Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum values of immunoreactive anodal trypsinogen (sAT) have been claimed to correlate well with rejection occurring in pancreatic allografts. We have studied the behavior of sAT in serial serum samples obtained from 39 type I diabetics undergoing whole-organ pancreas transplantation during the past 3 years. Patients had either received a pancreatic allograft simultaneously with a transplanted kidney (SPK, n = 33) or after a previous kidney transplant (pancreas after kidney [PAK] n = 6). The behavior of sAT was studied in relation to the clinical diagnosis of rejection. Graft amylase output for all 39 patients and serum creatinine for the 33 SPK recipients were also studied. Tissue biopsies were obtained from 11 patients with elevated sAT values and a presumptive diagnosis of rejection. Nine of these patients had SPK grafts and simultaneously elevated creatinine values. Tissue was obtained from the simultaneously transplanted kidney; all specimens revealed rejection. Two of the 11 patients had PAK allografts. Biopsies performed on the graft duodenum were consistent with acute rejection. Three additional patients with unchanged sAT values had biopsies for other reasons; these biopsies failed to demonstrate signs of acute rejection. Thus graft biopsy correlated exactly with sAT behavior in every case in which rejection was suspected. Five patients had elevations of sAT not associated with rejection: one resulted from direct trauma, two had outlet obstruction, and two had clinical diagnoses of graft pancreatitis. The sAT was more sensitive and specific than GAO and as sensitive as creatinine for SPK recipients. These studies confirm that sAT is a reliable, graft-specific biochemical marker for the early diagnosis of pancreatic rejection. The use of sAT should allow for the proper timing of graft biopsies and the judicious use of immunosuppressive agents, which will result in increased allograft survival for PAK and pancreas-alone allografts.
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PMID:A three-year experience with serum anodal trypsinogen as a biochemical marker for rejection in pancreatic allografts. False positives, tissue biopsy, comparison with other markers, and diagnostic strategies. 137 Nov 96

The average platelet counts in our patients with functioning SPK were significantly higher during postoperative week 2 and the interval of weeks 5 through 9 compared with a matched group of KTA recipients. The thrombocyte values in the SPK group were consistently elevated above the normal range (except postoperative week 1) but less than a platelet level typically requiring therapeutic intervention (greater than 1 mil/mm3). However, because potential pathology both locally (graft pancreatitis, endothelial damage of preservation and operative trauma, diminished graft blood flow) as well as systemically (atherosclerosis, hypertension) is present in SPK patients, we consider them at high risk for thromboembolic complications and therefore support prophylaxis of post-SPK thrombocytosis with platelet inhibitors.
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PMID:Thrombocytosis following segmental duct-occluded pancreatic transplantation. 232 12

We examined a group of SPK recipients that had early (<90 d post-transplant) pancreas graft failure caused by a technical complication, and looked at outcomes of the kidney graft in these recipients. Of 289 SPK transplants, 36 (12.5%) had early pancreas graft failure because of a technical complication: thrombosis (n = 16), leak (n = 5), infection (n = 14), and pancreatitis (n = 1). Once the pancreas was lost, there was a high incidence of subsequent kidney graft failure. Kidney graft survival in these 36 recipients was 71.4% at one yr and 59.5% at three yr, significantly inferior compared to recipients that did not have early failure of the pancreas (86% at one yr and 82% at three yr, p < 0.001). Of the 36 recipients with early pancreas loss, 18 have gone on to failure of the kidney graft. Causes included thrombosis (n = 3), infection (n = 1), death with function (n = 6), chronic rejection (n = 4), ischemia (n = 1), and other (n = 3). Of the 18 kidney graft failures, nine occurred within three months after loss of the pancreas graft, usually either because of graft thrombosis, or patient death (usually from systemic sepsis). Multivariate analysis showed technical failure of the pancreas to be the most significant risk factor for kidney graft loss (HR = 2.08, p = 0.006).
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PMID:What happens to the kidney in an SPK transplant when the pancreas fails due to a technical complication? 1831 38

Histidine-tryptophan-ketoglutarate solution (HTK) has been scrutinized for use in pancreas transplantation. A recent case series and a United Network for Organ Sharing data base review have suggested an increased incidence of allograft pancreatitis and graft loss with HTK compared to the University of Wisconsin solution (UW). Conversely, a recent randomized, controlled study failed to show any significant difference between HTK and UW for pancreas allograft preservation. This study was a retrospective review of all pancreas transplants performed at Indiana University between 2003 and 2009 comparing preservation with HTK or UW. Data included recipient and donor demographics, 7-day, 90-day and 1-year graft survival, peak 30-day serum amylase and lipase, HbA1c and C-peptide levels. Of the 308 pancreas transplants, 84% used HTK and 16% UW. There were more SPK compared to pancreas after kidney and pancreas transplant alone in the HTK group. Donor and recipient demographics were similar. There was no significant difference in 7-day, 90-day or 1-year graft survival, 30-day peak serum amylase and lipase, HbA1c or C-peptide. No clinically significant difference between HTK and UW for pancreas allograft preservation was identified. Specifically, in the context of low-to-moderate flush volume and short cold ischemia time (<or=10 h), no increased incidence of allograft pancreatitis or graft loss was observed.
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PMID:Histidine-tryptophan-ketoglutarate for pancreas allograft preservation: the Indiana University experience. 2035 71

Ninety-eight percent of the whole pancreas does not serve the purpose of pancreatic transplantation and it is a major cause of surgical complications. Up to 30% of pancreas transplant recipients experience surgical complications and require reoperation. Graft thrombosis and pancreatitis are the most common complications of pancreas transplantation (PT). Thus, different surgical techniques have been described to overcome the surgical hurdles and reduce surgical complications. In this study, for the first time, we report short- and long-term outcomes of PT with inferior vena cava (IVC) venous drainage. Forty-five PTs (22 simultaneous pancreas and kidney [SPK] transplantations and 23 pancreas after kidney [PAK] transplantations) were performed with this technique in our center. Sixty-eight percent of the donors were imported from outside of our area after they were declined by their local transplantation center. Patient and graft survival rates were 100% at 1 year. No graft thrombosis or pancreatitis occurred with this technique. Six patients (13.3%) required reoperation (3 bleeding, 2 anastomotic leak, and 1 small bowel perforation). No patient or graft loss occurred due to surgical complications. We conclude that this technique provides fast and easy dissection of the venous drainage of the PT without the need of complete occlusion of venous outflow. Surgical complication rates were lower with this technique compared with other reported techniques.
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PMID:Short and long-term outcomes of systemic drainage to IVC: a new technique for pancreas transplantation. 2513 Oct 66