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Motility

Depletion of enteric gonadotropin-releasing hormone is found in a few patients suffering from severe gastrointestinal dysmotility

, , , , &
Pages 1165-1173 | Received 09 Feb 2012, Accepted 19 Jun 2012, Published online: 27 Jul 2012
 

Abstract

Objective. Many patients, especially women, suffer from severe gastrointestinal pain and dysmotility for several years without being diagnosed. Depletion of gonadotropin-releasing hormone (GnRH) in the enteric nervous system (ENS) has been described in some patients. The aim of this study was to examine the expression of GnRH in ENS and antibodies against GnRH in serum, in a dysmotility patient cohort of southern Sweden. Materials and methods. All consecutive patients (n = 35) referred for laparoscopic full-thickness biopsy because of symptoms or signs of severe dysmotility between 1998 and 2009, or patients with a severe dysmotility disorder having had a bowel resection within the time frame, were considered for inclusion. In 22 cases, representative biopsy material containing ganglia was available, and these patients were included. Medical records were scrutinized. The expression of GnRH was determined by immunohistochemistry in bowel biopsies from these patients and in patients with carcinoma or diverticulosis without ENS histopathology. Antibodies against GnRH in serum were determined by ELISA in patients and controls. Results. 14 patients were diagnosed with enteric dysmotility (ED) and 8 with chronic intestinal pseudo-obstruction due to varying etiology. Immunostained biopsies showed expression of GnRH in the ENS. A reduced expression of GnRH-containing neurons was found in 5 patients, as well as antibodies against GnRH in serum. 3 of these patients had a history of in vitro fertilization (IVF) using GnRH analogs. Conclusions. A subgroup of patients with severe dysmotility had a reduced expression of GnRH-containing neurons in the ENS and expressed antibodies against GnRH in serum.

Acknowledgements

This study was sponsored by grants from the Crafoord Foundation, Bengt Ihre Foundation and the Development Foundation of Region Skane. Maria Nilsson and Annika Jönsson are acknowledged for excellent technical support in performing the immunostaining. Klas Sjöberg is acknowledged for providing control sera. The study was designed by OH, BO, BV and AM. Analysis and interpretation of clinical data was performed by OH, BO and AM. Drafting of the manuscript was performed by OH, BO and AM. Immunhistochemistry was analyzed by BV and ELISA by RA and GNF. BO obtained funding for the study. All authors contributed to the intellectual content of the manuscript and accepted the final version of it. This study was sponsored by grants from the Crafoord Foundation, Bengt Ihre Foundation and the Development Foundation of Region Skane.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

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