Quantifying the extent of fistulotomy. How much sphincter can we safely divide? A three-dimensional endosonographic study

Purpose

To quantify the longitudinal division of the internal anal sphincter (IAS) and external anal sphincter (EAS) after fistulotomy using three-dimensional endoanal ultrasound (3D-EAUS) and correlate the results with postoperative faecal incontinence.

Methods

A prospective, consecutive study was performed from December 2008 to October 2010. All patients underwent 3D-EAUS before and 8?weeks after surgery. Thirty-six patients with simple perianal fistula were included. Patients with an intersphincteric or low transphincteric fistula (<66% sphincter involved) without risk factors for incontinence underwent fistulotomy. The outcome measures were the longitudinal extent of division of the IAS and EAS in relation to total sphincter length and continence (Jorge and Wexner scores).

Results

One-year follow-up revealed a 0% recurrence rate. There was a strong correlation between preoperative 3D-EAUS measurement of fistula height with intraoperative and postoperative 3D-EAUS measurement of IAS and EAS division (p?p?>?0.05).

Conclusions

In patients without risk factors, division of the EAS during fistulotomy limited to the lower two thirds of the EAS is associated with excellent continence and cure rates.     

Hypertension and aortorenal disease in Alagille syndrome

Alagille syndrome is a rare congenital multisystem disorder that may involve heart disease and pulmonary or peripheral artery stenosis. We report the clinical and radiological presentation of five adult patients with Alagille syndrome, hypertension and renal artery stenosis. All had systolic hypertension and a narrowing of the abdominal aorta, corresponding to a secondary midaortic syndrome. Renovascular disease progressed during follow-up, with increases in blood pressure, decreases in glomerular filtration rate and/or kidney atrophy. A literature review identified several anecdotal reports of Alagille syndrome associated with hypertension, renal artery stenosis and/or midaortic syndrome. We discuss this condition, focusing on diagnosis, differential diagnosis, associated conditions and management. Cardiologists, nephrologists and radiologists should be aware of this rare cause of renovascular hypertension and of the need for clinical, biological and echographic follow-up.     

Connecting liver and gut: murine liver sinusoidal endothelium induces gut tropism of CD4+ T cells via retinoic acid

Gut-activated T cells migrating into the liver can cause extraintestinal manifestations of inflammatory bowel disease. T cells acquire a gut-homing phenotype dependent on retinoic acid (RA) provided by intestinal dendritic cells (DC). We investigated whether liver antigen-presenting cells can induce gut tropism supporting an enterohepatic lymphocyte circulation. Priming of CD4(+) T cells by liver sinusoidal endothelial cells (LSEC) supported migration into gut and gut-associated lymphoid tissue. As observed for T cells primed by intestinal DCs, this gut tropism depended on α(4) β(7) integrin and CC chemokine receptor 9 (CCR9) expression by LSEC-primed CD4(+) T cells. The induction of gut-homing molecules was mediated by RA, a derivate of vitamin A that is stored in large amounts within the liver. LSECs expressed functional retinal dehydrogenases and could convert vitamin A to RA. Conversely, the lack of signaling via the RA receptor prevented the expression of α(4) β(7) integrin and CCR9 on LSEC-primed CD4(+) T cells, consequently reducing their in vivo migration to the intestine. Other liver antigen-presenting cells failed to support high expression of α(4) β(7) integrin on CD4(+) T cells, thus, the potential to induce gut homing is restricted to LSECs. CONCLUSION: The capacity to promote gut tropism via vitamin A use is not unique for intestinal DCs but is also a feature of LSECs. Our data support the assumption that CD4(+) T cells can migrate from the liver to the gut as one branch of a postulated enterohepatic lymphocyte circulation.     

Antimicrobial therapy for bronchiectasis

Antibiotics have a role in the management of acute exacerbations of bronchiectasis and may also benefit selected subsets of patients with bronchiectasis as a part of a long-term maintenance strategy. At present, there are no Food and Drug Administration-approved antibiotics for acute or chronic management of bronchiectasis. Clinical trials are underway to determine the efficacy and safety of various inhaled antibiotics for chronic therapy for bronchiectasis. Until those results are available, clinicians need to tailor their therapies to individual patients based on their best clinical judgment and information from data and guidelines currently available in the published literature.