H pylori and duodenal ulcer

SIR,-I have read with great interest the instructive article by Zentler-Munro et al' about an association of vascular abnormalities and hepatic fibrosis in Osler's disease. Above all, I was impressed by their photographs. In Figure 3, there are dilated vascular spaces practically devoid of erythrocytes and still other ones full of red blood cells. I covered the latter by white stain and looked with astonishment how few hepatocytes remained from original hepatic tissue. To all appearances, a tissue of hepatic lobules was almost destroyed by vessels the aggressive character of which reminds of tumoral growth instead of telangiectases. As we believe that hyperplastic capillaries are involved in a pathogenesis of fibrosis, I looked for them in the article of Zentler-Munro et al. 2 Having been unable to identify them, I turned to other articles concerning Osler's disease. I found them in an article by Tedesco et al' who had described an angioma in the submucosa of a stomach and telangiectases associated with fibrosis in the liver. Further, I was attracted by an article by Nodle4 who had studied cutaneous telangiectases. His outstanding photographs of pathological vessels surrounded by nonhaematopoietic mesenchymal cells (Figs 2, 3, 4, 5, 6, 7, 8) reminded me immediately of similar vessels that I had observed when I studied cutaneous vascular tumours. At that time, I described hyperplastic capillaries composed of epithelioid undifferentiated endothelial cells and situated in the vicinity of a capillary haemangioma, a haemangiopericytoma, and an angioleiomyoma. The capillaries were so similar to sweat glands that a careful morphological analysis was needed in order to distinguish these two structures. These hyperplastic capillaries could give rise: (a) to long narrow strips of smooth muscle tissue by an in situ differentiation of their cells into smooth muscle cells; (b) to pathological muscular vessels by a short distance centrifugal migration and a differentiation of their cells into vascular wall muscular cells'; and (c) to ectatic capillaries surrounded by fibroblast-like cells by a migration of their cells into the extravascular space and their differentiation there. ' A similarity between the vessels described by Nodl4 and the vessels I have observed suggests that Nodl described in reality tumoral lesions. I looked, therefore, for hyperplastic capillaries in his article. I found them in Figs 3, 4, 6c, 6d, 7, 8. Nodl does not mention them because he considers them to be sweat glands. Why I believe that at least some of these structures are hyperplastic capillaries: (1) a number, a location, and a morphology of pathological muscular vessels indicate that they are not formed by remodelling pre-existing normal vessels; (2) some of them are collapsed and undergoing involution suggesting their high turnover; (3) there are structures clearly recognisable as mesenchymal but similar to sweat gland tubules (Figs 3, 4, 6d in the middle, 7a large tubule on the right side, 8 on the right side); (4) referring to my previous observation,' endothelial cells in the 'sweat glands' often degenerate, most probably because of hypoxia, and their nuclei form clusters leaving empty space in their vicinity (Fig 7 in the upper right corner); (5) endothelial cell nuclei often possess an elongated form. When they are oriented longitudinally hyperplastic capillaries manifest histopathological patterns incompatible with genuine sweat glands (Fig 7 in the upper right corner). Finally, there is a remnant of an original hyperplastic capillary composed of several layers of undifferentiated epithelioid endothelial cells (Figs 9, 10). Because there is no other pathological process present, the remnant is not a reactive hyperplasia but a manifestation of tumoural growth. If Osler's disease is a vascular tumour antiangiogenesis9"' may be tried in its therapy. This proposition is supported by a successful treatment of this disease by medroxyprogesterone acetate," an angiostatic steroid. " There are several other diseases which present themselves as telangiectases but derive from hyperplastic tumoural capillaries. They are the senile haemangioma, Cutis marmorata telangiectatica,' the vascular spider," and generalised essential telangiectasia (unpublished personal observation). J T BERANEK Division of'Cardiothoracic Surgery, Harper Hospital, Department ofSurgerv, Wavne State University Medical Center, Detroit, MI 48201, USA