Table 3.
Effect | Disease/state | Mechanism |
---|---|---|
Antimicrobial | Chronic Q fever endocarditis | Alkalinization of phagosome |
Human immunodeficiency virus | Inhibition of virus replication | |
Human corona virus | Inhibition of replication | |
Metabolic and cardiovascular | Hypoglycemic in diabetes mellitus | Decreasing insulin clearance and increasing secretion of C-peptide |
Improves lipid profile in SLE and RA and in steroid use | ||
Improve endothelial function | ||
Antithrombotic | Prevention of thromboembolism in immobilized patients | Inhibition of platelet aggregation and arachidonic acid release |
Prevention of thrombosis in antiphospholipid syndrome | ||
Inhibition of platelets activation by aPL antibodies, reducing binding of aPL-beta2-GPI to antiphospholipids and disruption of annexin A5 by aPL antibodies | ||
Antineoplastic | Prevention of lymphoma in mice | Induction of p53-dependentcell death |
Induction of apoptosis in CLL cells | Activation of caspase-3 | |
Solid tumors: e.g., breast, colon, glioblastoma multiforme, lung | ||
Sensitization of cancer cells to radiation and chemotherapy | ||
Other | Prevention of GVHD disease | Inhibition of T cell response to MHC antigens |
Kikuchi–Fujimoto disease | ||
Sarcoidosis | ||
Subglottic stenosis | ||
Sensory neuropathy | ||
Decreases risk of fetal cardiac lupus |
Where known, the mechanism is described
aPL antiphospholipid, GP glycoprotein, CLL chronic lymphocytic leukemia, GVHD graft versus host disease, MHC major histocompatibility complex