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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Progressive degrees of metabolic alterations are frequent in cirrhosis impairing peripheral tissue and body composition. Hepatocellular carcinoma worsens protein wasting and malnutrition. A normal energy production rate and an abnormal substrate oxidation rate are well-known findings in cirrhosis; however, no data are available on cirrhotic patients with hepatocellular carcinoma. The aim of this study was to measure oxidative metabolism in cirrhotic patients with and without hepatocellular carcinoma and to investigate the correlation between energy production rate, respiratory quotient and nutritional state. Thirteen male cirrhotic patients with hepatocellular carcinoma (8 well-nourished and 5 malnourished) were compared with 17 cirrhotic patients without hepatocellular carcinoma (11 well-nourished and 6 malnourished) and six controls who were age and sex matched. A diagnosis of malnutrition was made if the fat mass percentage was reduced to less than 20% of the patient's body weight. Indirect calorimetry was performed between 8 and 10 AM, after a 12-hr fast, for 30 min (with a 10-min steady-state period), and measured energy production rate was calculated according to Weir's formula. Body composition was assessed by means of the Durnin and Womersley formula. Anthropometry and bioelectric impedance analysis showed no variations in kilograms of fat-free mass in our malnourished patients. Our data show that, when the energy production rate is measured while the patient is at rest and corrected for fat-free mass, the energy requirements of cirrhotic patients and cirrhotic patients with hepatocellular carcinoma matched that of the controls, regardless of nutritional state.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxidative metabolism in cirrhotic patients with and without hepatocellular carcinoma: effects of malnutrition. 133 Aug 66

Renal vein thrombosis in early infancy is a complication of dehydration and prolonged hypotension. The onset is usually acute and the most common clinical signs are uni- or bilateral frank masses, hematuria, proteinuria and thrombocytopenia. In most cases, with conservative management, the late outcome is favorable. In the adult, renal vein thrombosis is often a silent complication of the nephrotic syndrome, the hypercoagulability of which may be an important factor in the pathogenesis of the thrombosis. Clinically, the presentation of a sudden complete occlusion is that of severe abdominal and lumbar pain with hematuria and loss of function of the kidney that suffers hemorrhagic infarction. Physical examination often reveals an enlarged kidney. With gradual occlusion, renal function is preserved. The initial diagnostic approach is with ultrasound studies and computed tomography; definitive diagnosis is established by renal venography or by selective renal arteriography. In general, a conservative approach including the use of anticoagulant treatment is preferred to surgical intervention. Priapism is a persistent painful penile erection due to ischemic or non-ischemic causes; therapeutic intracavernosal injection of papaverine is becoming the most common cause. In early and mild stages, aspiration of blood from the corpora cavernosa supplemented with intracavernosal irrigation with alpha-stimulating agents is the procedure of first choice; in late and severe ischemia, a shunt procedure may become necessary. Hepatic vein thrombosis occurs in association with a number of conditions considered predisposing factors including the use of oral contraceptives. The clinical picture may be that of an acute illness with abdominal pain, hepatomegaly, ascites and hepatic failure as well as early death. More often, the onset is insidious with slowly developing ascites and wasting. For the diagnosis, hepatic scintigraphy may be helpful but, at present, ultrasonography, computed tomography and magnetic resonance scanning are procedures of choice. There is, as yet, no adequate treatment. A fatal outcome may be prevented by surgical decompression of the congested liver and, in recent years, liver transplantation has been employed. Portal vein thrombosis, in children, is usually considered a complication of umbilical sepsis or a result of a congenital abnormality of the portal vein. In adults, the most frequent causes are hepatic cirrhosis and neoplasia. Clinically, there may be a sudden appearance of ascites with resolution in a symptom-free interval until the onset of other features of portal hypertension occur. Currently, ultrasound real-time imaging supplemented with Doppler capability, computed tomography and magnetic resonance scanning provide the necessary diagnostic information. Variceal hemorrhage is often the first major complication requiring treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Thrombosis in particular organ veins. 268 Aug 53

