Disease relevance of Diabetic Foot

• The combination of amdinocillin and cefoxitin was effective in mixed soft tissue infections including diabetic foot infections [1].
• Streptococcus sanguis bacteremia during ciprofloxacin therapy of a diabetic foot ulcer [2].
• The Biogun: A novel way of eradicating methicillin-resistant Staphylococcus aureus colonization in diabetic foot ulcers [3].
• Penetration of fosfomycin into inflammatory lesions in patients with cellulitis or diabetic foot syndrome [4].
• It has similar efficacy to comparator antibacterials such as piperacillin/tazobactam in cSSSI (including diabetic foot infection), cIAI and acute pelvic infection and ceftriaxone with or without metronidazole in cIAI, cUTI and CAP [5].

High impact information on Diabetic Foot

• As loss of nociception and axon-reflex vasodilation contribute to diabetic foot ulceration, early and prolonged NGF treatment at an appropriate dose may provide rational prophylaxis for this condition [6].
• Interestingly, we documented the absence of leptin receptor expression in human diabetic foot ulcers [7].
• Effect of medial arterial calcification on O2 supply to exercising diabetic feet [8].
• Evaluation of granulocyte-colony stimulating factor (Filgrastim) in infected diabetic foot ulcers [9].
• RESULTS: The concentration of MMP-1 was increased 65-fold in biopsies of diabetic foot ulcers compared with the concentrations measured in biopsies of traumatic wounds [10].

Chemical compound and disease context of Diabetic Foot

• Response to "Topical phenytoin in diabetic foot ulcers" [11].
• OBJECTIVE--To determine the effectiveness and safety of arginine-glycine-aspartic acid (RGD) peptide matrix in the treatment of diabetic foot ulcers [12].
• Penetration of piperacillin and tazobactam into inflamed soft tissue of patients with diabetic foot infection [13].
• Evaluation of infectious diabetic foot complications with indium-111-labeled human nonspecific immunoglobulin G [14].
• In vitro activities of moxifloxacin against 900 aerobic and anaerobic surgical isolates from patients with intra-abdominal and diabetic foot infections [15].

Biological context of Diabetic Foot

• 2003 William J. Stickel Silver Award. Skin temperatures as a one-time screening tool do not predict future diabetic foot complications [16].
• Bacteriology of 100 consecutive diabetic foot infections and in vitro susceptibility to ampicillin/sulbactam versus cefoxitin [17].
• The cells actively proliferate and lay down extracellular matrix to generate a papillary dermis-like device that shows a combination of angiogenic, growth factor and cell adhesion properties that enhance healing in diabetic foot ulcers [18].
• CONCLUSIONS: The plantar dermo-fat pad flap promotes primary wound healing after central ray amputation in diabetic foot ulcers by filling the dead space [19].

Anatomical context of Diabetic Foot

• Lower-limb peripheral arterial occlusive disease (PAOD) is a major risk factor in diabetic foot disease [20].
• Lack of insulin-like growth factor 1 (IGF1) in the basal keratinocyte layer of diabetic skin and diabetic foot ulcers [21].
• Computed tomography to visualize and quantify the plantar aponeurosis and flexor hallucis longus tendon in the diabetic foot [22].
• OBJECTIVE: To evaluate the role of granulocyte colony-stimulating factor (G-CSF) as adjunctive therapy for the treatment of diabetic foot infections in non-neutropenic patients [23].
• Use of indium-111-labeled white blood cells in the diagnosis of diabetic foot infections [24].

Gene context of Diabetic Foot

• However, TGF-beta1 expression was not increased in diabetic foot ulcers and chronic venous ulcers, and was comparable to diabetic and normal skin [25].
• Staining for IGF2 was intense in both normal and diabetic skin as well as in diabetic foot ulcers, being greatest at the ulcer edge [21].
• CONCLUSION/INTERPRETATION: The combination of increased concentrations of MMPs with decreased concentrations of TIMP-2 in chronic diabetic foot ulcers compared with healing wounds in normal patients suggests that the increased proteolytic environment contributes to the failure of diabetic wounds to heal [10].
• CONCLUSIONS: MRSA and enterococci are now a common cause of diabetic foot infections, and the increased prevalence may be due to antimicrobial use [26].
• Becaplermin: recombinant platelet derived growth factor, a new treatment for healing diabetic foot ulcers [27].

Analytical, diagnostic and therapeutic context of Diabetic Foot

• CONCLUSIONS: Adjunctive G-CSF treatment does not appear to hasten the clinical resolution of diabetic foot infection or ulceration but is associated with a reduced rate of amputation and other surgical procedures [28].
• Monoclonal antibodies to insulin-like growth factors 1 and 2 (IGF1 and IGF2) were used to investigate their distribution in diabetic foot ulcers and surrounding tissues by immunohistochemistry, compared with diabetic and non-diabetic uninjured skin [21].
• We investigated the distribution of the broad-spectrum antibiotic fosfomycin in infected soft tissue of patients with uncomplicated cellulitis of the lower extremities or diabetic foot infection using in vivo microdialysis [4].
• Epidermal sheets obtained from suction blisters of each patient were grafted on to diabetic foot ulcers without exposed bones (n = 10) and were compared with the standard treatment of local wound care, debridement with a scalpel when indicated, bed rest and parenteral antibiotics (n = 8) [29].
• Comparison of Tc-99m methylene diphosphonate, Tc-99m human immune globulin, and Tc-99m-labeled white blood cell scintigraphy in the diabetic foot [30].

References