25-Hydroxyvitamin D Deficiency: Impacting Deep-Wound Infection and Poor Healing Outcomes in Patients with Diabetes

SLR - November 2019 - Michael J. Blutfield

Reference: Smart H., AlGhareeb AM., Smart SA. 25-Hydroxyvitamin D Deficiency: Impacting Deep-Wound Infection and Poor Healing Outcomes in Patients with Diabetes. J Advances in Skin and Wound Care. 2019 June 13; 32 (7),321–328

Scientific Literature Review

Reviewed By: Michael J. Blutfield, DPM
Residency Program: Cooper University Hospital – Camden, NJ

Podiatric Relevance: Diabetic foot ulcerations (DFU) are a common cause of morbidity and mortality in diabetics which can lead to complications such as infections, gangrene, and lower extremity amputations. Previous studies have shown that deficiencies in 25(OH)D can influence the immune response in the body and potentially play a role in the pathogenesis of diabetic foot wounds. This study investigated how 25(OH)D deficiency in diabetics with foot wounds was associated with the negative wound bed status indicators and poor wound healing outcomes. This study aimed to determine baseline 25(OH)D levels in consecutive patients with an existing or newly developed wounds over a period of 31 days. It also aimed to examine the relationships among 25(OH)D status, glycemic control, and local wound bed indicators (superficial or deep and surrounding infection) on healing outcomes.

Methods: This study was a prospective, analytic, cross-sectional pilot study. 80 consecutive patients who presented to a regional wound care center in Bahrain with either an existing or new wound were included in this study.  In this study the primary outcomes measured were 25(OH)D levels and glycemic control. They were compared with the secondary outcomes of quantifiable wound healing; including 3D wound photography, NERDS and STONEES criteria, and an X-ray with a positive probe-to-bone test.

Results: Ninety percent of the sample population in this study were diabetics. Of the patients in this study, none had normal 25(OH)D levels; 15 percent had insufficient levels, and 85 percent had a deficiency. Poor glycemic control (HbA1c levels >6.8 percent) was found in 69.4 percent of diabetic population in the sample. 76.3 percent of the study population had 25(OH)D deficiency and diabetes. Of this group 40.9 percent demonstrated wound healing difficulties and 44.2 percent showed stalled or deteriorating wound healing. Exposed bone was found in 50 percent of the study group. General linear modeling statistical analysis linked poor wound healing in the diabetic sample population to three of the variables studied: 25(OH)D deficiency, poor glycemic control, and an exposed bone in the wound bed.

Conclusions: From this study the authors concluded that vitamin D deficiency may play a significant role in wound healing and the pathogenesis of diabetic foot ulcerations. They believe that this is an often overlooked factor in the pathophysiology and treatment of diabetic foot wounds. The authors state that 25(OH)D deficiency should be addressed as a potential contributing factor in the workup of diabetic foot wounds. They believe that treating these vitamin D deficiencies with supplementation can help to prevent the development of and improve the prognosis for diabetic foot wounds. Further studies are needed in regards to vitamin D supplementation on deficient diabetic patients and its effect on overall wound healing and prognosis.