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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We performed a prospective study including cytochemical, bacteriologic and pathologic observations in 25 patients with ascites of different causes. Activity of adenosine deaminase in ascitic fluid was higher in tuberculous (103 +/- 61 mu/l) than in neoplastic (16 +/- 8), inflammatory (16 +/- 13) and portal hypertension (15 +/- 6) etiologies (p less than 0.05). Inflammatory cases included patients with lupus and spontaneous peritonitis. Activity of adenosine deaminase was higher in every patient with tuberculosis than in any other patient. Thus, a high sensitivity and specificity of this test in the diagnosis of tuberculous peritonitis is confirmed.
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PMID:[Adenosine deaminase activity in peritoneal tuberculosis]. 251 74

A young woman with systemic lupus erythematosus developed portal hypertension and pulmonary hypertension. This is the first report of such a case. We suggest that the presence of the lupus anticoagulant may have been related to the development of these two unusual features of her illness.
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PMID:Portal and pulmonary hypertension in a case of systematic lupus erythematosus: possible relationship with a clotting abnormality. 644 58

A 26-year-old man with systemic lupus erythematosus (SLE) and a history of acute myocardial infarction developed portal hypertension accompanied by abnormal liver function and esophageal varices. As his clinical course suggested the possibility of antiphospholipid syndrome, a titer of anticardiolipin antibody (aCL) was serially measured using an enzyme immunoassay with beta 2-glycoprotein I as a cofactor. The titer of aCL increased with the development of portal hypertension, and promptly decreased with the improvement of liver function just after corticosteroid therapy. The long-term course in this case suggests that aCL may cause portal hypertension associated with SLE.
Lupus 1995 Jun
PMID:Portal hypertension associated with anticardiolipin antibodies in a case of systemic lupus erythematosus. 765 97

Patients with systemic lupus erythematosus (SLE) have a 25-50% chance of developing abnormal liver tests in their lifetime. This percentage does not include unconjugated hyperbilirubinaemia due to haemolysis associated with SLE, or elevated aspartate-aminotransferase caused by SLE-associated myositis. The most common cause is drug-induced hepatitis, while mild, predominantly lobular-but sometimes also portal and periportal-hepatitis reflecting SLE activity is another possibility. Other liver disease in SLE can be related to thrombotic events, whether or not associated with the lupus anticoagulant, including Budd-Chiari syndrome and veno-occlusive disease. Other liver abnormalities have been more or less frequently associated with SLE, such as nodular regenerative hyperplasia, perihepatitis, and hepatic or splenic rupture. Also viral hepatitis, obstructive jaundice, autoimmune hepatitis, primary biliary cirrhosis, granulomatous hepatitis, cryptococcus infection of the liver, chronic hepatitis with IgA or IgD deficiency, porphyria or idiopathic portal hypertension co-existing with SLE have been described.
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PMID:The spectrum of liver disease in systemic lupus erythematosus. 871 47

Sixty-five abdominal computed tomography (CT) scans of 54 systemic lupus erythrematosus (SLE) patients were retrospectively evaluated together with their clinical records. This was to assess the spectrum of CT findings and to determine the value of abdominal CT in this group of patients. Over a 3.5-year period, abdominal CT scans had been requested for suspected renal vein or inferior vena cava thrombosis (n = 52, 80%), sepsis, mesenteric ischaemia, Conn's syndrome, evaluation of hepatosplenomegaly, portal hypertension and hydronephrosis. The most frequent indication for CT was suspected renal vein thrombosis (RVT). An SLE patient with previously stable renal function who rapidly develops nephrotic syndrome with deteriorating renal function has an increased risk of thromboembolic phenomenon. Also, renal vein thrombosis is difficult to diagnose clinically and prompt anticoagulation can help preserve remaining renal function. Of these with suspected RVT, two had RVT only and five had thrombosis in both renal veins and inferior vena cava. Two patients had CT features strongly suggestive of mesenteric ischaemia, one had bilateral hydronephrosis thought to be secondary to lupus cystitis and CT confirmed two abdominal abscesses. Other incidental CT findings were: subscapular renal haematoma, overall enlargement or diminution of renal size, serositis, bowel wall thickening, splenic, hepatic and pancreatic enlargement and mild para-aortic lymphadenopathy. Abdominal CT revealed many diverse findings and aided the management of these SLE patients.
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PMID:Abdominal computed tomography in systemic lupus erythematosus. 911 46

