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 liver has a particular ability to regenerate and demonstrate hypertrophy under several circumstances. The aim of this essay is to illustrate the computed tomographic (CT) appearances of the hypertrophic changes in hepatic morphology and to focus on the broad spectrum of etiologies. One thousand seven hundred and twenty-one patients who had CT of the abdomen were retrospectively studied. One hundred and fifty-three (9% of them (82 men, 71 women), with a mean age of 50 years (range: 18 to 87 years), had hypertrophic changes in the liver. The different final diagnoses included liver cirrhosis (n = 75), Budd-Chiari syndrome (n = 35), partial hepatectomy (n = 25), cholangiocarcinoma (n = 10), liver metastasis (n = 1), preoperative portal vein embolization (n = 3), schistosomiasis (n = 1), and congenital hypertrophy (n = 3). Hypertrophic changes in hepatic morphology are not uncommon conditions and CT is likely to afford the opportunity to detect them. The discovery of such an abnormality must prompt the radiologist to eliminate the possibility of neoplastic etiology or underlying portal hypertension.
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PMID:The variable of hypertrophic changes in hepatic morphology: CT appearance. 825 50

Ninety seven patients with liver cirrhosis of schistosomiasis were collected. Its CT findings and features were analysed on the clinicopathological basis including (1) the high percentage of the hepatomegaly and of the enlargement of the left lobe; (2) occurrence of deposition and calcification of eggs in large bowel wall (5/5), the portal vein system (22/97), the root of the mesentery (9/97) and the liver (93/97); (3) the variety and characteristics of the appearances of the intrahepatic calcification; (4) widened and fibrotic changes in the portal canal region. It was also noted that high percentage of hepatocellular carcinoma associated with this disease in the present series (25/97).
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PMID:[Hepatic schistosomiasis. X-ray computed tomographic aspects. Apropos of 97 cases]. 839 1

Bleeding from esophageal varices is a common and serious problem in Schistosomiasis mansoni. A simple and accurate method of detection would facilitate measurement of individual and community morbidity and allow institution of preventive measures. An ultrasonographic scoring system grading periportal fibrosis, portal vein diameter, spleen size, and portasystemic anastomoses was evaluated as a predictor of esophageal varices and a past history of upper gastrointestinal hemorrhage in 43 patients with hepatosplenic schistosomiasis. Ultrasonographic variceal score correlated (r = 0.86, p < 0.001) with the endoscopic variceal grade. Patients with a sonographic score of 5 or greater were highly likely (21 of 23) to have varices of grade II or greater (sensitivity, 91.3%; specificity, 94.7%). Only those with sonographic scores of 5 or greater (15 of 23) had bled from esophageal varices. The ultrasonographic score provided a simple, inexpensive, accurate, and noninvasive means of screening individuals with hepatosplenic schistosomiasis for esophageal varices, and correlated strongly with prior gastrointestinal hemorrhage. It is not known whether a similar score would be useful in hepatic cirrhosis.
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PMID:Ultrasonographic prediction of esophageal varices in Schistosomiasis mansoni. 847 Jun 38

