Summary and Recommendations of the Fifth International Workshop-Conference on Gestational Diabetes Mellitus

  1. Boyd E. Metzger, MD1,
  2. Thomas A. Buchanan, MD2,
  3. Donald R. Coustan, MD3,
  4. Alberto de Leiva, MD, PHD4,
  5. David B. Dunger, MBBS, MD, FRCP5,
  6. David R. Hadden, MD, FRCP6,
  7. Moshe Hod, MD7,
  8. John L. Kitzmiller, MD8,
  9. Siri L. Kjos, MD9,
  10. Jeremy N. Oats, DM10,
  11. David J. Pettitt, MD11,
  12. David A. Sacks, MD12 and
  13. Christos Zoupas, MD13
  1. 1Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois
  2. 2Department of Medicine, University of Southern California Keck School of Medicine, Los Angeles, California
  3. 3Brown Medical School, Women and Infant's Hospital of Rhode Island, Providence, Rhode Island
  4. 4Department of Endocrinology, Hospital de la Santa Creui Sant Pau, Universitat Autònoma, Barcelona, Spain
  5. 5Department of Pediatrics, University of Cambridge, Addenbrooke's Hospital, Cambridge, U.K.
  6. 6Regional Endocrinology and Diabetes Centre, Royal Victoria Hospital, Belfast, U.K.
  7. 7Perinatal Division, Helen Schneider Hospital for Women, Rabin Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
  8. 8Division of Maternal-Fetal Medicine, Santa Clara County Health System, San Jose, California
  9. 9Department of Obstetrics and Gynecology, Harbor-UCLA Medical Center, Torrance, California
  10. 10Division of Maternity Services, The Royal Women's Hospital, Carlton, Victoria, Australia
  11. 11Sansum Diabetes Research Institute, Santa Barbara, California
  12. 12Department of Obstetrics and Gynecology, Kaiser Foundation Hospital, Bellflower, California
  13. 13Diabetes Center, Hygeia General Hospital, Athens, Greece
  1. Address correspondence and reprint requests to Boyd E. Metzger, MD, Northwestern University Feinberg School of Medicine, Tarry Building 15-735, 303 East Chicago Ave., Chicago, IL 60611. E-mail: bem{at}northwestern.edu

The Fifth International Workshop-Conference on Gestational Diabetes Mellitus (GDM) was held in Chicago, IL, 11–13 November 2005 under the sponsorship of the American Diabetes Association. The meeting provided a forum for review of new information concerning GDM in the areas of pathophysiology, epidemiology, perinatal outcome, long-range implications for mother and her offspring, and management strategies. New information and recommendations related to each of these major topics are summarized in the report that follows.

The issues regarding strategies and criteria for the detection and diagnosis of GDM were not reviewed or discussed in detail, since it is anticipated that the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study will provide data in mid-2007 that will foster the development of criteria for the diagnosis of GDM that are based on perinatal outcomes. Thus, for the interim, the participants of the Fifth International Workshop-Conference on GDM endorsed a motion to continue use of the definition, classification criteria, and strategies for detection and diagnosis of GDM that were recommended at the Fourth Workshop-Conference. Those guidelines are reproduced (with minor modifications) in this article in appendix Tables 1 and 2.

SUMMARY AND RECOMMENDATIONS—

The invited lectures, topical discussions, and posters presented at the conference and the invited manuscripts that appear in this issue of Diabetes Care served as the basis for the following summary and recommendations.

PANEL I: PATHOPHYSIOLOGY AND EPIDEMIOLOGY

Pathophysiology

General considerations.

Current diagnostic criteria assign the diagnosis of GDM to women with glucose levels in the upper ∼5–10% of the population distribution. The hyperglycemia varies in severity from glucose concentrations that would be diagnostic of diabetes outside of pregnancy to concentrations that are asymptomatic and only slightly above normal, but associated with some increased risk of fetal morbidity.

Like all forms of hyperglycemia, GDM is characterized by insulin levels that are insufficient to meet insulin demands. The causes of pancreatic β-cell dysfunction that …

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