Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021345 (infectious mononucleosis)
 3,358 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 19-year-old girl fell ill with a high temperature and cervical lymphadenopathy. The detection of heterophile antibodies as well as Epstein-Barr-virus-specific antibodies confirmed the diagnosis of infectious mononucleosis. In the course of the infection, the patient developed severe hemolytic anemia with her hemoglobin falling from 14 to 8 g/dl. High-dose corticosteroid therapy did not stop hemolysis; this could only be achieved by seven plasmapheresis sessions. Antibodies against triosephosphate isomerase (TPI) and the blood group marker 'i' were found in the patient's serum. Anti-i cold agglutinins were not active at 37 degrees C, whereas antibodies against TPI caused increased 51Cr release from marked patient's erythrocytes in vitro. Plasmapheresis removed the autoantibodies effectively and stopped the hemolysis. After 8 weeks, the patient gradually recovered.
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PMID:Successful plasmapheresis in corticosteroid-resistant hemolysis in infectious mononucleosis: role of autoantibodies against triosephosphate isomerase. 146 97

Generalized adenopathy and splenomegaly developed in an 18-year-old youth after a severe tonsillitis followed by headache, tiredness and weight loss for several weeks. Infectious mononucleosis (acute Epstein-Barr virus infection) was confirmed by the demonstration of virus-specific antibodies. A reticulocytosis (24%), decreased haptoglobin concentration (0.6 mg/dl) and increased lactate dehydrogenase activity (657 U/l) indicated marked haemolysis. The bone marrow showed increased erythropoiesis with abnormal maturation. Antibodies against triosephosphate isomerase and against blood group marker "i" were demonstrated in the patient's serum. Antibodies against triosephosphate isomerase from the patient's serum were purified by affinity-chromatography. They strongly reacted with the patient's erythrocytes and under complement activation induced an increased 51Cr liberation from marked erythrocytes. No corresponding effect of anti-i-antibodies was noted at 37 degrees C. With the fall in antibodies against triosephosphate isomerase the haemolysis receded and the patient became free of symptoms after 7 weeks.
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PMID:[Infectious mononucleosis: hemolysis by autoantibodies against triosephosphate isomerase]. 217 94

In sera from patients with acute EBV, infection and the clinical symptoms of infectious mononucleosis antibodies of the Ig class M were found that are directed against two cellular proteins. The molecular mass of these proteins was determined to be 29 (p29) and 26 kD (p26), respectively, in SDS-PAGE. P29 was identified as part of the glycolytic enzyme triosephosphate isomerase (TPI) by comparison of the NH2-terminal amino acid sequences. A purified antibody against TPI induces a 51Cr release from human erythrocytes. Possibly, anti-TPI causes hemolysis, which is an infrequent but serious symptom of infectious mononucleosis.
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PMID:Autoantibodies against triosephosphate isomerase. A possible clue to pathogenesis of hemolytic anemia in infectious mononucleosis. 230 86

Haemolysis has been observed frequently as a complication of acute hepatitis A virus (HAV) infection. However, the pathogenic mechanism has not been elucidated completely. In individual cases the detection of anti-erythrocyte antibodies of unknown specificity was described. The raised serum IgM fraction was shown to consist partially of autoantibodies. Previously, we detected autoantibodies of immunoglobulin class M directed against triosephosphate isomerase (IgM anti-TPI) in patients with infectious mononucleosis. These autoantibodies are able to induce haemolysis. In this study the occurrence of IgM anti-TPI in acute HAV infections and other viral diseases has been investigated. In 33 of 134 patients suffering from HAV infection (IgM anti-TPI was detected. Haematological and chemical data were available from seven of these 33 patients. Mild-to-moderate signs of haemolysis correlating with the IgM anti-TPI titre in the follow-up examinations were demonstrated. The presence of IgM anti-TPI in HAV infections is connected with a reactivation of a latent persistent EBV infection. In other viral infections both the detection of IgM anti-TPI and evidence of a reactivated EBV infection is rare. Thus, we anticipate that IgM anti-TPI antibodies occurring with the reactivation of a latent persistent EBV infection take part in provoking haemolysis in acute HAV infections.
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PMID:Haemolysis in hepatitis A virus infections coinciding with the occurrence of autoantibodies against triosephosphate isomerase and the reactivation of latent persistent Epstein-Barr virus infection. 892 93