LAUSR

ing. Indeed, the physiopathology remains elusive. One suggested hypothesis involves an adrenaline-induced constriction of periglandular vessels, followed by an exacerbated dilatation which allows blood to fill the eccrine ducts. This theory is supported by the improvement, reported in literature, following beta-blockers-based treatments,usually with propranolol with daily dosage ranging from 10 to 20 mg when reported. This case represents an exception, since our patient had only mucosal involvement, without reported episodes of bleeding from intact skin. Since we don’t know the exact anatomic site involved and considering the time taken for endoscopic procedures, taking a biopsy during a bleed had proved impossible. An isolated platelet deficit after ADP stimulation is not consistent with the clinical presentation, and we excluded Glanzmann’s thrombasthenia because of the normal platelet function following epinephrine, collagen, thromboxane A2, and thrombin receptor agonists stimulation. In fact, to date the diagnosis remains of exclusion, while a personalized multidisciplinary treatment is ideal.