Anorectal function testing and anal endosonography in the diagnostic work-up of patients with primary pelvic organ prolapse

AIM: To study the pathophysiology of defecation disorders in patients with primary pelvic organ prolapse (POP) and the diagnostic potential of anorectal function testing (AFT) including endosonography in the work-up of these patients. METHODS: 59 Patients were evaluated with a validated questionnaire, clinical examination, AFT and endosonography. RESULTS: Women with POP showed lower squeezing pressure, postponed first sensation and desire, lower capacity and prolonged pudendal nerve terminal latency time compared to healthy controls (all p < 0.01). Manometric findings did not differ significantly between patients with and without constipation. Patients with fecal incontinence had significantly lower resting and squeezing pressures than patients without fecal incontinence and an increased risk of an external sphincter defect (odds ratio = 12.75, 95% confidence interval 2.40-66.67). Although digital rectal examination could quantify absent, decreased and normal squeezing pressure, the positive predictive value for external sphincter defects was low (0.32). CONCLUSION: AFT indicates the presence of neuromuscular damage of the anorectal region in patients with POP. AFT is not useful in the work-up of patients with POP and constipation, because it fails to discriminate between symptomatic and asymptomatic patients. In cases of fecal incontinence, AFT and endosonography are helpful to distinguish between functional and anatomical problems

The mast cell stabiliser ketotifen decreases visceral hypersensitivity and improves intestinal symptoms in patients with irritable bowel syndrome

Background Mast cell activation is thought to be involved in visceral hypersensitivity, one of the main characteristics of the irritable bowel syndrome (IBS). A study was therefore undertaken to investigate the effect of the mast cell stabiliser ketotifen on rectal sensitivity and symptoms in patients with IBS. Methods 60 patients with IBS underwent a barostat study to assess rectal sensitivity before and after 8 weeks of treatment. After the initial barostat, patients were randomised to receive ketotifen or placebo. IBS symptoms and health-related quality of life were scored. In addition, mast cells were quantified and spontaneous release of tryptase and histamine was determined in rectal biopsies and compared with biopsies from 22 age- and gender-matched healthy volunteers. Results Ketotifen but not placebo increased the threshold for discomfort in patients with IBS with visceral hypersensitivity. This effect was not observed in normosensitive patients with IBS. Ketotifen significantly decreased abdominal pain and other IBS symptoms and improved quality of life. The number of mast cells in rectal biopsies and spontaneous release of tryptase were lower in patients with IBS than in healthy volunteers. Spontaneous release of histamine was mostly undetectable but was slightly increased in patients with IBS compared with healthy volunteers. Histamine and tryptase release were not altered by ketotifen. Conclusions This study shows that ketotifen increases the threshold for discomfort in patients with IBS with visceral hypersensitivity, reduces IBS symptoms and improves health-related quality of life. Whether this effect is secondary to the mast cell stabilising properties of ketotifen or H-1 receptor antagonism remains to be further investigate

The position of the acid pocket as a major risk factor for acidic reflux in healthy subjects and patients with GORD

Gastro-oesophageal reflux occurs twice as much during transient lower oesophageal sphincter relaxations (TLOSRs) in patients with gastro-oesophageal reflux disease (GORD) compared to healthy volunteers (HVs). Our aim was to assess whether the localisation of the postprandial acid pocket and its interaction with a hiatal hernia (HH) play a role in the occurrence of acidic reflux during TLOSRs. Ten HVs and 22 patients with GORD (12 with HH or =3 cm (l-HH)) were studied. The squamocolumnar junction and diaphragmatic impression were marked with a radioactively labelled clip. To visualise the acid pocket, (99m)Tc-pertechnetate was injected intravenously and images were acquired up to 2 h postprandial. Concurrently, combined manometry/impedance and four-channel pH-metry were performed, with pH pull-through at multiple time-points. The rate of TLOSRs and the per cent associated with reflux was comparable between all groups. However, acidic reflux was significantly increased in patients, especially in patients with l-HH. Acid pocket length was significantly enlarged in patients. Moreover, immediately before a TLOSR, the acid pocket was more frequently located within the hiatus or above the diaphragm in patients with GORD (s-HH, 54%; l-HH, 77%) compared to HVs (22% of TLOSRs). Acidic reflux was significantly increased when the acid pocket was located above the diaphragm in all groups compared to a sub-diaphragmatic localisation. The position of the acid pocket is largely determined by the presence of a HH. Entrapment of the pocket above the diaphragm, especially in patients with l-HH, is a major risk factor underlying the increased occurrence of acidic reflux during a TLOSR in patients with GOR