Serum Activity Of Lipase Research Articles

Administration of Warfarin Inhibits the Development of Cerulein-Induced Edematous Acute Pancreatitis in Rats.

Acute pancreatitis (AP) is a severe disease with high morbidity and mortality in which inflammation and coagulation play crucial roles. The development of inflammation leads to vascular injury, endothelium and leukocytes stimulation, and an increased level of tissue factor, which results in the activation of the coagulation process. For this reason, anticoagulants may be considered as a therapeutic option in AP. Previous studies have shown that pretreatment with heparin, low-molecular-weight heparin (LMWH), or acenocoumarol inhibits the development of AP. The aim of the present study was to check if pretreatment with warfarin affects the development of edematous pancreatitis evoked by cerulein. Warfarin (90, 180, or 270 µg/kg/dose) or saline were administered intragastrically once a day for 7 days consecutively before the induction of AP. AP was evoked by the intraperitoneal administration of cerulein. The pre-administration of warfarin at doses of 90 or 180 µg/kg/dose reduced the histological signs of pancreatic damage in animals with the induction of AP. Additionally, other parameters of AP, such as an increase in the serum activity of lipase and amylase, the plasma concentration of D-dimer, and interleukin-1β, were decreased. In addition, pretreatment with warfarin administered at doses of 90 or 180 µg/kg/dose reversed the limitation of pancreatic blood flow evoked by AP development. Warfarin administered at a dose of 270 µg/kg/dose did not exhibit a preventive effect in cerulein-induced AP. Conclusion: Pretreatment with low doses of warfarin inhibits the development of AP evoked by the intraperitoneal administration of cerulein.

Astaxanthin and Coenzyme Q10 are not synergistic against oxidative damage in cerulein-induced acute pancreatitis

Background/Aim: The anti-inflammatory effects of Astaxanthin (ATX) and Coenzyme Q10 (Ubiquinone) are studied in different inflammation models. The study aims to investigate the synergistic effect of astaxanthin and Coenzyme Q10 in a rat model of acute pancreatitis. Methods: Twenty-four female Wistar rats were grouped as control (C), carrier-treated control (AP), astaxanthin-treated (ATX; 40 mg/kg), astaxanthin+coenzyme Q10- treated (ATX+Q10; 40 mg/kg and 1 gr/kg) groups. Cerulein was administered (50 µg/kg) twice, one hour apart. Seven hours after the first cerulein injection, the rats were sacrificed. Pancreatic oxidative damage was evaluated with an increase in the serum activity of lipase and amylase, tissue levels of myeloperoxidase activity (MPO), malondialdehyde (MDA), luminol and lucigenin and decrease of glutathione. Results: In all AP groups, MDA and MPO increased while GSH decreased (P<0.001). ATX and ATX+Q10 both decreased MDA and MPO (P<0.001) and increased GSH (P<0.01). Both therapies significantly increased luminol levels (P<0.001, and P<0.01, respectively). Lucigenin markedly decreased in the ATX+Q10 group (P<0.01). Conclusion: Antioxidant combination therapy does not alleviate oxidative damage in pancreatic tissue better than astaxanthin alone.

Myrtus communis leaf extract protects against cerulein-induced acute pancreatitis in rats.

In this study, the aim was to examine the potential protective effects of Myrtus communis subsp. communis leaf ethanol extract (MC) treatment against acute pancreatitis (AP) in rats. Thirty-two rats were grouped as the saline-pretreated control (C), MC-pretreated control (MC), saline-pretreated AP (AP), and MC-pretreated AP (MC+AP) groups. To induce AP, cerulein was administered (50µg/kg) two times. The rats were given MC for 14days before cerulein injection. Six hours after the final cerulein injection, the rats were sacrificed. Pancreatic damage was associated with an increase in the serum activity of lipase and amylase, the pancreatic activity of myeloperoxidase, and the pancreatic level of malondialdehyde, interleukin-1β, and interleukin-6. AP also led to a decrease in the pancreatic level of anti-inflammatory interleukin-10 and glutathione. Pretreatment with MC before the induction of AP significantly reduced the pancreatic damage observed during the histological examination as well as reversed the biochemical changes evoked by AP. PRACTICAL APPLICATIONS: Acute pancreatitis is characterized by high mortality (average about 5%; severe cases may reach about 30%). The current treatment for acute pancreatitis is mainly symptomatic. The introduction of herbal drugs may lead to the development of a new strategy in the treatment of this disease. This study revealed that MC reduced pancreatic injury by decreasing pro-inflammatory cytokines, increasing antioxidant capacity and anti-inflammatory cytokine, IL-10. To the authors' knowledge, this research is the first report showing that MC inhibits the development of AP. This observation suggests that MC may be useful in the prevention and the treatment of AP in clinical settings.

