Assessment of Financial Conflicts of Interest Related to the Use of Dermal Substitutes in Burn Management

Author(s):  
Jacob Radparvar ◽  
Tina Tian ◽  
Manish Karamchandani ◽  
Jeffrey Aalberg ◽  
Daniel Driscoll ◽  
...  

Abstract This study aims to systematically review the accuracy of the self-reporting of conflicts of interest (COI) among studies related to the use of dermal substitute products in burn management and evaluate factors associated with increased discrepancies. To do so, a literature search was done to identify studies investigating the use of dermal substitutes in burn management published between 2015 – 2019. Industry payments were collected using the Centers for Medicare & Medicaid Services Open Payments database. Declared COI were then compared with the listed payments. Studies and authors were considered to have a COI if they received payments totaling >$100 for each company. A total of 51 studies (322 authors) were included for analysis. Thirty-eight studies (75%) had at least one author received an undisclosed payment from industry. From 2015 to 2019, 1391 general payments (totaling $1,696,848) and 108 research payments (totaling $1,849,537) were made by 82 companies. When increasing the threshold on what would be considered an undisclosed payment, the proportion of authors with discrepancies gradually decreased, from 88% of authors with undisclosed payments >$100 to 27% of authors with undisclosed payments >$10,000. Author order, journal impact factor, and study type were not significantly associated with increased risk of discrepancy. We found that the majority of studies investigating the use of dermal substitute products for burn management did not accurately declare COI, highlighting the need for a uniform declaration process and greater transparency of industry sponsorship by authors when publishing peer-reviewed burn surgery research papers.

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 3714-3714
Author(s):  
Lei Zhang ◽  
Huacheng Luo ◽  
Jing Li ◽  
Hong-Min Ni ◽  
Mark Sellin ◽  
...  

Background: Among all tissues, bone marrow (BM) is the most sensitive tissue to ionizing radiation (IR)-induced acute tissue damage (ATD) and chronic long-term residual damage (LT-RD). BM failure and a significant reduction in blood cells (pancytopenia) often occurs within days after exposure to IR due to the massive death of proliferative hematopoietic progenitor cells (HPCs). However, due to their quiescent cell cycle status and reduced fidelity of DNA repair feature, many hematopoietic stem cells (HSCs) cannot fully eliminate such damage and enter senescence; this results in LT-RD. Abnormal dysplastic hematopoiesis is the most common LT-RD in most victims of IR, followed by an increased risk of leukemia/lymphoma development. Thus IR exposure is an established cause of BM failure and leukemia. A significant increase in the production of inflammatory cytokines is induced by IR which contributes to the pathogenesis of both ATD and LT-RD. Such inflammatory cytokines induce the activation of Ripk3-Mlkl-mediated necroptotic signaling in HSCs. However, the role of Ripk3-Mlkl signaling in IR-induced damage has not studied. Experimental procedures: The self-renewal capacity of HSCs among Ripk3-/-, Mlkl-/- and WT mice were examined and compared by serial transplantation assay. The phenotypes of ATD and LT-RD induced by different dosages of IR were compared among Ripk3-/-, Mlkl-/- and WT mice. The mechanism by which Ripk3 signaling prevents IR-induced leukemia development was studied. Results: Ripk3-Mlkl signaling is not required for hematopoiesis during homeostatic condition. However, during serial transplantation, inactivation of such signaling prevents stress-induced loss of HSCs. Interestingly, Ripk3 signaling also induces an Mlkl-independent ROS-p38-p16-mediated senescence in HSCs. Thus Ripk3-/- HSCs showed better competitive hematopoietic ability compared to Mlkl-/- and WT HSCs during serial transplantation. A sub-lethal dosage of IR (6Gy) induces Ripk3-dependent NF-κB activation and pro-survival gene expression in HSCs, which is necessary for the survival of damaged HSCs. After 6Gy IR, although DNA damage is repaired in most HSCs within 2 days, a proportion of HSCs in WT and Mlkl-/- mice fail to fully repair the damage and undergo p53-p21-dependent senescence. However such cells in Ripk3-/- mice die from apoptosis. Thus the remaining HSCs in Ripk3-/- mice should be functionally normal, while a proportion of the remaining HSCs in Mlkl-/- and WT mice remain damaged but senescent, all as demonstrated by competitive hematopoietic reconstitution assay. Multiple low-doses of IR (1.75Gy once week × 4) induce HSC exhaustion in WT mice but not in Ripk3-/- and Mlkl-/- mice. Interestingly, almost all Ripk3-/- mice develop acute lymphoblastic leukemia within 200 days after such low dose IR, while 45% of WT and 60% of Mlkl-/- mice develop thymomas within 360 days (see Figure). Mechanistically, such low-dose IR stimulates chronic inflammatory cytokine production. Such cytokines induce Ripk3-Mlkl-mediated necroptosis in response to HSC exhaustion observed in WT mice. These cytokines also induce Ripk3-ROS-p38-p16-mediated senescence in response to impaired HSC functioning observed in both WT and Mlkl-/- mice. In Ripk3-/- mice, due to the lack of both necroptotic and senescent signaling, mutant HSCs accumulate and leukemia development is accelerated. Conclusion: Ripk3 signaling plays distinct roles in HSCs in response to different doses of IR. High-dose IR induces Ripk3-dependent NF-κB/survival signaling, which is required for the survival of HSCs which fail to repair the damage. Thus temporal inhibition of Ripk3-NF-κB signaling might help to remove the damaged HSCs thus preventing the occurrence of LT-RD. However multiple low-doses of IR induces Ripk3 activation in HSCs which represses leukemia development by inducing both ROS-p38-p16-mediated senescence and Ripk3-Mlkl-mediated necroptosis. Induced activation of Mlkl-necroptosis might help to repress leukemia development by removing damaged HSCs. Disclosures No relevant conflicts of interest to declare.


Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 2162-2162
Author(s):  
Kamelah Abushalha ◽  
Sawsan Abulaimoun ◽  
Ryan Walters ◽  
Sara Albagoush ◽  
Hussain I Rangoonwala ◽  
...  

Background: Patients with hepatocellular carcinoma (HCC) are at an increased risk for developing venous thromboembolism (VTE)- mainly portal venous thrombosis (PVT). Malignancy and liver cirrhosis ( 80%-90% of HCC cases are related to cirrhosis) are conditions that can perturb the hemostatic balance towards a prothrombotic state. Also, these patients with HCC are at high risk for gastrointestinal bleeding (GIB), making thromboprophylaxis and anticoagulation a treatment challenge. Additional information regarding the outcomes and severity of both VTE and GIB in patients with HCC would be useful to guide clinical decision-making Aim: To determine the rates, inpatient mortality, length of stay (LOS) and hospital cost of VTE and GIB-related admissions in patients with hepatocellular carcinoma. Method: We used ICD-9-CM and ICD-10-CM codes to identify hospitalizations from 2007 to 2016 that included HCC with primary discharge diagnoses of GIB or VTE. Linear trends in the rate of GIB and VTE, as well as in-hospital mortality, LOS, and inflation-adjusted hospital cost (in 2016 US dollars), were evaluated using Daniel's test; piecewise slopes were used as needed. All analyses accounted for the NIS sampling design with updated hospital trend weights used as appropriate. SAS v. 9.4 was used for all analyses. Results: Between 2007 and 2016, we identified 6,527,871 hospitalizations with HCC and a primary discharge diagnosis of GIB (3,517,059; 53.9%) or VTE (3,010,812; 46.1%). From 2007 to 2010, a decreasing trend was observed in the rate of GIB diagnoses (55.5% to 51.6%, ptrend < .001), whereas an increasing trend was observed for VTE diagnoses (44.5% to 48.4%, ptrend < .001). By contrast, from 2010 to 2016, an increasing trend was observed in GIB (51.6% to 55.2%, ptrend < .001), whereas a decreasing trend was observed in VTE (48.4% to 44.8%, ptrend < .001). For in-hospital mortality, a decreasing trend was observed for GIB (2.3% to 1.9%, ptrend < .001), whereas a decreasing trend was observed in VTE until 2012 (1.8% to 1.5%, ptrend < .001), after which no trend was indicated (1.5% to 1.6%, ptrend = .337). Although decreasing trends in LOS were observed for GIB (3.4 days to 3.2 days, ptrend < .001) and VTE (4.3 days to 3.3 days, ptrend < .001), increasing trends were observed for inflation-adjusted hospital cost for both GIB ($6,996 to $7,707, ptrend < .001) and VTE ($7,283 to $7,584, ptrend = .048). Conclusion: In this NIS cohort of hospitalized patients with HCC, GIB was more frequently observed than VTE. Trends observed in the rates of GIB and VTE went in opposite directions. In general decreasing trends were observed in in-hospital mortality and LOS for both VTE and GIB. By contrast, increasing trends were observed in the hospital cost for both diagnoses. Clinicians should balance benefits against risks when deciding VTE prophylaxis and treatment in patients with HCC. Future studies are needed to determine the ideal agent and specific dosages to treat HCC-associated VTE. Disclosures No relevant conflicts of interest to declare.


Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 4903-4903 ◽  
Author(s):  
Ibraheem H Motabi ◽  
Syed Ziauddin A. Zaidi ◽  
Mamoun Hassan Ibrahim ◽  
Imran K Tailor ◽  
Nawal Faiez Alshehry ◽  
...  

Abstract Introduction Respiratory viruses are an important cause of outbreaks of pneumonia in hematological malignancy patients. Recently, novel Middle East respiratory syndrome coronavirus (MERS-CoV) caused a cluster of life-threatening infections in Saudi Arabia (688 confirmed MERS-CoV infection cases with 282 deaths were reported to WHO by June 6, 2014 including 28% cases in HCW). Most patients had upper &/or lower respiratory tract symptoms but other features included abdominal pain, diarrhea, acute kidney injury & shock. Few hematology units were closed due to havoc. Here we report clinical features & outcome of 4 patients diagnosed at our unit during the peak period (mid-March through May 2015) including 2 who got chemotherapy (chemo) soon after recovery. Patient #1 A 62-yr-old male had free λ light chain multiple myeloma (MM) with spinal cord compression. After surgery & local radiation, he was sent to us with paraplegia & grade 4 infected sacral bedsore that needed inpatient care. He was started on CyBorD Cycle 2 on April 24, 2014. On May 2, he had a fever spike with shortness of breath (SOB) & cough. He was started on antibiotics. CXR revealed bilateral infiltrates & right sided pleural effusion. His O2 sat dropped & he needed CPAP. Oseltamivir was started & sputum was positive for MERS-CoV RT-PCR. He became afebrile with decreasing O2 requirement, CXR normalized & RT-PCR for MERS-CoV turned negative. Later he was able to receive 3rdcycle of CyBorD. Patient #2 A 65-yr-old lady came to us with B symptoms & huge organomegaly due to stage-IV DLBCL. On May 2, 2014 RCVP chemo was started. On day 6, she spiked fever with SOB, cough & was started on imipenem. CXR showed consolidation in right lower lobe. She needed 4L of O2/min. On May 10, 2014, she worsened with RR 32/min, O2 sat 79% on 15L O2/min & BP 79/47 mmHg. CXR revealed bilateral consolidation. She needed intubation & inotropic support in ICU. Vancomycin & oseltamivir were started & RT-PCR was positive for MERS-CoV on two nasopharyngeal swabs (NPS). LFT & RFT were normal but she continued to decline & died on May 13, 2014. Patient # 3 A 22-yr-old lady with past H/O AML t(8;21) was admitted on April 27, 2014 with 3 day H/O cough, fever & SOB. CXR had infiltrates in left lower lobe. She had severe pancytopenia & BMB confirmed relapsed AML. She had slightly raised LFT. Urine grew Ent. fecium. Antibiotics & voriconazole were used. She remained febrile over next 2 days. CT chest revealed extensive bilateral consolidation. She needed O2 up to 5L/Min for few days. RT-PCR for MERS-CoV was positive from NPS. She was initiated on oseltamivir. She became afebrile after 2 days & repeated RT-PCR for MERS-CoV was negative. Fludara, Ara-C (FA) chemo was started. She remained neutropenic for next 4 weeks but there was no recurrence of respiratory symptoms. BMB on day 28 of FA confirmed CR. CT chest revealed complete resolution of air space opacities. She was discharged with plan to undergo matched sibling donor Allo-HSCT. Patient #4 A 76-yr-old male with H/O HTN & CKD was diagnosed to have IgA κ MM. He was started on MPV chemo as inpatient due to logistic reasons. After 3 cycles of MPV, serum free κ chains decreased by 91% but remained on dialysis. On 21 April, 2014 he developed cough, SOB & fever. CXR revealed bilateral infiltrates & antibiotics were started. He worsened over next few days & CXR showed worsening bilateral consolidation. Eventually he needed intubation. He was treated with antimicrobials including voriconazole & oseltamir. RT-PCR for MERS-CoV was positive from NPS. Unfortunately he died few days later. Discussion: Patients with hematological malignancies are at increased risk of community & hospital-acquired infections. Recent outbreak of MERS-CoV infection has created a havoc among hematologists community. There is uncertainty about impact of MERS-CoV infection on continuation of chemo. We report 4 cases of hematological malignancies with MERS-CoV infection. Three of the 4 patients developed severe pneumonia & required intubation (2 died later) & one had milder form of pneumonia treated in isolation room. In addition to supportive care, all 4 received antimicrobials & oseltamivir. Chemo was safe soon after recovery from infection in the surviving 2 patients. We propose that during MERS-CoV epidemics, pneumonia can be treated with supportive care, antibiotics & oseltamivir. Chemo can be continued for the malignant disease soon after recovery. Further reports are needed to confirm our findings. Disclosures No relevant conflicts of interest to declare.


