Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From October 1982 to June 1985 158 hospitalized patients in the National Hospital of Niamey, Republic of Niger, were selected whenever one of the following signs was found: hepatomegaly, jaundice, ascites, oesophageal varices, abdominal venous pattern, or splenomegaly. Investigations included hepatic echography (158/158), needle liver biopsy (68/158), radioimmunoassays for serum hepatitis B surface antigen (HBsAg; 158/158), anti-HBs (152/158), anti-HBc (129/158) and anti-delta antibody (anti-HD; 158/158). 112 patients with liver diseases comprised 28 with chronic hepatitis, 55 with non-alcoholic hepatic cirrhosis, and 29 with hepatocellular carcinoma (HCC). 46 patients with other diagnoses were used as controls. 71/112 liver disease patients were positive for HBsAg in serum compared with 1/46 controls (P less than 10(-9)). Prevalences of delta superinfection in patients with serum HBsAg (+) and anti-HD (+) were 45/112 (40.2%) in liver disease patients versus 1/46 (2.2%) in controls (P less than 10(-9)). Delta superinfection was very frequent in chronic hepatitis (8/28), non-alcoholic cirrhosis (24/55) and HCC (14/29). In chronic hepatitis, delta superinfection was more frequent in the chronic active form than in the chronic persistent type (not significant). Cirrhosis patients with delta superinfection were younger (10 years in males, 11 years in females) than those without (P less than 0.05).
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PMID:Delta superinfection in patients with chronic hepatitis, liver cirrhosis and hepatocellular carcinoma in a Sahelian area. Study of 112 cases versus 46 controls. 284 9

Primary sclerosing cholangitis is a chronic cholestatic liver disease that is commonly associated with chronic ulcerative colitis. We observed the development of varices in the abdominal wall surrounding the ileostomy stoma of patients with primary sclerosing cholangitis who underwent proctocolectomy and ileostomy for chronic ulcerative colitis. In 10 of 19 patients, the development of peristomal varices was documented 12-133 mo after operation. Risk factors for the development of peristomal varices included splenomegaly, esophageal varices, advanced histologic stage at liver biopsy, low serum albumin, thrombocytopenia, and an increased prothrombin time. Recurrent bleeding from peristomal varices was a major problem; 7 of 10 patients required repeated blood transfusions. The only therapy of long-term benefit was surgical decompression of the portal venous system in 1 patient and liver transplantation in a second patient. In contrast, there was no perirectal bleeding in 4 patients with primary sclerosing cholangitis who underwent proctocolectomy with an ileoanal anastomosis.
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PMID:Peristomal varices after proctocolectomy in patients with primary sclerosing cholangitis. 293 90

Thirty six patients with culture-proven enteric fever and 15 patients of fever with etiology other than enteric fever as a control group were studied, with special reference to hepatic dysfunction and its relation to clinical features of the disease. Hepatomegaly was observed in 55% of enteric fever patients, and was slightly more common than splenomegaly (50%). Its incidence in typhoid fever (67%) was three times higher than in paratyphoid fever (22%). Hepatic dysfunction occurred in 55% of cases. Jaundice was noted in only 8% of the cases, whereas hyperbilirubinemia (serum bilirubin greater than 1.8 mg %) was present in 17%. Although hepatic manifestations of enteric fever were mild, a small but important group had sufficient hepatic involvement to mimick the clinical picture seen in viral hepatitis, amebic liver disease, and malaria with jaundice. It may be considered of clinical significance, since enteric hepatitis responds very well to specific therapy.
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PMID:The spectrum of hepatic injury in enteric fever. 312 48

In 117 patients affected by chronic alcoholic liver disease, we have histomorphometrically determined hepatocyte and nuclear areas, total amount of fat and total amount of fibrosis, comparing them with the following clinical and biochemical parameters: ascites, encephalopathy, jaundice, spiders, collateral circulation, splenomegaly, prothrombin activity, serum albumin, gammaglobulin, bilirubin, ASAT, ALAT, GGT, leukocyte and platelet count, and daily consumption of ethanol. Both hepatocyte and nuclear areas closely correlated with most of the parameters indicative of hepatic function derangement, whereas fat amount correlated with them inversely, but positively with the daily consumption of ethanol. The degree of fibrosis was greater in patients with a worse hepatic function, and there was a direct relationship between the degree of fibrosis and hepatocyte and nuclear areas, and an inverse one between the degree of fibrosis and the total amount of fat.
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PMID:Hepatocyte and nuclear areas and fatty infiltration of the liver in chronic alcoholic liver disease. 323 42

