The annual cost to the NHS of managing 3.8 million patients with a wound was estimated in 2020 to be £8.3 billion, of which £5.6 billion was spent on the 30% of wounds that did not heal and £2.7 billion on the 70% of wounds that healed (Guest, 2020). One of the main symptoms associated with chronic \'hard-to-heal\' wounds is the production of excess exudate (Atkin et al, 2019). This is due to a prolonged chronic inflammatory response stimulated by a physiological cause. This article describes what exudate is and its importance in the wound healing process, highlighting the consequences of too little or excessive wound exudate associated with any wound. The article goes on to describe a case series observational study involving a range of patients (n=47; 33 male/14 female), aged between 33 and 91 years (mean 67.4 years), with a variety of acute (n=11) and chronic exuding wounds (n=44). In total, 55 wounds of various aetiologies were managed with DryMax Super (a dressing whose design includes superabsorbent polymers) in order to evaluate and report on the absorption and fluid-handling properties of the product.

Treatment of infected wounds remains a major challenge for clinicians. Antimicrobial stewardship is an important pillar in wound treatment and, as the role of bacteria in wound repair is not well understood, new treatment options and products are constantly being developed to tackle local infection and biofilm. This case report describes a case of antibiotic-resistant Burkholderia cepacia skin infection and subsequent leg ulceration in an 86-year-old man during the COVID pandemic in Italy, which was successfully treated in a conservative way using 1% acetic acid and silver oxysalts in conjunction with compression bandage.

Time-driven activity-based costing (TDABC) is suggested to assess costs within the value-based healthcare approach, but there is a paucity of applications in chronic diseases such as deep vein thrombosis (DVT) and leg ulcers. In this context, we applied TDABC in a cost-effectiveness analysis comparing venous stenting to compression ± anticoagulation (standard of care-SOC) from both hospital and societal perspectives in Italy. TDABC was applied to both treatments to assess costs that were included in a cost-effectiveness model. Clinical inputs were retrieved from the literature and integrated with real-world data. The Incremental Cost Utility Ratio (ICUR) of stenting compared to SOC was EUR 10,270/QALY and EUR 8962/QALY for hospital and societal perspectives, respectively. The mean cost per patient for venous stenting of EUR 5082 was higher than the Diagnosis-Related Group (DRG) reimbursement (EUR 4742). For SOC, an ulcer healing in 3 months costs EUR 1892, of which EUR 302 (16%) is borne by the patient versus a reimbursement of EUR 1132. TDABC showed that venous stenting may be cost-effective compared with SOC but that reimbursement rates may not completely cover the real costs, which are partially sustained by the patients. A more efficient policy for covering the real costs may be beneficial for both clinical centers and patients.

Elevated levels of inflammatory mediators-including the interleukin IL-23-are implicated in the pathogenesis of pyoderma gangrenosum (PG), an autoinflammatory neutrophilic dermatosis characterized by rapidly enlarging, suppurative ulcers and cribriform scarring. Here, we present the first case report of significant response of isolated ulcerative PG with tildrakizumab, a biologic agent directed against the p19 subunit of IL-23, in an elderly woman with extensive treatment-refractory PG on her left leg. Tildrakizumab (100 mg subcutaneously at weeks 0 and 4, then every 8 weeks, and eventually increased in frequency to every 6 weeks), combined with acetic acid soaks each morning and chemical debridement every evening with 3% hydrogen peroxide, resulted in progressive decrease in ulcer size and depth, re-epithelialization, and recovery of sensory perception. This report describes the dramatic clinical response of ulcerative PG on the leg with tildrakizumab.

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The chronic use of hydroxyurea (HU) in some oncologic and non-oncologic diseases (psoriasis, sickle cell anemia) can be accompanied by side effects, both systemic and mucocutaneous. The most severe adverse events known in HU therapy are leg ulcers and cutaneous carcinomas. At skin level may also appear: xerosis, persistent pruritus, skin color changes (erythema, hyperpigmentation), cutaneous atrophy. Likewise, oral ulcerations and stomatitis may occur at mucosal level. Hair damage can be expressed through alopecia and nail damage through melanonychia and oncycholysis. First case, a 63-year-old woman with severe psoriasis vulgaris and chronic granulocytic leukemia, with 5 years of HU therapy, was admitted to hospital for submammary and palmoplantar ulcers, superinfected with methicillin-resistant Staphylococcus aureus and Proteus mirabilis. Clinical exam showed that the patient had also cutaneous atrophy, marked palmoplantar xerosis and melanonychia. The second case, a 72-year-old woman with primary thrombocytemia, treated with HU for 3 years, presented with necrotic leg ulcers that were superinfected with Pseudomonas aeruginosa, Enterobacter and E. Coli. The patient associates cellulitis, microbial eczema and xeroderma. In both cases, after HU discontinuation, systemic antibiotics, topical epithelizing agents and emollients, the ulcers had a slow favorable evolution. In our cases, the ulcers appeared after 5, respectively 3 years of HU therapy. It is stressed that in the first case, which had associated psoriasis, after 1 year of 1 g of HU/day, the psoriatic lesions completely disappeared. The severe progression of the ulcers was also favored by the superinfection of the ulcers with 2, respectively, 3 identified germs for which appropriate systemic antibiotics was required.

