Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sonography and duplex Doppler frequently fail to identify a cause for right upper quadrant pain, liver dysfunction, or ascites. The aim of our study was to describe and analyze the pulsatile portal venous waveform in which minimum velocity dropped to or below zero on duplex Doppler sonography and to investigate its possible association with tricuspid regurgitation, one of the causes of liver dysfunction. We correlated the findings in 15 patients in whom this duplex Doppler waveform was seen with the findings on Doppler echocardiography (n = 14) or ultrafast CT (n = 1). All patients had biochemical liver abnormalities or sudden onset of ascites, rapid weight gain, increased abdominal girth, and hepatomegaly. They were referred for sonography to rule out liver metastases, biliary disease, portal vein thrombosis, or Budd-Chiari syndrome. All examinations were done with a 3-MHz phased-array sector transducer with duplex Doppler capability. Seventeen volunteers with no known liver or heart disease served as a control group. We correlated maximum and minimum flow velocities on the portal venous Doppler waveform with the portal vein diameters of the study and control groups. Thirteen patients were later proved to have tricuspid regurgitation, one patient had an aortic-right atrial fistula owing to rupture of an aneurysm of the sinus of Valsalva, and one patient was proved to be normal. In none of the 17 control subjects was this pulsatile portal venous waveform seen. Our study shows that detection of a pulsatile portal venous waveform on duplex Doppler sonography in patients with liver dysfunction should raise the possibility of tricuspid regurgitation.
 ...
PMID:Pulsatile portal vein flow: a sign of tricuspid regurgitation on duplex Doppler sonography. 211 8

From 1984 to 1989, 52 cases with Budd-Chiari syndrome were surgically treated at the PUMC Hospital. Among them there were 31 cases of membranous obstruction of the inferior vena cava (MOVC, 59.6%). There were 24 males and 7 females, ase ranging from 24 to 36 years. Diagnosis was confirmed by inferior venocavagraphy. According to Sugiura's Classification, there were type Ia and Ib in 26 cases, and type II in 5. Edema and varicosity on both legs, the chest, the abdomen, and the back were found in 93.5% (29/31), and hepatomegaly, splenomegaly, and large amount of ascites were found in 61.3% (19/31), 64.5% (20/31), and 54.8% (17/31), respectively. Transcardiac membranotomy was performed in 27 cases, and the remaining 4 cases were treated by percutaneous transluminal angioplasty using balloon catheters both without operative mortality. Four to sixty months' follow-up in 29 cases revealed satisfactory results. The authors belief that membranotomy can be successfully performed in cases of MOVC when the stricture is located well above the level of T-9th vertebra, and with a length of less than 2 cm.
 ...
PMID:[Diagnosis and treatment of membraneous obstruction of the inferior vena cava]. 215 Jul 99

Budd-Chiari syndrome is caused by the obstruction of the hepatic veins or of the inferior vena cava. It is characterized by the classic symptomatological triad: ascites, hepatomegaly, and abdominal pain. In 2/3 cases its etiology remains unknown. Budd-Chiari syndrome may be associated with polycythemia vera, neoplasms, chronic leukemia, congenital abnormalities, hypercoagulation conditions, pregnancy, oral contraceptives, and constrictive pericarditis. Even though its clinical diagnosis is difficult, radiology plays a decisive role with US, CT, MR imaging and, above all, angiography; the latter, together with liver biopsy, generally provides with an unquestionable diagnosis. Through the definition of stage of the disease, of level (intrahepatic, venous, caval, cardiac), of type (intrinsic or extrinsic), and degree of both obstruction and consequent development of collateral channels, radiology determines which patients should undergo a medical or a surgical treatment. In some case, percutaneous angioplasty can be performed. Four cases of Budd-Chiari syndrome, including two children, were investigated with US, CT, angiography, and liver biopsy; MR imaging was also employed in one case. The underlying cause was identified in 3 patients: constrictive pericarditis of probable congenital origin and web occlusion of the inferior vena cava near the right atrium in the 2 children; hepatic vein thrombosis due to essential thrombocythemia in the third case. In the fourth patient, thrombosis of the inferior vena cava and hepatic veins was unexplained. The diagnosis was established by means of liver biopsy and phlebography of the hepatic veins. Good diagnostic information was also supplied by non-invasive techniques, such as US, CT, and MR imaging.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Diagnostic imaging of Budd-Chiari syndrome in adults and children]. 218 5