Therapeutic Effect of Low Doses of Acenocoumarol in the Course of Ischemia/Reperfusion-Induced Acute Pancreatitis in Rats.

Intravascular activation of coagulation is observed in acute pancreatitis and is related to the severity of this inflammation. The aim of our study was to evaluate the impact of acenocoumarol therapy on the course of acute pancreatitis induced in male rats by pancreatic ischemia followed by reperfusion. Acenocoumarol at a dose of 50, 100, or 150 µg/kg/dose was administered intragastrically once a day, starting the first dose 24 h after the initiation of pancreatic reperfusion. Results: Histological examination showed that treatment with acenocoumarol reduces pancreatic edema, necrosis, and hemorrhages in rats with pancreatitis. Moreover, the administration of acenocoumarol decreased pancreatic inflammatory infiltration and vacuolization of pancreatic acinar cells. These findings were accompanied with a reduction in the serum activity of lipase and amylase, concentration of interleukin-1β, and plasma d-Dimer concentration. Moreover, the administration of acenocoumarol improved pancreatic blood flow and pancreatic DNA synthesis. Acenocoumarol given at a dose of 150 µg/kg/dose was the most effective in the treatment of early phase acute pancreatitis. However later, acenocoumarol given at the highest dose failed to exhibit any therapeutic effect; whereas lower doses of acenocoumarol were still effective in the treatment of acute pancreatitis. Conclusion: Treatment with acenocoumarol accelerates the recovery of ischemia/reperfusion-induced acute pancreatitis in rats.

Is the pancreas affected in patients with septic shock? — a prospective study

Hyperamylasemia can be observed anecdotally during the course of severe sepsis or septic shock. This study aimed to investigate the possibility of pancreatic involvement in patients with septic shock using serum pancreatic enzyme determinations and imaging techniques in 21 consecutive patients with septic shock and 21 healthy subjects as controls. The serum activity of pancreatic amylase and lipase was assayed initially in all subjects and 24 and 48 hours after the initial observation in the 21 patients with septic shock. All patients also underwent radiological examination to detect pancreatic abnormalities. The serum activity of pancreatic amylase was significantly higher in the 21 patients with septic shock than in the 21 control subjects during the study period, while the serum activity of lipase was similar to that of the control subjects. Amylase and lipase serum activity did not significantly changed throughout the study period in the 21 patients with septic shock. None of the patients with pancreatic hyperenzymemia had clinical signs or morphological alterations compatible with acute pancreatitis. The presence of pancreatic hyperenzymemia in septic shock patients is not a biochemical manifestation of acute pancreatic damage, and the management of these patients should be dependent on the clinical situation and not merely the biochemical results.

Involvement of sensory nerves in the protective effect of growth hormone on acute pancreatitis

Growth hormone (GH) has been shown to protect the intestinal barrier integrity and to stimulate the production of insulin-like growth factor 1 (IGF-1), which inhibits the development of acute pancreatitis. Sensory nerves are implicated in the protection of pancreatic tissue against acute inflammation. The aim of this study was to investigate the influence of exogenous GH on acute pancreatitis (AP) and to assess the involvement of sensory nerves and IGF-1 in above effect. Studies were performed on Wistar rats. AP was induced by subcutaneous administration of caerulein (25 μg/kg) to the conscious animals. GH (1 or 2 mg/kg) was administered to the rats as an intraperitoneal injection 30 min prior to the start of AP. To deactivate sensory nerves capsaicin was given at total dose of 100 mg/kg 10 days before the experiments. AP was confirmed by histological examination and manifested by the significant rises of pancreatic weight, and serum activities of lipase, TNFα and IL-10 (by 550%, 300% and 50%, respectively), whereas IGF-1 blood concentration was markedly reduced. Administration of GH prior to the caerulein infusion significantly increased GH, IGF-1 and IL-10 blood levels, attenuated harmful effects of AP and reduced histological manifestations of pancreatitis in the rats with intact sensory nerves. This was accompanied by the reduction of serum lipase, and TNFα activities. In the AP rats with capsaicin-deactivated sensory nerves GH failed to protect the pancreas against acute damage and, as a consequence of above deactivation, IGF-1 was low. Conclusion GH modulates the development of acute pancreatitis in the presence of active sensory nerves probably via stimulation of IGF-1 release.

