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Deranged smooth muscle α-actin expression as a biomarker of intestinal pseudo-obstruction
  1. E Jaynes,
  2. N J Carr,
  3. A C Bateman
  1. Department of Cellular Pathology, Southampton General Hospital, Southampton, UK
  1. Correspondence to:
    Dr A C Bateman
    Department of Cellular Pathology, Mailpoint 2, Southampton General Hospital, Level E, South Academic Block, Tremona Road, Southampton SO16 6YD, UK;

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We read with interest the article by Knowles and colleagues (Gut 2004;53:1583–9) in which the authors concluded that immunostaining of the adult jejunum with smooth muscle α-actin (ASMA) may be a valuable biomarker of chronic idiopathic intestinal pseudo-obstruction (CIIP). We recently published a similar study in which 17 archival formalin fixed, paraffin wax embedded samples of small intestine and 12 samples of large intestine were immunostained with ASMA, desmin, and smooth muscle myosin heavy chain, using the same antibody for ASMA as Knowles and colleagues.1 In two of the three cases investigated in our study, ileal samples were examined from patients with clinical evidence of intestinal pseudo-obstruction. We found that both of these CIIP cases and all 15 control ileal samples showed weak or absent ASMA expression within the inner circular layer of the muscularis propria, with an identical pattern to that identified within the case and control ileal samples examined by Knowles et al.

Knowles et al found that 24% of CIIP cases showed absent or partial inner circular muscle ASMA expression within the jejunum while this pattern was not identified in any control jejunal samples. However, in the ileum, absent or weak ASMA expression was universal in their controls and present in 69% of CIIP cases.

It is possible that absent or weak inner circular muscle ASMA expression within the jejunum may represent a biomarker of CIIP. However, the universal incidence of this phenomenon within the ileum in both studies and its presence at this site in a greater proportion of controls than cases, according to Knowles et al, indicates that ASMA expression should be interpreted with caution in these patients. In particular, although Knowles et al suggest that this phenomenon may be a biomarker of CIIP when identified within the jejunum, a definitive study of the geographical variation in ASMA expression within the muscularis propria of the small intestine is now indicated to determine the precise significance of this finding. The observation that manometric studies have shown pressure tracing patterns more suggestive of a neural defect than a primary muscular abnormality in most CIIP patients casts further doubt on the biological significance of apparent alterations in ASMA expression.



  • Conflict of interest: None declared.

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