AimsTo validate the perfusion, extent, depth, infection and sensation (PEDIS) classification system and to make the clinical practice easier, we created a score system and compared this system with two previously published common score systems.MethodsA retrospective cohort study was conducted on patients with diabetic foot ulcer (DFU) attending our hospital (n=364) from May 2007 to September 2013. Participants’ characteristics and all variables composing the PEDIS classification system were assessed.ResultsDuring a median follow-up of 25 months (range 6-82), ulcers healed in 217 of the 364 patients (59.6%), remained unhealed in 37 patients (10.2%), and were resolved by amputation in 62 patients (17.0%); 48 patients (13.2%) died. When measured using the PEDIS classification system, the outcome of DFU deteriorated with increasing severity of each subcategory. Additionally, longer ulcer history, worse perfusion of lower limb, a larger extent of the ulcer, a deeper wound, more severe infection, and loss of protective sensation were independent predictors of adverse outcome. More importantly, the new PEDIS score system showed good diagnostic accuracy, especially when compared with the SINBAD and Wagner score systems.ConclusionsThe PEDIS classification system, which encompasses relevant variables that contribute to the outcome of DFU and has excellent capacity for predicting the ulcer outcome, demonstrated acceptable accuracy. The PEDIS classification system might be useful in clinical practice and research both for the anticipation of health care costs and for comparing patient subgroups.

The aim of this study was to describe the characteristics of diabetic foot ulcer (DFU) patients with anemia and assess the relationship between anemia and DFU outcome. A retrospective cohort study was conducted on patients with DFU who attended our hospital from May 2007 to September 2014. All of the variables in the DFU patients with and without anemia were compared. In this study, 353 subjects were included, anemia was present in 236 patients (66.9%). These patients were significantly male, more likely to be a smoker, had a lower level of serum albumin and worse kidney function, more likely to use at least 2 types of antibiotics and had a worse perfusion of the lower limb, a larger and deeper ulcer and a more severe infection. A multivariate analysis showed that male sex, lower serum albumin, and worse kidney function were independent predictors of anemia in DFU patients. Additionally, in multivariate models, anemia was one of the variables that was most significantly associated with adverse outcomes and with similar findings for secondary outcomes. Receiver operating characteristic analysis determined a hemoglobin cutoff of 12.3 g/dL (females) and 12.1 g/dL (males) to identify a high-risk population of DFU patients who would have adverse outcomes. So anemia is common in patients with DFU. Although typically mild or moderate, anemia has been associated with substantial morbidity and mortality in patients with DFU.

Matricellular proteins, a group of extracellular matrix (ECM) proteins, are key regulators of skin repair and their dysregulation impairs wound healing in diabetes. Tubulointerstitial nephritis antigen like 1 (TINAGL1) is a new member of matricellular protein family, and the understanding of its functional role is still relatively limited. In the current study, we detected the expression of TINAGL1 in diabetic skin wound tissues through RT‐PCR, ELISA and Western blot analysis, investigated the contribution of TINAGL1 to wound healing through cutaneous administration of recombinant TINAGL1 protein, and characterized its regulation by hyperglycemia through RNA‐seq and signal pathway inhibition assay. We showed that TINAGL1 expression has dynamic change and reaching a peak on day‐9 after wound during the wound healing process in wild‐type (WT) mice. Interestingly, decreased TINAGL1 expression is detected in skin tissues of diabetic patients and mice after wound. Then, we found that high glucose (HG), an important factor that impairs wound healing, reduces the expression of TINAGL1 in fibroblasts through JNK pathway. Notably, the histology analysis, Masson trichrome assay and IHC assay showed that exogenous TINAGL1 promotes wound healing in diabetic mice by accelerating the formation of granulation tissues. Our study provides evidence that TINAGL1 has an essential role in diabetic wound healing, and meanwhile, indicates that manipulation of TINAGL1 might be a possible therapeutic approach.

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