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

Acute and/or recurrent gastrointestinal bleeding due to ruptured gastric varices from an isolated thrombosed splenic vein is a distinct entity. Incidence of this syndrome is probably less than 1%. Typical clinical features of this syndrome include evidence of splenic hypertension without liver disease and no demonstrable cause of gastrointestinal hemorrhage. Diagnosis can easily be missed unless the surgeon is familiar with this syndrome. Typical findings at the time of surgery are an enlarged spleen, varicose veins usually involving the upper third of the stomach, and pancreatic and peripancreatic inflammation. Portal vein and portal pressure will be normal. Meso-portography is a convenient and safe procedure and will lend support to suspicion when a retrograde nonfilling of the splenic vein is present. Splenectomy offers the expectation of a long-range cure. A representative case of a 39-year-old man is discussed. He had at least six episodes of gastric bleeding in less than 3 years. At a previous laparotomy, the cause of bleeding could not be determined. A splenectomy in December 1970 has been able to control the gastric bleeding since then.
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PMID:Splenic vein thrombosis: an unusual case of gastric bleeding. 30 66

In 5 patients with portal hypertension caused by schistosomiasis, the sinusoidal pressure (wedged hepatic pressure) varied from 20.7 to 35.4 mm Hg. While the catheter was in an occluded position within the hepatic vein and the patients were undergoing splenectomy, the main trunk of the hepatic artery was clamped. The sinusoidal pressures then fell to levels that varied from 3.7 to 7.4 mm Hg but returned to previous levels when the clamping was released. Wedged hepatic venous pressure levels, which were significantly greater than portal venous pressure values, decreased minimally after splenectomy. Portal venous pressure levels, however, fell to 63% of presplenectomy levels. In a control case with an enlarged spleen (cavernous hemangioma, but with a normal liver, the wedged hepatic pressure was 7.4 mm Hg and showed no alteration after clamping of hepatic artery. These data point out the importance of hepatic artery hypertrophy, that has already been demonstrated in other studies, in causing elevation of the wedged hepatic pressure in advanced hepatic schistosomiasis.
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PMID:Hepatic artery hypertrophy and sinusoidal hypertension in advanced schistosomiasis. 31 79

Nodular regenerative hyperplasia of the liver was identified at autopsy in a patient with myelofibrosis with extramedulary hematopoiesis, an association not previously reported. Portal venous hypertension, documented during the patient's terminal hospitalization, was ascribed, in part, to a high rate of blood flow through the enlarged spleen. Possible mechanisms accounting for the development of nodular regenerative hyperplasia of the liver, and evidence provided by this case pertinent to these mechanisms, are discussed.
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PMID:Nodular regenerative hyperplasia of the liver in a case of myelofibrosis with extramedullary hematopoiesis and secondary portal venous hypertension. 45 99

A total of 13 cases of ASL have been documented to date among VC workers in four different plants in the United States. In this particular industrial population, this number of cases represents at least a 400-fold increase over expected incidence for this extremely rare tumor. The first case occurred in 1961. Average age at diagnosis is 48.2 years. Average length of time between initial VC work and diagnosis has been 20.3 years. A detailed review of 7 cases associated with one plant revealed that clinical features varied from little or no overt illness prior to diagnosis to advanced liver disease with portal hypertension and marked splenomegaly. Portal fibrosis was present in all 7 of these ASL cases as well as in 4 additional cases with non-malignant liver disease among VC workers at the same plant. These findings suggest that exposure to VCM in industrial settings can produce hepatic fibrosis with angiosarcoma as a late manifestation. Conventional liver function tests may not be sensitive indicators of such liver impairment, at least in its early stages.
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PMID:Characteristics of cases of angiosarcoma of the liver among vinyl chloride workers in the United States. 105 56

Portal haemodynamic studies were carried out in 11 subjects, seven with chronic myeloid leukaemia and four with chronic lymphatic leukaemia, and results compared with those obtained in five patients with 'idiopathic' splenomegaly and with control subjects. All 11 patients with chronic leukaemia had intrasplenic pressures above 11 mmHg and of these four had pressures above 20 mmHg. Portosystemic collaterals were seen on splenovenography in four of these patients. Hepatic vein wedge pressure was above 7 mmHg in nine patients and these high levels were a result of increased free hepatic vein pressure. The corrected sinusoidal pressure and post sinusoidal resistance were essentially normal in all patients. Evidence of increased pre-sinusoidal resistance was seen in six patients. Estimated hepatic blood flow above 1500 ml/min was seen in six patients and all had evidence of histological portal or sinusoidal infilatration. Patients with 'idiopathic' splenomegaly regardless of increased liver blood flow did not have a significant increase in intrasplenic pressure and no alteration in other haemodynamic parameters. It appears that increased liver blood flow alone in a normal liver can only minimally elevate intrasplenic pressure but can play a significant part in the pathogenesis of portal hypertension when liver structure is altered.
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PMID:Portal hypertension in chronic leukaemia. 105 78

