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Diabetes & Metabolism
Volume 34, n° 2
pages 182-183 (avril 2008)
Doi : 10.1016/j.diabet.2008.01.001
Received : 18 December 2007 ; 
Uneventful pregnancy in a patient with ketosis-prone type 2 diabetes mellitus
Déroulement normal d’une grossesse chez une patiente ayant un diabète de type 2 cétosique
 

E. Carreira
Department of Diabetology, hôpital Cochin-Saint-Vincent-de-Paul and Université Paris Descartes, 27, rue du Faubourg-Saint-Jacques, 75014 Paris, France 

J. Lepercq
Department of Obstetrics, hôpital Cochin-Saint-Vincent de Paul and Université Paris Descartes, 27, rue du Faubourg-Saint-Jacques, 75014 Paris, France 

C. Bouché, D. Dubois-Laforgue, J. Timsit
Department of Diabetology, hôpital Cochin-Saint-Vincent-de-Paul and Université Paris Descartes, 27, rue du Faubourg-Saint-Jacques, 75014 Paris, France 

Corresponding author.

Keywords : Ketosis-prone type 2 diabetes, Pregnancy, Insulin resistance

Mots clés : Diabète de type 2 cétosique, Grossesse, Insulinorésistance


Ketosis-prone type 2 diabetes is typically revealed by acute metabolic decompensation, followed by remission and subsequent relapse [1]. The mechanisms of this phasic course are not fully understood, but may involve both a progressive defect of insulin secretion and insulin resistance [2]. Since pregnancy is associated with insulin resistance, it may be a situation at high risk for decompensation in such patients. However, there have been no reports on the prognosis of pregnancy in patients with this particular form of diabetes.

History and examination

A 30-year-old woman from Mali was admitted with metabolic decompensation revealing diabetes. She had no significant past medical history and no known family history of diabetes. Her body weight was previously normal (70kg, BMI 24.2kg/m2). She reported the onset of polyuria and mouth dryness, followed by vomiting and abdominal discomfort, eight days before admission. On admission, her physical examination was unremarkable apart from signs of dehydration. The patient had lost 8kg of body weight. Plasma glucose concentration was 40mmol/L and urine ketone bodies were 4+. Arterial pH was 7.32 and bicarbonates were 7mmol/L. Plasma sodium was 151mmol/L, potassium was 4.8mmol/L, protides were 103g/L and creatinine was 148μmol/L. Liver and pancreas enzymes were normal. No precipitating factor was identified. HbA1c was 13.2% (normal 4.3–5.7%).

The diagnosis of diabetic ketoacidosis with moderate hyperosmolarity (calculated plasma osmolarity was 361mmol/L) was made, and the patient was treated by fluid and potassium replacement, and intravenous regular insulin. Insulin requirements were 240IU during the first 24h, and 120IU the next day. Thereafter, insulin was administered subcutaneously. Good glycaemic control was achieved with 66IU/day of insulin on day 4 after admission. Metformin (2550mg/day) and glyburide (15mg/day) were then instituted while the insulin dosage was tapered. The patient was discharged on day 10 while taking insulin therapy and oral hypoglycaemic agents, with normal glycaemic control. Islet-cell antibodies, anti-GAD and anti-IA-2 antibodies were all negative.

During the following six weeks, insulin therapy and glyburide were progressively tapered, and the patient remained on metformin alone with good glycaemic control. She was followed-up for 15 months and remained in remission (HbA1c 5.2–5.6%). At this time, the patient had regained her initial weight loss. Because the patient planned a pregnancy, metformin was discontinued with no deterioration of glycaemic control (preconceptional HbA1c 5.3%). Throughout the entire pregnancy, the patient was treated with diet alone and glycaemic control remained good, as indicated by capillary blood glucose self-monitoring (mean value of four to six daily determinations: 5.6–6.1mmol/L) and HbA1c values (5.1–5.7%). Total weight gain during the pregnancy was 10kg. Pregnancy was uneventful and the patient spontaneously delivered, at 40 weeks of gestation, a healthy 3710-g girl, who had no neonatal hypoglycaemia. Thirty months after the initial decompensation, the patient remains in remission.

Conclusion

In this patient, the diagnosis of ketosis-prone type 2 diabetes was established on the basis of her ethnicity, the uncovering of diabetes by severe decompensation in the absence of a precipitating event, the subsequent progression to complete remission within a few weeks, and the absence of type 1 diabetes-associated autoantibodies.

The definite pathophysiology of ketosis-prone type 2 diabetes remains unknown. It has been shown that insulin secretion and insulin sensitivity, which are deeply suppressed at presentation, both recover at least partially after treatment with insulin. However, after the first remission and cessation of insulin therapy, up to 60% of patients with ketosis-prone type 2 diabetes have a recurrence of hyperglycaemia within two years when treated by diet alone [1]. In patients in remission, progressive hyperglycaemia precedes, and is a strong risk factor for subsequent relapse [2]. More recently, short-term studies have shown that glucotoxicity, but not lipotoxicity, is involved in the occurrence of β-cell dysfunction and abnormal muscle insulin signalling [3]. Thus, both insulin secretion defect and insulin resistance may be involved in relapse.

The case we have described shows that the insulin resistance normally associated with pregnancy was not sufficient to trigger metabolic decompensation in our patient. This suggests that, despite the severe initial presentation, recovery of β-cell function was near-normal, or at least able to counteract insulin resistance. Since glucotoxicity is a major determinant of the insulin secretion defect observed in ketosis-prone type 2 diabetes, maintenance of normal glucose control is crucial to avoid relapse of metabolic decompensation. In this respect, monotherapy with metformin, which is not associated with the risk of hypoglycaemia, should be used during the remission phase in patients who have ketosis-prone type 2 diabetes.

References

Umpierrez G.E., Smiley D., Kitabchi A.E. Narrative review: ketosis-prone type 2 diabetes mellitus Ann Intern Med 2006 ;  144 : 350-357 [cross-ref]
Mauvais-Jarvis F., Sobngwi E., Porcher R., Riveline J.P., Kevorkian J.P., Vaisse C., and al. Ketosis-prone type 2 diabetes in patients of sub-saharan origin. Clinical pathophysiology and natural history of β-cell dysfunction and insulin resistance Diabetes 2004 ;  53 : 645-653 [cross-ref]
Umpierrez G.E., Smiley D., Gosmanov A., Thomason D. Ketosis-prone type 2 diabetes: effect of hyperglycemia on beta-cell function and skeletal muscle insulin signaling Endocr Prat 2007 ;  13 : 283-290 [cross-ref]



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