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Query: UMLS:C0038002 (splenomegaly)
9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Splenectomy for massive splenomegaly and hypersplenism carries a significant morbidity and mortality. We have used partial splenic embolization (PSE) as an effective alternative to splenectomy. Ten PSE procedures were performed on nine patients without mortality and with minimal morbidity. The age of the patients ranged from 8 months to 32 years (mean 14 years). The causes of splenomegaly and hypersplenism included cystic fibrosis with cirrhosis (2), tyrosinemia and cirrhosis (1); thalassemia (1), hemophilia with Human Immune Deficiency Virus infection (2), chronic hepatitis with portal hypertension (1), malignant histiocytosis (1), and Wiskott-Aldrich Syndrome (1). All procedures were performed under local anesthesia with sedation. A percutaneous femoral artery approach to the splenic artery was used to deliver Ivalon sponge particles (280-800 microns) into the spleen. Splenic infarction was assessed by postembolization angiograms. All of the patients except one demonstrated improvement of hematologic parameters. In one patient, however, cytopenia improved only after a second embolization. In the total series, there was an early mean rise of 8,600/mm3 in the leukocyte count (range 2,900-14,900) and 212,000/mm3 in the platelet count (range 30,000-718,000). Follow-up ranged from 4 months to 7 years. Improvement of the blood picture has been persistent in seven of the eight patients who showed initial improvement. Transient procedural complications included fever (5), pleural effusion (2), pneumonia (1), and splenic abscess (1). One patient had paralytic ileus lasting for 10 days and one patient developed a streptococcal peritonitis 3 weeks after embolization. No patient developed pancreatitis or vascular compromise of other abdominal viscera.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Partial splenic embolization. An effective alternative to splenectomy for hypersplenism. 226 5

Although restricted transhepatic portal flow is necessary for development of generalized portal hypertension (GPH), increased splanchnic arterial inflow also contributes to GPH and its clinical sequelae. In this context, we describe 7 male and 6 female patients (mean age 48 years) in whom the lesser splanchnic (gastrosplenic) system played a key role in the signs and symptoms of GPH. These 13 patients (9 with hepatic cirrhosis, 3 with primary myeloproliferative disorder, and 1 with extrahepatic portal block) shared common features of massive splenomegaly, huge splenofundic gastric varices, often with a prominent natural shunt to the left renal vein. Total or near total splenectomy alone or combined where appropriate with coronary vein ligation was effective in controlling varix hemorrhage (10 patients), ascites (3), or complications of an enlarged spleen-anorexia and abdominal pain (3), hemolytic anemia (1) and profound thrombocytopenia with severe epistaxis (1). Intraoperative jejunal portal venography was crucial in operative management in order to establish definitively the presence or absence of coronary venous collaterals, and when present, to verify their operative ligation. These distinctive patients illustrate: 1) GPH is a heterogeneous syndrome of divergent splanchnic circulatory patterns, a feature which should be taken into account in selecting operative treatment; 2) one well-defined subgroup displays prominent hyperdynamic lesser splanchnic and specifically, splenic blood flow as a major contributor to clinical complications; and 3) within this subgroup, splenectomy combined with documented absence or surgical interruption of coronary venous collaterals as corroborated by intraoperative portography is effective alternative treatment.
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PMID:Preeminence of lesser splanchnic blood flow in selected patients with generalized portal hypertension. 227 22

The prevalence of splenomegaly associated with portal hypertension was examined in a consecutive population of 111 patients who had portal hypertension diagnosed using specific endoscopic, sonographic, and Doppler signs. Splenic size was measured objectively via its cranio-caudal length on coronal section using ultrasound and by clinical examination. Sonographically, 52% of patients had a definitely large spleen and 35% a spleen less than one standard deviation from the normal mean, while a further 13% had equivocal splenomegaly. Only 52% of patients had splenomegaly on clinical assessment. Splenomegaly was less common in patients with alcoholic (41% definite, 15% equivocal) than in those with non-alcoholic liver disease (66% definite, 17% equivocal, p = 0.02) and splenic length was significantly smaller in alcoholic patients (12.7 +/- 0.5 cm) compared to patients with either non-alcoholic liver disease (15.0 +/- 0.6 cm, p = 0.003) or portal hypertension due to vascular occlusive diseases (16.5 +/- 2.0 cm, p = 0.006). Splenomegaly, whether assessed sonographically or clinically, is an insensitive sign of portal hypertension and its absence cannot be used as a negative predictor of the presence of portal hypertension in patients with chronic liver disease.
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PMID:Splenomegaly--an insensitive sign of portal hypertension. 229 25

We describe the history of a man aged 73 with a myeloproliferative syndrome and massive splenomegaly, who was admitted with bleeding oesophageal varices. After sclerotherapy and other conservative measures had failed to stop the bleeding, splenectomy was performed. Liver biopsy obtained at the time of splenectomy showed extramedullary haematopoiesis and no signs of cirrhosis. Six weeks after the operation no varices were present any more. Studies of the pathogenesis of portal hypertension in splenomegaly of different causes show the importance of the increased splenic blood flow as one of the main contributory causes to this specific type of portal hypertension. Therefore this type of portal hypertension can probably be cured by splenectomy, as we saw in our patient and as has been described in several case reports.
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PMID:[Splenectomy as therapy for esophageal varices in a myeloproliferative syndrome]. 230 91

