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

Chronic liver disease due to obstructive lesion of the hepatic inferior vena cava (IVC) is common in Nepal. This study presents 10 patients with cavographically documented membranous obstruction of the hepatic IVC with minimal symptoms and a benign course. One patient with an incomplete membrane had balloon dilation of the lesion. The duration of the disease among these patients varied from 5 months to 23 yr; eight patients have been followed for periods varying from 1 to 15 yr, with an average of 6 yr. In developing countries, the possibility of hepatic IVC obstruction should be considered in the differential diagnosis of hepatomegaly or hepatosplenomegaly, even in the absence of ascites and external cava-caval collateral. Routine liver and hematology tests in these patients usually are normal, and liver biopsy findings may not always be specific. Ultrasound, however, has proved to be the best diagnostic procedure for the condition. The lesion can be demonstrated easily by cavography. The disease runs a chronic course, and, in the absence of resistant ascites or repeated variceal bleeding, surgical procedures such as cavoatrial bypass, which are a significant cause of death in developing countries, may be contra-indicated.
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PMID:Membranous obstruction of the hepatic portion of the inferior vena cava: is this an underdiagnosed entity in developing countries? 867 37

Intra hepatic inferior venacaval (IVC) obstruction at the site or just above hepatic vein opening in the IVC, is a common hepatic problem in Nepal. These patients either present as a chronic IVC obstruction with insidious onset or may present with rapid onset disease (acute/subacute disease). The former type may be asymptomatic (20%) or may have features of chronic liver dysfunction. The latter presents with rapid onset ascites. Presence of hepatomegaly with flank/back veins are characteristic clinical features of the disease. The disease is invariably encountered amongst rural poor, alcoholic and in the peripartum period. Ultrasonography, IVC graphy hepatogram and liver biopsies are the usual diagnostic modalities. Twenty four percent of the 126 chronic hepatic IVC disease had associated liver cell cancer at our centre. The aetiology of the disease is unclear. Presently it is believed that local thrombophlebitis in IVC causes such obstruction. Despite, surgical and radiological intervention, the ideal management in such patients is yet to be established. We believe conservative therapy, particularly prevention and early therapy of sepsis in such patients prolongs survival.
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PMID:Hepatic venous outflow obstruction in Nepal. 898 5

Hepatic venous outflow obstruction also called the Budd-Chiari syndrome is increasingly being recognized as a cause of portal hypertension. In western countries the obstruction is usually in the hepatic veins while in reports from South Africa, Japan and India the predominant cause is a block in the IVC at the level of the diaphragm above the entry of the hepatic veins. A hypercoagulable state caused by myeloproliferative haematological disorders, clonal defects in haemopoietic stem cells, lupus anticoagulant, contraceptive pills and postpartum state are some of the aetiological conditions described. However in 25% to 75% cases no cause can be identified. The predominant presenting features in patients with hepatic vein obstruction are hepatomegaly and ascites while those with IVC obstruction show prominent veins on the trunk and back. Ultrasound examination should be the first investigative step. However a liver biopsy is the gold standard of diagnosis. To confirm the site of obstruction inferior vena cavography or functional hepatography may be required. In the acute phase thrombolytic therapy may be useful but for established cases either surgical intervention in the form of shunts or recently balloon angioplasty may be helpful. For patients with established cirrhosis and end-stage liver failure the only alternative is liver transplantation. All these patients however should be put on long term anticoagulants to prevent rethrombosis. Some series have reported that upto 45% of patients may develop hepatocellular carcinoma on long term followup. With proper management a larger proportion of patients can be returned to a useful productive life.
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PMID:Hepatic venous outflow obstruction. 982 3

This study was to evaluate the clinical effects of percutaneous balloon angioplasty of Budd-Chiari syndrome (BCS) caused by inferior vena cava (IVC) obstruction. Between 1993 and 1999, 28 men and 14 women with mean age of 44+/-12 years underwent percutaneous balloon angioplasty for primary BCS. Color Doppler ultrasound and venography showed membranous and segmental obstruction of IVC in 29 and 13 patients, respectively. Fourteen patients also had left- and/or mid-hepatic vein obstruction. Angioplasty of IVC was successful in 41 patients (97.6%), resulting in a reduction of pressure gradient between IVC and the right atrium from 15.0+/-2.5 to 5.5+/-0.8 mmHg (P<0.01). A stent was placed in the site of obstruction in the patient with unsuccessful balloon angioplasty. Patients with successful angioplasty or stent placement had significant improvement in clinical symptoms indicated by a reduction in hepatomegaly and the degree of ascites. No specific attempt was made to treat the occluded left- and/or mid-hepatic vein due to the presence of potent right hepatic vein. Over the follow-up period of 32+/-12 months, restenosis of IVC occurred in only one patient (2.4%), which was redilated successfully. Percutaneous balloon angioplasty is a safe and effective therapy for Budd-Chiari syndrome caused by IVC obstruction, therefore should be the first choice of treatment for this condition.
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PMID:Percutaneous balloon angioplasty of inferior vena cava in Budd-Chiari syndrome-R1. 1200 92

Abdominal pain with elevated transaminases from inferior vena cava (IVC) obstruction is a relatively common reason for referral and further workup by a hepatologist. The differential for the cause of IVC obstruction is extensive, and the most common etiologies include clotting disorders or recent trauma. In some situations the common etiologies have been ruled out, and the underlying process for the patient's symptoms is still not explained. We present one unique case of abdominal pain and hepatomegaly secondary to IVC constriction from extrinsic compression of the diaphragm. Based on this patient's presentation, we urge that physicians be cognizant of the IVC diameter and consider extrinsic compression as a contributor to the patient's symptoms. If IVC compression from the diaphragm is confirmed, early referral to vascular surgery is strongly advised for further surgical intervention.
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PMID:Trapped vessel of abdominal pain with hepatomegaly: A case report. 3053 89