JAMA ◽  
2018 ◽  
Vol 319 (4) ◽  
pp. 408 ◽  
Author(s):  
Quinn Grundy ◽  
Adam G. Dunn ◽  
Florence T. Bourgeois ◽  
Enrico Coiera ◽  
Lisa Bero

Blood ◽  
2017 ◽  
Vol 130 (Suppl_1) ◽  
pp. 915-915
Author(s):  
Qian Wang ◽  
Changchuan Jiang ◽  
Yaning Zhang ◽  
Stuthi Perimbeti ◽  
Prateeth Pati ◽  
...  

Abstract Introduction: Previous studies have shown that uninsured and Medicaid patients had higher morbidity and mortality due to limited access to healthcare. Disparities in cancer-related treatment and survival outcome by different insurance have been well established (Celie et al. J Surg Oncol.,2017). There are approximately 8,260 newly diagnosed HL cases in the US yearly (Master et al. Anticancer Res.2017). Therefore, we aim to investigate the variation of survival outcome and insurance status among HL patients. Methods: We extracted data from the US National Cancer Institute's Surveillance, Epidemiology and End Results (SEER) 18 program. HL patients who were diagnosed from 2007-2014 were included. Demographic information including age, sex, race, annual household income, education and insurance were also collected. Insurance includes uninsured, insured and any Medicaid. Race/ethnicity includes white, black and other (including American Indian/AK native, Asian/Pacific Islander). HL is categorized by using International Classification of Disease for Oncology (ICD-O-3) into classical HL NOS (CHL NOS), nodular lymphocyte predominant HL (NLP), lymphocyte rich (LR), mixed cellularity (MC), lymphocyte depleted (LD), and nodular sclerosis (NS). Treatment modality included RT alone, CT alone, RT and CT combined, and no RT or CT. Survival time was estimated by using the date of diagnosis and one of the following dates: date of death, date last known to be alive or date of the study cutoff (December 31, 2014). Chi-square test and multivariate Cox regression were performed by using SAS 9.4 (SAS Institute Inc., Cary, NC, USA). Exclusion criteria include: 1) patients with unknown or unspecified race; 2) patients who survived less than 6 months because time of radiotherapy/chemotherapy was not known to the time of diagnosis; 3) patients with any other type of cancer prior to the diagnosis of HL; 4) patients with second or later primaries, and who were not actively followed. Results: A total of 14.286 HL patients were included in the analysis. Table 1 indicates the insurance status and demographic and tumor characteristics among HL patients diagnosed between 2007 and 2014. Patients with black race, male sex, and B symptoms were more likely to be uninsured and on any Medicaid compared to other races, female sex and without B symptoms (p&lt;0.01). As stage of disease increased, the percentage of insured patients decreased from 82.0% to 71.7%, (p&lt;0.01). As with year of diagnosis advanced, the percentage of uninsured did not appear to be changed however the proportion of both those with insurance and any Medicaid decreased slightly by 2.4% (p&lt;0.01). Those who received RT only were most likely to have insurance (89.6%) followed by combination modality (80.1%). As expected, uninsured status was associated with lower income and education level (p&lt;0.01). Table 2 shows the insurance and hazard ratio among HL patients by year of diagnosis adjusting for race, sex, histology type, income, education, and year of diagnosis. Any Medicaid patients had the highest HR of death from 2007-2010 compared to insured patients. Without insurance was also associated with increased risk of death but only significant in 2008, HR=2.26, 95% CI (1.35, 3.80). The survival outcomes comparing different insurance status by age groups (&lt;=29 and 30-64) were demonstrated in Kaplan-Meier Curve. In the age 29 or less group, insured patient showed has the best survival outcome followed by any Medicaid and then the uninsured. In the age 30-64 group, Medicaid patients had the worst survival outcome compared to those with or without insurance. Conclusion: Insurance status is one of the most important contributors of health disparity, especially in malignancy given the significant financial toxicity of therapies. We found that the proportion of the uninsured was trending up before the Affordable Care Act (ACA). Regarding the HL outcome, insured patients had the best survival across all age groups even though not significantly while Medicaid patients had the worst outcomes in almost all age groups, even worse than the uninsured after adjusting for the disease stage at diagnosis and sociodemographic factors. It would be of interest to explore the reason behind Medicaid patients' relatively poor outcomes. Future studies may also investigate how ACA, Medicaid expansion, and the possible upcoming republican healthcare reform influence HL outcome. Disclosures No relevant conflicts of interest to declare.


