Urinary Amylase Values Research Articles

Improving monitoring after pancreas transplantation alone: fine-tuning of an old technique.

Graft survival after pancreas transplantation alone (PTA) is significantly poorer than graft survival after simultaneous pancreas kidney (SPK) and is particularly affected by difficulty in monitoring rejection. Exocrine bladder drainage allows assessment of pancreas graft function as urinary amylase (UA). However, standards for UA collection and interpretation are not well defined. In this study, 21 bladder-drained PTA recipients were monitored with daily values for UA and urine creatinine (Creat) concentration from post-transplant 10-mL samples and 24-h collections. Clinical events were documented and correlated to UA measurements. UA values were found to increase post-transplant until day 15, and large interpatient variability was noted (median 12676IU/L, range 668-60369IU/L). A strong correlation was found total 24-h UA production and spot UA/Creat ratio (r=0.80, p<0.001). UA/Creat ratio showed less variation during episodes of impaired renal function; therefore, urinary amylase baseline was defined as the median UA/Creat ratio after day 15. A>25% decrease of UA predicted 9/13 (69%) events. We conclude that individual baselines should be set once the values have stabilized after 15d post-transplant and that spot UA/Creat measures are reliable, patient friendly and indicate potential events after PTA.

Interruption of gallbladder wall with pericholecystic fluid: a CT finding of perforation

In this report, we present an unusual case of gallbladder perforation due to acalculous cholecystitis, masked clinically by acute pancreatitis. Severe abdominal pain referred to the patient's back, nausea, vomiting, and high serum and urinary amylase values were compatible with acute pancreatitis. However, on contrast-enhanced CT, the size and appearance of the pancreas were normal while the gallbladder was abnormally enlarged with a wall defect indicating perforation, soon afterward confirmed by surgery.

Preferential rejection of the kidney in a simultaneous kidney-pancreas transplant.

A case of selective kidney allograft rejection with stable pancreas function in a patient who received simultaneous kidney-pancreas allograft from the same donor is reported. Pancreas function was shown to be normal within the first month posttransplant by both a glucose tolerance test (despite a high corticosteroid dose) and stable urinary amylase values during biopsy-proven acute renal allograft rejection. This patient subsequently rejected his kidney allograft as documented by histopathologic evidence of severe chronic vascular rejection and acute tubulointerstitial rejection, yet his pancreas function remained intact. He subsequently received a six-antigen-matched kidney, continues to have normal fasting glucose and normal glucose tolerance by oral glucose tolerance test, and is without evidence of glucosuria. He has never had a clinical rejection of his pancreas, as evidenced by either a decline in urinary amylase or hyperglycemia, and has not required insulin except in the perioperative period of his second kidney transplant, at which time he was receiving high doses of both corticosteroids and cyclosporin. It is suggested that preferential rejection and subsequent loss of the kidney, although infrequent, do occur in combined renal-pancreas allografts and that maintenance of immunosuppression is justified until retransplant of kidney is available.

SERUM IMMUNOREACTIVE ANODAL TRYPSINOGEN AND URINARY AMYLASE AS BIOCHEMICAL MARKERS FOR REJECTION OF CLINICAL WHOLE-ORGAN PANCREAS ALLOGRAFTS HAVING EXOCRINE DRAINAGE INTO THE URINARY BLADDER

