Ulcerating stasis dermatitis of the forearm associated with arteriovenous graft and central vein stenosis.

INTRODUCTION: Stasis dermatitis is a pathologic condition of the skin that most commonly occurs in the lower limb, where it is caused by chronic venous insufficiency. Stasis dermatitis of the upper limb is rare. CASE REPORT: A 45-year-old male, resident in Angola, presented to the emergency department with an ulcer encompassing the entire left forearm. Past medical history comprised arterial hypertension and end stage renal disease treated with hemodialysis. Dialysis access consisted of a left brachial-basilic AV graft obtained 4 years before. The patient also reported that a right internal jugular vein catheter was used previously during the maturation of the left brachial-basilic AV graft. Stenosis of the left brachiocephalic vein was documented at angiography. Angioplasty was performed, with complete resolution of the wound 2 months after admission. CONCLUSION: The differential diagnosis of extensive ulcer of the forearm must include neoplasms, cellulitis, and/or deep tissue infection with secondary ulceration, but it is also important to maintain suspicion for venous stasis syndrome as a rare but possible cause of these lesions.

Brain-derived neurotrophic factor mediates neuroprotection against Aß-induced toxicity through a mechanism independent on adenosine 2A receptor activation.

Brain-derived neurotrophic factor (BDNF) promotes neuronal survival through TrkB-FL activation. The activation of adenosine A2A receptors (A2AR) is essential for most of BDNF-mediated synaptic actions, such as synaptic plasticity, transmission and neurotransmitter release. We now aimed at evaluating the A2AR influence upon BDNF-mediated neuroprotection against Aß25-35 toxicity in cultured neurons. Results showed that BDNF increases cell survival and reduces the caspase-3 and calpain activation induced by amyloid-ß (Aß) peptide, in a mechanism probably dependent on PLCγ pathway. This BDNF-mediated neuroprotection is not affected by A2AR activation or inhibition. Moreover neither activation nor inhibition of A2AR, per se, significantly influenced Aß-induced neuronal death on calpain-mediated cleavage of TrkB induced by Aß. In conclusion, these results suggest that, in opposition to the fast synaptic actions of BDNF, the neuroprotective actions of this neurotrophin against a strong Aß insult do not require the activation of A2AR.