Seventeen cases of segmental portal hypertension due to splenic vein thrombosis are reported. This syndrome may be asymptomatic for a long time and then present suddenly in the form of a serious picture of high digestive haemorrhage due to rupture of gastric fundus varices as a result of hypertrophied submucous collateral drainage circulation. Useful for diagnosis are oesophagogastroduodenoscopy, which points to stomach varices, and splenoportography or splenic artery angiography with venous phase, which highlight pathognomonic dilatation and tortuosity of the gastroepiploic veins. Surgical exploration typically shows: presence of large epiploic vessels, splenomegaly, absence of changes in the liver and in the portal and mesenteric circulation. Curative treatment of choice is splenectomy.
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PMID:[Segmental portal hypertension caused by splenic vein thrombosis]. 233 52

A 60-year-old man with primary splenic hemangiosarcoma (PSH) presented with weakness, weight loss, abdominal pain, and anemia. Physical examination revealed hepatomegaly, ascites, and firm, huge splenomegaly. Ultrasonography showed many nodular structures characterized by hypoechogenic and hyperechogenic areas. The patient also had portal hypertension, which was confirmed by physical findings and by measurement of portal vein pressure during operation. A liver-spleen scan using Tc-99m sulfur colloid and Tc-99m labeled heat denatured erythrocytes failed to demonstrate any splenic uptake, a reliable feature of functional asplenia. Although on a total body scan with Ga-67 citrate there was no splenic uptake, there was gallium uptake in the liver, where the presence of the metastatic lesion was histopathologically verified and confirmed by operation. There was also uptake in the middle zones of the lungs. Ga-67 citrate imaging appears to be helpful in the diagnosis of metastasis of PSH, and PSH can rarely cause portal hypertension.
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PMID:Functional asplenia and portal hypertension in a patient with primary splenic hemangiosarcoma. 234 Jun 75

Between 1973 and 1983 6 children with portal hypertension were treated at the University Children's Hospital Medical Centre in Teheran by transpositioning the spleen into the thorax. In one case with splenomegaly, ascites and 4 years of severe bleeding, this procedure was not possible. We therefore performed a partial splenectomy 7 years ago, with the view of a transpositioning into the thorax at a later date. Follow-up examinations revealed disappearance of the symptoms of portal hypertension. This led us to believe that this procedure could be adopted for the treatment of portal hypertension as an alternative to splenic transpositioning into the thorax and shunt operation. The precipitation and increase in collateral circulation with this method leads to rapid improvement.
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PMID:Partial splenectomy and partial splenic attachment for the treatment of portal hypertension. 236 Mar 73

It was discovered that eight patients with complications of non-cirrhotic portal hypertension had received an arsenical preparation for psoriasis as Fowler's solution some years age. Seven of them were admitted for bleeding oesophageal varices. Upon admission, splenomegaly and hypersplenism were present. Liver tests were normal and palmar skin keratosis and melanosis were noted. Liver biopsy of six patients showed features of incomplete septal cirrhosis. Malignant skin lesions were present in half of the patients. One patient died from lung carcinoma and another from an ovarium neoplasm. Chronic arsenic intake should be actively looked for in all patients with psoriasis and non-cirrhotic portal hypertension. They should be followed up for many years for development of malignant lesions in skin, lung and liver. Liver abnormalities present in the biopsies are often minor and may escape detection.
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PMID:Arsenic and non-cirrhotic portal hypertension. A report of eight cases. 180 30

DIC in patients affected by cirrhosis, accompanied by portal hypertension and splenomegaly, has been suspected in the past. The main aim of this study is to ascertain the incidence of this phenomenon. We carried out coagulation and fibrinolytic tests in 113 cirrhotic patients and 20 healthy control persons. We found chronic consumption coagulopathy at analysis level in 28 cases (24.8%) with a decrease of fibrinogen, factor V, kallikrein, platelets, prothrombin complex activity, increase of PDF, partial thromboplastic time and euglobulin lysis. 25 cases had active cirrhosis, with ascites, variceal bleeding and/or hepatic encephalopathy; 3 were non-active cirrhosis. Only 7 patients had clinical DIC. We observed that coagulation disorders increased with more active cirrhosis.
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PMID:[The incidence of consumption coagulopathy in liver cirrhosis]. 256 20

A case of idiopathic portal hypertension associated with connective disease resembling systemic lupus erythematosus is described. The patient was a 50-year-old woman with splenomegaly, ascites, esophageal varices, and pancytopenia, but without extrahepatic portal obstruction or cirrhosis of the liver. Electron microscopy of the liver showed perisinusoidal fibrosis. High titers of autoantibodies against proliferating cell nuclear antigen (PCNA) were found in the sera as well as in ascites; anti-DNA antibodies appeared after anti-PCNA antibodies and remained thereafter at a moderate titer. The possibility of an immunological process in the pathogenesis of idiopathic portal hypertension is discussed.
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PMID:[Idiopathic portal hypertension associated with connective tissue disease similar to systemic lupus erythematosus]. 259 83


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