Vitamin K deficiency thus activate) certain enzymes involved in coagulation: Factors II, VII, IX, X, and protein C and protein S. Inability to activate the clotting cascade via these factors leads to the bleeding symptoms mentioned above. Notably, when one examines the lab values in Vitamin K deficiency [see below] the prothrombin time is elevated, but the partial thromboplastin time is normal or only mildly prolonged. This may seem counterintuitive given that the deficiency leads to decreased activity in factors of both the intrinsic pathway (F-IX) which is monitored by PTT, as well as the extrinsic pathway (F-VII) which is monitored by PT.
Vitamin A deficiency reference point for the extent of deficiency (with mortality increasing with severity of the eye disease). In a longitudinal study of preschool Indonesian children, susceptibility to disease increased nine times when severe VAD was present. The reason for the increased infection rate in vitamin A deficient populations is the T-killer cells require retinoids to proliferate correctly. Retinoic acid binds the promoter region of specific genes, so activates the transcription process and cell replication. A vitamin A-deficient diet will have a very limited surplus of retinol, so cell proliferation and replication will be suppressed, contributing to a reduced number of T-cells