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

Rash, lymphadenopaty, splenomegaly, periorbital edema, and hepatitis occurred in an 18-year-old woman who was taking phenobarbital and hydrochlorothiazide. Tests for fluorescent antinuclear antibody and hepatitis-associated antigen and antibody were negative. Liver biopsy was not characteristic of viral hepatitis. Clinical recovery occurred within two weeks. Treatment consisted of withdrawal of the above drugs plus the administration of methylprednisolone and diphenhydramine.
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PMID:Jaundice and rash associated with the use of phenobarbital and hydrochlorothiazide. 12 22

One hundred forty-four of 166 adults with acute viral hepatitis (AVH) admitted to an Egyptian fever hospital were followed for 12 months. The hepatitis B surface antigen (HBsAg) carrier rate in 95 with hepatitis B virus (HBV) hepatitis decreased from 53% at three months to 13% at 12 months. At 12 months, 22% of the male patients had persistent HBsAg compared with only 7% of the female patients. The HBsAg carrier rate was 25% at 12 months in those with schistosomiasis compared with 9% in those with only acute HBV infection. Splenomegaly persisted in those with palpable spleens at the initial examination and others developed splenomegaly. The prevalence of splenomegaly increased from 11% on admission to 20% at 12 months in those with only AVH, and from 40% to 69% in those with concomitant schistosomiasis. Patients with concomitant schistosomiasis had higher mean values for liver function test results and a greater proportion had abnormal liver function test results during hospitalization and follow-up than those with AVH only. Concomitant schistosomiasis increased the prevalence and prolonged splenomegaly and morbidity due to AVH. Both male sex and concomitant schistosomiasis prolonged the HBsAg carrier state. We propose that AVH frequently converts uncomplicated intestinal schistosomiasis to hepatosplenic schistosomiasis.
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PMID:The impact of endemic schistosomiasis on acute viral hepatitis. 176 2

For the detection of mild liver disease (acute viral hepatitis, chronic persistent hepatitis, fatty liver) serum bile acids levels have not proved to be superior to transaminases or other common liver tests with almost similar sensitivity and/or specificity. Indeed it has been possible to show in patients with compensated cirrhosis of the liver that the serum bile acids concentration is related to the degree of intrahepatic shunts and that there was a significant relationship between the fasting serum bile acids and the intrinsic clearance of ICG. Measurement of serum bile acids appear to be more sensitive for detection of cirrhosis than commonly used tests. The elevation of bile acids concentration in cirrhotic patients is thought to result from a reduced hepatic clearance and/or from portosystemic shunting. In order to determine the role of serum bile acid estimation in the indirect assessment of portal hypertension, fasting and two-hour postprandial serum bile acids concentration were measured in 36 patients with liver cirrhosis, classified according to Child-Pugh's criteria. Real time ultrasonography, esophagogastroscopy and static liver scintigraphy of the liver were carried out in all patients. The size of esophageal varices, the portal vein and its related structure, the nuclear criteria were graded according to the common methods. Between the clinical findings, splenomegaly, was noted and graded, though the size of spleen does not correlate well with the level of portal pressure. In our patients a good correlation (p less than 0.001) existed between the two hour postprandial bile acids concentration and ultrasonographic findings of portal hypertension. Fasting serum bile acids (SBA) were significantly higher in severe than in mild liver cirrhosis according to Pugh's criteria (p less than 0.001). In conclusion we think that SBA concentrations have a great prognostic value in assessment of major complications (upper gastrointestinal hemorrhage particularly). The reduced liver blood flow, for intra-and extrahepatic porto-systemic shuntings, is probably the main cause of reduced hepatic clearance of bile acids.
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PMID:[Serum concentration of bile acids and portal hypertension in cirrhotic patients. Possible correlations]. 264 42

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

Spleen size in patients with infectious mononucleosis (IM) was measured using ultrasound, and the findings were compared with data obtained in cases of acute viral hepatitis (AVH). The size was expressed as the spleen index (SI) or the product of the longitudinal and transverse diameters, expressed in cm2, of the maximum cross-sectional area of the spleen. A normal value obtained from 28 healthy individuals was 15 +/- 7 cm2. The SI (mean +/- SD) of patients with AVH and IM were 38 +/- 7 cm2 and 88 +/- 26 cm2, respectively. When the SIs were divided into five groups--grade 0 (0-25), grade I (26-50), grade II (51-75), grade III (76-100), and grade IV (100+), 83.3% of the patients with AVH were graded as Grade 0 or I, whereas 88.9% patients with IM belonged to higher grades. Splenomegaly with a SI value over 75, grade III or IV, strongly suggests IM when IM and AVH are being considered in the absence of other potential causes of splenomegaly. Because the clinical features of IM sometimes resemble those of AVH, it is often difficult to differentiate the two entities. The measurement of spleen size could be a significant supplemental aid in the diagnosis of IM in primary medicine, before clinical data can be obtained.
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PMID:Differentiation of mononucleosis from hepatitis by sonographic measurement of spleen size. 314 58

