Table 1.

Clinical studies with NAC in patients with peripheral vascular disease (PVD).

Patient Information	Intervention	Outcome	Ref.
Pts (6 M and 16 F, YOA: 18–75) with RP secondary to SSc	NAC i.v. starting with a 2 h loading dose of 150 mg/kg, then 15 mg/kg/h for 5 days	Both frequency and severity of RP attacks, active ulcers, and old challenge test mean recovery time decreased	[11]
Pts (7 M and 43 F; YOA: 35–67) with RP secondary to SSc	NAC i.v. 15 mg/kg/h for 5 h in every 14 days for about 3 years	Reduction of DU, RP attacks, and RP DU ulcer visual analog scale	[12]
Pts (4 M and 22 F, YOA: 25–68) with RP secondary to SSc	NAC i.v. 15 mg/kg/h for 5 h, every 2 weeks for 2 years	Increased global hands perfusion and decreased plasma adrenomedullin concentrations, frequency and severity of RP attacks	[13]
Pts (42 M, YOA: 32–58) with RP secondary to SSc	NAC oral 600 mg tid for 4 weeks	Decreased DU but no vasodilator effect on hands’ microcirculation	[14]
Pts (20 M and 4 F, YOA: 56–78) with stage 5 CKD during hemolysis	NAC i.v. 5 g in 5% glucose in a final volume of 50 mL during one hemodialysis session	Improved arterial vascular reactivity during reactive hyperemia with decreased reflective index	[8]
Pts (total 36, YOA: 56–76, without or with only minor signs of preoperative ischemia of the lower body) undergoing elective infrarenal AAA	NAC i.v. 150 mg/kg b.m. 30 min before infrarenal aortic clamping	Prevented elevation of plasma lipid peroxide, thromboxane, and prostacyclin levels after declamping with increased plasma GSH concentration for over 12 h	[10]

NAC: N-acetylcysteine; Pts: patients; M: male; F: female; YOA: years of age; RP: Raynaud’s phenomenon; SSc: systemic sclerosis; mg: milligram; kg: kilogram; h: hour; Ref: references; i.v.: intravenous infusion; DU: digital ulcer; tid: three times a day; AAA: abdominal aortic aneurysm; b.m.: body mass; b.w.: body weight; CKD: chronic kidney disease; GSH: glutathione.