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D Bourdet

Publications and source records attributed to D Bourdet.

3 recordsLinked to original sources

[Perforating generalized granuloma annulare. A two case study (author's transl)].

This article deals with two new cases of perforating generalized granuloma annulare characterized, from a clinical and biological standpoint, by a long course of evolution for one case and the presence of diabetes and dyslipidemia for the other case. Histologic study confirms the possible coexistence of typical granuloma annulare lesions with epidermic corbelar aspects pinching necrotic material which could lead to complete epidermic perforation. Based on the study of previous cases in the literature, the process of transepidermic elimination and the actual pathophysiologic concepts of granuloma annulare are reviewed. From the therapeutic standpoint, if the first case did not appear to profit from the administration of an alkylating agent, the second case seems to be presently improved through gluco-lipid re-equilibrium associated with lipocaic heparin.

Aged↗

[Piebaldism. Clinical, pathological and ultrastructural study of three cases (author's transl)].

Comparative study of achromic and normally pigmented skin of three piebald patients from two families is reported here. DOPA-positive cells were not seen in the achromic areas, but the number of ATPase sites appeared to be normal; therefore the assumption of the replacement of the melanocytes by Langerhans cells cannot be supported. Through electron microscope, Langerhans cells looked strictly normal. Melanosomes appeared reduced in size and some alterations were noticed in their shape and contents. Ultrastructurally, a more prominent change consisted in increased undefined clear cells in the achromic skin. These dendritic suprabasal cells were devoid of melanosomes or Langerhans granules and might represent undifferentiated melanocytes. These features were discussed according to previous literature.

Adenosine Triphosphate↗

[Kaposi's disease. Ultrastructural study of 4 cases].

An ultrastructural study of Kaposi's disease showed often immature vascular proliferation bordered by large globular or fusiform endothelial cells. Other cell types participated in this proliferation: inflammatory cells, pericytes and fibroblasts. These various cell types are the site of active erythrophagocytosis. It is reasonable to accept that the disease is the result of reticulo-endothelial proliferation with multiple morphological types and predominant vascular differentiation.

Blood Vessels↗