Chronic asymptomatic pancreatic hyperenzymemia (CAPH) may be associated with different clinical circumstances, both pancreatic and extrapancreatic, ranging from a laboratory abnormality without clinical significance to the rare eventuality of an association with neoplastic lesions. This chapter summarizes the clinical circumstances that can initiate CAPH and provides an algorithm for clinical management. Up to 20% of patients with inflammatory bowel disease have been reported to present pancreatic hyperenzymemia without overt pancreatic disease. These enzyme elevations can be explained by subclinical extraintestinal involvement of the pancreas and by drug-induced hyperenzymemia, but some authors have proposed a more general mechanism based on increased reabsorption of amylase or lipase through the inflamed “leaky” gut. In 1978, different authors began reporting cohorts of patients with chronic increases in serum pancreatic enzymes. This elevation was frequently of nonpancreatic origin and that when isoenzyme profiling presumed a pancreatic origin, it often occurred in the absence of pancreatic abnormalities.
Asymptomatic Chronic Elevation of Serum Pancreatic Enzymes: How to Deal with It? / Vanella, G.; Arcidiacono, P. G.; Capurso, G.. - (2021), pp. 158-167. [10.1002/9781119570097.ch22]
Asymptomatic Chronic Elevation of Serum Pancreatic Enzymes: How to Deal with It?
Vanella G.Primo
;Arcidiacono P. G.Penultimo
;Capurso G.
2021-01-01
Abstract
Chronic asymptomatic pancreatic hyperenzymemia (CAPH) may be associated with different clinical circumstances, both pancreatic and extrapancreatic, ranging from a laboratory abnormality without clinical significance to the rare eventuality of an association with neoplastic lesions. This chapter summarizes the clinical circumstances that can initiate CAPH and provides an algorithm for clinical management. Up to 20% of patients with inflammatory bowel disease have been reported to present pancreatic hyperenzymemia without overt pancreatic disease. These enzyme elevations can be explained by subclinical extraintestinal involvement of the pancreas and by drug-induced hyperenzymemia, but some authors have proposed a more general mechanism based on increased reabsorption of amylase or lipase through the inflamed “leaky” gut. In 1978, different authors began reporting cohorts of patients with chronic increases in serum pancreatic enzymes. This elevation was frequently of nonpancreatic origin and that when isoenzyme profiling presumed a pancreatic origin, it often occurred in the absence of pancreatic abnormalities.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.