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)

In order to investigate the changes in phosphoglucose metabolism in acute experimental pancreatitis, the authors utilized the measuring cell NMR spectroscopy. The experimental pancreatitis had been evoked by both the method of ligature of lateral pancreas ducts and that of the duodenal blind loop. These methods evoke a morphological response, namely edematous and necrotizing pancreatitis. Gradual reduction of macroergic phosphate binds and augmentation of anorganic phosphates represent the principal change in NMR spectrum. The clinical picture provides evidence of the exhaustion of highly energetic phosphate compounds which are necessary for the maintenance of integrity of the pancreas tissue in acute experimental pancreatitis. The discussion includes the possibilities and limitations of the NMR spectroscopy.
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PMID:[31P NMR spectroscopy in acute experimental pancreatitis]. 781 17

Data from basic science and clinical studies suggest that hydroxyurea (hydroxycarbamide)-based regimens are effective treatment options for patients with HIV at various stages of disease. In vitro studies of HIV-infected lymphocytes have shown that hydroxyurea: (i) inhibits viral DNA synthesis; (ii) synergistically interacts with nucleoside reverse transcriptase inhibitors (NRTI); and (iii) increases the antiviral activity of didanosine. Clinical studies have confirmed that hydroxyurea in combination with didanosine produces potent and sustained viral suppression in patients with HIV infection. However, some concerns have been recently raised on the use of hydroxyurea in association with NRTI. Hydroxyurea can cause myelosuppression, skin toxicities, mild gastrointestinal toxicity, and abnormalities of renal and liver functions. In addition, hydroxyurea may accentuate the toxic effects of nucleoside analogues. In fact, some clinical data seem to indicate an increased risk of pancreatitis and neuropathy when hydroxyurea is combined with didanosine and stavudine. Since hydroxyurea-related toxicity is dose dependent, a systematic study of hydroxyurea optimal dosage and schedule was initiated to monitor patients for possible nucleoside toxicity. In the Research Institute for Genetic and Human Therapy (RIGHT) 702 study it was shown that a low, well-tolerated hydroxyurea dose (600 mg daily) achieved better antiretroviral activity than higher doses, together with better CD4+ cell count increase and fewer adverse effects. In this paper the effects of hydroxyurea as salvage therapy for heavily pretreated patients with advanced HIV disease are presented. These studies have shown that some patients with extensive pretreatment experience and advanced disease can respond substantially to the addition of hydroxyurea. The addition of hydroxyurea to didanosine does not prevent the emergence of resistance to didanosine; nonetheless, the efficacy of this therapeutic regimen may not be attenuated by the presence of didanosine-resistant HIV mutants. Since CD4 T lymphocyte activation is essential for virus replication and CD8 T lymphocyte activation may contribute to pathogenesis, the combination of hydroxyurea with other drugs may lead to the inhibition of HIV, by blocking the 'cell activation-virus production-pathogenesis' cycle. Clinical data indicate that hydroxyurea may play a role in attenuation of viral rebound and immune reconstitution by decreasing CD4 T cell proliferation, as well as preventing the exhaustion of CD8 T cell populations that may result from excessive activation during HIV infection. While the combination of hydroxyurea with didanosine has provided hope, future studies including those that evaluate optimal dosing and long-term toxicity are needed to define the role for this agent in the treatment of HIV infection.
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PMID:Hydroxyurea in the treatment of HIV infection: clinical efficacy and safety concerns. 1281 30

BACKGROUND The effective and safe treatment of chronic frequently relapsing pancreatitis is challenging. CASE REPORT We present the case of a 63-year-old male patient with severe complications of this variant of the disease: parapancreatitis with the formation of an inflammatory mass, fermentative ascites-peritonitis, 2-sided pleural effusions, sepsis, and cachexia. Conservative treatment was ineffective, and emergency surgery was chosen. A novel surgical procedure - open internal stenting of the main pancreatic duct via pancreatowirsungotomy and duodenotomy - was used successfully in this difficult case. The elimination of pancreatic ductal hypertension and maintenance of maximum physiological pancreatic juice outflow, achieved via surgery, led to rapid improvement in the patient's condition. He was discharged on the 26th day after surgery. The clinical outcome was good at the 2-year follow-up. CONCLUSIONS Open stenting of the main pancreatic duct can be recommended for treating patients similar to the patient described in this paper - having severe complications of CP against the background of a relapse, exhaustion, and being in a severely or critically ill general condition. This surgical procedure is especially important when minimally invasive methods of eliminating pancreatic hypertension are technically unsuccessful or impossible due to the lack of necessary equipment and staff.
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PMID:Open Internal Stenting of the Main Pancreatic Duct as Life-Saving Surgery in a Critically Ill Patient with Chronic Frequently Relapsing Pancreatitis and Pancreatic Ductal Hypertension. 3123 Nov 18

Acute biliary pancreatitis (ABP) with a high mortality rate is an incurable digestive system disease induced by abnormal bile acid regurgitation due to the biliary obstruction. Dehydrocholic acid (DA) alleviates the severity of cholestatic hepatitis related to biliary inflammation, suggesting DA is potential to develop for the incurable ABP management. Here we identified DA potency and explored the underlying mechanism in ABP. Our data showed that DA administration not only reduced typically clinicopathological parameters including serum levels of amylase and lipase but also suppressed pancreatic tissue edema, necrosis and trypsin activation in ABP mice. We also found that DA significantly reduced the necrosis of pancreatic acinar cells induced by sodium taurocholate (NaT). Further experimental data showed the significant inhibitions of DA on mitochondrial membrane potential depolarization, ATP exhaustion, calcium overload and reactive oxygen species (ROS) erupted in acinar cells induced by NaT, indicating DA could avert acinar cell death through protecting the mitochondrial function, scavenging excessive oxidative stress and balancing calcium. The comprehensive study found DA elevated the expression of transcription factor EB (TFEB) in vitro thus to increase the functional lysosome content. Indeed, DA decreased the Microtubule-associated protein light chain 3 (LC3) II/I ratio as well as ubiquitin-binding protein p62 and Parkin expressions in vivo and in vitro, revealing autophagy restoration maybe through the improvement of TFEB-mediated lysosome biogenesis. These data indicate that DA improves ABP through the mitochondrial protection, antioxidant ability enhancement and autophagy recovery. In conclusion, our study proposes a potential therapy strategy for the incurable ABP.
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PMID:Dehydrocholic Acid Ameliorates Sodium Taurocholate-Induced Acute Biliary Pancreatitis in Mice. 3247 20