Cases reported "Polycythemia Vera"

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1/25. Anemic infarction of the liver resulting from hepatic and portal vein thrombosis.

    True anemic infarction of the liver is a rare lesion. Most of the reported cases are due to occlusion of the hepatic artery. Whether venous occlusion can result in such anemic infarcts has been disputed although few authentic cases have been reported. A case of polycytheia vera complicated by hepatic and portal vein thrombosis with anemic infarction of a large segment of the liver is presented. The case illustrates that anemic infarcts of the liver can result from venous occlusion. The intense congestion secondary to hepatic vein occlusion may cause secondary arterial hypoperfusion unless the portal vein is available as an outflow tract.
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ranking = 1
keywords = hepatic
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2/25. Spontaneous cervical hematoma: a report of two cases.

    Cervical hematomas are generally associated with trauma, surgery, and tumors. Although they are rare, they can be life-threatening because they put the patient at risk for great-vessel compression and upper airway obstruction. We describe two cases of spontaneous cervical hematoma--one in an 81-year-old man and the other in a 30-year-old woman. The man reported dysphonia, dysphagia, and neck swelling of 5 hours' duration. He had been taking 100 mg/day of aspirin for a cardiovascular condition. Examination revealed that the man had polycythemia vera. The woman was found to have neck ache, odynophagia, and cervical ecchymosis; portal hypertension, schistosomiasis, and blood dyscrasia were also found. Both patients denied trauma. A suspected diagnosis of cervical hematoma was confirmed by computed tomography, and treatment was instituted. The hematomas resolved in about 2 weeks. The treatment of cervical hematoma is controversial, although it is agreed that the evaluation of upper airway obstruction and its permeability is mandatory. Surgical treatment is generally reserved for complicated cases because of the risk of infection or bleeding.
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ranking = 0.1564241518415
keywords = obstruction
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3/25. budd-chiari syndrome complicating restorative proctocolectomy for ulcerative colitis: report of a case.

    PURPOSE: This is a case of hepatic vein thrombosis presenting in a delayed fashion after proctocolectomy with ileal pouch-anal anastomosis for ulcerative colitis. Search for a causative thrombotic condition resulted in the diagnosis of polycythemia vera, a myeloproliferative disorder associated with hypercoagulability. The polycythemia was masked by an iron deficiency associated with the ulcerative colitis. methods: The history, physical, diagnostic modalities, and treatment for this patient are described, and the literature of budd-chiari syndrome associated with ulcerative colitis is reviewed. RESULTS: Six cases of budd-chiari syndrome in the setting of ulcerative colitis are reported in the literature from 1945 to 1997. CONCLUSIONS: Hepatic vein thrombosis is a rare complication of ulcerative colitis. The diagnosis of budd-chiari syndrome demands a thorough search for a hematologic condition predisposing to thrombosis. Our patient had a myeloproliferative disorder, polycythemia vera, that is associated with a hypercoagulable state. The disorder was masked by an iron deficiency associated with the ulcerative colitis. Recognition of the entity will permit successful treatment.
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ranking = 0.14285714285714
keywords = hepatic
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4/25. Early medical treatment is life saving in acute Budd-Chiari due to polycythemia vera.

    Here we describe two women with polycythemia vera presented with fulminant hepatic failure due to acute budd-chiari syndrome. Both had a history of severe abdominal pain and distention of short duration. Clinical and laboratory findings showed fulminant hepatic failure due to acute budd-chiari syndrome. Diagnosis was confirmed with abdominal ultrasonography and Doppler ultrasonography showing ascites, hepatomegaly, portal hypertension and total occlusion of hepatic veins. Complete blood count and other clinical findings were compatible with polycythemia vera in both patients. patients were treated successfully with early administration of continuous heparin infusion, repeated phlebotomies and hydroxyurea. We emphasize here early diagnosis and effective treatment in such fulminant cases may be life saving.
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ranking = 0.42857142857143
keywords = hepatic
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5/25. Familial polycythemia vera with budd-chiari syndrome in childhood.

    polycythemia vera is a myeloproliferative disorder that, in most cases, occurs sporadically with a median age at presentation of 60 years. Familial cases are very rare and usually manifest in elderly family members. The budd-chiari syndrome, characterized by the obstruction and occlusion of the suprahepatic veins, is a rare typical complication in polycythemia vera patients. To date, only two children or adolescents with polycythemia vera and budd-chiari syndrome have been described. Here, we report an 11-year-old girl with budd-chiari syndrome as the initial symptom of familial polycythemia vera, which was also found in the girl's grandmother. Details of the diagnostic procedures used and the clinical course are reported. The patient underwent orthotopic liver transplantation and is being treated with hydroxyurea. The available literature on familial polycythemia vera and polycythemia vera in childhood with and without budd-chiari syndrome is reviewed.
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ranking = 0.22106921877789
keywords = hepatic, obstruction
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6/25. polycythemia vera in a child following treatment for acute lymphoblastic leukemia.

