Rapid Responses to:

PRACTICE: Lucy C Chappell and Sarah J Germain Commentary: Controversies in management of diabetes from preconception to the postnatal period BMJ 2008; 336: 717-718 [Full text]

Rapid Responses: Submit a response to this article

Rapid Responses published:

Associations and causes in diabetic pregnancy.

Martin Quinn   (2 April 2008)

Associations and causes in diabetic pregnancy. 2 April 2008
Martin Quinn, Consultant in Gynaecology Bridge, Fertility, Gynaecology & Genetics Clinic, 1 St Thomas Street, London. Send response to journal: Re: Associations and causes in diabetic pregnancy.	Improved maternal glycaemic control has not reduced adverse fetal outcomes, including miscarriage, preeclampsia, and preterm labour, in diabetic pregnancy (1). Raised maternal glucose levels may not be the source of these complications. An alternative explanation is that maternal diabetes and adverse fetal outcomes are simply associations - it is possible that similar mechanisms cause diabetes in one woman, adverse fetal outcomes in a second, and, both diabetes and adverse fetal outcomes, in a third. Pelvic nerves, derived from large autonomic plexi on the pelvic side wall, are susceptible to injury by persistent straining to achieve defaecation (2). Uterine denervation has been associated with adverse pregnancy outcomes, including miscarriage, preeclampsia, and, impaired fetal growth (3). Patchy loss of islets of Langerhans is the histological hallmark of type 1 diabetes mellitus that may result from injury to autonomic (sympathetic) nerves closely applied to the posterior surface of the pancreas (4). Within this hypothesis, both maternal diabetes and adverse fetal outcomes have a common cause; injury to the autonomic nerves of the coeliac and hypogastric plexi respectively. Straining may cause injury to the nerves of a womans’ pancreas in early childhood. Recurrent straining may cause an injury to uterine nerves in her reproductive years when her body has achieved adult proportions. Connecting two events in two different organs at two different ages by a single mechanism, may explain some of the difficulties in improving outcomes in diabetic pregnancy over the past twenty years (1). (1) Chappell LC, Germain SJ Commentary: Controversies in management of diabetes from preconception to the postnatal period. BMJ 2008; 338:717-8. (2) Quinn MJ Perivascular nerve fibre proliferation; the consequence of persistent straining. J Obstet Gynecol 2007; 27(2):185-8 (3) Khong TY, Tee JH, Kelly AJ Absence of innervation of the uteroplacental arteries in normal and abnormal human pregnancies. Gynecol Obstet Invest. 1997;43(2):89-93. (4) Mei Q, Foulis AK, Fligner C, Hull R, Nguyen H, Gilliam L, Taborsky GJ Selective Loss of Sympathetic Nerves from the Islet in Human Type 1 Diabetes: a Potential Mechanism for Impaired Glucagon Responses to Hypoglycemia. Paper presented at The American Diabetic Association, 2006 Competing interests: None declared