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Altered Regulation of Fibrinolysis in Scleroderma and Potential for Thrombolytic Therapy
Published in Pia Glas-Greenwalt, Fibrinolysis in Disease Molecular and Hemovascular Aspects of Fibrinolysis, 2019
Marvin J. Fritzler, David A. Hart
Recently Khmiuk et al.126 have reported that administration of t-PA (1 mg/kg/24 h) to selected scleroderma patients led to short-lived, but significant improvements in skin blood flow. Some patients were reinfused with t-PA and experienced no side effects. In another study of livedoid vasculitis, t-PA therapy proved to be efficacious.127 Therefore, there is evidence that thrombolytics may be effective therapeutic modalities in scleroderma. Considerably more investigation is needed to identify the best fibrinolytic agent to use and the optimal treatment protocol. At the present time, only t-PA has been employed. As discussed elsewhere,128,129 urokinase-like enzymes are the most prevalent in connective tissues and therefore may be the fibrinolytic of choice if one is trying to modify the extravascular fibrotic tissue. However, if the changes observed after therapy are primarily intravascular, and are due to increased blood flow and oxygenation of the tissues, then t-PA may be the preferred therapeutic. Another possibility is that a combined UK/t-PA protocol may be needed to target both the vascular and fibrotic components of the disease.
Multifactorial aetiology for non-uremic calciphylaxis: a case report
Published in Journal of Community Hospital Internal Medicine Perspectives, 2018
Sijan Basnet, Niranjan Tachamo, Rashmi Dhital, Biswaraj Tharu
A 71-year-old female presented to the emergency department (ED) with left leg pain, swelling and fever for 1 day. It was preceded by recent unroofing of the nail bed of the great toe. She had poorly controlled type II diabetes mellitus, hypertension and coronary artery disease. In the ED, she was febrile (temperature 103.1°F) with blood pressure of 188/120 mm Hg and pulse of 106/min. Physical examination revealed barely palpable peripheral pulses. The left leg appeared bluish and was extremely tender. White blood cell count on admission was 19,500/µl with neutrophilia. Ultrasound of left lower extremity (LLE) was negative for deep vein thrombosis. She was septic on presentation and was started on vancomycin, cefepime and metronidazole. CT scan of LLE showed diffuse cellulitis/oedema without abscess or osteomyelitis. She underwent LLE arterial duplex which did not show any hemodynamically significant stenosis. The ankle-brachial index showed moderate arterial insufficiency but no evidence of rest pain or critical limb ischemia. On day 3 of presentation, three patches and a bulla appeared on the left leg. Cutaneous vasculitis was suspected. ANA, ANCA, serum C3, C4, Rheumatoid factor, homocysteine, hypercoagulability panel, lipid panel, hepatitis B and hepatitis C were unremarkable. A transesophageal echocardiogram done to rule out septic emboli from infective endocarditis was negative for vegetation. A punch biopsy done from the posteromedial aspect of the left leg showed superficial and deep inflammation with areas of superficial epidermal necrosis and was diagnosed as livedoid vasculitis. Cultures of the skin biopsy were negative. The diagnosis was met with scepticism and the slides were sent to a dermatopathologist. The patient was discharged on wound care and pain control with a review pending.