LAUSR

We thank Atamanalp for his interest in and thoughtful comments [1] on our case report [2]. His valuable comments made us further reflect on the relationship between sigmoid colon volvulus (SV) and liver atrophy. We previously reported that a preceding partial liver defect induced secondary liver atrophy based on sequential imaging observations with computed tomography and magnetic resonance imaging [2]. We further speculated that the surplus intra-abdominal void generated after liver atrophy may predispose to SV development. Contrary to our speculation, Atamanalp argues that SV development is unlikely in a wide intra-abdominal void than in a tight one because a wider void can allow the twisted intestinal loop, which occurs physiologically and resolves spontaneously, to untwist more easily and consequently prevents SV development. Atamanalp wonders whether SV occurrence in our case may be indifferent to hepatic volume reduction from atrophy. The pathogenesis of SV is complex and has not been fully elucidated because of its multifactorial etiology. Furthermore, the pathogenic association between liver volume loss and SV remains a matter of speculation because of limited past literature [3, 4]. Reduced liver volume due to atrophy certainly provides a surplus intra-abdominal void where the sigmoid colon intrudes and twists, readying for SV occurrence. On the other hand, in cases where the colonic wall is lax, i.e., having high elasticity, the sigmoid colon becomes larger and elongated due to the pressure gradient from intraintestinal gas retention and expands into the redundant void after liver atrophy. The overextended sigmoid colon eventually cannot restore the once-twisted intestinal loop and causes SV. This speculation is supported by our sequential imaging observation in which the enlarged colon came to manifest as an intestinal interposition between the liver and the diaphragm, called Chilaiditi’s sign [4], as the liver atrophy progressed. This radiographic sign represents occupancy of the redundant void by the expanded colon. It also agrees with our speculation that the SV occurred exactly when the liver atrophy became severe. Hence, this case suggests that a redundant intra-abdominal void concomitant with a high-elasticity colonic wall also causes SV, although further investigations on the relationship between liver volume loss and SV are required by accumulation of similar cases.