Renal sodium and potassium handling, plasma aldosterone and cortisol concentrations, and urine free norepinephrine excretion were determined every 4 h for 24 h in 15 cirrhotics (7 without ascites, group 1; 8 with ascites, group 2) and 7 healthy controls during controlled salt intake and recumbency. Renal sodium excretion was significantly reduced in group 2, whereas it exceeded threefold the salt intake in group 1. Its circadian rhythm was disrupted in both groups of patients. Significant inverse correlations with plasma aldosterone were found erratically in controls, never in group 1, and at every 4-h interval in group 2. In the latter, the indexes of tubular activity and effectiveness of aldosterone were also significantly increased. Urine norepinephrine excretion was never related to sodium excretion in either controls or patients; in group 2 it was directly correlated with glomerular filtration rate in many instances. The cortisol-related circadian rhythm of kaliuresis was retained only in group 1. The 24-h renal potassium excretion of controls and patients was comparable, in spite of the striking hyperaldosteronism, and the more than doubled contribution of aldosterone to kaliuresis shown in group 2. The influence of aldosterone on potassium excretion was also witnessed by the direct correlation between these variables found in group 1 and, when kaliuresis was corrected by the distal sodium delivery, group 2. Renal sodium handling in cirrhosis is altered even before ascites formation and compensated patients can undergo "spontaneous natriuresis." Aldosterone is the main cause of sodium retention in nonazotemic ascitic patients, while sympathoadrenergic hyperactivity may contribute to preserve renal perfusion. The influence of aldosterone on kaliuresis is enhanced, but renal potassium wasting in patients with ascites and hyperaldosteronism is prevented by reduced distal tubular availability of sodium.
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PMID:Circadian variation in renal sodium and potassium handling in cirrhosis. The role of aldosterone, cortisol, sympathoadrenergic tone, and intratubular factors. 292 63

Clinical findings, symptoms and predisposing factors were studied in 43 patients with oesophageal candidiasis, 40 patients with peptic oesophagitis and 40 normal controls. Oesophageal candidiasis was confirmed cytologically. 2.4% of patients who had undergone gastroscopy had oesophageal candidiasis; only three of them had simultaneous candidiasis of the oral cavity. Cardiac failure, oesophageal varices, hiatus hernia and gastric ulcer were common associated disorders. 42% of patients with candidal oesophagitis were symptom-free. Most common symptoms were vomiting, retrosternal and epigastric pain. Peptic oesophagitis was more frequently associated with symptoms. Predisposing factors were present in 88% of cases of oesophageal candidiasis: alcoholism, hepatic cirrhosis, diabetes mellitus, malignant tumours and other wasting diseases. 18 patients had had treatment with cimetidine; they included all 13 patients whose candidiasis was first detected at check endoscopy.
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PMID:[Candidiasis of the esophagus. Prospective study of incidence, type of complaints and predisposing factors]. 373 73

Muscle weakness, neuropathy, and transient rises in hepatic enzyme activity have been reported with the use of the antiarrhythmic agent amiodarone. A 68 year old teetotaller with normal liver function was given amiodarone for resistant supraventricular arrhythmias. He presented 19 months later with vomiting, muscle weakness and wasting, sensory neuropathy, and hepatomegaly. Liver biopsy showed fibrosis and the presence of hyaline. The amiodarone was withdrawn. Three months later he developed ascites. Oesophageal varices were found and he later died. The liver showed micronodular cirrhosis. The large volume of distribution and long half life of amiodarone may explain the persistence of toxicity, which may have been aggravated by simultaneously administered doxepin in this case. Amiodarone should be withdrawn if abnormal liver function or neuropathy develops.
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PMID:Neuropathy and fatal hepatitis in a patient receiving amiodarone. 632 31

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.
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PMID:Piretanide: a loop-active diuretic. Pharmacology, therapeutic efficacy and adverse effects. 638 44

Alterations of calcium and bone metabolisms have been observed in numerous studies of small groups of male HIV-infected patients. However, our knowledge regarding the manifestation of AIDS-associated hypoparathyroidism in female subjects is limited. In order to investigate the influence of heroin on the calciotropic hormones we performed a cross-sectional study on 45 female patients with proven HIV infection. The following criteria were used for exclusion from the study: age less than 20/ more than 50 years; confinement to bed; wasting symptoms; treatment with agents containing ketoconazole, renal or hepatic insufficiency; clinical or echographic signs of liver cirrhosis; endocrine diseases, or treatment with drugs known to influence calcium metabolism. A reduced parathormone (PTH) level was found among the female HIV-infected patients. Additional long-term use of heroin resulted in a significant increase of PTH compared to sex- and age matched controls and a second group of non-HIV-afflicted heroin dependent females. Significantly lowered serum magnesium concentrations were found in all three groups. Both serum calcium and urinary excretion of calcium were elevated in the group of HIV-infected heroin addicts and were independent from low vitamin D3 levels (1,25-dihydroxycholecalciferol) and alterations of protein metabolism. Therefore, it is concluded that the changes of PTH secretion are mainly due to mechanisms both of the impaired immune defense of HIV-infected females and the additional effect of opiates.
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PMID:Elevated serum-calcium and parathormone-levels in HIV afflicted female heroin addicts. 926 87