Growth rate and histology of splenic autotransplants in subcutaneous pockets were compared with those of autotransplants in the extrahepatic portal bed in splenectomized mice infected with cercariae of Schistosoma mansoni and in splenectomized uninfected controls. By the fifteenth week after transplantation (and tenth week after injection of cercariae) subcutaneous transplants gained 6.5 times and omental transplants 8.2 times more weight in infected animals than corresponding transplants in uninfected animals. Portal pressures averaged 11 to 13 cm of water in infected animals with transplants and 17 cm in those with intact spleens (compared to that of 6 to 7 cm in controls). Hyperplasia of white pulp with increase in germinal center activity characterized transplants as well as intact spleens of infected animals. The results suggest that a) During the first 10 weeks of experimentally induced infection, portal congestion is not the predominant mechanism regulating increased spleen growth; and b) An intact enlarged spleen appears to contribute to elevated portal pressure.
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PMID:Regulation of spleen growth and portal pressure in hepatic shcistosomiasis. 111 19

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 sonographic parameters in portal hypertension (PHT) were examined in a consecutive population of 118 patients who had PHT diagnosed using specific endoscopic, sonographic and Doppler signs. A patent or enlarged paraumbilical vein was found in 85.6% of patients overall and 82.5% of patients with varices indicating a relatively high sensitivity. A portal vein diameter greater than or equal to 13mm was found in only 41.1% and greater than or equal to 15mm in only 20% of patients. A thrombosed portal vein and reversed portal vein flow were present in 3.4% and 5.3% of patients respectively. These signs have only been reported in the context of PHT and are felt to be specific for PHT, but both have a very low sensitivity. Portal vein velocities were highly variable suggesting that this is not a useful predictor of PHT. Splenomegaly was found in only 53.5% of patients demonstrating its poor sensitivity as a sign of PHT. Varices were found in 73.3% of patients overall, and in 100% of patients with a patent or enlarged paraumbilical vein combined with ascites. No other statistically significant correlation between varices and sonographic findings was demonstrated. We conclude that the presence of a patent or enlarged paraumbilical vein is a practical, useful and sensitive ultrasound sign to look for in the diagnosis of PHT.
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PMID:Duplex Doppler ultrasound signs of portal hypertension: relative diagnostic value of examination of paraumbilical vein, portal vein and spleen. 152 Jan 64

The microsomal content and activity of the principal male-specific cytochrome P450 2C11 are reduced in cirrhotic rat liver. In order to define the pathophysiological mechanism for such changes, the present study was undertaken to determine the time course of impaired P450 2C11 expression in relation to the development of cirrhosis during intake of a choline-deficient diet. Fatty infiltration of the liver was evident after 6 weeks of intake but hepatic fibrosis was not present until 10 weeks, when fine fibrotic bands in a perisinusoidal distribution were observed. Fibrotic bands were progressively more prominent at 20 and 25 weeks and cirrhosis was established by 30 weeks of dietary intake. Portal pressure, as measured by saline manometry and indicated by splenomegaly, appeared to increase gradually after 6 weeks and by 25 weeks values were significantly greater than controls. The microsomal content of P450 2C11 and its associated steroid 16 alpha-hydroxylase activity were unchanged at 6 weeks but were decreased to around 30% of control from 10 weeks of intake of the choline-deficient diet to the end of the experimental period (30 weeks). Serum bile acids were approximately 2-fold greater in choline-deficient rats from 10 weeks. Similarly, serum estradiol concentrations were elevated (to 2.5-fold of control) in male rats after 10 weeks intake of the choline-deficient diet; this increase was sustained in 30-week cirrhotic rats. On the other hand, there was no evidence of altered serum testosterone until 30 weeks of dietary deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impaired expression of microsomal cytochrome P450 2C11 in choline-deficient rat liver during the development of cirrhosis. 156 Mar 81

A comparative study of portal hemodynamics was made in 79 cirrhotics (24 cirrhotics with a large spleen greater than or equal to 500 cm3 in volume, 55 cirrhotics with a spleen less than 500 cm3 in volume), 22 patients with idiopathic portal hypertension, and 63 healthy adults who served as the control for portal and splenic venous flows. Portal and splenic venous flows were significantly increased in the group order of the cirrhosis without splenomegaly group, the cirrhosis with splenomegaly group, and idiopathic portal hypertension group. Intrahepatic shunt index was significantly greater in the cirrhosis with splenomegaly group than in the cirrhosis without splenomegaly group, and it was negligible in the idiopathic portal hypertension group. Portal vein pressure was significantly elevated in the cirrhosis with splenomegaly group than in the cirrhosis without splenomegaly and idiopathic portal hypertension groups. Postsinusoidal resistances were significantly greater in the two groups of cirrhosis than in the idiopathic portal hypertension group, whereas presinusoidal resistance was significantly greater in the idiopathic portal hypertension group than in the two groups with cirrhosis. It is concluded that these differences are inconsistent with the view that cirrhosis with splenomegaly comes from idiopathic portal hypertension.
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PMID:Differences in portal hemodynamics in cirrhosis and idiopathic portal hypertension. 292 62


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