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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Splenomegaly is a common finding in patients with portal hypertension. In the present study the relation between spleen size and blood flow in the splenic and portal vein was evaluated in 33 patients with alcoholic liver cirrhosis and portal hypertension using pulsed Doppler sonography (Ultramark 9, ATL, Solingen, FRG). There was a significant positive correlation between hilar spleen diameter (HD) and splenic vein diameter (r = .73, p less than .001) as expected as the consequence of portal hypertension. However, a positive correlation between HD and splenic vein flow (SBF) was found (r = .67, p less than .001). Furthermore, there was no negative correlation between HD and flow velocity in the splenic vein (r = .01, n.s.). Portal blood flow (830 +/- 360 ml/min) was fairly constant in spite of considerable variations in SBF (range: 120 to 1200 ml/min). The data of the present study indicate that splenomegaly in patients with liver cirrhosis and portal hypertension is not simply the consequence of portal congestion resulting in decreased SBF. Rather, increased SBF serves to maintain portal blood flow and thereby contributes to portal hypertension. In few patients (15%) SBF increased to more than 11/min may be an important factor for the severity of portal hypertension. Surgical shunt treatment should be adjusted in these patients.
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PMID:[Splenic size and duplex sonography determination of blood flow in the vena lienalis and vena portae in liver cirrhosis]. 151 Dec 15

The caliber of the splenic and hepatic arteries, the hepatic to splenic artery ratio and the spleen size (area of widest spleen section) were evaluated by real time ultrasonography (US) in 88 patients affected by liver cirrhosis of different etiology (26 alcoholic cirrhosis, 43 hepatitis B virus (HBV) related cirrhosis, 8 cryptogenic cirrhosis and 11 primary biliary cirrhosis) and in a control group of 21 normal subjects, in order to assess the possible influence of the etiology of the disease on these morphological parameters. The mean caliber of the hepatic artery was larger, and the mean caliber of the splenic artery smaller in alcoholic than in HBV-related, cryptogenic and in primary biliary cirrhosis. This difference is emphasized when considering the hepatic to splenic artery ratio: this parameter was never greater than 0.9 in all cases of primary biliary cirrhosis, in 38 out of 43 patients with HBV-related cirrhosis and in 6 out of 8 cryptogenic cirrhosis, while in the alcoholic group only in one out of 26 was it less than 0.9. The sensitivity, specificity and accuracy of this ratio in differentiating alcoholic from non-alcoholic cirrhosis was 96%, 88% and 91%, respectively. Splenomegaly resulted more in primary biliary cirrhosis, in HBV-related cirrhosis and in cryptogenic cirrhosis than in the alcoholic form. Finally, a significant correlation was found in all groups of cirrhotic patients between the diameter of the splenic artery and the spleen size. These results show that some ultrasonographic morphological features of liver cirrhosis differ according to its varied etiology, probably reflecting different pathophysiological mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Caliber of splenic and hepatic arteries and spleen size in cirrhosis of different etiology. 194 2

A 40-year-old man with rheumatoid arthritis, splenomegaly and mild thrombocytopenia presented with gross ascites and a history of excess alcohol consumption. Oesophageal varices were documented endoscopically. Alcoholic cirrhosis was suspected and laparoscopy revealed a macronodular liver surface. Liver biopsy disclosed subtle microscopic structural variations which together with the laparoscopic findings were consistent with the diagnosis of nodular regenerative hyperplasia. The importance in diagnosis of macroscopic appearance combined with histological findings is emphasised. Clinically significant portal hypertension may be present at a histologically early stage of this condition.
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PMID:Nodular regenerative hyperplasia of the liver: the importance of combined macroscopic and microscopic findings. 200 57

Liver disease, particularly alcoholic cirrhosis, is associated with a number of interesting chemical changes which result in structural and metabolic abnormalities of the erythrocyte membrane leading to microscopically observable cell shape changes and hemolytic anemia varying from very mild to potentially lethal. Increase in unesterified serum cholesterol owing to lecithin cholesterol acyl transferase (LCAT) deficiency in cirrhosis leads to expansion of the lipid bilayer and macrocytosis without megaloblastic changes in precursors. Substitutions of phosphatidyl choline (PC) moieties in the erythrocyte lipid bilayer lead to echinocytes (disaturated PC) or to stomatocytes (diunsaturated PC). In some patients, high density lipoprotein (HDL) abnormalities lead to erythrocyte surface changes causing rapid formation of echinocytes. The rapidity and reversibility of these changes suggest blockade of metabolic transport channels critical to the maintenance of erythrocyte membrane shape. Metabolic changes involving vitamin E deficiency leading to lipid peroxidation and pyruvate kinase instability leading to adenosine triphosphate (ATP) reduction have also been invoked to explain hemolysis associated with acute liver damage. The most severe hemolysis in liver disease is associated with acanthocytes (spur cells) and a marked imbalance in cholesterol-phospholipid ratio. These patients usually have hypersplenism, as well as rigid erythrocyte membrane transformations which are irreversible. Any of the other erythrocyte membrane shape changes described appear to be reversible if the liver disease abates, but they too may become irreversible if bits of projecting membrane are repeatedly removed by the macrophages of an enlarged spleen.
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PMID:Mechanisms of hemolysis in liver disease. 218 63

