Background/AimsChronic intestinal pseudo-obstruction (CIPO) is a serious, life-threatening motility disorder that is often related to bacterial overgrowth. Fecal microbiota transplantation (FMT) results in restoration of the normal intestinal microbial community structure. We investigated the efficacy of FMT in the treatment of CIPO patients. MethodsNine patients (age 18-53 years) with CIPO were enrolled in this prospective, open-label study. Patients received FMT for 6 consecutive days through nasojejunal (NJ) tubes and were followed up for 8 weeks after treatment. We evaluated the rate of clinical improvement and remission, feeding tolerance of enteral nutrition, and CT imaging scores of intestinal obstructions. Lactulose hydrogen breath tests were performed before FMT and 8 weeks after FMT to evaluate for the presence small intestinal bacterial overgrowth (SIBO). ResultsFMT significantly alleviated bloating symptoms, and symptoms of pain were relieved 2 weeks after FMT. Enteral nutrition administered through a NJ tube after FMT was well-tolerated by 66.7% (6/9) of patients. CT scores of intestinal obstructions were significantly reduced after FMT (P = 0.014). SIBO was eliminated in 71.0% (5/7) of patients. ConclusionsThis pilot study demonstrated the safety of using FMT. FMT may relieve symptoms in selected patients with CIPO. FMT may also improve patient tolerance of enteral nutrition delivered via a NJ tube.

Non-obstructive azoospermia (NOA) severely affects male infertility, however, the deep mechanisms of this disease are rarely interpreted. In this study, we find that undifferentiated spermatogonial stem cells (SSCs) still exist in the basal compartment of the seminiferous tubules and the blood–testis barrier (BTB) formed by the interaction of neighbor Sertoli cells (SCs) is incomplete in NOA patients with spermatogenic maturation arrest. The adhesions between SCs and germ cells (GCs) are also broken in NOA patients. Meanwhile, the expression level of geranylgeranyl diphosphate synthase ( Ggpps ), a key enzyme in mevalonate metabolic pathway, is lower in NOA patients than that in obstructive azoospermia (OA) patients. After Ggpps deletion specifically in SCs, the mice are infertile and the phenotype of the SC- Ggpps −/− mice is similar to the NOA patients, where the BTB and the SC–GC adhesions are severely destroyed. Although SSCs are still found in the basal compartment of the seminiferous tubules, fewer mature spermatocyte and spermatid are found in SC- Ggpps −/− mice. Further examination suggests that the defect is mediated by the aberrant protein isoprenylation of RhoA and Ras family after Ggpps deletion. The exciting finding is that when the knockout mice are injected with berberine, the abnormal cell adhesions are ameliorated and spermatogenesis is partially restored. Our data suggest that the reconstruction of disrupted BTB is an effective treatment strategy for NOA patients with spermatogenic maturation arrest and hypospermatogenesis.

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