Adult cystic fibrosis (CF) patients are increasingly diagnosed with hepatic cirrhosis, cholecystitis, and cholelithiasis. A continuing diagnostic problem is the early detection of cirrhosis prior to diffuse liver involvement. Sonography has been used in evaluating the pancreas, gallbladder, liver, and spleen in cystic fibrosis patients. We used a real-time mechanical sector scanner to study the portal veins in adult CF patients randomly selected from our CF population and correlated the portal vein diameters with liver function studies. A measurement greater than 12 mm was interpreted as a probable sign of portal hypertension. Of 21 patients studied, 14 had portal veins that measured greater than 12 mm, and 12 patients had (although not necessarily at the time of the exam) elevated serum alkaline phosphatase levels. Three patients had associated splenomegaly and thrombocytopenia, and 10 patients also exhibited cholelithiasis and abnormal gallbladders on sonography. Initial results indicate that portal vein measurement may be a sensitive indicator of early portal hypertension. Sonography may, thus, isolate patients at high risk for possible future complications. Serial sonograms can be performed easily in evaluating the progress of liver disease.
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PMID:Portal vein measurement by ultrasonography in patients with long-standing cystic fibrosis: preliminary observations. 354 Feb 61

Forty-one black patients aged 21 to 75 years with hepatic tuberculosis diagnosed at liver biopsy were studied prospectively. The liver varied in size and consistency and was tender in 44 per cent of patients. Abdominal symptoms, weight loss, pyrexia, hepatomegaly, splenomegaly and anaemia were absent in 54, 39, 37, 5, 68 and 27 per cent of patients respectively. Twenty-two per cent of chest radiographs were normal. Liver function tests were of little diagnostic value and hepatic imaging techniques often gave normal results. Acid-fast bacilli, caseation and coexistent liver disease were detected in 59, 51 and 37 per cent of patients respectively. Since there was no consistent clinical pattern a high index of suspicion is necessary if this disease is to be detected in communities in which tuberculosis is endemic. In patients with unexplained hepatomegaly or hepatosplenomegaly or pyrexia of unknown origin liver biopsy provides the only means of making this diagnosis.
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PMID:A prospective study of hepatic tuberculosis in 41 black patients. 365 66

The clinical, biochemical, and histological features of 27 children with syndromic paucity of the interlobular bile ducts are described. All presented in the first 5 months of life, 21 with jaundice, two with spontaneous bleeding due to vitamin K malabsorption in addition to jaundice, two with pruritus, and two with failure to thrive. Interlobular bile ducts were abundant in liver biopsies from five (18% of cases) in the first 6 months of life. The degree of portal fibrosis and cellular infiltrate was mild in all except three patients. Clinically significant heart lesions occurred in 52% but only 22% had peripheral pulmonary stenosis. Characteristic facial appearances were present in only 70%; embryotoxon and vertebral anomalies were present in 56 and 33%, respectively. Two infants died of cardiovascular complications, one of alimentary bleeding and one of progressive liver disease. Complications of vitamin K deficiency occurred in 15%, vitamin D deficiency in 30%, and vitamin E deficiency in 37%. Survivors at ages of 19 months to 16.5 years had considerable morbidity with pruritus occurring in 70%, jaundice in 48%, xanthomas in 30%, 74% having hepatomegaly and 63% splenomegaly. All had abnormal biochemical tests of liver function, 90% had growth retardation, and 50% developmental delay. We conclude that differentiation from extrahepatic biliary atresia can be difficult if biliary flow cannot be demonstrated. Prevention of fat-soluble vitamin deficiency is essential. Further research is required to decrease the morbidity associated with this syndrome in infancy.
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PMID:Syndromic paucity of the intrahepatic bile ducts: diagnostic difficulty; severe morbidity throughout early childhood. 368 72