Lipasa y amilasa total y sus isoenzimas como marcadores de daño pancreático en pacientes tratados con fármacos antiepilépticos

The study of the serum lipase and total amylase and its isoenzymes as biochemical markers of pancreatic injury in patients treated with valproic acid and other enzyme-inducing antiepileptic drugs. The serum activities of lipase and total amylase and its isoenzymes were determined in 41 patients treated in monotherapy with valproic acid, 50 patients in mono/polytherapy with phenytoin, phenobarbital and carbamazepine, and 30 healthy controls. In the first group of patients a clinically significant difference in relation to the control group was not obtained for any of the enzyme activities studied; however, in the group of patients treated with enzyme-inducing antiepileptic drugs clinically significant differences were obtained for lipase and pancreatic amylase. In this group of patients, the activity of pancreatic amylase was clearly increased in two cases (4%), suggesting the existence of a pancreatic damage. In the patients studied, the total amylase showed a poor specificity as a biochemical marker for pancreatic injury, and the greater serum activity observed in one case corresponds to an increase of the salivar isoenzyme. The sensitivity of the lipase is smaller than amylase pancreatic isoenzyme. In patients treated with antiepileptic drugs, the determination of the pancreatic isoenzyme of amylase would be of interest even in absence of clinical signs for acute pancreatitis.

Feline Exocrine Pancreatic Disorders

Despite the uncommon clinical diagnosis, cats frequently suffer from disorders of the exocrine pancreas. Pancreatitis is the most common feline exocrine pancreatic disorder. Pancreatitis can be acute or chronic and mild or severe. The etiology of most cases of feline pancreatitis is idiopathic. Some cases have been associated with severe abdominal trauma, infectious diseases, cholangiohepatitis, and organophosphate and other drug intoxication. The clinical presentation of cats with pancreatitis is nonspecific. Vomiting and signs of abdominal pain, which are the clinical signs most commonly observed in humans and dogs with pancreatitis, are only uncommonly observed in cats with pancreatitis. Routine laboratory findings are also nonspecific. Abdominal ultrasonography is a valuable diagnostic tool in feline patients with pancreatitis. Serum activities of lipase and amylase are rarely increased in cats with pancreatitis; however, these cats often have elevated serum fTLI concentrations. The goals of management are removal of the inciting cause, provision of supportive and symptomatic therapy, and careful monitoring for and aggressive treatment of systemic complications. Exocrine pancreatic insufficiency is a syndrome caused by insufficient synthesis of pancreatic digestive enzymes by the exocrine portion of the pancrease. The clinical signs most commonly reported are weight loss, loose and voluminous stools, and greasy soiling of the hair coat. Serum fTLI is subnormal in affected cats. Treatment of cats with EPI consists of enzyme supplementation with powdered pancreatic extracts or raw beef pancreas. Many cats with EPI have concurrent small intestinal disease. Most cats with EPI also have severely decreased serum cobalamin concentrations and may require parenteral cobalamin supplementation. Pancreatic adenocarcinoma is the most common neoplastic condition of the exocrine pancreas in the cat. At the time of diagnosis, the tumor has already metastasized in most cases, and the prognosis is poor. Pancreatic pseudocyst, pancreatic abscess, pancreatic parasites, pancreatic bladder, and nodular hyperplasia are other exocrine pancreatic disorders, that are less commonly seen in cats.

Serum lipase and amylase activity after endoscopic retrograde pancreatography (author's transl)

Serum activities of lipase and amylase were measured in 11 patients at short time intervals (-10 min; + 10, 30, 60 min; 2,3,4,6,8,24,48 hours) after an endoscopic retrograde pancreatography. Lipase activity increased rapidly in 9 patients in 10 min after the contrast instillation and obtained its maximum at the first hour of investigation. Amylase activity elevation occurred in 5 patients only and was significantly lower than that of lipase with a flat peak at 1-6 hours.