[Vitamin C deficiency and leg ulcers. A case control study].
ABSTRACT Vitamin C is a necessary cofactor for collagen synthesis. A deficiency of vitamin C results in the breakdown of connective tissue in and around the walls of blood vessels. The disease is thus characterized by poor healing of wounds. Chronic leg ulcers are defined as wounds that do not heal.
To investigate whether patients with chronic leg ulcers have vitamin C deficiency.
Case control study; vitamin C was assayed in peripheral blood samples of 42 consecutive patients with chronic leg ulcers and in 37 consecutive patients without chronic leg ulcers. Patients without leg ulcers had peripheral vascular disease, or hypertension, or connective disorders. Patients with diabetes, immunodepression (cancer, HIV infection, corticosteroid therapy) and aged under 65 years were excluded. Reference range for plasma vitamin C was above 26 micromol/l (normal levels, group I), hypovitaminosis C as 6-26 micromol/l (group II) and concentrations<6 micromol/l as scurvy (group III).
Mean age was 77.2 years in the ulcers group and 73.8 in the control group (NS), mean weight 73.1 kg in the ulcers group and 67.5 kg in the control group (NS). Smoking was more frequent in the control group (P<0.001). Mean vitamin C levels were lower in the leg ulcers group: 23.9 vs 33.8 micromol/l (P<0.003). Normal levels of vitamin C (group I) were more frequent in the control group: 78.4 vs 50% (P<0.01). Hypovitaminosis C (group II) was more frequent in the leg ulcers group: 23.8 vs 16.2% (P<0.01). Scurvy was more frequent in the leg ulcers group: 26.2 vs 5.4% (P<0.01). C reactive protein levels were higher in the leg ulcers group: 31.8 vs 9.3 mg (P=0.002) and albumin levels were lower in the leg ulcers group: 25 vs 38 g/l (P=0.01) [retrospective data].
Patients with chronic leg ulcers have lower levels of vitamin C than patients without leg ulcers, although smoking was more frequent in patients without leg ulcers. The question is whether vitamin C deficiency is a cofactor of impaired healing or is a simple marker of poor healing? It would be interesting to conduct a randomized controlled study about treatment of chronic leg ulcers with vitamin C.
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ABSTRACT: Significance: Chronic wounds represent a major burden on global healthcare systems and reduce the quality of life of those affected. Significant advances have been made in our understanding of the biochemistry of wound healing progression. However, knowledge regarding the specific molecular processes influencing chronic wound formation and persistence remains limited. Recent Advances: Generally, healing of acute wounds begins with hemostasis and the deposition of a plasma-derived provisional matrix into the wound. The deposition of plasma matrix proteins is known to occur around the microvasculature of the lower limb as a result of venous insufficiency. This appears to alter limb cutaneous tissue physiology and consequently drives the tissue into a 'preconditioned' state that negatively influences the response to wounding. Critical Issues: Processes, such as oxygen and nutrient suppression, edema, inflammatory cell trapping/extravasation, diffuse inflammation, and tissue necrosis are thought to contribute to the advent of a chronic wound. Healing of the wound then becomes difficult in the context of an internally injured limb. Thus, interventions and therapies for promoting healing of the limb is a growing area of interest. For venous ulcers, treatment using compression bandaging encourages venous return and improves healing processes within the limb, critically however, once treatment concludes ulcers often reoccur. Future Directions: Improved understanding of the composition and role of pericapillary matrix deposits in facilitating internal limb injury and subsequent development of chronic wounds will be critical for informing and enhancing current best practice therapies and preventative action in the wound care field.Advances in wound care: the journal for prevention and healing 10/2013; Ahead of Print(3). DOI:10.1089/wound.2013.0462
Article: Nutrition and skin ulcers.[Show abstract] [Hide abstract]
ABSTRACT: Skin ulcerations cause significant morbidity and mortality, while driving up healthcare utilization and costs. Interventions to prevent ulcers and improve wound healing times are needed to reduce the burden on patients and healthcare systems. It has been well established that weight loss, protein-calorie malnutrition, and dehydration are risk factors for pressure ulcers. Many nutritional interventions have been studied, with studies being of variable quality and producing mixed results. This review aims to clarify the current evidence and highlights the recent advances in the area of nutrition for the prevention and management of skin ulceration. Markers for assessing nutritional status will be reviewed first, followed by a discussion on the theoretical benefit of various nutritional interventions on wound healing. Recommendations for nutrient repletion are also included. Finally, the most recent or important literature will be highlighted and the risks and benefits of supplementation are debated. There is mixed evidence for most nutritional interventions, with most studies being of poor quality with variable study designs, lack of control groups, small sample sizes, and short study lengths. Long-term randomized trials of individual nutrients and clinically relevant endpoints are needed to definitively show the benefit of additional nutritional supplementation over dietary interventions. Until those studies become available, best evidence suggests the importance of screening for malnutrition, calculating resting energy expenditure and caloric needs, and monitoring dietary intake of essential nutrients.01/2013; 16(1):39-49. DOI:10.1097/MCO.0b013e32835bc0a1
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ABSTRACT: The aim of this study was to systematically screen hospitalized elderly patients for clinical symptoms of scurvy and to confirm the diagnosis with biological measures. Geriatric acute care ward. Scurvy symptoms (one or more among perifollicular hyperkeratosis, petechiae or bruises, haemorrhagic features caused by venous puncture, severe gingivitis). We compared associated diseases, nutritional status, need for assistance for feeding, serum albumin, transthyretin, B9 and B12 vitamins, iron status and Serum Ascorbic Acid Level (SAAL) and outcome (in-hospital mortality) between scurvy and scurvy free patients. 18 patients with clinical symptoms of scurvy (scurvy group) were identified out of 145 consecutive patients (12%). They were compared to 23 consecutive control patients with no clinical symptoms of scurvy (scurvy-free group). SAAL was significantly lower (1.09 +/- 1.06 vs 4.87 +/- 4.2 mg x L-1, p < .001) and vitamin C deficiency more frequent (94 vs 30 %, p < .001) in the scurvy group. Moreover, in scurvy group, coronary heart disease (39 vs 9 %, p=.028), need for assistance for feeding (56 vs 13 %, p=.006) and in-hospital deaths (44 vs 9 %, p=.012) were more frequent. Ninety-four percent of patients with clinical symptoms of scurvy had vitamin C deficiency. Our results suggest that in hospitalized elderly patients, clinical symptoms allow scurvy diagnosis. Scurvy could be a frequent disease in elderly patients admitted to acute geriatric ward.The Journal of Nutrition Health and Aging 06/2010; 14(6):407-10. DOI:10.1007/s12603-010-0032-y · 2.66 Impact Factor