Hepatic metabolism is the primary process of elimination of propafenone. It therefore is important to understand the effect of altered liver function on the disposition and elimination kinetics of this drug. Patients with abnormal liver function probably will require treatment with propafenone for cardiac arrhythmias; an understanding of the relationship between liver function and the pharmacokinetics of propafenone will provide a rational basis for optimal dosage adjustments in these individuals. Our results demonstrate that both systemic clearance and bioavailability of propafenone are sensitive to variability in liver function. The bioavailability of propafenone is inversely related to the clearance of indocyanine green (ICG), whereas a direct relationship exists between systemic clearance of propafenone and ICG clearance. Comparisons of clinical parameters with the propafenone data yielded interesting results. An overall clinical grading of severity of liver disease based on the presence or absence of portal hypertension (i.e., varices and/or splenomegaly), prior encephalopathy, and ascites did not correlate well with propafenone results. However, albumin, total bilirubin, serum glutamic oxaloacetic transaminase (SGOT) concentrations and prothrombin time values correlated strongly with the overall results. No definite relationships with subjects' age; weight; and hemoglobin, alkaline phosphatase, lactic acid dehydrogenose, cholesterol, blood urea nitrogen, or creatinine levels were detected. These results demonstrate that moderate to severe liver disease significantly affects the absorption and disposition of propafenone. In patients with cirrhosis, and presumably other forms of hepatic dysfunction, careful adjustments of propafenone doses are needed to optimize therapy.
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PMID:Influence of hepatic dysfunction on the pharmacokinetics of propafenone. 369 82

Agreement among six physicians for 18 clinical signs in 50 alcoholic patients was prospectively studied. Twenty patients had alcoholic cirrhosis, 14 noncirrhotic alcoholic liver disease, and 16 alcoholics had no clinical or biochemical abnormalities. Agreement was assessed by kappa index for categorical variables and by intraclass correlation coefficient for the others. A good agreement was observed for ascites (r = 0.75) and splenomegaly (r = 0.75). It was fair for jaundice (r = 0.65), Dupuytren's contracture (r = 0.65), and vascular spiders (r = 0.64). However, it was poor for white nails (r = 0.27) and hepatic consistency (r = 0.11). Agreement was better among senior physician's than junior physicians. In order to assess which signs contributed to differentiate the three groups of patients, a stepwise discriminant analysis was realized; it identified three variables: vascular spiders (P less than 0.001), splenomegaly (P less than 0.001), and abdominal wall collateral veins (P less than 0.01). These results suggest that studies based on physical findings must be cautiously considered.
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PMID:Interobserver agreement in the physical diagnosis of alcoholic liver disease. 381 79

In the past 10 years we have examined 20 children with inflammatory liver disease associated with high serum titers of anti-liver-kidney microsome antibody (anti-LKM). The first hepatic symptoms were progressive fatigue and jaundice, the fortuitous finding of hepatomegaly or splenomegaly with raised transaminase activity, or an acute hepatitis-like illness. At the time of diagnosis, hepatomegaly was present in 18 children, splenomegaly in 16, jaundice in nine, and ascites in two. Serum alanine transferase activities were elevated in all but two, who had already received steroids. Serum total gammaglobulin values were greater than 2.0 gm/dl in 16 children, prothrombin activity less than or equal to 60% in six, and serum titer of anti-LKM between 1:100 and 1:100,000. All children but one had cirrhosis, and histologic signs of aggressivity were present in 14. In 11 children one or more extrahepatic diseases were present, including type 1 diabetes, vitiligo, glomerulonephritis, autoimmune hemolytic anemia, hypoglycemia with hyperinsulinism, autoimmune thyroiditis, chronic mucocutaneous candidiasis with hypoparathyroidism, and multiple cutaneous and visceral telangiectasias. Treatment with prednisone and azathioprine improved the liver condition in 16 of the 18 patients given treatment. In eight of them discontinuation of treatment resulted in rapid relapse; 14 are still receiving treatment and have stable hepatic function with follow-up from 8 months to 6 1/2 years. Only two are free of treatment. Four children died, two in spite of immunosuppressive therapy, one during a relapse, and one of extrahepatic disease. These results indicate that this autoimmune inflammatory liver disease may have onset early in life, with several clinical patterns; is frequently associated with certain types of extrahepatic manifestations of autoimmune origin; and is a potentially fatal disease for which immunosuppressive treatment must be started early.
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PMID:Liver disease associated with anti-liver-kidney microsome antibody in children. 395 Aug 19


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