Parenchymal liver cells from emphysema patients with an inherited deficiency of alpha(1)-antitrypsin contain globules of glycoprotein that bind fluorescent antibody to alpha(1)-antitrypsin. The globules can be seen after hematoxylin and eosinstaining or on electron microscopy, but are more readily demonstrated by PAS stain of amylase-treated liver sections. It appears that an inappropriately large amount of alpha(1)-antitrypsin is found in the liver even when there is a deficiency in the serum. Genetic variants of the normal antitrypsin molecule may be unable to leave their site of synthesis in the liver cell because of some molecular aberration.
A 4\m=1/2\-year-oldboy experienced the acute onset of fever, generalized lymphandenopathy, apparent respiratory obstruction, and hepatosplenomegaly. Laboratory studies were compatible with infectious mononucleosis. In order to rule out the possibility of a fulminant lymphoma and govern the therapy, a cervical lymph node biopsy was performed. Histological examination revealed architectural distortion and engorgement with atypical reticulum cells, some of which were indistinguishable from Reed\x=req-\ Sternberg cells. However, an interpretation of Hodgkin's disease was deferred, and the patient was treated conservatively. Thirteen months later he was asymptomatic, and his abnormal physical findings and laboratory tests returned to normal. This patient is presented, therefore, as an instance of the presence of Reed-Sternberg cells in a disease other than Hodgkin's.
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