Paroxysmal nocturnal hemoglobinuria in an identical twin.
The presentation of symptoms, laboratory findings and possible precipitating factors are reviewed in an 18-year-old patient with the onset of typical paroxysmal nocturnal hemoglobinuria. The opportunity was taken to study the physiology in his normal identical twin sibling who showed no hematological abnormalities on exhaustive studies, including photoscanning of the erythrocytes. These observations strengthen the evidence that PNH is an acquired disease with no basic measurable abnormalities of a hereditary or genetic nature.
D000293:Adolescent; D000728:Androgens / Q000627:therapeutic use; D000743:Anemia, Hemolytic / Q000209:etiology; D000747:Anemia, Hypochromic / Q000209:etiology; D001803:Blood Transfusion; D001854:Bone Marrow Cells; D001856:Bone Marrow Examination; D016026:Bone Marrow Transplantation; D002462:Cell Membrane; D004200:Diseases in Twins; D004781:Environmental Exposure; D004913:Erythrocytes, Abnormal / Q000166:cytology; D005492:Folic Acid / Q000627:therapeutic use; D006452:Hemoglobinometry; D006457:Hemoglobinuria, Paroxysmal / Q000150:complications / Q000235:genetics* / Q000628:therapy; D006461:Hemolysis; D006485:Hemosiderin / Q000652:urine; D006801:Humans; D007501:Iron / Q000627:therapeutic use; D008297:Male; D008855:Microscopy, Electron, Scanning; D013924:Thrombophlebitis / Q000209:etiology; D014184:Transplantation, Homologous
D000728:Androgens; D006485:Hemosiderin; D005492:Folic Acid; D007501:Iron