Leiden Factor V mutation, associated with resistance to activated protein C, is a prothrombotic state found in 20% of the patients with a first episode of deep-vein thrombosis. We report the case of a 30-Year-old woman with a history of intermittent abdominal pain who developed small bowel infarction requiring extensive small bowel resection. Biological search for prothrombotic disorder showed resistance to activated protein C due to homozygosity for the factor V Leiden mutation.
View Article and Find Full Text PDFPurpose: Haptoglobin (H) and orosomucoid (O) are acute phase proteins that increase in a parallel manner. When hemolysis and inflammation are both present, study of the O-H couple on the protein profile may reveal an unknown hemolysis.
Methods: To determine if hemolysis is more frequent during infectious endocarditis than during septicemia without valvulopathy or during valvulopathy without septicemia.
Zidovudine is known to be responsible for a mitochondrial myopathy with ragged-red fibres and mitochondrial DNA depletion in muscle. Lactic acidosis alone or associated with hepatic abnormalities has also been reported. A single report mentioned the concomitant occurrence of muscular and hepatic disturbances and lactic acidosis in a patient receiving zidovudine, but muscle and liver tissues were not studied.
View Article and Find Full Text PDFIntroduction: Hemolysis and red cell fragmentation accompanying vitamin B12 deficiency may misdirect the diagnosis. Signs of malabsorption and abnormalities related to folic acid metabolism characterized by discrepancies between folic acid normal serum levels and erythrocytic folic acid levels may also exist.
Exegesis: We report the occurrence of hemolysis and red cell fragmentation mimicking microangiopathic hemolytic anemia, malabsorption and folic acid deficiency in the course of vitamin B12 deficiency.