Rheumatology ◽  
2019 ◽  
Vol 58 (Supplement_4) ◽  
Author(s):  
Kishore Warrier1 ◽  
Catherine Salvesani ◽  
Samundeeswari Deepak

Abstract Background Rituximab is a chimeric monoclonal antibody that depletes the B cell population by targeting cells bearing the CD20 surface marker and is used widely in the management of paediatric rheumatological conditions like juvenile systemic lupus erythematosus (JSLE), juvenile dermatomyositis (JDM), mixed connective tissue disease (MCTD) and juvenile idiopathic arthritis (JIA). Pneumocystis jirovecii pneumonia (PCP) is a potentially fatal opportunistic infection associated with congenital and acquired defects in T cell–mediated immunity. Our guideline did not recommend prophylaxis against PCP for patients on rituximab, unlike patients on cyclophosphamide, who are on cotrimoxazole until three months after cessation of the treatment. Cyclophosphamide is an alkylating agent which affects both B and T lymphocytes. Following the death of 16 year-old girl with JSLE due to PCP, the team reviewed the possible contributing factors, undertook a review of literature and discussed this at multi-disciplinary meetings involving the microbiology and immunology teams. This patient was found to have other risk factors for PCP – low CD4 T cells, concomitant use of corticosteroids and hypogammaglobulinaemia (IgG 3.0g/L). Although there is limited evidence that rituximab on its own increases the risk of PCP, there is emerging data that B cells may have a role in the protection against pneumocystis. Following the review, it was concluded that children on rituximab and an additional immunosuppressant (including corticosteroids) should receive prophylactic cotrimoxazole to cover PCP. Methods Retrospective audit carried out by the team to look at adherence to the new guideline regarding the use of cotrimoxazole for PCP prophylaxis in patients who have had rituximab between August 2017 and May 2019. Results P54 Table 1 Total number of patients who had rituximab 10 Number of patients who had other immunosuppressants concomitantly / recently (within previous 3 months) 7 Number of patients on rituximab monotherapy 2 Number of patients who are 6 months post-treatment 1 Number of patients with other risk factors for PCP 1 (hypogammaglobulinaemia) Number of patients who are eligible for prophylaxis, as per the guideline 8 (7 for concomitant immunosuppression and 1 for hypogammaglobulinaemia) Number of patients on cotrimoxazole 7 (87.5%) - one of the patients is on methotrexate, which is advised not to combine with cotrimoxazole We achieved 87.5% compliance in prescribing cotrimoxazole for PCP prophylaxis to all rheumatology patients receiving rituximab alongside another immunosuppressant agent; the one patient who this was not adhered to was due to potential adverse drug pharmacodynamic interaction between cotrimoxazole and methotrexate. Conclusion Although the current evidence points to increased risk of PCP in patients with inherited and iatrogenic defect of T cell function, there is emerging evidence that B cells may have a role too. Hence more work is required to determine the risk of PCP in patients on B cell targeted therapy (BCTT) and the need for prophylaxis. Conflicts of Interest The authors declare no conflicts of interest.


