Diabetic foot ulcers (DFUs) are among the most serious and costly complications of diabetes, characterised by delayed healing, frequent infections, and a high risk of recurrence. Despite advances in wound care, many current therapies fail to address the multifactorial pathophysiology of diabetic wounds, including vascular dysfunction, immune dysregulation, chronic inflammation, and microbial imbalance. In this context, topical probiotics have emerged as a promising microbiome-based strategy aimed at restoring microbial balance while promoting tissue repair. This review summarises current evidence on the use of topical probiotics in diabetic wound healing, with a particular focus on DFUs, outlining key pathophysiological barriers to healing and examining how probiotic therapies may counteract these processes through antimicrobial, antibiofilm, immunomodulatory, and pro-angiogenic mechanisms. Preclinical studies suggest that topical probiotics may promote accelerated wound closure, reduce bacterial burden, modulate inflammatory responses, and enhance collagen deposition and angiogenesis following topical probiotic application. Early clinical studies investigations remain limited to small pilot studies and case series but have reported preliminary signals of enhanced healing and acceptable short-term tolerability in small exploratory cohorts. In addition, recent advances in probiotic delivery, such as bioengineered dressings, postbiotic formulations, and nano-enabled systems designed to improve stability and therapeutic performance, are also discussed. While existing data indicate biological plausibility and early clinical feasibility, larger, well-designed randomized controlled trials and deeper mechanistic investigations are still required to confirm efficacy, clarify safety in high-risk populations, and enable responsible clinical translation.

Diabetic foot ulcers (DFUs) are among the most serious and costly complications of diabetes, characterised by delayed healing, frequent infections, and a high risk of recurrence. Despite advances in wound care, many current therapies fail to address the multifactorial pathophysiology of diabetic wounds, including vascular dysfunction, immune dysregulation, chronic inflammation, and microbial imbalance. In this context, topical probiotics have emerged as a promising microbiome-based strategy aimed at restoring microbial balance while promoting tissue repair. This review summarises current evidence on the use of topical probiotics in diabetic wound healing, with a particular focus on DFUs, outlining key pathophysiological barriers to healing and examining how probiotic therapies may counteract these processes through antimicrobial, antibiofilm, immunomodulatory, and pro-angiogenic mechanisms. Preclinical studies consistently report accelerated wound closure, reduced bacterial burden, modulation of inflammatory responses, and enhanced collagen deposition and angiogenesis following topical probiotic application, while early clinical studies report encouraging outcomes, including improved healing rates and favourable safety profiles. In addition, recent advances in probiotic delivery, such as bioengineered dressings, postbiotic formulations, and nano-enabled systems designed to improve stability and therapeutic effectiveness, are discussed. While existing data support the potential of topical probiotics as promising adjuncts in DFU management, larger, well-designed clinical trials and deeper mechanistic studies are still needed to define optimal formulations, confirm long-term safety, and enable successful clinical translation.

Chronic diabetic foot ulcers remain a major clinical challenge due to persistent inflammation, impaired tissue repair, and microbial dysbiosis. We report the case of a 62-year-old male with diabetes mellitus presenting with two chronic diabetic foot ulcers managed using different local treatment strategies within the same patient. One wound received conventional wound care, while the second was treated with topical probiotic therapy containing Enterococcus faecium and Saccharomyces boulardii. Wound progression was assessed over eight weeks using the RESVECH 2.0 scale (Results Expected from Chronic Wound Healing), serial wound measurements, and microbiological cultures obtained before and after treatment. Although baseline wound characteristics differed between lesions—with the probiotic-treated ulcer being smaller and less severe at presentation—the probiotic-treated plantar ulcer demonstrated progressive reduction in RESVECH 2.0 scores and complete closure by week 8, whereas the conventionally treated ulcer remained partially open at the end of follow-up. Serial microbiological assessment demonstrated persistent colonization with Providencia stuartii and changes in antimicrobial susceptibility profiles during follow-up. Although limited to a single-patient observation, these findings support further investigation of microbiome-targeted approaches as adjunctive strategies in chronic wound management.

Introduction: Mycophenolate mofetil and its active metabolite mycophenolic acid are routinely used as immunosuppressant drugs in solid organ transplantation in a fixed daily dose regimen in association with cyclosporine, tacrolimus and steroids. Therapeutic drug monitoring for mycophenolic acid concentration has been suggested to optimize outcomes by reducing rejection and drug related toxicities in clinical renal transplantation. Aim: To determine the predose concentration of mycophenolic acid in renal transplanted patients by a validated proposed high-performance liquid chromatography (HPLC) method and to estimate the interindividual variability based on the therapeutic target. Materials and methods: An HPLC method combined with protein precipitation has been validated for mycophenolic acid determination in the human plasma obtained from 21 renal transplant recipients. HPLC analysis was carried out using the chromatographic system Agilent Technologies 1200 DAD. Samples were injected manually, and the compounds were separated on a LiChrosphere® select B C18 analytical column. The mobile phase was 45:55 (v/v) acetonitrile-buffer phosphate, pH 2.5, flow rate of 1.0 mL/min and column temperature of 30°C. Detection was performed at 215 nm. Whole blood samples were collected into vacutainers containing EDTA and separated at 6000 g for 10 minutes. A 200-μL aliquot of patient plasma was transferred to a tube, followed by addition of 10 μL of naproxen as internal standard and 400 μL of acetonitrile (v/v) as a protein precipitating agent. Each tube was vortex-mixed for 30 sec and then centrifuged for 10 min at 10000 rpm. 20 μL of the supernatant was injected into the HPLC system for analysis. Results: The method showed appropriate linearity for MPA with correlation coefficient greater than 0.999. High inter-patient variability is observed with 18% of patients within the target trough concentration range, 27% of patients below the target trough concentration range and 54% over the range with risk of toxicity. Conclusions: Therapeutic monitoring of MPA might contribute to a better management of renal transplant recipient with the goal of optimizing therapeutic regimens in order to reduce the risk of rejection and MPA‐related toxicity.