ArticlePlastic and reconstructive surgery. Global open2026
Rapid Wound Healing Observed Following Oral LathMized NAD+ Supplementation: A Case Study.
Article in Plastic and reconstructive surgery. Global open, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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5 authors.
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Abstract
Postoperative wound infections after common body contouring procedures are a key contributor to chronic open wounds, placing major burdens on patients and presenting serious challenges to plastic surgeons. Patients may experience consequent serial infections, prolonged treatment plans, readmissions, high medical costs, and decreased quality of life. An aging population and rising prevalence of obesity and metabolic syndrome contribute to growing risks of developing postoperative wound infections and chronic wounds. We present the case of a 59-year-old woman with hypertension, hyperlipidemia, and a distant history of a prolonged postoperative complications and hospitalization who underwent implant removal, bilateral mastopexies with capsulectomies, and concurrent bilateral brachioplasties with liposuction. Despite use of evidence-based perioperative and postoperative interventions, the patient presented with significant incisional dehiscence and fibrinous exudate at postoperative day (POD) 14. On POD 18, the patient, on her own initiative, began 1500 mg of modulated oral LathMized NAD+ (LNAD+) and continued dosage throughout the wound healing period. Healing progressed from full-thickness wound dehiscence before supplementation to granulation on days 2-5 of supplementation (POD 19-22) and complete closure without scar formation on day 22 (POD 40). No adverse reactions were reported. To our knowledge, this case represents the first reported use of oral LNAD+ that potentially supported reduced healing time of deep surgical wound dehiscence in a patient predisposed to delayed healing and scarring. Proposed mechanisms of action might involve suppression of inflammatory mediators known to impede wound healing and metabolic upregulation via an increase in SIRT1 levels and activity.
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