RESUMEN
CONTEXT: The elevation of serum amylase and lipase are generally associated with pancreatic diseases. However they can be associated with different pathologies unrelated with amylase and lipase. CASE REPORT: This paper aims to report a case of a patient diagnosed with nonspecific hyperamylasemia and warn of this possibility in the differentiation of hyperamylasemia. CONCLUSION: The correct diagnosis of silent hyperamylasemia is important in order to determine whether there is the risk of pancreatic disease or if we are just ahead of a benign hyperenzymemia.
Asunto(s)
Amilasas/sangre , Hiperamilasemia/sangre , Adulto , Diagnóstico Diferencial , Femenino , Humanos , Hiperamilasemia/diagnóstico , Hiperamilasemia/enzimología , Páncreas/diagnóstico por imagen , Páncreas/enzimología , Enfermedades Pancreáticas/sangre , Enfermedades Pancreáticas/diagnóstico , Enfermedades Pancreáticas/enzimología , Radiografía , UltrasonografíaRESUMEN
BACKGROUND AND OBJECTIVES: It was proposed that occult pancreaticobiliary reflux (OPBR) was associated with precancerous mucosal changes in the gallbladder, hence the importance of this disorder. There are no published reports investigating the incidence of OPBR in patients operated on for the entire spectrum of benign gallbladder diseases and gallbladder cancer. Our aim was to determine the incidence of OPBR and measure the levels of active pancreatic enzymes (amylase and lipase) in gallbladder bile of patients undergoing cholecystectomy for benign and malignant gallbladder diseases. METHODS: One hundred eight patients with normal pancreaticobiliary junction evidenced by operative cholangiography were included in the study. RESULTS: According to gallbladder bile amylase and lipase levels, 84.2% and 89% patients respectively had OPBR. OPBR was present in all gallbladder cancer patients; in these patients the biliary levels of amylase and lipase were significantly higher than the levels found in patients with benign gallbladder pathology (P < 0.0001). CONCLUSIONS: OPBR could lead to inflammatory changes of the biliary epithelium and progress towards the development of precancerous mucosal changes and gallbladder cancer. The reason why such high levels of pancreatic enzymes are regurgitated into the biliary tree of patients with gallbladder cancer should be clarified.
Asunto(s)
Amilasas/análisis , Enfermedades de los Conductos Biliares/etiología , Reflujo Biliar/etiología , Bilis/enzimología , Enfermedades de la Vesícula Biliar/complicaciones , Neoplasias de la Vesícula Biliar/complicaciones , Lipasa/análisis , Enfermedades Pancreáticas/etiología , Adulto , Anciano , Anciano de 80 o más Años , Enfermedades de los Conductos Biliares/enzimología , Reflujo Biliar/enzimología , Colecistitis/complicaciones , Colecistitis/enzimología , Femenino , Enfermedades de la Vesícula Biliar/enzimología , Humanos , Masculino , Persona de Mediana Edad , Enfermedades Pancreáticas/enzimologíaRESUMEN
Streptozotocin-induced pancreatic damage involves nitric oxide (NO) and prostaglandins (PGs) overproduction. In this work we aim to evaluate a putative relationship between the elevated NO levels and the altered prostanoid production in pancreatic tissue from streptozotocin-diabetic rats. Total NOS activity and nitrate/nitrite pancreatic levels in tissues from diabetic rats are decreased when the cyclooxygenase (COX) inhibitor indomethacin (INDO) is added to the incubating medium, while the addition of PGE(2)increases nitrate/nitrite production and NOS levels. INDO and PGE(2)selectively affect Ca(2+)-dependent NOS (iNOS) activity in diabetic tissues, and they have not been able to modify nitrate/nitrite levels, iNOS or Ca(2+)-dependent (cNOS) in control tissues. When the NOS inhibitor L-NMMA was present in the incubating medium, control pancreatic [(14)C]-Arachidonic Acid ([(14)C]-AA) conversion to 6-keto PGF(1 alpha)and to TXB(2)was lower, and PGF(2 alpha), PGE(2)and TXB(2)production from diabetic tissues diminished. The NO donors, spermine nonoate (SN) and SIN-1, enhanced TXB(2)levels in control tissues, while PGF(2 alpha), PGE(2)and TXB(2)levels from diabetic tissues were increased. PGE(2)production from control and diabetic tissues was assessed in the presence of the NO donor SN plus INDO or NS398, a specific PG synthase 2 inhibitor. When SN combined with INDO or NS398 was added, the increment of PGE(2)production was abolished by both inhibitors in equal amounts, indicating that the activating effect of nitric oxide is exerted on the inducible isoform of cyclooxygenase. In the diabetic rat, prostaglandins and NO seem to stimulate the generation of each other, suggesting a lack of regulatory mechanisms that control the levels of vasoactive substances in acute phase of beta-cell destruction.
