Islet autotransplantation after total pancreatectomy in a child

• Published in: Journal of pediatric surgery 1996, Vol.31 (1), p.132-136
• Main Authors: Wahoff, David C, Papalois, Basil E, Najarian, John S, Farney, Alan C, Leonard, Arnold S, Kendall, David M, Robertson, R.Paul, Sutherland, David E.R
• Format: Article
• Language: English
• Subjects: Blood Glucose - metabolism; Child; Chronic Disease; Diabetes Mellitus, Type 1 - etiology; Diabetes Mellitus, Type 1 - prevention & control; Humans; Islets of Langerhans Transplantation; Male; Pain, Intractable - etiology; Pain, Intractable - surgery; Pancreatectomy - adverse effects; Pancreatitis - complications; Pancreatitis - surgery; Transplantation, Autologous
• ISSN: 0022-3468; 1531-5037
• DOI: 10.1016/S0022-3468(96)90335-8

Islet autotransplantation can prevent surgically induced diabetes after total pancreatectomy in adults; however, the efficacy of this procedure has not been established in children. The authors report the case of a 12-year-old boy who underwent total pancreatectomy and islet autotransplantation for intractable pain caused by idiopathic chronic pancreatitis. Islets were prepared from the excised pancreas by collagenase digestion and mechanical dispersion. The resultant preparation, containing 109,500 islets, was injected into the recipient's liver via the portal vein. No complication from the pancreatectomy or transplant occurred. Postoperatively, the patient had complete relief of abdominal pain. He remained insulin-independent, with normal fasting blood glucose and hemoglobin A 1c levels, for 2 1 2 years. Preoperatively, the acute insulin response and the rate of glucose disappearance (K g) were 213 μU/mL and 2.14% (respectively) after intravenous administration of 20 g of glucose. Although lower than pretransplantation values, both insulin response and K g remained normal at 4 months (88 μU/mL; K g, 1.01%); however, these decreased further, to below normal, by 2 years posttransplantation (10 μU/mL; K g, 0.67%). Two-and-a-half years after transplantation, fasting hyperglycemia (>200 mg/dL) was evident, and the patient was begun on exogenous insulin. Five years posttransplantation he remains insulin-dependent with a fasting serum C-peptide level of 0.20 ng/mL, which increased to 0.35 ng/mL in response to intravenous arginine, indicating sustained islet function. During the documented decreases in insulin secretion and K g posttransplantation, the patient's body weight increased by 65% (from 34 to 56 kg) as a result of normal growth; the number of transplanted islets relative to body mass decreased accordingly, from 3,200 to 1,950 islets per kilogram of body weight. In this case, the number of islets transplanted likely could not meet the increased insulin demands of the larger body mass. Thus, exogenous insulin supplementation was needed to prevent hyperglycemia. In conclusion, insulin independence was initially established in a child by islet autotransplantation after total pancreatectomy. The failure of the islets to maintain normoglycemia long-term suggests that a sufficient number must be transplanted (to meet the demands of normal growth and development) for sustained insulin independence.