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Drugs causing cutaneous necrosis
Published in Biju Vasudevan, Rajesh Verma, Dermatological Emergencies, 2019
Alternatively, drug-induced vascular injury may be associated with livedoid skin lesions. The red or hyperpigmented cutaneous streaks are subtle and are referred to as microlivedo and are clinically different from the full-blown net-like hyperpigmentation in livedo reticularis. Microvascular occlusion due to cryofibrinogenemia, antiphospholipid antibody syndrome and hypercoagulable states from protein C and S deficiency have to be considered as differentials in such a clinical scenario [25].
Wound Healing and Tissue Engineering: Physiology of Wound Healing
Published in Armstrong Milton B., Lower extremity Trauma, 2006
Panthaki Zubin J., Okpaku Anire
Pentoxifylline (800 mg three times a day) may be a helpful adjunct in the healing of lower extremity wounds (8). As an inhibitor of tumor necrosis factor-a, pentoxifylline acts to reduce leukocyte adhesion and improve red blood cell flow through the microvasculature (9). Unfortunately, the clinical data have not shown this agent to be effective in increasing healing rates of leg wounds (9). The anabolic steroid stanozolol may be effective in treating ulcers due to lipodermatosclerosis and cryofibrinogenemia, but has no effect on other types of leg wounds (4).
Short-Term Outcomes of Transcatheter Aortic Valve Replacement in Kidney Transplant Recipients: A Nationwide Representative Study
Published in Structural Heart, 2021
Mohamed Hassanein, Omar M. Abdelfattah, Anas M. Saad, Toshiaki Isogai, Mohamed M. Gad, Keerat R. Ahuja, Taha Ahmed, Shashank Shekhar, Richard Fatica, Emilio Poggio, Samir R. Kapadia
In our cohort, we aimed to identify the predictors of IHS to effectively allocate resources targeting the prevention of such events in this high-risk population following TAVR. In our analysis, KTRs had the greatest OR for IHS, even after adjustment for all other factors. Moreover, our findings support those of others that female sex,18,19 carotid artery disease,20 CKD stage 4 and ESRD requiring dialysis19,21,22 and transapical (TA) access23 as independent predictors of IHS following TAVR. However, several reports described comparable rates of IHS following TA-TAVR versus transfemoral TAVR.18,24,25 Our results demonstrated an increased risk of both ischemic and hemorrhagic IHS among KTRs, despite a lower incidence of atrial fibrillation and lower CAD2DS2-VASc score among the KTRs. This increased IHS might be attributed to the increased prothrombotic state associated with KT. Fox et al. reported stroke occurrence in one patient in a cohort of 8 KTR patients undergoing TAVR.15 It has been suggested that KTRs are prone to increased risk of thromboembolism (TE). Indeed, in 1997, Irish et al. identified KT as a chronic prothrombotic state, mainly due to increased blood levels of D-dimer, fibrinogen, factor, factor VII coagulant activity, and other prothrombotic factors when compared to controls.26 Other risk factors for hypercoagulability in KTR include protein C and S deficiency, antiphospholipid antibodies, cryoglobulinemia, cryofibrinogenemia, sepsis, disseminated intravascular coagulation, liver disease, nephrotic syndrome, and malignancy.27 More recently, Verhave et al. compared KTRs to controls and concluded that the risk of thromboembolism (TE) in KTR was eight-fold higher than the general population, especially during the first year post-transplant but remained elevated after that.28 Another possible explanation for the dramatically increased stroke risk in KTRs is the higher progression of aortic valve calcifications among ESKD and KTRs compared to the general population undergoing TAVR.8,29