Islet Autotransplantation Restores Normal Glucose Tolerance in a Patient With Chronic Pancreatitis
Impaired glucose tolerance is a frequent complication of chronic pancreatitis (CP) that over time leads to diabetes (1). Intractable abdominal pain from CP that can no longer be managed by oral pancreatic enzymes and by narcotic analgesics is treated by surgery. To avoid diabetes onset following pancreatectomy, combined islet autotransplantation has been offered to the patients who suffered from CP in Leicester, U.K., since 1994 (2,3) (http://hpb.org.uk/hpbunitspecialist.php?page_id=11).
Here, we present a case report of a patient that suffered from CP and had an abnormal oral glucose tolerance test (OGTT) before pancreatectomy (showing diabetes and impaired glucose tolerance) but since surgery has had normal results. Indeed, OGTT results of stimulated blood glucose were 11.9 and 8 mmol/l at 19 and 11 months presurgery, respectively.
At the time of the surgery, the patient was a 43-year-old woman. The etiology of CP was idiopathic, and the patient suffered from chronic epigastric pain for more than 2 years before surgery. On 28 May 2002, the patient underwent a total pancreatectomy combined with islet autotransplantation during an 8-h operation (including the islet preparation process, as previously described [2,3]). The weight of the pancreas was 55 g, and after digestion, 14 ml pancreatic tissue (tissue-packed volume) was obtained. A total of 232,721 islets, corresponding to 57,296 islet equivalents (IEQ), 18% free of acinar tissue, was infused into the left branch of the portal vein.
The patient remains insulin independent 5 years after autoislet transplantation with 954.93 IEQ/kg body wt. Intravenous insulin was stopped 8 days postoperatively; her blood glucose levels were monitored every 4 h and remained stable throughout her hospital stay (21 days). She did not experience any perioperative complications. By 2 years postoperation, she began to experience regular postprandial hypoglycemic episodes, which is a well-known prolonged insulin response of transplanted islets due to a defective glucagon secretion (4,5).
Annual follow-up visits revealed normal OGTT results. Her fasting C-peptide levels have remained detectable, and the C-peptide production in response to an oral glucose load is significantly higher than basal levels (1.44 and 5.02 ng/ml, respectively, at 5 years postsurgery).
To our knowledge, this is the first case report of a CP patient, with abnormal OGTT before surgery, who has become insulin independent after autoislet transplantation with less than 1,000 IEQ/kg body wt. These results show that it is possible to restore normal glucose tolerance with total pancreatectomy combined with islet autotransplantation in CP patients with borderline diabetes. Furthermore, these results support the concept that insulin independence can be achieved in patients with islet cell autograft of a low number of islets. Indeed, from our series, no correlation was found between the islet number and the outcome of the islet transplant in terms of insulin independence (2).
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