{'fraction_non_alphanumeric': 0.024649092776446422, 'fraction_numerical': 0.016775077028414926, 'mean_word_length': 5.522321428571429, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Uniform vascular response to different aetiological factors

Sir: We have read with great interest the instructive article on vascular changes in thrombocythaemic erythromelalgia by Michiels er al. (1984). Having studied the influence of amnionconditioned medium on the healing of venous ulcers (Beranek er al. 1984) we are very impressed by a similarity between venous stasis muscular sclerotic vessels in our material (Figure 1) and muscular sclerotic vessels in erythromelalgia (Michiels el al. 1984, Figure 6). This suggests to us that different aetiological factors may induce a uniform vascular response in both diseases. Venous stasis dermatitis is characterized by a proliferation of hyperplastic capillaries (Graham el al. 1972) composed entirely of endothelial cells (Beranek et al. 1984). Their appearance may be understood as a consequence of the capillary damage inducing the production of angiogenic factors stimulating endothelial cells with the highest capacity of proliferation. Thanks to the well known antagonism between cell division and cell differentiation, this process may lead successively to a selection of highly undifferentiated cells and to a production of hyperplastic capillaries (Beranek, Hsi & Ortonne, 1985, in press). Venous stasis muscular vessels most probably develop from hyperplastic capillaries (Figure 2) by a differentiation of their medial endothelial cells into smooth muscle cells and, eventually, of their external endothelial cells into concentrically orientated fibroblast-like cells. Some of the figures of Michiels el al. (1984) suggest that erythromelalgia muscular vessels develop in the same way. The capillaries in their Figure 9a seem to be hyperplastic (cf the capillaries in their Figure 9b) and the vessels are very numerous suggesting stimulation by angiogenic factors (their Figures 8, 9a). There are intermediate forms between capillaries and muscular vessels (their Figures 1, 8. 9a) and the muscular vessel in their Figure 1 resembles a vein rather than an artery. The proposals regarding histogenesis, based on an absence of antigenic marker, are precarious ones and we believe that a relative positivity of Factor VIII-R:Ag favours the endothelial origin of vascular muscular cells (their Figure 10). The sclerosis of erythromelalgia muscular vessels and the sclerosis of venous stasis muscular vessels may be understood in the light of the fact that hyperplastic capillaries often do not contain blood (Beranek er al. 1984); the scleroses of both venous stasis and erythromelalgia muscular vessels thus resemble disuse arteriosclerosis rather than the hyperplastic arteriosclerosis of functional arterioles. Moreover, sclerotic arterioles of ageing or hypertension are not surrounded by concentrically orientated fibroblast-like cells (Fontaine. Bollack & Chadad 1967) in the way sclerotic venous stasis or erythromelalgia muscular vessels often are. One