Twenty-two patients with HBsAg positive acute viral hepatitis have been followed-up for two years after the acute episode. Besides the usual clinical, pathological and biological examinations, the following tests were carried out: serum HBsAg: circulating T and B lymphocytes: serum IgG, IgA, IgM: leukocyte migration test to HBsAg; serum complement: autoantibodies, rheumatoid factors, cryoglobulins, alpha-fetoprotein. Serum HBsAg persistence was correlated with some features of the acute episode: protracted clinical form: recurrences or relapses; splenomegaly; decrease of circulating T-lymphocytes; presence of lymphocyte sensibilization to HBsAg. Among the seven serum HBsAg carriers, three developed a chronic hepatitis. The state of healthy chronic HBsAg carrier was associated with high levels of serum IgA (over 300 IU/ml). A chronic hepatitis has been also diagnosed in four out of the 15 patients who cleared their serum HBsAg. The presence, on the one hand, of a chronic hepatitis among the patients who cleared their HBsAg and, on the other hand, its absence in some of the HBsAg carriers suggest that HBsAg persistence is not a sine qua non condition for the development of the chronic liver disease. The onset of autoimmune phenomena due to the disturbance of immunologic homeostasis and perhaps other genetic or environmental factors seemingly allow the perpetuation of a hepatic damage.
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PMID:A prospective study of postacute viral hepatitis: the role of HBsAg. 370 99

78 hospitalized patients were selected when presenting with at least one of these signs: hepatomegaly, jaundice, ascites, oesophageal varices, abdominal venous pattern, splenomegaly. All had radioimmunoassays for hepatitis B surface antigen (HBsAg) and antidelta antibody (78/78). Acute or chronic hepatic disease was diagnosed in 56 patients: 7 acute viral hepatitis, 13 chronic hepatitis, 23 non alcoholic hepatic cirrhosis, and 13 hepatocellular carcinoma. Twenty-two patients with other diagnoses served as controls. Serum antidelta was present in each group: acute viral hepatitis (2/7), chronic hepatitis (2/13), non alcoholic hepatic cirrhosis (9/23), hepatocellular carcinoma (3/13), controls (2/22). Every patient with acute or chronic hepatic disease and positive serum anti-delta was positive for serum HBsAg. Amony controls, 2 patients with positive serum antidelta were negative for serum HBsAg but positive for antiHBs. Delta superinfection is present in the sahelian region; Patients with acute viral hepatitis, chronic hepatitis, non alcoholic hepatic cirrhosis, and hepatocellular carcinoma are electively infected. Patients with acute or chronic hepatitis and positive serum antidelta have hepatitis B virus evolutive infection (positive serum HBsAg).
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PMID:[HB virus infection and delta surinfection in Sahelian Africa]. 380 84

The weights of the spleens of series of patients with various disorders of children dating from birth or early infancy and causing splenomegaly, with or without cirrhosis of the liver, were analyzed. The linear regression equation for spleen weight versus age in months for each disease was derived, and the rate constants from these equations were adjusted for the age range of the patients in each group. The original data of Coppoletta and Wolbach were used for normal values. The rates of splenic growth of appropriate entities for which the regression equation could be computed fell into three groups, with adjusted rate constants (growth of spleen in grams per month) of 6.53-6.95 (biliary atresia, thalassemia, and cirrhosis following neonatal hepatitis), 2.30-2.62 (cirrhosis of alpha-1-antitrypsin deficiency, infantile polycystic disease, and spherocytosis), and 1.06-1.11 (cystic fibrosis and idiopathic thrombocytopenic purpura). These classes of splenic growth rates are approximately 10, 3.7, and 1.6 times the normal growth rate (0.67 g/mo). Rate constants could not be computed for the categories cirrhosis following viral hepatitis and hemolytic anemia other than spherocytosis and sickle cell anemia, and the numbers of patients with splenic vein obstruction, cirrhosis with the cholestatic syndrome of parenteral alimentation, hypoplastic anemia with hemosiderosis, tyrosinemia, Byler's disease, congenital hepatic fibrosis, and Wilson's disease were too few for analysis. The significance of the finding of classes or "quantum groups" of splenic growth rates in disorders of children, dating from birth or early infancy and causing splenomegaly, is uncertain. Comparable data on adequate series of patients with other appropriate disorders will be necessary.
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PMID:Splenic growth rates in cirrhotic and other splenomegalic diseases of childhood. 384 62

Four adolescents presented with leucopenia, thrombocytopenia, and splenomegaly; three had associated congenital abnormalities and two had a cirrhosis. They provide further evidence of an association between hepatic disease and bone marrow dysfunction. It is considered that these patients suffer from a genetic or constitutional disorder which may result in a susceptibility of their bone marrow to hypoplasia following viral hepatitis or other infections.
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PMID:Marrow hypoplasia with splenomegaly in adolescence. 743 Mar 85

We report a 20 year-old woman with hemophagocytic syndrome. In February 1993, she developed high fever, arthralgia, salmon-like pink eruption, leukocytosis and splenomegaly. She was diagnosed as adult Still's disease and successfully treated with intravenous immunoglobulin and oral prednisolone. In September 1993, she was re-admitted to our hospital complaining of general fatigue and low grade fever and treated with oral prednisolone at a daily dose of 15 mg. On October 2, 1993, she suddenly developed high fever and salmon-like pink eruption on her leg followed by the marked increase of serum transaminase and LDH levels (GOT 3,270 IU/l, GPT 1,880 IU/l, LDH 5,480 IU/l) on October 7. Since hepatic failure progressed, we started methylprednisolone pulse therapy and plasmapheresis. However, because of the progression of pancytopenia caused by hemophagocytosis, the treatment with VP-16 was initiated. However, she died of DIC on November 2, 1993. Autopsy revealed submassive necrosis of the hepatocytes with moderate infiltration of histiocytes. She was retrospectively diagnosed as hemophagocytic syndrome whose manifestations are very similar to those in adult Still's disease and acute viral hepatitis.
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PMID:[A case of hemophagocytic syndrome manifesting adult Still's disease and acute hepatitis]. 755 62


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