Venous damage is an uncommon cause of intestinal ischaemia. We report on a 44-year-old woman who presented signs and symptoms of acute intestinal ischaemia requiring surgical treatment. Histological examination of the resected right colon showed features of an intramural lymphocytic venulitis with no other demonstrable causes of ischaemic injury of the bowel. Extramural mesenteric veins appeared dilated and congested, without evidence of thrombotic occlusion or of inflammatory involvement. The patient, who was not taking any long-term medication and had no clinical evidence of collagen-vascular disease, promptly recovered after surgery. Follow-up for 7 months with no recurrences suggested a self-limited or indolent process. We propose the name 'intramural mesenteric venulitis' for this condition and believe that it could represent one extreme (the microscopic variant or intramural phase) of the spectrum comprising entero-colic phlebitis and mesenteric inflammatory veno-occlusive disease. The immunohistochemical evidence of a marked preponderance of T phenotype in the perivenular lymphocytes suggests lymphocyte-mediated vascular damage as the pathogenesis of the lesion.
Intramural mesenteric venulitis. A new cause of intestinal ischaemia / Corsi, Alessandro; Ribaldi, S; Coletti, M; Bosman, C.. - In: VIRCHOWS ARCHIV. - ISSN 0945-6317. - 427:(1995), pp. 65-69.
Intramural mesenteric venulitis. A new cause of intestinal ischaemia.
CORSI, ALESSANDRO;
1995
Abstract
Venous damage is an uncommon cause of intestinal ischaemia. We report on a 44-year-old woman who presented signs and symptoms of acute intestinal ischaemia requiring surgical treatment. Histological examination of the resected right colon showed features of an intramural lymphocytic venulitis with no other demonstrable causes of ischaemic injury of the bowel. Extramural mesenteric veins appeared dilated and congested, without evidence of thrombotic occlusion or of inflammatory involvement. The patient, who was not taking any long-term medication and had no clinical evidence of collagen-vascular disease, promptly recovered after surgery. Follow-up for 7 months with no recurrences suggested a self-limited or indolent process. We propose the name 'intramural mesenteric venulitis' for this condition and believe that it could represent one extreme (the microscopic variant or intramural phase) of the spectrum comprising entero-colic phlebitis and mesenteric inflammatory veno-occlusive disease. The immunohistochemical evidence of a marked preponderance of T phenotype in the perivenular lymphocytes suggests lymphocyte-mediated vascular damage as the pathogenesis of the lesion.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.