Laboratory findings associated with thrombophilia are not more common in inflammatory bowel disease.

Thromboembolic disease (TED) has been recognized as a complication of inflammatory bowel disease (IBD) since the 1930s (Bargen & Barker 1936). The relative contributions of inherited or acquired thrombophilia and the inflammatory response to the mechanism of this tendency is unclear. Thrombotic events are more common in active disease although significant numbers also occur spontaneously, when the disease is in clinical remission (Talbot et al. 1986; Jackson et al. 1997). Studies looking at the prevalence of specific thrombophilic states such as Antithrombin III deficiency (Jackson et al. 1997; Lake, Stauffer & Stuart 1978; Cianco et al. 1996; Ghosh et al. 1983), Factor V Leiden mutation (APC Resistance) (Jackson et al. 1997; Probert et al. 1997; Ardizzone et al. 1998; Liebman et al. 1998), anticardiolipin antibodies (Ciancio et al. 1996), Protein C (Wyshock, Caldwell & Crowley 1988; Korsten & Reis 1992) and Protein S deficiencies (Jorens et al. 1990; Aadland et al. 1992) in IBD have been contradictory or equivocal. We had previously found that IBD patients with a history of TED are not more likely to have a laboratory thrombophilic abnormality than those with uncomplicated disease. We also demonstrated that the prevalence of heterogenous laboratory thrombophilic abnormalities (usually minor) in all IBD patients may be as high as 60%, much higher than the recognized prevalence of TED (Lim, Jones & Gould 1996). We wondered how this would compare with the healthy non-IBD population. We have therefore explored the prevalence of such thrombophilic abnormalities in a group of IBD patients who had no history of TED and compared them with healthy age and sex matched controls.

Erythrocyte-reactive T-cell lines and clones from normal mice recognize serum-derived antigens.

T-cell clones and cell lines which apparently respond to autologous (syngeneic) erythrocytes have been generated from the spleens of normal mice. The response showed considerable cross-reactivity with red blood cells (RBC) from other species, including chicken, and was 'heteroclitic' in that reactivity against some species of RBC, notably rat and monkey, was greater than to mouse. The clones were Thy-1+ L3T4+ Lyt-2- and recognized antigen in association with I-Ak or I-Ek. At least three specificities were identified on the basis of reactivity to crude lysates of mouse and rat RBC. One of the putative clones, M0.5/1/D2, showed a change in reactivity during culture, proliferating strongly against antigen-presenting cells (APC) without added erythrocytes. Analysis of the clones and lines using an I-Ak I-Ek expressing hybridoma, HB-98, has indicated that only one, M5/1/F5, was likely to be erythrocyte-specific; the remainder were responding to antigens present in foetal calf serum (FCS). The data demonstrate that apparent erythrocyte specificity can be a result of serum components being presented to T lymphocytes via red blood cells.