    polycythemia vera (PV), a hematologic stem cell disorder characterized by predominant erythroid proliferation, is extremely rare in childhood. Some PV patients develop acute leukemia, especially acute myelogenous leukemia, but cases of PV occurring after treatment of acute leukemia are rare. The authors describe a girl with an atrioventricular canal who was diagnosed with acute lymphoblastic leukemia (ALL) at 23 months of age, was cured with chemotherapy, and developed PV 7 years later. She went on to develop hepatic complications of PV that culminated in death from liver disease at 20 years of age, without recurrence of ALL.
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ranking = 0.14285714285714
keywords = hepatic
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7/25. A case of budd-chiari syndrome secondary to multiple thrombogenic conditions: a case report and review of literature.

    This report describes a case of budd-chiari syndrome caused by latent polycythemia vera and factor v Leiden mutation. This syndrome usually occurs due to thrombosis of hepatic veins or membranous obstruction of inferior vena cava. The most common reasons for thrombosis are manifest polycythemia vera and the other prothrombotic conditions. Recently, latent polycythemia vera and factor v Leiden mutation have been reported in increasing frequency. In this report, we aimed to emphasize that all prothrombotic conditions must be evaluated while investigating the etiology of budd-chiari syndrome, including latent polycythemia vera and factor v Leiden mutation, and appropriate antithrombotic and surgical therapies must be performed without delay.
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ranking = 0.22106921877789
keywords = hepatic, obstruction
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8/25. Colonic obstruction caused by adhesive splenomegaly: report of a case.

    INTRODUCTION: splenomegaly caused by hematologic or infectious diseases is a well-known complication that may cause discomfort because of increased intra-abdominal pressure; however, complete obstruction of the large bowel usually never occurs. methods: We present a case of a 76-year-old male with polycythemia vera admitted with symptoms of complete colonic obstruction. At operation, the descending colon was found to be completely obstructed by a large adhesive spleen. Incision of the adhesions, complete colonoscopy, and mobilization of the colon was performed. RESULTS: Afterward, the patient had a normal colonic function; however, four days later he had a magnetic resonance-confirmed cerebral thrombosis followed by an episode of aspiration pneumonia, which he died of ten days after the operation. CONCLUSIONS: Colonic obstruction caused by splenomegaly is extremely rare, but may happen in patients with hematologic diseases.
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ranking = 0.54748453144526
keywords = obstruction
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9/25. Resolution of budd-chiari syndrome due to activation of endogenous fibrinolysis that may be induced by weight reduction.

    We describe a 45-year-old female with polycythemia vera and Leiden factor v mutation, who suffered the subacute form of budd-chiari syndrome and was treated with anticoagulants and diuretics. Surprisingly, after 3 months clinical signs of budd-chiari syndrome resolved; venography disclosed the resolution of thrombosis in the vena cava inferior and hepatic veins. This was associated with considerable increase of endogenous fibrinolytic activity, documented by a substantial change in the euglobulin clot lysis time, and a decrease of plasminogen activator inhibitor antigen and activity. During the disease the patient followed a diet and significantly reduced her body weight. Putting all data together it could be speculated that weight reduction (along with anticoagulants) considerably activated endogenous fibrinolysis, resulting in spontaneous resolution of budd-chiari syndrome. The validity of this explanation should be explored in a larger clinical study.
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ranking = 0.14285714285714
keywords = hepatic
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10/25. Quantification of changes in electroencephalographic power spectra in a patient with Budd-Chiari-syndrome after implantation of a transjugular intrahepatic portosystemic stent shunt (TIPSS).

    We examined a 41-year-old female with a subacute budd-chiari syndrome (BCS) before and after implantation of a transjugular intrahepatic portosystemic stent shunt (TIPSS) by means of digital electroencephalography (EEG). After TIPSS implantation hepatic decompression had been achieved and the liver function as well as the clinical status improved daily. Simultaneously, the digital EEG showed a decrease in the power of the theta band and an increase in the physiological alpha frequency band. The theta/alpha ratio decreased after TIPSS, despite an elevated arterial ammonia level. The patient had a well-preserved liver parenchyma before the occurrence of the BCS. After portal decompression by TIPSS, the liver function normalized and the liver resumed efficient synthesis and parts of its detoxification task. This regeneration capacity was documented by a rise in cholinesterase after TIPSS. After temporary substitution of albumin the serum albumin concentration returned to normal. Thus, some neurotoxic substances with high albumin-binding capacity may not be absorbed by the central nervous system (CNS). Furthermore, it appears likely that the length of time the brain is exposed to neurotoxic substances plays a role in the clinical and electroencephalographic changes. Compared to the conventional EEG the theta/alpha ratio reflected better metabolically conditioned electroencephalographic changes after TIPSS.
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ranking = 0.85714285714286
keywords = hepatic
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