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Query: UMLS:C0023890 (cirrhosis)
42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a patient with liver cirrhosis and severe hypersplenism resistent to corticosteroids splenectomy was attempted but proved impossible. Embolisation of the splenic artery with tiny fragments of absorbable gelatin sponge induced gradual restitution of haematological function to normal after 6 wk. Abdominal pain, paralytic ileus of short duration, transient pyrexia, and pleural effusion ensued but were well tolerated. The patient has remained well, 2 1/2 mo later. It is suggested that this simple method may prove rewarding and could safely be used, if necessary, more than once in patients for whom other treatments are unsuitable or have failed.
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PMID:Treatment of hypersplenism by embolus placement in the splenic artery. 6 45

The effect of portasystemic shunts on hypersplenism has been evaluated in 129 patients who were operated upon. Correction of hypersplenism was obtained in 79 per cent of patients with shunting procedures without splenectomy and 90 per cent of those with splenectomy. The improvement was significant and lasting. These results confirm the beneficial effect of splenic decompression on hypersplenism after simple portasystemic shunt. On the basis of these data, we feel that a difficult splenectomy can also be avoided in patients who have cirrhosis with striking hypersplenism.
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PMID:Effect of portasystemic shunt on hypersplenism: clinical study in 129 patients with cirrhosis. 46 92

The influence of the spleen on the blood has been assessed in a series of 187 consecutive patients with chronic liver disease. Patients were described as having 'hypersplenism' if the white blood count and/or platelet count were below 4.0 X 10(9)/1 and 100 X 10(9)/1 respectively at the time of biopsy diagnosis and on at least one subsequent occasion. Using this definition 17 per cent of patients with alcoholic cirrhosis had hypersplenism, compared with 38 per cent with cryptogenic cirrhosis and 26 per cent with active chronic hepatitis. Studies with 51Cr labelled autogenous erythrocytes in 36 of the patients with different types of chronic liver disease showed that the spleen rarely caused anaemia either by excessive splenic pooling or splenic haemolysis. Further studies with 51Cr labelled platelets in 20 other patients showed that the splenic platelet pool was usually considerably increased and the platelet life span reduced. Some patients showed excessive destruction of platelets in the spleen but none of these features consistently related to thrombocytopenia. Splenic enlargement per se did not cause expansion of the plasma volume in chronic liver disease. Of a total of 17 patients who underwent surgical operations for reduction of portal pressure five had hypersplenism but in these the haematological state was not significantly improved at one month. However, none of the survivors of these operations subsequently developed hypersplenism. One patient with severe hypersplenism who underwent simple splenectomy was cured of leucopenia but not of thrombocytopenia.
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PMID:Splenic influences on the blood in chronic liver disease. 53 22

The relationship between platelet count and aggregability was serially evaluated after splenectomy in patients with normosplenism and hypersplenism, and the results were compared with those found in patients undergoing only upper abdominal surgery. The preoperative count and aggregability of platelets were significantly suppressed in patients with cirrhosis of the liver, idiopathic portal hypertension, and prehepatic portal obstruction. However, the platelet aggregability of these patients markedly increased in accordance with the platelet counts after splenectomy. In the patients with normal splenic function preoperatively, splenectomy caused a simultaneous increase in platelet count and aggregability. The platelet function was not always reflected by the count in the patients with idiopathic thrombocytopenic purpura. On the other hand, in the control patients undergoing only laparatomy the platelet count substantially increased two weeks after operation, but platelet aggregability did not differ from the preoperative value. The present results suggest that additional factors for thromboembolism such as hypotension, acidosis, or stagnant blood flow should be avoided during the peak period of reactive thrombocytosis after splenectomy, and that an appropriate use of anticoagulants or inhibitors of platelet aggregation is recommended if and when necessary.
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PMID:Platelet aggregability after splenectomy in patients with normosplenism and hypersplenism. 56 40

Cruveilhier-Baumgarten Disease is a rare clinical entity. The distinction between C-B Disease and C-B syndrome rests solely on the liver morphology. In C-B Disease, the liver is morphologically normal. A case of a 27-year-old juvenile diabetic female with C-B Disease is presented. She manifested many of the metabolic and hemodynamic changes of cirrhosis including portal hypertension, encephalopathy, and a hyperdynamic cardiovascular state. There was also associated splenomegaly, hypersplenism, and splenic artery aneurysms. Splenectomy and splenic artery ligation were performed. Liver biopsies had normal morphology. The patient has had no recurrence of her symptoms. The pathogenesis of C-B Disease is unknown.
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PMID:Cruveilhier-Baumgarten disease with associated splenic artery aneurysms. 86 36

