The acronym IBD identifies the ulcerative colitis (URC), Crohn's disease (CD) and the undeterminate colitis (UC) 7. Inflammatory bowel diseases are characterized by variegated etiopathogenesis, probably autoimmune. They have in common a histological damage of a granulomatous/ulcerative kind and also the same manifestations which includes the alternation of remissions and exacerbations 1. They have a remarkable familiarity (13.5%) although it is more evident in CD than in URC. The incidence of IBD varies according to different geographical areas but with a steady increasing trend above all in CD and the diffusion seems to be linked to genetic factors (association with HLA-A2 and B 18) and to geographical factors. Today the etiopathogenesis is still debated. The latest theories seem to confirm an autoimmune genesis. IBD show a remarkable tendency in developing secondary remote manifestations in a different location from the intestinal one: extraintestinal manifestations (EM). They can appear simultaneously with the primitive intestinal manifestation or they can precede or follow after years. According to the most reliable etiopathogenetic hypothesis, EM give rise to "metastasizations" of autoantibodies activated in the bowel from the "ideational intestinal brain"; once the autoantibodies are activated, they are able to attack any organ, tissue or system causing damage directly or mediated. In support of this theory there is the evidence that almost all EM regress with a cortison-based/immunosuppressant treatment. In literature we have descriptions of the extraintestinal remissions of symptoms after total proctolectomia and ileo-anal pouch. Among EM we find following manifestations: hepatobiliary, osteoarticular, muscular, dermatological, stomatological, ophthamological, gynaecological, urological, metabolic, perianal etc. Recently another manifestation has appeared which consists in a remarkable thromboembolic tendency (TE) in IBD patients. TE and IBD are an important field of research as TE occurs in young patients aggressively causing significant morbidity (stroke, retinal vascular occlusive thrombus deposition in cerebral, retinal and mesenteric vessels, massive pulmonary embolism). Several studies describe thrombosis in venous and arterial district in IBD patients as 4% but according to autopsy studies the percentage is more than 30% 2. Among the causes of the TE disease we have: thrombocytosis, increase of the coagulation factors, mutation of V factor of Laiden 8, hyperhomocysteinemia (due to the combined deficit of methylene-hydrofolate-tetra reductase (MTHFR), B12 vitamin and folate) observed mutation of MTHFR gene in some IBD patients. Finally, surgery determines an additional TE risk in these patients compared to non-IBD patients who have the same operation. Some studies describe mortality of 1-1,2% after restorative proctolectomia due to TE complications (pulmonary-cerebral and mesenteric district.
Thromboembolic tendency (TE) in IBD (Inflammatory bowel disease) patients
AVENIA, Nicola;
2012
Abstract
The acronym IBD identifies the ulcerative colitis (URC), Crohn's disease (CD) and the undeterminate colitis (UC) 7. Inflammatory bowel diseases are characterized by variegated etiopathogenesis, probably autoimmune. They have in common a histological damage of a granulomatous/ulcerative kind and also the same manifestations which includes the alternation of remissions and exacerbations 1. They have a remarkable familiarity (13.5%) although it is more evident in CD than in URC. The incidence of IBD varies according to different geographical areas but with a steady increasing trend above all in CD and the diffusion seems to be linked to genetic factors (association with HLA-A2 and B 18) and to geographical factors. Today the etiopathogenesis is still debated. The latest theories seem to confirm an autoimmune genesis. IBD show a remarkable tendency in developing secondary remote manifestations in a different location from the intestinal one: extraintestinal manifestations (EM). They can appear simultaneously with the primitive intestinal manifestation or they can precede or follow after years. According to the most reliable etiopathogenetic hypothesis, EM give rise to "metastasizations" of autoantibodies activated in the bowel from the "ideational intestinal brain"; once the autoantibodies are activated, they are able to attack any organ, tissue or system causing damage directly or mediated. In support of this theory there is the evidence that almost all EM regress with a cortison-based/immunosuppressant treatment. In literature we have descriptions of the extraintestinal remissions of symptoms after total proctolectomia and ileo-anal pouch. Among EM we find following manifestations: hepatobiliary, osteoarticular, muscular, dermatological, stomatological, ophthamological, gynaecological, urological, metabolic, perianal etc. Recently another manifestation has appeared which consists in a remarkable thromboembolic tendency (TE) in IBD patients. TE and IBD are an important field of research as TE occurs in young patients aggressively causing significant morbidity (stroke, retinal vascular occlusive thrombus deposition in cerebral, retinal and mesenteric vessels, massive pulmonary embolism). Several studies describe thrombosis in venous and arterial district in IBD patients as 4% but according to autopsy studies the percentage is more than 30% 2. Among the causes of the TE disease we have: thrombocytosis, increase of the coagulation factors, mutation of V factor of Laiden 8, hyperhomocysteinemia (due to the combined deficit of methylene-hydrofolate-tetra reductase (MTHFR), B12 vitamin and folate) observed mutation of MTHFR gene in some IBD patients. Finally, surgery determines an additional TE risk in these patients compared to non-IBD patients who have the same operation. Some studies describe mortality of 1-1,2% after restorative proctolectomia due to TE complications (pulmonary-cerebral and mesenteric district.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
