Anatomical condition mimicking superior mesenteric artery syndrome might cause duodenal involvement in Henoch–Schönlein purpura

The authors thank Dr Fujii for his voluminous contribution to the literature in general and to our article in particular. The excellent and comprehensive discussion in his letter of the anatomical condition similar to superior mesenteric artery syndrome (SMA) and duodenal lesion in Henoch–Schönlein purpura (HSP) provides an illuminating framework on our study. We would like to offer a few comments. Dr Fujii indicated that HSP patients with abdominal pain and duodenal lesion by ultrasound showed hypoperistalsis, which was not consistent with characteristics of SMA syndrome. We have also observed bowel abnormalities (BA) on ultrasound in HSP that were inflammatory, and paralytic findings of the intestine. Thus, in our manuscript, BA were defined as bowel wall thickness of more than 3 mm and signs of paralytic ileus, such as hypoperistalsis of thickened bowel and bowel fluid stagnation in the proximal side, which differ from small bowel series criteria for SMA syndrome. We referred to ultrasound criteria for SMA syndrome, only to emphasize and explain the correlation between the anatomical condition mimicking SMA syndrome and duodenal involvement in HSP, not to diagnose SMA syndrome. Moreover, we are afraid that duodenal BA never develop merely due to the anatomical condition mimicking SMA syndrome, and we think BA develop due to this anatomical condition concomitant with systemic leukocytoclastic vasculitis. As described in our manuscript, ultrasound criteria for SMA are just one set of the required criteria to diagnose SMA syndrome. In one of twelve HSP patients with abdominal pain and duodenal lesions by ultrasound in our study, we measured the aortomesenteric angle (AMA) and the aortomesenteric distance (AMD) both on admission and at the time of discharge. Decrease of AMA (23°→12°) and AMD (5.3 mm→3.3 mm) at the time of discharge compared with those on admission was observed in this patient, because bowel edema resolved after prednisolone therapy. We used the values of AMA and AMD measured on admission in all HSP patients in our study. The difference between patients and controls might have been more significant in AMA and AMD after resolution of intestinal edema, if we had adopted the values at the time of discharge or the asymptomatic state in all HSP patients. Thus, the significant differences in AMA and AMD between the two groups would not be overestimated but rather underestimated. Strictly speaking, we should adopt the values at the asymptomatic state, not the edematous state, because we would research the causality of duodenal lesion in an HSP patient with abdominal pain. However, since the number of HSP patients assessed in our study was small, we are now planning an extended study.