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

The haemolytic process in hepatosplenic schistosomiasis is often regarded as a result of splenomegaly that can be increased by spontaneous or surgical shunts. The importance of splenomegaly and/or shunt on the etiology of haemolysis was studied in a group of 74 patients with hepatosplenic schistosomiasis and portal hypertension. They were divided into 4 groups: Group I (22 cases) - pre-operative; Group II (15 cases) - classic splenorenal shunt; Group III (22 cases) - selective portal decompression and Group IV (15 cases) - azygoportal disconnection with splenectomy. The first group is characterized by the presence of splenomegaly and the absence of shunt; the second by the presence of shunt and absence of splenomegaly; the third, by the presence of both splenomegaly and shunt and the last by absence of both, shunt and splenomegaly. In all cases, the levels of sensitive markers of haemolysis, such as haptoglobin and hemopexin as well as non-conjugated and total bilirubins were determined. Biochemical and coagulation parameters, used to evaluate the hepatic function, were also studied. The data was initially analysed according to a factorial experiment of 2 and standard least squares techniques were used to evaluate the effects of splenomegaly, shunt and their interaction. The results showed that the shunts always provoked haemolysis, even in the absence of splenomegaly, but the presence of both, splenomegaly and shunt, always increased the process of haemolysis.
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PMID:Systemic surgical shunts and splenomegaly as causes of haemolysis in portal hypertension in mansonic schistosomiasis. Evaluation through serum levels of haptoglobin, hemopexin and bilirubins. 308 93

Intravascular hemolysis is associated with several pathologic conditions that include hemoglobinopathies, trauma, malaria, and bacterial infections. Among plasma-protective proteins against oxidative damage caused by red blood cell rupture, haptoglobin and hemopexin are thought to play a crucial role. Haptoglobin and hemopexin, by binding with high-affinity hemoglobin and heme, respectively, exert an antioxidant action by preventing heme-catalyzed free radical production. Moreover, these proteins prevent iron loss by inhibiting glomerular filtration of hemoglobin and heme diffusion through plasma membranes. Analysis of single-null mice demonstrated the antioxidant action of haptoglobin and hemopexin in vivo and suggests that the 2 proteins cooperate in the resolution of hemolytic stress. To evaluate the physiological relevance of the haptoglobin-hemopexin system and the principal targets of its action, we generated haptoglobin-hemopexin double-knockout mice and analyzed them under basal conditions and after acute hemolysis. Whereas haptoglobin-hemopexin double-null mice displayed no obvious alteration in phenotype under basal conditions, nonlethal hemolytic stress in these animals led to pronounced splenomegaly as well as liver inflammation and fibrosis. These data demonstrate that haptoglobin and hemopexin together are essential for protection from splenomegaly and liver fibrosis resulting from intravascular hemolysis.
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PMID:Enhanced splenomegaly and severe liver inflammation in haptoglobin/hemopexin double-null mice after acute hemolysis. 1239 71