Nine out of 10 patients with primary lymphoma of the liver presented in a manner that did not suggest a tumour. The initial diagnoses were chronic active hepatitis in three cases and "granulomatous cholangitis", inflammatory pseudotumour, and anaplastic carcinoma in one case each. Moreover, extensive haemorrhagic necrosis in three cases initially suggested the Budd-Chiari syndrome. All the tumours were diffuse non-Hodgkin's lymphomas like the 50 cases reported previously, but they differed from most of these in that nine were of T cell phenotype. Five were pleomorphic small T cell, two T zone, and two T lymphoblastic lymphomas: only one was centrocytic and of B cell lineage. This report extends the range of clinical manifestations (diffuse hepatomegaly without a tumour), histological appearances (resemblance to chronic inflammatory or vascular liver diseases) and phenotype (of T cell lineage) of primary lymphoma of the liver: these features seemed to be related in this series. Recognition is important as prognosis remains favourable in appropriately treated cases. Although the appearances of the liver biopsy specimens may be difficult to interpret, the destructiveness of the infiltrate is an important clue to the diagnosis.
 ...
PMID:Primary lymphoma of the liver: clinical and pathological features of 10 patients. 226 72

The authors describe a child with Budd-Chiari syndrome secondary to membranous obstruction of the hepatic veins and a web in the inferior vena cava. Transhepatic catheter venography demonstrated the occlusion, which was recanalized and dilated percutaneously via a transhepatic approach. Hepatomegaly and ascites decreased promptly and the prothrombin time became normal.
 ...
PMID:Budd-Chiari syndrome: treatment with percutaneous transhepatic recanalization and dilation. 252 37

Renal vein thrombosis in early infancy is a complication of dehydration and prolonged hypotension. The onset is usually acute and the most common clinical signs are uni- or bilateral frank masses, hematuria, proteinuria and thrombocytopenia. In most cases, with conservative management, the late outcome is favorable. In the adult, renal vein thrombosis is often a silent complication of the nephrotic syndrome, the hypercoagulability of which may be an important factor in the pathogenesis of the thrombosis. Clinically, the presentation of a sudden complete occlusion is that of severe abdominal and lumbar pain with hematuria and loss of function of the kidney that suffers hemorrhagic infarction. Physical examination often reveals an enlarged kidney. With gradual occlusion, renal function is preserved. The initial diagnostic approach is with ultrasound studies and computed tomography; definitive diagnosis is established by renal venography or by selective renal arteriography. In general, a conservative approach including the use of anticoagulant treatment is preferred to surgical intervention. Priapism is a persistent painful penile erection due to ischemic or non-ischemic causes; therapeutic intracavernosal injection of papaverine is becoming the most common cause. In early and mild stages, aspiration of blood from the corpora cavernosa supplemented with intracavernosal irrigation with alpha-stimulating agents is the procedure of first choice; in late and severe ischemia, a shunt procedure may become necessary. Hepatic vein thrombosis occurs in association with a number of conditions considered predisposing factors including the use of oral contraceptives. The clinical picture may be that of an acute illness with abdominal pain, hepatomegaly, ascites and hepatic failure as well as early death. More often, the onset is insidious with slowly developing ascites and wasting. For the diagnosis, hepatic scintigraphy may be helpful but, at present, ultrasonography, computed tomography and magnetic resonance scanning are procedures of choice. There is, as yet, no adequate treatment. A fatal outcome may be prevented by surgical decompression of the congested liver and, in recent years, liver transplantation has been employed. Portal vein thrombosis, in children, is usually considered a complication of umbilical sepsis or a result of a congenital abnormality of the portal vein. In adults, the most frequent causes are hepatic cirrhosis and neoplasia. Clinically, there may be a sudden appearance of ascites with resolution in a symptom-free interval until the onset of other features of portal hypertension occur. Currently, ultrasound real-time imaging supplemented with Doppler capability, computed tomography and magnetic resonance scanning provide the necessary diagnostic information. Variceal hemorrhage is often the first major complication requiring treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Thrombosis in particular organ veins. 268 Aug 53

