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[Microcirculatory changes in Bureau-Barrière disease and alcoholic polyneuropathy. Preliminary note: correlations and
S Bilancini1, M Lucchi, S B Curri
1Centre d'Etude des Maladies Vasculaires, Frosinone-Italie, Milan.
Abstract:
Nosologically, in ulcerative-mutilating acropathies (U.M.A.), it is customary to differentiate the usual forms of the disease (Thevenard's disease) which develop primarily and the secondary forms (U.M.A. or, better, pseudo-U.M.A.), in which the syndrome is secondary to a known pathologic process and which represent a symptom and not a disease. The link between these two nosological entities is the pseudo-syringomyeli U.M.A. of the lower extremities, or Bureau-Barrier's disease. This disease is exclusively seen in alcoholics and is similar to the neurological alterations observed in alcoholic polyneuropathies. Some authors consider this form as an ulcerative-mutilating acropathy (symptomatic U.M.A.). The objective of our research is to demonstrate the similarity between the microcirculation alterations in patients with Bureau-Barriere's disease and patients with alcoholic polyneuropathy without trophic lesions. For this purpose, we have biopsied the pulp of the great toe, according to the method described by Curri-Schendorf in three patients with Bureau-Barriere's disease, 46, 50 and 65 year-old respectively, and three patients with alcoholic polyneuropathy, 34, 54 and 63 years-old respectively. All these patients presented a normal macrocirculation, without any diabetes, nor disease prone to alter the microcirculation. The results obtained, in a limited series however, permit to state that it is possible to unify alcoholic polyneuropathy and Bureau-Barriere's disease in a single clinical and nosological entity, and to say that the latter only represents an evolution of the former. Besides, we have notices that microcirculation alterations, although non-specific, are extensive and occur early, permitting to suspect a pathogenic process related to a true alcoholic histo-angeitis which, for us, represent the pathogenic basis of Bureau-Barriere's disease.