The authors collected 41 cases of cirrhosis in native Tibetans with pathological verification. It is found that 60.98% of the cases were alcoholic cirrhosis, with an incidence significantly higher than that of 7.6% reported in the inland (P less than 0.01). 74.19% and 20% of the cirrhosis in male and female patients respectively were alcoholic, while 50% of the cirrhosis in the female were due to malnutrition. Among the Tibetan cirrhotics 12.2% was due to hepatitis and 4.88% each to hydatid disease and tuberculosis. The average age of these cirrhotics was 47.05. The frequent occurring age was between 41-50 (about 41.46%). The Tibetan cirrhosis in peasants and herdsmen were 51.28%. At the first admission, 84.49% got jaundice and 90.2% got ascites. These percentages were higher respectively than 43.2% and 50.5% from the Lanzou report (P less than 0.01). Ascites was serious, portal vein expanded, but splenomegaly were merely 17.07% (normal were 82.93%). These spleens expanded just a little, macrosplenopathy was not found.
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PMID:[Analysis of the etiology and clinical characteristics of Tibetan cirrhosis in Tibet]. 262 23

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

Blood platelets were assayed in 56 cirrhosis patients divided into two groups: alcoholic cirrhosis (20 cases) and non-alcoholic cirrhosis (36 cases). Each group was also divided into two sub-groups: with and without clinical signs of portal hypertension. Low platelet counts were found in both groups (greater than 70%), the incidence being high in the sub-group with clinical signs of portal hypertension. Alcohol appeared to have no influence on the development of platelet insufficiency which was rather correlated with the severity of the hepatopathy, the presence of splenomegaly (splenic sequestration), immunological factors, (presence of circulating antiplatelet antibodies) and "consumption" phenomena (significant incidence of circulating FDP, and indicator of chronic Disseminated Intravascular Coagulation).
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PMID:[Thrombopenia and cirrhosis. Study of 56 cases]. 367 Jun 96

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 patients with liver cirrhosis, there were various symptoms in decompensated state, but not in compensated state. Most of symptoms were due to liver cell dysfunction and portal hypertension. Jaundice, ascites, edema, bleeding tendency and endocrinological symptoms were due to liver cell dysfunction. Hepatic encephalopathy, esophageal varices and splenomegaly were related to portal hypertension. Vascular spiders and palmar erythema were found in patients with alcoholic liver cirrhosis more frequently than in patients with viral liver cirrhosis. Jaundice was a sign of poor prognosis. There were no difference in clinical symptoms between aged patients and young patients. Careful observation of the symptoms is important to care the patients with liver cirrhosis.
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PMID:[Clinical symptoms of patients with liver cirrhosis]. 811 8

Hundred-forty-one patients, 78 affected by alcoholic liver cirrhosis and 63 by posthepatitic cirrhosis were studied in order to assess the degree of portal hypertension in liver cirrhosis of different etiology taking into account the developing stages of the disease. Etiological assessment was based on anamnesis, laboratory data, needle liver biopsy and patients of each group were divided into 3 subgroups (grade A, B, C) according to Child-Turcotte classification. A > 1.3 cm diameter of portal vein and a > 13 cm spleen size evaluated by means of real-time ultrasonography together with the occurrence of esophageal varices at endoscopy were considered as signs of portal hypertension. Our study shows that such signs are more frequent in patients affected by posthepatitic cirrhosis in comparison with those affected by alcoholic cirrhosis. If the severity of the disease was considered, at the early stage (grade A) no significant difference was reported in portal diameters while splenomegaly and esophageal varices appeared more frequent in posthepatitic cirrhosis. In grade B patients the increase of portal and spleen size proved significantly greater in posthepatitic cirrhosis whereas prevalence of esophageal varices was similar in the two groups. The lack of differences in the three considered parameters at the end stage of the disease may be due to severe changes in liver morphology actually similar in the 2 groups apart from etiological factors.
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PMID:[Assessment of portal hypertension in hepatic cirrhosis in relation to etiologic factors]. 835 80


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