The chronic inflammatory status that features lupus erythematosus leads to a higher susceptibility to cardiovascular complications. Lupus, indeed, is often characterized by endothelial dysfunction, the earliest marker of cardiovascular disease, as well as hypertension and renal damage. In a NZB/W F1 mice model of lupus, oral HCQ gavage of 10 mg/kg/day for five weeks reduced the incidence of thromboembolic events. Moreover, improvements in hypertension, renal damage, and heart hypertrophy occurred, probably due to the normalized endothelium response and reduction of Reactive Oxygen Species (ROS) attributable to HCQ intake [90]. The same effect of normalizing nitric oxide and ROS production have been confirmed in a NZB/W F1 murine model at different times. HCQ at 3 mg/kg/day p.o. protected vascular endothelium, with a strong improvement of endothelial dysfunction [91]. The benefits on atherosclerosis also pass through the lipid-lowering power of HCQ. A clinical study on 155 autoimmune patients revealed a statistically significant association between HCQ (400 mg/day) and a lessening of triglyceride and cholesterol levels, mainly LDL, while no HDL changes were observed [92]. By contrast, HCQ in patients with a mild or inactive condition had no significant effects on lipid profile. A survey involving 65 Chinese lupus patients, treated with HCQ (244 ± 86 mg/day), demonstrated that only triglycerides tended to be lowered, while no statistically significant changes are observable in cholesterol levels [119]. The use of HCQ may be helpful in minimizing cardiovascular risk by improving glycemic homeostasis in lupus patients. A cross-sectional study performed between 2000 and 2005 on 149 nondiabetic women affected by lupus estimated that a mean dose of 400 mg of HCQ affects insulin sensitivity and resistance, as assessed by HOMA index, as well as fasting glucose levels [82].