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A case of Budd-Chiari syndrome with high antiphospholipid antibody in a patient with systemic lupus erythematosus.

Yun YY, Yoh KA, Yang HI, Park SH, Lee SH, Cho CS, Kim HY - Korean J. Intern. Med. (1996)

Bottom Line: Antiphospholipid syndrome is characterized by recurrent episodes of arterial and venous thrombosis, spontaneous fetal losses, thrombocytopenia and persistently elevated levels of antiphospholipid antibodies.The clinical and laboratory findings were compatible with the cirteria for systemic lupus erythematosus (SLE) and she was found to have anticardiolipin antibody, thrombocytopenia and prolonged partial thromboplastin time.Initially, she was treated with intravenous heparin and uroki nase and she was followed up with warfarin, baby aspirin and steroids.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, Catholic University Medical College, Seoul, Korea.

ABSTRACT
Antiphospholipid syndrome is characterized by recurrent episodes of arterial and venous thrombosis, spontaneous fetal losses, thrombocytopenia and persistently elevated levels of antiphospholipid antibodies. We experienced a case of Budd-Chiari syndrome in a 32-year old female lupus patient who was presented with left leg edema, ascites and esophageal varix. The clinical and laboratory findings were compatible with the cirteria for systemic lupus erythematosus (SLE) and she was found to have anticardiolipin antibody, thrombocytopenia and prolonged partial thromboplastin time. Initially, she was treated with intravenous heparin and uroki nase and she was followed up with warfarin, baby aspirin and steroids.

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Inferior venocavogram.
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f2-kjim-11-1-82-10: Inferior venocavogram.

Mentions: On laboratory findings, hemoglobin was 10.6 g/dl, hematocrit 32%, white blood cell 8.1×103/mm3 (neutrophil 82%. lymphocyte 10%) and platelet 122×103/mm3. Renal function showed blood urea nitorgen 5.3 mg/dl, creatinine 0.9 mg/dl and 24hr urine protein 6.18 g/day. Urinanalysis showed 0 to 2 white cells and 10 to 20 red cells per high power fields. Lipid profile revealed total cholesterol 170 mg/dl. triglyceride 98 mg/dl and HDL-cholesterol 51 mg/dl. The AST was 16 IU/L. ALT 12 IU/L, alkaline phosphatase 229 IU/L, total bilirubin 0.7 mg/dl, total protein 4.1 g/dl and albumin 2.1 g/dl. The prothrombin time was 11.8 sec (control 12.1 sec) and activated partial thromboplastin time 59.2 sec (control 26.6 sec). On immunologic studies, FANA was positive (homogenous pattern, titer 1 : 1280), anti-ds DNA antibody 5 IU/ml, C3 21 mg/dl and C4 15 mg/dl. Rheumatoid factor was negative and ANCA was positive (GS-ANA, titer 1 : 80). Anti-cardiolipin antibody Ig G was 100 GPL IU/ml. Lupus anticoagulant was positive by the Kaolin clotting test. Anti-ENA and anti-Ro antibodies were all negative. The direct and indirect Coombs’ tests were all negative. The erythrocyte sedimentation rate was 18 mm/hr and C-reactive protein 2.4 mg/l. The immunoglobulin G, A, M levels revelaed 928, 274, 106 mg/dl, respectively. The serum viral hepatitis markers revealed that HBs antigen was negative, HBs antibody positive and HCV antibody negative. Gastrofiberscope showed esophageal varix, grade 2, and gastric fundal varix. Abdominal ultrasonography showed a moderate amount of ascites, moderate splenomegaly and marked coarse increased liver echogenecity. At computed tomography of the abdomen, we could not trace the inferior vena cava at the intrahepatic portion(Fig. 1). Doppler ultrasonography of the left leg showed no thrombosis in the superficial femoral vein and popliteal vein. Inferior and superior venocavograms showed obstructions at the intrahepatic portion of IVC and at both subclavian veins and abnormal collateral vessels were found around the obstructions (Fig. 2, 3). We injected Heparin 5,000 units and Urokinase 500,000 units intravenously at the bolus during venocavogram and further thrombolytic therapy (Heparin 5,000 units/day and Urokinase 500,000 units/day continuously all day long) was done for additional two days. We followed the venocavogram to evaluate the extent of thrombosis, compared with pre-thrombolytic therapy, but we could not find any interval change. We decided to give the patient Warfarin 5 mg/day, Prednisolone 1 mg/kg and baby aspirin 100 mg/day and to follow her up at the outpatient clinic.