Rejection of pancreas allografts is best measured today by co-monitoring the creatinine of a simultaneously transplanted kidney allograft from the same donor. This methodology discourages pancreas transplantation for patients who have previously received a kidney allograft and preuremic patients. Thus, an early, graft-specific marker of rejection is desirable. In this study we compared 2 putative biochemical markers for rejection of pancreas allografts, serum immunoreactive anodal trypsinogen and urinary amylase, with serum creatinine in 15 simultaneously transplanted type I diabetics. Serial values during hospitalizations were determined. Follow-up ranged from 18 to 134 postoperative days. Rejection was diagnosed clinically and considered real if the patient received a course of anti-rejection medication. Ten of these 15 patients experienced a total of 21 rejection episodes. For all episodes of rejection, serum trypsinogen rose from a baseline of 398.1 +/- 25 ng/ml to 1686.2 +/- 317.9 ng/ml (P less than 0.001) on the day of rejection. Urinary amylase fell from 88,310 +/- 7877 U/24 hr to 37,508 +/- 7142 U/24 hr (P less than 0.001). For 10 patients in whom rejection was diagnosed on the initial hospitalization so that serial prediagnosis sera and urines were available, anodal trypsinogen rose from a baseline of 756 +/- 263 ng/ml to 1936 +/- 582 ng/ml (P less than 0.001). Urinary amylase values for these same 10 patients did not change significantly (baseline = 55,788 +/- 18,404 U/24 hr, rejection = 47,133 +/- 14,737 U/24 hr, (P = 0.7). We conclude that serum anodal trypsinogen behaves as a graft-specific biochemical marker for rejection of vascularized pancreas allografts.

EXPERIMENTAL AND CLINICAL EXPERIENCE WITH URINE AMYLASE MONITORING FOR EARLY DIAGNOSIS OF REJECTION IN PANCREAS TRANSPLANTATION

Pancreas allograft rejection in dogs with pancreaticocystostomy can be predicted in advance of hyperglycemia by monitoring the urinary amylase (UA) concentration (U/L): In initial experiments, UA values declined to less than 1000 1.3 +/- 0.2 days before hyperglycemia in nonimmunosuppressed dogs, 3.3 +/- 1.0 days in dogs treated with cyclosporine (CsA), and 9.3 +/- 0.7 days in dogs treated with CsA, azathioprine (Aza), and prednisone (triple therapy). Autotransplanted control dogs maintained high urine amylase concentrations indefinitely (mean 125,544 +/- 36,931). In a subsequent experiment, in 19 dogs with bladder-drained pancreas allografts on CsA only for prophylactic immunosuppression, a five-day course of antirejection treatment with Aza (5.0 mg/kg) and antilymphocyte globulin ALG (1 mg/kg) was started in group A (n = 10) when a raise in serum glucose was detected, and in group B (n = 9) when a drop of UA below 1000 was observed. The functional allograft survival rate was 9.2 +/- 0.5 days in group A (treatment started after hyperglycemia) and 29.0 +/- 5.7 days in group B (treatment started after drop in UA) (P = .002). The UA dropped in all dogs before hyperglycemia, at a mean of 2.7 days in group A and 20.8 days in group B. Clinically, 8 patients received a whole cadaver pancreas transplant with urinary drainage of the exocrine secretions. All were followed with UA monitoring. Three recipients lost the grafts for technical reasons. Three recipients lost the grafts for technical reasons. One had a primary non-function and UA was below 1000 U/24 hr; two developed abscesses and the grafts were removed while functioning with high UA values. Five grafts are currently functioning; 3 recipients had no rejection episodes and their UA values ranged from 30,000 to 100,000 U/24 hr during their entire postoperative course. The other two had rejection episodes. In both cases UA decreased to baseline levels 1 and 4 days in advance of the hyperglycemia. After antirejection treatment UA rose again to high values and plasma glucose levels declined. Both patients are currently insulin-independent, with UA values ranging from 10,000 to 200,000 U/24 hr. Both experimentally and clinically UA is an early predictor of pancreas allograft rejection. The institution of early treatment of rejection episodes in dogs, based on UA, significantly improved allograft survival. Urine amylase monitoring in pancreas transplant recipients could lead to an early treatment of rejection and improve graft survival.

Iatrogenic pancreatitis. A fatal complication in the induction therapy for acute lymphocytic leukemia

A patient with acute lymphocytic leukemia developed acute pancreatitis during induction therapy with corticosteroids and asparaginase. Postmortem examination showed changes consistent with hemorrhagic pancreatitis and fat necrosis over the pancreas and omentum. Corticosteroids were thought to be responsible for pancreatitis in this patient since "hemorrhagic pancreatitis" has not been previously described with asparaginase. We recommend careful follow-up of serum and urinary amylase values in patients receiving induction therapy with these agents.