Asunto(s)
Isoenzimas/farmacología , Óxido Nítrico Sintasa/metabolismo , Enfermedades Pancreáticas/metabolismo , Prostaglandina-Endoperóxido Sintasas/farmacología , Animales , Ácido Araquidónico/metabolismo , Radioisótopos de Carbono , Ciclooxigenasa 2 , Inhibidores de la Ciclooxigenasa 2 , Inhibidores de la Ciclooxigenasa/farmacología , Diabetes Mellitus Experimental/enzimología , Diabetes Mellitus Experimental/metabolismo , Diabetes Mellitus Experimental/patología , Dinoprostona/biosíntesis , Modelos Animales de Enfermedad , Interacciones Farmacológicas , Femenino , Isoenzimas/antagonistas & inhibidores , Óxido Nítrico/metabolismo , Óxido Nítrico Sintasa/efectos de los fármacos , Óxido Nítrico Sintasa de Tipo II , Enfermedades Pancreáticas/inducido químicamente , Enfermedades Pancreáticas/enzimología , Enfermedades Pancreáticas/patología , Prostaglandinas/metabolismo , Prostaglandinas/farmacología , Ratas , Ratas Wistar , EstreptozocinaRESUMEN
We compared pancreatic acinar and ductal secretion in two patients with Johanson-Blizzard syndrome, age-matched control subjects, and patients with other primary pancreatic diseases. Patients with Johanson-Blizzard syndrome had preservation of ductular output of fluid and electrolytes, as in patients with Shwachman syndrome but differing from those with cystic fibrosis, who have a primary ductular defect. They also had decreased acinar secretion of trypsin, colipase and total lipase, and low serum immunoreactive trypsinogen levels, consistent with a primary acinar cell defect.
Asunto(s)
Insuficiencia Pancreática Exocrina/fisiopatología , Páncreas/fisiopatología , Estudios de Casos y Controles , Colipasas/análisis , Consanguinidad , Fibrosis Quística/enzimología , Fibrosis Quística/fisiopatología , Insuficiencia Pancreática Exocrina/enzimología , Femenino , Humanos , Lactante , Recién Nacido , Lipasa/análisis , Síndromes de Malabsorción/enzimología , Síndromes de Malabsorción/fisiopatología , Masculino , Páncreas/enzimología , Páncreas/metabolismo , Enfermedades Pancreáticas/enzimología , Enfermedades Pancreáticas/fisiopatología , Conductos Pancreáticos/enzimología , Conductos Pancreáticos/metabolismo , Síndrome , Tripsina/análisis , Tripsinógeno/sangreRESUMEN
These data suggest that an improved understanding of the relationship between high dietary carbohydrate and the rate of lipid peroxidation may give some insight into possible treatment modalities for pancreatic damages and may shed light on molecular mechanisms underlying certain pathological processes. High dietary carbohydrate lesions are age related and induced alterations on ceruloplasmin, phospholipids, total proteins, copper and zinc serum levels. Significantly increased serum and pancreatic amylase, and lipoperoxide determinations were observed in 20 month old rats. Cu-Zn superoxide dismutase was decreased in these animals. Daily injection of Cu-Zn superoxide dismutase conjugated with polyethylene glycol (SOD-PEG) prevented the serum and pancreatic changes, indicating that superoxide radical is an important intermediate to high dietary carbohydrate lesion.