Passive liver congestion secondary to increased hepatic venous pressure may accompany congestive heart failure. Abnormal patterns of hepatic parenchymal contrast medium enhancement in 25 patients with advanced congestive heart failure who were studied with computed tomography (CT) include a lobulated, patchy, inhomogeneous pattern in all 25 patients, an irregular perivascular enhancement in 14, and a global delay in parenchymal enhancement in nine. CT examinations showed cardiomegaly in the 20 patients with cardiac failure and pericardial effusion or thickening in the five patients with pericardial disease. Also noted were distention of the inferior vena cava (IVC) in 24 patients, hepatomegaly in 23, early reflux of contrast medium into the IVC in 21 and hepatic veins in 16, and hepatic perivascular lymph-edema in six. The abnormal patterns are thought to be due to slowing of hepatic blood flow. Confusion with Budd-Chiari syndrome and other forms of multifocal hepatic disease is avoidable with clinical and radiologic correlation.
 ...
PMID:Inhomogeneous enhancement of liver parenchyma secondary to passive congestion: contrast-enhanced CT. 291 31

Ascites, hepatomegaly, and abdominal pain constitute the classic triad of the Budd-Chiari syndrome of hepatic-vein or inferior-vena-cava obstruction. This condition was first mentioned by Budd in the mid 1800s and additional information was provided by Chiari in the 1890s. In nearly two-thirds of patients the exact etiology cannot be determined. The syndrome has, however, been associated with hypercoagulable states, neoplasms, trauma, medications, and congenital abnormalities. The diagnosis is difficult to make clinically; therefore, radiology plays a critical role in the workup of these patients. Nuclear medicine, sonography, CT, angiography, and MRI all provide valuable diagnostic information. These data combined with hepatic biopsy determine which patients should be treated by percutaneous angioplasty or surgery, and also determine the type of shunt to be performed (such as the mesoatrial shunt when the inferior vena cava is occluded or severely compressed). Noninvasive imaging is also useful in the follow-up of patients after both percutaneous angioplasty and surgery.
 ...
PMID:The Budd-Chiari syndrome: a review. 294 Aug 46

A rare chronic course of Budd-Chiari syndrome associated with thrombosis of the portal vein was observed in a 30-year-old male patient suffering from postmyocarditic cardiosclerosis. At the age of 24 the patient had infectious allergic myocarditis, was hospitalized and rehospitalized for circulatory insufficiency. Upon 3 years since the disease onset the patient was admitted to a hematological department for progressive enlargement of the spleen. The diagnosis on discharge was idiopathic myelofibrosis with portal hypertension. The treatment included prednisolone, blood transfusions, myelosan. In 1987 the patient presented with enlarged liver and spleen, ascites, gastric and esophageal varicosis, augmenting hepatic insufficiency clinically evaluated as hepatic cirrhosis. Postmortem examination revealed macrofocal cardiosclerosis, splenomegaly, ascites, portal varicosis, enlarged nutmeg liver with smooth surface. Microscopically there was phlebosclerosis and phlebothrombosis varying in duration and involving predominantly medial branches of the hepatic and portal veins, liver fibrosis. The findings provided evidence for the final diagnosis of Budd-Chiari syndrome running an uncommon chronic course.
 ...
PMID:[The chronic form of the Budd-Chiari syndrome]. 297 4

A 22-year-old female with active ulcerative colitis developed massive ascites, hypoalbuminemia, and hepatomegaly compatible with thrombosis of the hepatic veins. The diagnosis of Budd-Chiari syndrome was confirmed by ultrasonography, computed tomography, and by liver biopsy. A search of the literature disclosed only three previous reports of Budd-Chiari syndrome occurring in patients with ulcerative colitis. All patients have been young females with active colitis and no other known risk factor for the development of hepatic vein thrombosis. Our patient, unlike the previously reported patients who died, recovered sufficiently to be discharged from the hospital.
 ...
PMID:Recovery from hepatic vein thrombosis (Budd-Chiari syndrome) complicating ulcerative colitis. 319 87


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>