SummaryNecrobiosis lipoidica (NL) is a rare granulomatous disease of hitherto unclear etiology frequently seen in patients with diabetes. Characterized by its potential for ulcerations, it often presents a serious burden for those affected. There are currently neither German nor European guidelines for the treatment of NL. At the same time, standard treatment with topical or intralesional corticosteroids does not always show satisfactory results. We therefore set out to evaluate whether the various treatment regimens published since 2000 have actually expanded the therapeutic armamentarium in a relevant manner. Included were all publications that described more than one patient being treated with any given therapeutic modality. Overall, we analyzed data for 16 different treatment regimens reported in 49 publications.The largest amount of data exists for topical PUVA therapy, photodynamic therapy (PDT), and systemic treatment with fumaric acid esters. Remarkably, our analysis showed that with an increase in the number of documented patients treated with a given therapeutic modality, the proportion of those achieving a complete or partial response actually decreased. This was interpreted as publication bias. Thus, no clear recommendation can be given for second-line therapy in case topical or intralesional corticosteroids fail.

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Abstract:The treatment of chronic ulcers is a complex issue and presents an increasing problem for caregivers everywhere. This is especially true in Germany, where more than 4 million chronic wounds are treated each year. Therapeutic decisions must be patient-centered and reflect wound etiology, localization, and healing status. The practice of using the same wound dressing during the entire healing period is no longer reasonable. Instead, multiple types of dressings may be needed for a single wound over its healing trajectory. Selection of the most appropriate dressing should be based on wound phase, depth, signs of infection, and level of exudate. Moisture balance is critical in wound care; dryness will hamper epithelial cell migration while excessive generation of fluid causes maceration at the wound margins. Hence, exudate management is a key issue in chronic wound therapy, particularly given that exudate from chronic wounds has a composition different from that of acute wound fluid. Several studies have shown that exudates from non-healing wounds contain significantly elevated levels of protease activity, increased formation of free radicals, and abundant amounts of proinflammatory cytokines, while concentrations of growth factors and protease inhibitors are markedly decreased. Application of dressings that remove and sequester excess amounts of wound fluid may not only help in restoring the correct balance of moisture, but also support the wound healing process by preventing tissue deterioration caused by abundant protease activity. Several types of dressings, such as hydrogels, hydrocolloids, alginates, hydrofibers, foams, and superabsorbent dressings, are reviewed here and evaluated with regard to their efficacy for highly exuding wounds.

It is a general goal to improve wound healing, especially of chronic wounds. As light therapy has gained increasing attention, the positive influence on healing progression of water-filtered infrared A (wIRA), a special form of thermal radiation, has been investigated and compared to the detrimental effects of UV-B irradiation on wound closure in vitro. Models of keratinocyte and fibroblast scratches help to elucidate effects on epithelial and dermal healing. This study further used the simulation of non-optimal settings such as S. aureus infection, chronic inflammation, and anti-inflammatory conditions to determine how these affect scratch wound progression and whether wIRA treatment can improve healing. Gene expression analysis for cytokines (IL1A, IL6, CXCL8), growth (TGFB1, PDGFC) and transcription factors (NFKB1, TP53), heat shock proteins (HSP90AA1, HSPA1A, HSPD1), keratinocyte desmogleins (DSG1, DSG3), and fibroblast collagen (COL1A1, COL3A1) was performed. Keratinocyte and fibroblast wound healing under non-optimal conditions was found to be distinctly reduced in vitro. wIRA treatment could counteract the inflammatory response in infected keratinocytes as well as under chronic inflammatory conditions by decreasing pro-inflammatory cytokine gene expression and improve wound healing. In contrast, in the anti-inflammatory setting, wIRA radiation could re-initiate the acute inflammatory response necessary after injury to stimulate the regenerative processes and advance scratch closure.

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