Table 2.

Controversies concerning role of antimalarials and ACE inhibitors in KS onset: Pro and con

Favoring effect	Impeding effect
High prevalence of KS in malarial areas with widespread use of quinine and its derivates18	Quinolines are potential anticancer agents alone or in combination with other antineoplastic drugs: inhibition of autophagy and apoptosis92., 93., 94.
Low prevalence of KS in areas where malaria is rare and quinine derivates are rarely used19	Lysosomotropic effects of quinolines inhibit pH-dependent steps of viral entry and replication99., 100., 101.
Use of quinine to “cut” heroin in drug addicts affected by AIDS-KS85	Quinolines inhibit angiogenesis, hallmark of KS pathogenesis95
Well-known immunosuppressive properties of quinine and its derivatives, largely used in the treatment of autoimmune diseases (SLE, DLE, rheumatoid arthritis)82	Quinolines inhibit production of pro-inflammatory cytokines, involved in HHV-8 lytic cycle reactivation96
Antimalarials indirectly encourage the onset of KS, through their inhibitory effect on TNF-α expression103	Antimalarials indirectly prevent the onset of KS, through their inhibitory effect on TNF-α expression102
Chloroquine can reduce the antibody response to primary immunization83
ACE inhibitor intake can induce KS86., 87.	ACE inhibitor intake can protect from KS104

ACE, angiotensin-converting enzyme; DLE, discoid lupus erythematosus; HHV, human herpesvirus; KS, Kaposi’s sarcoma; SLE, Systemic lupus erythematosus; TNF, tumor necrosis factor.