The effects of liver disease on pharmacokinetics and pharmacodynamics are highly variable, and difficult to predict as the mechanisms of these effects are not well understood. Since the majority of the published literature is concerned with cirrhotic liver disease, this review also focuses mainly on this area. Four different theories have been proposed to account for the effects of chronic liver disease with cirrhosis on hepatic drug elimination: the sick cell theory; the intact hepatocyte theory; the impaired drug uptake theory; and the oxygen limitation theory. While some data in support of each of the first 2 theories have been published recently, a large amount of clinical data would appear to refute both of these theories. These clinical data are substantially consistent with the latter 2 theories, which regard the decreased permeability of the capillarised sinusoid as the critical feature in cirrhosis. Further work is required to determine the applicability of each of these theories. In cirrhosis, drug glucuronidation is spared relative to oxidative drug metabolism; however, in advanced cirrhosis this pathway may also be impaired substantially. There is evidence that in cirrhosis other conjugation pathways may also be impaired to variable degrees. Growing evidence suggests that biliary drug excretion is impaired in cirrhosis. Recent studies with several racemic drugs indicate that the disease can have different effects on the hepatic elimination of individual enantiomers, which may lead to a change in the concentration-response relationships of racemic drugs in cirrhosis. A major finding which has emerged in recent years is that, even with moderate degrees of hepatic impairment, there is a decrease in clearance of drugs or active metabolites normally cleared by the kidney. The effect on renal clearance of unbound drug may be masked if there is a concomitant decrease in plasma protein binding of the drug. Neither serum creatinine levels nor creatinine clearance are useful markers of the renal dysfunction associated with cirrhosis. Both may greatly overestimate renal function in patients with cirrhosis due to increased fractional renal tubular secretion of creatinine. Altered receptor sensitivity has been observed with some drugs in cirrhosis, while for other drugs there is no change in pharmacodynamics. Precise determination of drug dosage in cirrhosis requires information on changes in pharmacodynamics and plasma protein binding in addition to changes in drug elimination. Pharmacokinetic investigations in a variety of chronic liver diseases without cirrhosis (e.g. carcinoma, schistosomiasis and viral hepatitis) suggest that in the absence of cirrhosis, impairment of drug elimination is not sufficient to warrant reduction of drug dosage. However, if cirrhosis is present, 'safe' drug use requires an awareness of the possibility of multiple interactions between changes in hepatic and renal disposition and pharmacodynamics. In chronic liver disease with cirrhosis, dosage reduction is the general rule regardless of the route of elimination of drug or metabolite.
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PMID:Clinical pharmacokinetic and pharmacodynamic considerations in patients with liver disease. An update. 858 20

We report the results of sclerotherapy in 20 patients with bleeding gastric varices due to hepatic schistosomiasis. In an endemic area, patients with hepatic schistosomiasis, and bleeding gastric varices seen on endoscopy to be inferior extension of esophageal varices, were treated with emergency endoscopic injection just proximal to the cardia. Hemostasis was achieved in 17. Obliteration of varices was achieved in all patients with sclerotherapy, combined with surgery. Thirteen patients who had not been operated on in the past and consented to surgery underwent esophagogastric devascularization with splenectomy. Surgery was carried out as an emergency in the three patients who did not respond to sclerotherapy and electively in 10 patients after control of bleeding. After surgery, sclerotherapy was required for remnant varices. One patient with Child-Pugh grade C cirrhosis died of hepatic encephalopathy after control of the bleed. During a median follow-up of 9 months (range, 1-25 months), recurrence of bleeding in one patient and recurrent varices in two others were controlled with sclerotherapy. One patient had a fatal hemorrhage at home. We conclude that sclerotherapy effectively controls acutely bleeding type 1 gastric varices. Combined with esophagogastric devascularization and splenectomy, long-term results may be encouraging in patients with hepatic schistosomiasis.
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PMID:Sclerotherapy in bleeding gastric varices of hepatic schistosomiasis. 887 33

Familial and secondary deficiency of plasma lecithin-cholesterol acyltransferase (LCAT) produce circulating lipoprotein particles with gross structural and compositional abnormalities; these have adverse effects on a variety of cellular functions. Factors affecting hepatic synthesis and secretion of this plasma enzyme are largely unknown but, potentially, some of them can be investigated with monospecific antibodies. In the present study, enzymically active LCAT was purified 40,000-fold from human plasma and then used to raise polyclonal antibodies in New Zealand White rabbits. Addition of this antiserum (1 microliter) to human plasma (25 microlitres) completely inhibited LCAT activity, although it was less effective against plasma from other species. The antibodies appeared to be monospecific to plasma LCAT. They gave a single precipitin arc by crossed immunoelectrophoresis, while immunodiffusion established that there was no cross-reactivity with several apolipoproteins or with serum albumin. Moreover, the antiserum was successfully used to detect LCAT in normal human plasma by Laurell rocket immunoelectrophoresis. By contrast, Western blotting of plasma proteins using whole LCAT antiserum was largely unsuccessful because of high background staining, although this could be substantially reduced by use of an IgG fraction. However, the whole antiserum readily immunoprecipitated LCAT secreted into the culture medium of HepG2 cells, a human hepatoblastoma cell line, pre-labelled with [35S]methionine, the [35S]-labelled LCAT appearing as a narrow 65-kDa protein band by electrophoresis and fluorography. We conclude that polyclonal antibodies may be an important tool to investigate the characteristics and underlying mechanisms of secondary LCAT deficiencies, including those associated with hepatic cirrhosis and schistosomiasis.
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PMID:Characterization and potential uses of rabbit polyclonal antibodies against human plasma lecithin-cholesterol acyltransferase. 918 Oct 76