Hepatitis C virus (HCV) accounts for approximately 20% of cases of acute hepatitis, 70% of chronic hepatitis, and 30% of end-stage liver disease in the United States. The acute infection has an incubation period of 7 weeks (range, 4-20 weeks) and is symptomatic and icteric in only one third of patients. Serum aminotransferase levels generally increase greater than 10-fold elevated and as symptoms and signs resolve decrease into the normal range. Antibody to HCV is usually but not always present at the time of onset of symptoms. HCV RNA appears in the serum early during the incubation period, increases in titer and peaks at the time of symptoms, and then disappears in resolving disease. Importantly, 85% of patients with acute HCV infection develop chronic infection. In these patients, HCV RNA remains present and in approximately two thirds of patients, aminotransferases remain elevated in the range of 1.5- to 10-fold the upper limit of normal. The course of chronic hepatitis C is variable. Probably fewer than 20% of patients have symptoms and they are usually intermittent, vague, and nonspecific, largely being malaise and easy fatiguability. A small percentage of patients develop extrahepatic manifestations of hepatitis C, including cryoglobulinemia and glomerulonephritis. It is estimated that 20% to 30% of patients with chronic hepatitis C develop cirrhosis, but the process is generally slow and insidious. Once cirrhosis develops, symptoms are more common and the signs of end-stage liver disease can appear with jaundice, weakness, wasting, and gastrointestinal bleeding. Patients with cirrhosis are also at risk for developing hepatocellular carcinoma. Thus, this important liver disease has protean manifestations but is often insidious and can lead to end-stage liver disease despite the presence of few symptoms and signs of illness.
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PMID:Hepatitis C: the clinical spectrum of disease. 930 58

The prevalence of liver diseases is increasing in the United States, particularly as a result of the recent hepatitis C epidemic. In the past, patients who developed fulminant hepatic failure or cirrhosis owing to a chronic liver disease were likely to expire. During the last 15-20 years, liver transplantation has given these patients a chance at survival. Progressive nutrition deficiencies and muscle wasting are universal problems in these patients. Left untreated, the progressive wasting of liver disease leads to infection and an increased risk of death owing to infection both before and after transplantation. Aggressive nutritional support is essential to optimize the care of these patients and to enable them to obtain and survive a liver transplant and gain access to a new life following a successful liver engraftment.
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PMID:Nutrition support for individuals with liver failure. 1094 63

Data on the bone metabolism of human immunodeficiency virus (HIV)-infected patients are still extremely rare. To investigate the influence of HIV infection on the calciotropic hormones and markers of bone metabolism, we therefore performed a cross-sectional study on 100 patients (65 males and 35 females) with proven HIV infection. The following criteria were used for exclusion from the study: age less than 20/more than 50 years, confinement to bed, wasting symptoms, treatment with agents containing ketoconazole, renal or hepatic insufficiency, clinical or echographic signs of liver cirrhosis, endocrine diseases, or treatment with medications known to influence bone metabolism. Bone mineral content (BMC) was determined by single-photon absorptiometry on the left forearm. Reduced BMC was found among the male and female HIV-infected patients. Additional long-term use of heroin resulted in a severe loss of mineralization in the respective females. The markers of bone metabolism were determined in urine and serum samples. Significantly lower osteocalcin concentrations were found, indicating a reduced bone formation rate whose severity showed a significant correlation with the progressive loss of CD4 helper cells and was independent of low vitamin D3 levels (1,25-dihydroxycholecalciferol) and alterations of protein metabolism. Increased urinary excretion of cross-links as an expression of enhanced bone resorption was likewise significantly correlated with the loss of CD4 helper cells and independent of the vitamin D concentration and protein metabolism. It is therefore concluded that the changes in bone metabolism are mainly due to mechanisms of the impaired immune defense of HIV-infected patients.
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PMID:Changes in calciotropic hormones and biochemical markers of bone metabolism in patients with human immunodeficiency virus infection. 1101 93


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