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

One of the causes of portal hypertension is portal vein thrombosis (PVT). The aim of this study was to determine whether natural anticoagulant deficiencies, activated protein C resistance (APCR), and factor V Leiden play a role in the development of PVT, leading to cavernous transformation of the portal vein (CTPV). Twenty-three patients with idiopathic CTPV (group 1) seen at Hacettepe University Hospital during the past 12 years were identified and prospectively studied. These 23 patients underwent a detailed hematological evaluation including measurement of protein S, protein C, antithrombin III, activated protein C resistance (APCR), and factor V Leiden gene mutation. Additionally, all patients were tested for anticardiolipin antibodies (ACA), IgG, IgM, and lupus anticoagulant (LA). Natural anticoagulants and APCR were measured using available commercial kits, and factor V Leiden mutation (R506Q) was detected by Mnl I digestion of an amplified factor V DNA fragment. All parameters were measured at least 6 months after the diagnosis of CTPV was established. No patient was on anticoagulant or antiaggregant treatment while tested. The findings in these 23 patients were compared with those in 20 healthy control subjects (group 2), in whom all tests mentioned above were also performed. In 23 patients (group 1), who had no recognizable factor for portal vein thrombosis, considerably natural anticoagulant deficiencies and factor V Leiden mutation positivity were found when we compare them to those healthy controls (group 2). The protein C levels of six patients (26%), the protein S levels of 10 patients (43.5%), and the antithrombin III levels of five patients (26%) were lower than in control subjects. Two patients were found to have combined protein S and antithrombin III deficiency, and one had combined protein S and C deficiency and APCR. APCR was detected in seven of the 23 patients, and six of these seven patients were found to have R506Q factor V Leiden mutations. In group 1, ACA IgG levels were higher in four patients (17%) and ACA IgM level was higher in one (4%) compared with the control group. LA was positive in only one patient in group 1. Natural anticoagulant deficiencies and factor V Leiden mutation are strongly associated with PVT. The natural anticoagulant deficiencies and APCR (almost totally caused by R506Q mutation) produce a favorable medium for thrombus generation. PVT seems to be related to the natural anticoagulant deficiencies and factor V Leiden R506Q mutation. A combination of these defects increases the incidence of PVT and these factors should be evaluated carefully in patients with idiopathic CTPV.
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PMID:The role of natural anticoagulant deficiencies and factor V Leiden in the development of idiopathic portal vein thrombosis. 1063 14

A case of idiopathic portal hypertension (IPH) associated with systemic lupus erythematosus (SLE) is reported in a 38-year-old man who had been diagnosed with SLE and treated for 18 years. Esophageal varices. found in 1994 on endoscopic examination, had been followed up for 2 years. On July 16, 1996, he was admitted to Nagoya University Hospital because there was a high risk of bleeding from the esophageal varices due to severe thrombocytopenia. As partial splenic embolization had temporarily controlled the thrombocytopenia, splenectomy and devascularization of the stomach vessels were performed after endoscopic ligation of the esophageal varices. Histological specimens of wedge biopsied liver showed chronic inactive hepatitis without cirrhosis. The presence of anticardiolipin antibody, indicated by positivity for lupus anticoagulant, was suggestive of the presence of a common immunological mechanism in the etiology of SLE and IPH.
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PMID:Idiopathic portal hypertension associated with systemic lupus erythematosus. 1075 94

Nodular regenerative hyperplasia of the liver (NRH), characterized by multiple hepatic nodules in the absence of fibrosis, is a rare but important complication of systemic lupus erythematosus (SLE) associated with non-cirrhotic portal hypertension. The diagnosis of NRH is based on the pathological examination, and radiological findings of NRH are poorly documented. We report a case of a 40-year-old woman with SLE complicated with NRH. Sixteen years after diagnosis of SLE, esophageal varices were incidentally found and diagnosis of portal hypertension due to NRH was made by magnetic resonance imaging (MRI) and confirmed by needle liver biopsy. Although MRI showed the lesions as significant nodules, neither computed tomography nor ultrasonography could demonstrate the nodules. However, serial MRI showed significant enlargement of the nodules for 2 years Because NRH may lead to portal hypertension with life-threatening variceral haemorrhage in patients with SLE, MRI is a useful, non-invasive examination to screen the patients for its presence and follow-up. We reviewed the literature regarding NRH in SLE and discuss the management of the affected patients.
Lupus 2002
PMID:Significance of magnetic resonance imaging in the diagnosis of nodular regenerative hyperplasia of the liver complicated with systemic lupus erythematosus: a case report and review of the literature. 1199 86

A 37-year old woman with systemic lupus erythematosus (SLE) complicated by pulmonary hypertension (PHT) was admitted to evaluate abnormal liver function. Radiological imaging study, including ultrasonography, computed tomography and magnetic resonance imaging and upper gastrointestinal endoscopy, revealed multiple hepatic nodules, hepatosplenomegaly and esophageal varices. Percutaneous needle liver biopsy showed non-cirrhotic hepatic nodules with hyperplastic hepatocytes surrounded by atrophic hepatocytes, confirming the diagnosis of nodular regenerative hyperplasia (NRH) associated with non-cirrhotic portal hypertension (PT). NRH of the liver is known to be a very rare hepatic manifestation in rheumatic diseases. This case shows the association of NRH with porto-pulmonary hypertension in SLE.
Lupus 2006
PMID:Association of nodular regenerative hyperplasia of the liver with porto-pulmonary hypertension in a patient with systemic lupus erythematosus. 1712 May 97


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