Reporting 5 cases of Wilson' disease occuring in children and expressed by a major liver involvement, the practical aspects of therapy are discussed. In 4 cases, follow-up exceeded 3 years. 1. D-Penicillillamine, a chelating agent, is administered for the purpose of inverting the cupric balance. Cupruria has, therefore, no absolute value and must be interpreted according to multiple factors. 2. The effects of D-penicillamine on the liver, as assessed by clinical, biological and histological data, appears encouraging. Laparoscopic examinations, so as to appreciate the evolution of the cirrhosis are still lacking. 3. The decrease in spleen size and signs of hypersplenism probably illustrate the reversibility of the portal hypertension. In Wilson's disease, portal hypertension requires special measures which exclude surgical portal diversion.
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PMID:[Treatment of Wilson's disease in children. Five case reports]. 99 39

The authors report the incidence of portal thrombosis in their experience, of patients who have been operated on for splenectomy as treatment for portal hypertension with splenomegaly and hypersplenism without a portal systemic shunt. In 161 patients studied angiographically for portal hypertension due to cirrhosis, portal thrombosis was shown in 19 patients. Of these 19 patients 13 previously splenectomized. Only 6 were never operated upon.
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PMID:Portal thrombosis: high incidence following splenectomy for portal hypertension. 105 64

The effects of splenic artery ligation were studied in Sprague-Dawley rats and in eight selected symptomatic patients with hepatic cirrhosis. In rats, this maneuver induced splenic infarction, reduced functional splenic mass, transiently raised platelet and reticulocyte counts and was without local complications. In seven selected patients with cirrhosis and prominent splenomegaly, the splenic artery was markedly enlarged, splenic arterial flow was greatly increased and splenic artery ligation partially lowered portal pressure. In three patients with varying cytopenias secondary to hypersplenism splenic artery ligation uniformly improved peripheral blood elements, although varying degrees of hypersplenism later recurred necessitating splenectomy in one. In five other patients, splenic artery ligation in conjunction with coronary vein ligation in four was performed for bleeding esophageal varices. Two patients later required portacaval shunting, and one other in whom operation was undertaken in desperation died of hepatic failure. Celiac-mesenteric arterioportography, operative portography, hemodynamic measurements and examination of peripheral blood elements in these eight patients suggests that splenic artery ligation in conjunction, where appropriate, with coronary vein ligation has several potentially beneficial effects. Hypersplenism may be sufficiently controlled to alleviate clinical symptoms. Arterial inflow into the portal system is reduced tending to lower portal pressure. Transheptic portal flow from the mesenteric bed is preserved. Venous anastomotic channels still functioning around the splenic pedicle and no longer draining a hyperdynamic splenic circuit may be converted into an escape route for mesenteric venous blood entering the portal system under high pressure. Nonetheless, each of these effects and their interrelationships require further study before this operation assumes a larger role in the treatment of complications of portal hypertension.
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PMID:Splenic artery ligation in selected patients with hepatic cirrhosis and in Sprague-Dawley rats. 108 42

The growing scepticism about the use of portocaval anastomosis operations to prevent renewed bleeding of esophageal varices has led to the testing of new methods. This report describes subcutaneous transposition of the resected spleen in normal experimental animals with the Vena porta constricted with Ameroid rings and liver cirrhosis induced by DMNA. The report also covers 9 patients operated on from 1972 to 1973 with subcutaneous transposition of the spleen. A 77-year-old woman died postoperatively, one patient died after 2 years 4 months, and one had slight bleeding. All the other patients are alive 2-4 years after the operation, with no signs of renewed bleeding. The advantage of subcutaneous transposition of the spleen is that it eliminates hypersplenism.
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PMID:[Subcutaneous transposition of the spleen: an experimental and clinical study (author's transl)]. 108 39

Wilson's disease was diagnosed in a 16-year-old adolescent who presented with signs of hypersplenism due to cirrhosis, with marked hyperpigmentation of both lower legs and neurological disturbances. In view of progressive thrombocytopenia and leukocytopenia, splenectomy was performed during therapy with penicillamine later in the course, and the result was good. The patient's 12-year-old sister was found to have a hepatic form of Wilson's disease with typical biochemical findings. During the initial hospitalization a severe, spontaneous copper-induced hemolysis was noted. Another sister probably has a presymptomatic form of the disease. The parents are healthy but heterozygote carriers with regard to biochemical findings. The importance is stressed of hypersplenism, hyperpigmentation of the legs and especially of acute hemolysis in infancy as pointers in the diagnosis of Wilson's disease. Further diagnostic and therapeutic aspects are discussed.
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PMID:[Familial Wilson's disease: copper induced hemolysis, hypersplenism and hyperpigmentation as the main symptoms]. 121 85


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