DEFICIENT VASCULAR INNERVATION IN FAMILIAL DYSAUTONOMIA, AN EXPLANATION FOR VASOMOTOR INSTABILITY

Deficient vascular innervation in familial dysautonomia, an explanation for vasomotor instability
An ultrastructural study of peripheral blood vessels in familial dysautonomia demonstrates the absence of autonomic nerve terminals. In control subjects both sympathetic terminals containing dense-cored vesicles and presumptive cholinergic terminals containing agranular vesicles are readily shown. Lack of autonomic innervation of blood vessels in familial dysautonomia accounts for postural hypotension and other abnormalities of vasomotor reflexes. It also explains exaggerated responses to sympathomimetic and parasympathomimetic agents in terms of denervation hypersensitivity. Ultrastructural analysis of vascular nerve terminals may be of general value in the study of many diseases which show vasomotor instability.     

Melanocytic Nevus with Atypical Dermoscopic Features at the Site of Radiodermatitis

BACKGROUND: Radiation therapy can cause acute and chronic damage of the skin. OBJECTIVE: A 71-year-old woman presented with an atrophic and sclerotic plaque at a site previously treated with radiotherapy because of lung cancer. Inside the area affected by chronic radiodermatitis, she reported that a preexisting pigmentary lesion had gradually undergone morphologic changes after radiation therapy. MATERIALS AND METHODS: On dermoscopy, the lesion showed features highly suspicious for malignant melanoma. The lesion was excised and examined histopathologically. RESULTS: The histopathologic diagnosis was compound congenital melanocytic nevus associated with prominent dermal sclerosis and epidermal atrophy. CONCLUSIONS: The existence of melanocytes within an atrophic and fibrotic area is a finding typically associated with recurrent or persistent melanocytic lesions. It is likely that the "pseudomelanoma" features of the lesion observed in our patient might have been secondary to the skin changes induced by radiation therapy.