrospective study. The mean and range of increased anion gaps were 25 and 19-28 mmol/L. Values exceeding 30 mmol/L were uncommon and may indicate either acidosis or laboratory error. The most common causes of the increased anion gap among patients were chronic renal failure, congestive heart failure, malignant neoplasm, and diabetes mellitus. Increased anion gap in this study may be due to excess acids along with decreases in sodium, chloride, and carbon dioxide. The mean and range of decreased anion gap were 6 and 3-8 mmol/L. Anion-gap values less than 3 mmol/L were uncommon (one of 500 cases), and a high incidence of such values may indicate laboratory error. Nephrotic syndrome, liver cirrhosis, intestinal obstruction, and severe hemorrhage were the common disorders associated with decreased anion gap, which resulted from hypoalbuminemia and hyponatremia. Although most patients with decreased anion gap had hypoalbuminemia, hypoalbuminemic patients did not necessarily have decreased anion gap.
 ...
PMID:Value of the anion gap in clinical diagnosis and laboratory evaluation. 682 31

The authors examined in detail the clinical and laboratory data and pathologic findings for 12 patients with alcoholic cardiomyopathy who were autopsied in the preceding ten years to determine the types of liver disease prevalent in this population. Neither alcoholic hepatitis nor cirrhosis was present in any patient, and most of the hepatic changes could be related to the effects of acute and chronic congestive heart failure. The major hepatic lesions included centrilobular congestion and/or ischemic necrosis, cardiac sclerosis (fibrosis about central veins and in perisinusoidal spaces), mild canalicular cholestasis, portal fibrosis, and nodular regenerative hyperplasia. This last finding may account for macroscopic nodularity resembling cirrhosis as well as portal hypertension in patients with alcoholic cardiomyopathy. Although alcoholic cardiomyopathy and alcoholic hepatitis or cirrhosis were mutually exclusive in the patients studied, the factors responsible for this are at present uncertain.
 ...
PMID:Liver disease in alcoholic cardiomyopathy: evidence against cirrhosis. 684 Jul 53


<< Previous 1 2 3 4 5 6 7 8 9 10