Paroxymal noctural hemoglobinuria is due to -

Paroxysmal Nocturnal hemoglobinuria (PNH). PNH is the only hemolytic anemia caused by an acquired intrinsic defect in the cell membrane. PNH results from an acquired mutation that inhibits the synthesis of Glycosylphosphatidylinositol (GPI). Several protective proteins called complement-regulating proteins are anchored to the cell membrane by GPI. These protective proteins prevent activation of complement and thereby complement-mediated lysis of blood cells. Deficiency of GPI results in absence of these proteins and blood cells become unusually sensitive to complement-mediated lysis. The GPI - linked proteins that are missing are : - Inhibitor of reactive lysis (CD-59) → Their absence results in hemolysis Decay-accelerating factor (CD 55) → Their absence results in hemolysis C8 binding protein. → Their absence results in hemolysis Urokinase plasminogen activator receptor - Its absence promotes thrombosis. Leukocyte alkaline phosphatase (LAP) → Decreased LAP score. Because the causative somatic mutations occur in pluripotent stem cells, all its clonal progeny i.e., red cells, white cells, and platelets are deficient in GPI linked protein. So, all these cells are sensitive to complement-mediated lysis that results in  - Anemia, Leucopenia, Granulocytopenia, Thrombocytopenia