A case of Budd-Chiari syndrome with high antiphospholipid antibody in a patient with systemic lupus erythematosus.

Yun YY, Yoh KA, Yang HI, Park SH, Lee SH, Cho CS, Kim HY - Korean J. Intern. Med. (1996)

Inferior venocavogram.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4532003&req=5

f2-kjim-11-1-82-10: Inferior venocavogram.
Mentions: On laboratory findings, hemoglobin was 10.6 g/dl, hematocrit 32%, white blood cell 8.1×103/mm3 (neutrophil 82%. lymphocyte 10%) and platelet 122×103/mm3. Renal function showed blood urea nitorgen 5.3 mg/dl, creatinine 0.9 mg/dl and 24hr urine protein 6.18 g/day. Urinanalysis showed 0 to 2 white cells and 10 to 20 red cells per high power fields. Lipid profile revealed total cholesterol 170 mg/dl. triglyceride 98 mg/dl and HDL-cholesterol 51 mg/dl. The AST was 16 IU/L. ALT 12 IU/L, alkaline phosphatase 229 IU/L, total bilirubin 0.7 mg/dl, total protein 4.1 g/dl and albumin 2.1 g/dl. The prothrombin time was 11.8 sec (control 12.1 sec) and activated partial thromboplastin time 59.2 sec (control 26.6 sec). On immunologic studies, FANA was positive (homogenous pattern, titer 1 : 1280), anti-ds DNA antibody 5 IU/ml, C3 21 mg/dl and C4 15 mg/dl. Rheumatoid factor was negative and ANCA was positive (GS-ANA, titer 1 : 80). Anti-cardiolipin antibody Ig G was 100 GPL IU/ml. Lupus anticoagulant was positive by the Kaolin clotting test. Anti-ENA and anti-Ro antibodies were all negative. The direct and indirect Coombs’ tests were all negative. The erythrocyte sedimentation rate was 18 mm/hr and C-reactive protein 2.4 mg/l. The immunoglobulin G, A, M levels revelaed 928, 274, 106 mg/dl, respectively. The serum viral hepatitis markers revealed that HBs antigen was negative, HBs antibody positive and HCV antibody negative. Gastrofiberscope showed esophageal varix, grade 2, and gastric fundal varix. Abdominal ultrasonography showed a moderate amount of ascites, moderate splenomegaly and marked coarse increased liver echogenecity. At computed tomography of the abdomen, we could not trace the inferior vena cava at the intrahepatic portion(Fig. 1). Doppler ultrasonography of the left leg showed no thrombosis in the superficial femoral vein and popliteal vein. Inferior and superior venocavograms showed obstructions at the intrahepatic portion of IVC and at both subclavian veins and abnormal collateral vessels were found around the obstructions (Fig. 2, 3). We injected Heparin 5,000 units and Urokinase 500,000 units intravenously at the bolus during venocavogram and further thrombolytic therapy (Heparin 5,000 units/day and Urokinase 500,000 units/day continuously all day long) was done for additional two days. We followed the venocavogram to evaluate the extent of thrombosis, compared with pre-thrombolytic therapy, but we could not find any interval change. We decided to give the patient Warfarin 5 mg/day, Prednisolone 1 mg/kg and baby aspirin 100 mg/day and to follow her up at the outpatient clinic.

Bottom Line: Antiphospholipid syndrome is characterized by recurrent episodes of arterial and venous thrombosis, spontaneous fetal losses, thrombocytopenia and persistently elevated levels of antiphospholipid antibodies.The clinical and laboratory findings were compatible with the cirteria for systemic lupus erythematosus (SLE) and she was found to have anticardiolipin antibody, thrombocytopenia and prolonged partial thromboplastin time.Initially, she was treated with intravenous heparin and uroki nase and she was followed up with warfarin, baby aspirin and steroids.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, Catholic University Medical College, Seoul, Korea.

ABSTRACT
Antiphospholipid syndrome is characterized by recurrent episodes of arterial and venous thrombosis, spontaneous fetal losses, thrombocytopenia and persistently elevated levels of antiphospholipid antibodies. We experienced a case of Budd-Chiari syndrome in a 32-year old female lupus patient who was presented with left leg edema, ascites and esophageal varix. The clinical and laboratory findings were compatible with the cirteria for systemic lupus erythematosus (SLE) and she was found to have anticardiolipin antibody, thrombocytopenia and prolonged partial thromboplastin time. Initially, she was treated with intravenous heparin and uroki nase and she was followed up with warfarin, baby aspirin and steroids.

Show MeSH
Related in: MedlinePlus