Pancreatitis in childhood

Thirty cases of pancreatitis in children are reviewed. Diagnosis is based on the clinical findings of pancreatic inflammation, laboratory confirmation with elevated serum and/or urinary amylase values, and in some cases surgical or postmortem tissue substantiation. Four major classes of pancreatitis are defined in children: (1) traumatic; (2) systemic-disease associated; (3) drug-induced, caused by drug therapy for various life-threatening diseases, and (4) chronic pancreatitis, with or without an anatomic abnormality. If cases of traumatic pancreatitis are excluded, females outnumber males 5 to 1. A high index of suspicion is necessary to make the diagnosis, and this is very important if the mortality for pancreatitis in children is to be lowered. Awareness and consistent early aggressive intervention should increase the salvage rate.

Blood Amylase and Diabetic Ketoacidosis

To the Editor.— In their article on prolonged high blood amylase levels in a case of diabetic ketoacidosis, Drs vanSonnenberg and Pitchumoni discuss a possible causal connection between diabetes and pancreatitis. Since they refer to Somogyi's pioneer work on low serum amylase levels in diabetic ketoacidosis, it may be of more than historic interest that this puzzling altered amylase level in diabetes had intrigued the investigator as early as 1929. 1 At that time it was already known that, in experimental as well as clinical nonketotic diabetes, urinary amylase values can be low. This was explained by diminished renal filtration. Perhaps vanSonnenberg and Pitchumoni, as clinicians, can take comfort in the fact that, in the experimental phlorizin diabetes of the rabbit, the increase in urine amylase had then also been found to be oddly protracted.

Macroamylasemia: clinical and laboratory features in 7 patients.

The clinical features of patients with macroamylasemia are diverse. A certain correlation between macroamylasemia and the disease of the pancreas or hepato-biliary system may exist, because among 7 patients in this series 4 patients were diagnosed as acute pancreatitis or relapsing pancreatitis and another patient was performed choledochotomy and manipulation of papilla of Vater may had a effect on pancreas. Among other 2 patients, one was completely symptomless and had no abnormal findings and in another the action of anticancer drugs is suspected. The course of macroamylasemia is usually chronic but in this series one patient had acute transient macroamylasemia and another one had intermittent macroamylasemia during exacerbations of pancreatitis. The serum amylase levels are mostly 2-4 times above normal with one exception (192 Somogyi units) and urinary amylase values are low with one exception (1922 Somogyi units) during exacerbation of pancreatitis. Characteristic zymogram of macroamylase on electrophoresis is also reported.

Macroamylasemia in the postoperative patient. A source of confusion and concern.

Macroamylasemia is a recently described condition of unknown cause characterized by elevated serum amylase concentrations without hyperamylasuria. No particular clinical signs or symptoms accompany this finding. However, postoperative determinations of serum amylase in such patients may occasion great alarm, since the hyperamylasemia may be confused with that due to pancreatitis, perforated or ischemic bowel, or other serious condition. The simple practice of determining urinary amylase values at the same time as serum amylase will provide the major clue for diagnosis. A new method for rapid detection of the macroamylase complex found in this syndrome provides a definitive capability for separating patients with macroamylasemia from those with pathologic causes for the elevation of serum amylase.

Amylase in the management of pancreatic trauma.

Serum and urinary amylase values from 63 patients with pancreatic injuries were reviewed and correlated with clinical data. Forty-three patients were treated with debridement and drainage, 15 with distal pancreatectomy, and five with pancreatoduodenectomy. All of the latter survived. Of the 63 patients, six suffered injuries to other major structures and died. Serum amylase levels were elevated preoperatively in only 26% of the patients; postoperatively, they were routinely normal. Urinary amylase (diastase) levels were elevated in 93% of the patients immediately after operation and were the best indicator of postoperative pancreatitis. When nasogastric suction was discontinued on clinical grounds in the face of an elevated diastase level, 11 of 14 patients developed recurrent signs of pancreatitis. In patients with pancreatic injury, postoperative hyperamylasuria is an important indication for continued intensive therapy, including nasogastric suction even in asymptomatic patients.