ABSTRACT
Several factors may contribute to the pathogenesis of pancreatitis after transplantation (Table 13.1). There is a well-known association between end-stage renal disease and acute pancreatitis. Hyperparathyroidism is frequent in dialysis patients and may require time before reversing after transplantation. Hyperparathyroidism is associated with pancreatitis in 1.5-17% of cases. Although the relationship between these two entities is still under discussion, there are data suggesting that hypercalcemia, caused by hyperparathyroidism, is a major risk factor for the development of pancreatitis (Carnaille et al., 1998). A number of patients developed pancreatitis after parathyroidectomy (Mjaland and Normann, 2000). Many dialysis patients have silent gallstone disease (Badalamenti et al., 1994), which may increase the risk of acute pancreatitis either by obstruction or by reflux of biliary or duodenal contents, which stimulate pancreatic secretion. A possible role has been advocated for immunosuppressive drugs, including corticosteroids (Buchman, 2001), azathioprine (Siwach et al., 1999), cyclosporine (Ko et al., 1997), tacrolimus (Nieto et al., 2000; Ogunseinde et al., 2003), and mycophenolate mofetil (Furst, 1999). Rare cases of acute pancreatitis have developed after the administration of OKT3 (Scheinin et al., 1993) or antithymoglobulins (Lee et al., 2006). Changes consistent with the presence of cytomegalovirus in the gland and good response to ganciclovir have been reported in patients with post-transplant pancreatitis, suggesting an involvement of viral infection (Klassen et al., 2000; Sinha et al., 2003). Hypertriglyceridemia, which may be frequent in transplant patients, is also often associated with pancreatitis (Murphy et al., 2002; Grochowiecki et al., 2003).