The patient was a 58-year old man whose complaints were generalized malaise and right epigastralgia. He had liver cirrhosis and schistosomiasis japonica, previously diagnosed by laparoscopy. Computed tomography (CT) showed a high density funicular shadow in the liver. However no tumorous lesions in the liver were visualized. Ultrasonography (US) of the liver showed a reticulate or scaly pattern, but no images of tumorous lesions. Hepatic angiography showed a single, deeply colored image about 1cm in diameter, in the segmentum anterosuperior. Preoperative and intraoperative enhanced US with hepatic intraarterial injection of carbon dioxide gas was performed. It showed a hyperechoic tumor shadow about 1cm in the segmentum anterior. The segmentum anterosuperior including the tumor was partially resected. Pathologically, the tumor was found to be a hepatoma of Edmondson type II, caused by cirrhosis and schistosomiasis japonica. The patient's postoperative course was uneventful. Enhanced US with hepatic intraarterial injection of carbon dioxide gas was useful for the diagnosis and treatment of the microhepatoma associated with schistosomiasis japonica.
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PMID:A case of microhepatoma associated with schistosomiasis japonica diagnosed by enhanced ultrasonography after hepatic intraarterial injection of carbon dioxide gas. 923 10

Hepatitis C virus (HCV) infection prevalence was determined in 34 hepatocellular carcinoma (HCC) patients with underlying liver cirrhosis. Serum alfa-fetoprotein level was found to be more than 1000 ng/ml (3153 +/- 1451) in those patients. Anti-HCV antibodies were detected in 84% of patients sera negative for hepatitis B surface antigen (HBsAg), while HCV RNA was only detected in 28% of the sera of those patients. Schistosomiasis antibodies were found in 92% of the anti-HCV-positive HBsAg negative sera of HCC patients, while they were only detected in 61% of sera of control non HCC patients with anti-HCV antibodies and without HBsAg. HCV and hepatitis B virus (HBV) coinfection was found in 16% of the studied group, based on antibodies in sera, and in 9% based on the presence of HCV RNA. HBV (HBsAg) was found, on its own, in sera of 5.9% of the patients studied. These results show that HCV and schistosomiasis play a major role in the development of hepatocellular carcinoma in Egypt.
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PMID:Prevalence of hepatitis C infection and schistosomiasis in Egyptian patients with hepatocellular carcinoma. 940 30

Imaging can play an important role in the diagnosis and planning of treatment for patients with diffuse liver disease. In certain entities, such as iron overload disorders, fatty change, Budd-Chiari syndrome, and schistosomiasis, the imaging findings are characteristic and diagnostic. In others, the findings are less specific, but imaging still has utility in assessment for associated changes of cirrhosis and portal hypertension. In either case, familiarity with these diffuse hepatic diseases and their expected imaging findings enables an organized and thoughtful assessment, with careful attention paid to the key diagnostic features and the important sequlae, such as portal hypertension and the development of HCC.
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PMID:Imaging of diffuse liver disease. 952 Sep 88

A case of preeclampsia with fetal death at 32 weeks' gestation is reported. Liver examination of the patient revealed network patterns on ultrasonography and linear calcifications on unenhanced CT scans in the liver. These findings are typical of those of chronic schistosomal infection. Indeed, liver biopsy specimens showed eggs of schistosoma japonicum. We diagnosed her case as preeclampsia with liver cirrhosis due to chronic schistosomiasis japonica. Schistosomal placentitis may have been present and may have contributed to preeclampsia and fetal death.
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PMID:Preeclampsia with fetal death in a patient with schistosomiasis japonica. 954 76


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