Leg ulcers have been a common presentation in clinics; disruptions in the mechanism of ulcer healing are vascular insufficiency, anemia, metabolic disturbances, neuropathy, and autoimmunity. The term \'non-transfusion-dependent thalassemia\' encompasses the milder forms of thalassemia traits that require intermittent or no transfusion at all, and are mostly associated with leg ulcers. We present the case of a 19-year-old female with beta-thalassemia major who presented with non-healing leg ulcers and anemia. The clinical findings and lab evidence suggested hemolytic anemia evidenced by pathologic fractures, hepato-splenomegaly, and normal iron studies. Hemoglobin electrophoresis confirmed beta-thalassemia major with its complications including adrenal insufficiency and pathological fractures, all of which remained well compensated till the second decade of life.

Klinefelter syndrome (KS) is the most frequent type of congenital sex-chromosomal disorder caused by at least one extra X chromosome and commonly treated with lifetime testosterone therapy. Ulcerative lesions on lower extremities may occur as a complication of KS. The pathogenesis of ulcers in KS patients has not been clarified on a molecular level. Here we present a case of leg ulcers exacerbation associated with the administration of a high dose of acetylsalicylic acid in a 63-year-old KS patient with karyotype 47,XXY undergoing testosterone replacement therapy for the last 20 years. The appearance of the ulcer on the patient\'s leg occurred during one week of high oral acetylsalicylic acid intake (1.2 g daily). The patient was advised to return to his standard daily dose of 0.1 g of acetylsalicylic acid and significant improvement of his leg ulcer was observed after two weeks. We hypothesize that testosterone-mediated nitric oxide balance in KS patient is perturbed under the condition of acute high-dose acetylsalicylic acid administration. We propose that small standard doses of approximately 0.1 g/day of acetylsalicylic acid have no apparent effect on nitric oxide status, whereas higher doses may cause dysregulation of nitric oxide production and/or utilization, creating conditions which may cause the appearance of leg ulcers in the KS patients.

One of the biggest challenges faced by healthcare providers is the treatment of chronic, non-healing wounds. This paper reports for the first time in the UK the results of five case studies in which a novel regenerating matrix-based therapy, CACIPLIQ20, was used. CACIPLIQ20 is a heparan sulphate mimetic designed to replace the destroyed heparan sulphate in the extracellular matrix of wound cells. All five patients in this case series had chronic, non-healing ulcers that had not improved with conventional care. Treatment included two applications of CACIPLIQ20 per week, for a maximum of 12 weeks. Three of the five wounds healed completely, and the remaining two showed significant improvements in size and quality. The treatment was well tolerated by the patients and also led to a significant reduction in pain. Moreover, CACIPLIQ20 treatment was found to be highly cost-effective when compared to conventional care, with the potential to save healthcare systems significant resources. Further studies are needed to build a strong evidence base on the use of this product, but these preliminary findings are certainly promising.

Leg ulcers may occur due to many autoimmune, hereditary, inflammatory, and infectious causes including venous, arterial, and neuropathic ulcers. Hyperhomocysteinemia is a metabolic disorder caused by various enzyme defects in methionine metabolism. The most common cause is methylenetetrahydrofolatreductase (MTHFR) enzyme gene mutations. Hyperhomocysteinemia is an independent risk factor for deep vein thrombosis and peripheral arterial disease. The effects of endothelial cell damage on smooth muscle hypertrophy, platelet aggregation, coagulation, and fibrinolysis cause atherogenesis and thrombosis, leading to venous and arterial lower extremity ulcers. In this article, we report the case of a 47-year-old male patient who was admitted to our clinic due to painful leg ulcers that started 1 year ago. He had a history of vena cava inferior thrombosis, deep vein thrombosis, and 40 pack-year smoking. Histopathological examination of punch biopsy taken from ulcerative lesion showed intense inflammatory infiltration in the middle dermis, erythrocyte extravasation, leukocytoclasia, and thrombus formation in a small diameter venule lumen. There were nonspecific findings in direct immunofluorescence examination. He was found as having MTHFR C677T homozygote and plasminogen activator inhibitor-1 4G/5G heterozygote gene mutation with high homocysteine level of 22.90 µmol/L, and he was diagnosed as hyperhomocysteinemia. He was recommended to quit smoking because it triggered thrombosis in hyperhomocysteinemia. Herein, we present a case of hyperhomocysteinemia due to MTHFR mutation, which is one of the rare hereditary thrombophilia causes.