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Gut 52:1072-1073 doi:10.1136/gut.52.7.1072-a
  • Letter

Transient ischaemic colitis following an aeroplane flight

  1. I E Koutroubakis,
  2. A Theodoropoulou,
  3. E A Kouroumalis
  1. Department of Gastroenterology University Hospital, Heraklion, Greece
  1. Correspondence to:
    Dr I E Koutroubakis, Department of Gastroenterology, University Hospital Heraklion, PO Box 1352, 71110 Heraklion, Crete, Greece;
    ktjohn{at}her.forthnet.gr

    We read with interest the report of Butcher and colleagues (Gut 2002;51:746–7) of two cases of transient ischaemic colitis following an aeroplane flight. This report represents more evidence supporting the suggestion of a possible important role of acquired and hereditary thrombotic risk factors in the pathogenesis of ischaemic colitis.1,2 However, the largest study to date concerning these factors in patients with ischaemic colitis was not mentioned in the study.1 Moreover, the reported patients may also have other acquired or inherited thombophilic disorders which were not evaluated. Lipoprotein (a), anticardiolipin antibodies, the C677T methylenetetrahydrofolate reductase polymorphism, and the G20210A prothrombin gene mutation were not studied in both patients whereas in the second case even the very important factor V Leiden mutation as well as lupus anticoagulant and homocysteine levels were not evaluated. Although the aeroplane flight could be the most important risk factor in these cases, the rather incomplete thrombophilic screening does not permit us to conclude that it was “the only potential risk factor”.

    It is known that deep vein thrombosis (mainly symptomless) may occur in up to 10% of long haul airline travellers.3 In contrast, hypercoagulable states may play an important role in ischaemic colitis, leading to the development of thrombotic occlusion of the small vessels supplying the colon. In a recent study of comprehensive thrombophilic screening in patients with an established diagnosis of ischaemic colitis, we found the prevalence of acquired and hereditary thrombotic risk factors significantly higher compared with the prevalence of these factors in matched inflammatory and healthy controls.1 A thrombophilic tendency was demonstrated in the majority of patients and the most significant associations were with antiphospholipid antibodies and with the factor V Leiden mutation. Moreover, we recently found a high frequency of protein Z deficiency in patients with ischaemic colitis (unpublished data). Based on the recent data of the association of protein Z deficiency mainly with arterial thrombosis,4 protein Z deficiency may be involved in the development of the disease in a subgroup of patients by causing thrombosis in the small mesenteric arteries.

    Ischaemic colitis is considered the result of localised non-occlusive ischaemia of the small arteries. In contrast, the presence of hypercoagulable states suggests a possible role of venous obstruction. It is possible that future identification of subgroups in ischaemic colitis patients with sophisticated imaging techniques could distinguish cases with arterial or venous ischaemia.

    In conclusion, we suggest that the mechanism of ischaemic colitis is multifactorial. Acquired and genetic factors may interact leading to disease manifestation. Arrhythmia and embolic conditions, oral contraceptives, and other medications, as well long haul flights probably play a role in genetically predisposed individuals in the disease pathogenesis.

    References