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)

It is well established that damage to the outer membrane of cells is a common phenomenon allowing abnormal transmission of substances into the cytosol. Penetration of albumin into acinar cells has been detected in experimental acute pancreatitis, raising the possibility that membrane damage is a very early event, potentially representing the first changes leading to pancreatitis. To determine if direct damage to the cell membrane is a key factor during induction of acute pancreatitis, thus altering the balance of extra- and intracellular substances, fluorescein-dextran was administered with supramaximal doses of caerulein via the jugular vein or by injection directly into the pancreas. This tracer rapidly penetrates into cells. Two patterns of tracer penetration are observed: cytosolic and vesicular/vacuolar. Fluorescein-dextran administered intravenously with caerulein penetrates into the cytosol of acinar cells within 10 min. Strong cytoplasmic fluorescence occurs within 5 min after direct injection. It may be concluded that supramaximal caerulein, administered in vivo, damages the cell membrane of acinar cells, allowing large molecules to enter the cytosol. Thus Ca(2+) and other substances may enter the cells in abnormally high concentrations, initiating the cellular changes characteristic of pancreatitis. The results raise the question whether membrane wounding may play a role in the initiation of human pancreatitis.
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PMID:Cell wounding in early experimental acute pancreatitis. 1476 92

27 year old patient with a history of alcohol abuse after consumption of fat meal and wine following epigastric pain noticed sudden bilateral visual loss: right eye logMAR 0, 94, left eye logMAR 1, 22. Retinal examination revealed massive edema in the central part of the retina, multiple cotton wool spots in the posterior pole peripapillary and flame-shaped hemorrhages. On the OCT, there was edema most of all in the inner part of the retina, but also subretinal, hyperreflectivity in the nerve fibre layers corresponding to massive cotton wool spots. Fluorescein angiography in the early phases showed hypofluorescent ischemic areas of the retina subsequently leakage developed in the late phases. Immediately after antibiotic and spasmoanalgetic treatment of the pancreatitis visual acuity improved and 2 months after beginning of the therapy visual acuity is logMAR 0 bilateraly. We proposed that the most suspected cause of Purtscher-like retinopathy in this case is fat embolism.
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PMID:[Purtscher-like retinopathy in acute alcoholic pancreatitis: fluorescein angiography and optical coherence tomography findings]. 2139 69