Drug Research ◽  
2018 ◽  
Vol 69 (04) ◽  
pp. 185-193 ◽  
Author(s):  
Xingang Li ◽  
Shusen Sun ◽  
Xiaowei Xu ◽  
Zhigang Zhao ◽  
Wei Li

Abstract Background and study aim Genetic polymorphisms may play a role in muscular injury associated with simvastatin, but results were inconclusive. This study aimed to summarize evidence from the literature investigating the effects of genetic polymorphism on simvastatin-induced myopathy. Methods Studies regarding the association between genetic polymorphisms and simvastatin-induced myopathy were retrieved through electronic databases from February 1, 1990 to March 15, 2018. Two authors independently extracted data, including PMID, author, publication year, country, race, age, population characteristics, drugs, definition of case and control, gene, allele, SNP position, Hardy-Weinberg equilibrium, number of genotypes (case and control), minor allele frequency of cases and controls, association, study type and the Newcastle-Ottawa scale. Due to high heterogeneity in study design and outcome measurements among the included articles, a narrative synthesis of the evidence was conducted. Results A total of 10 association studies were identified in this study, including SLCO1B1, ABCB1, GATM, HTR3B, HTR7, RYR2 and HLA-DRB1. The evidence linking myopathy to rs4149056 in SLCO1B1 is of high quality, and this association has been reproduced in randomized trials and clinical practice-based cohorts. As for other candidate genetic markers, the evidences are limited or controversial, and additional well-designed studies with larger sample sizes, are required to further elucidate this association. Conclusion SLCO1B1 genotype is a useful biomarker for predicting an increased risk of simvastatin-induced myopathy.


2018 ◽  
Vol 31 (Supplement_1) ◽  
pp. 188-189
Author(s):  
Pei Yu ◽  
Su Zhang ◽  
Ming Wang ◽  
He Liang ◽  
Hu Fan ◽  
...  

Abstract Background Several studies have suggested an association between poor oral health and esophageal squamous cell carcinoma (ESCC). We conduct this study to further examine the association between oral hygiene and ESCC risk in Linxian, the high risk area of China. Methods We recruit 29,553 healthy and 3318 esophageal squamous dysplasia participants aged between 40 and 69 in 1985 and then followed up until April, 2015. Basic characteristics were collected and oral related diseases were examined by trained doctors. Cox regression models were used to calculate hazard rations (HRs) and 95% confidence intervals (CIs). Results In general group, 2577 participants’ dead for ESCC and the cumulative rate of ESCC death was 12.9%. Teeth loss more than 20, before age of 40, bleeding of teeth, chapped lips, oral leukoplakia were significantly associated with risk of death from ESCC, and with 1.28 (95% CI: 1.18–1.38), 1.12 (95% CI: 1.03–1.23), 1.28 (95% CI: 1.13–1.45), 1.14 (95% CI: 1.04–1.25), 1.23 (95% CI: 1.12–1.35) fold increased risk of death from ESCC respectively in models adjusted for potential confounders. In dysplasia group, 540 participants’ dead for ESCC and the cumulative rate was 24.7%. Those who loss teeth more than 20, before age of 40, bleeding of teeth, have 1.24 (95% CI: 1.02–1.51), 1.25 (95%CI: 1.02–1.52), 1.35(95%CI: 1.06–1.70) fold increased risk after adjustment. Association between chapped lips and ESCC death was not found. Conclusion Severe teeth loss, early age teeth loss and teeth bleeding were associated with ESCC death and excess risk increased as dysplasia occurred. Chapped lips loss association with ESCC death in dysplasia group, it may reveals that it react before dysplasia change. Further studies are warranted to find the mechanism association and improvements of protecting oral health should be done. Disclosure All authors have declared no conflicts of interest.


Author(s):  
Marianna Sallustro ◽  
Raffaele Polichetti ◽  
Anna Florio

Nonhealing leg ulcers are a major health problem worldwide with a high economic burden since they require human and material resources. Moreover, nonhealing ulcers are a major nontraumatic cause of lower limb amputations. Dermal substitutes have emerged as an effective therapeutic option for treatment of skin lesions, but data on leg ulcers are scarce. We evaluated safety and efficacy of a porcine-derived dermal substitute in the treatment of chronic vascular leg ulcers. Records of patients with nonhealing ulcers seen at our unit from 2018 to 2019 were retrospectively reviewed. Wound etiology, wound area, and complications were evaluated. Each patient received one application of porcine-derived dermal substitute and was followed-up. Six patients (5 females and 1 male) with a mean age of 61.3 (52-81) years presented with nonhealing leg ulcers. After surgical debridement and wound bed preparation, porcine-derived dermal substitute was applied onto the ulcer. Granulation was satisfactory within 10 days. All wounds healed after an average time of 14 weeks. Graft take was good, and no graft loss, rejection, or associated infection were observed. In conclusion, the data presented indicate that dermal substitutes are safe and effective for treatment of chronic nonhealing vascular leg ulcers.


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