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)

Cerebral fat embolism was established as the cause of death in a 34-year-old man with acute pancreatitis. Encephalopathy complicating pancreatitis may be due to hypoxia secondary to pulmonary fat embolism, cerebral fat embolism, or the complicating syndromes of disseminated intravascular coagulation or hyperosmolality.
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PMID:Pancreatic encephalopathy. 32 Jun 76

Hyponatremia and rapid correction of hyponatremia have often been proposed as pathogenetic mechanisms in the development of central pontine myelinolysis. We report the case of a 36-year-old man who died with acute hemorrhagic pancreatitis with the autopsy findings of central pontine and extrapontine myelinolysis. The patient had developed moderate serum hyperosmolality during the first 3 days of his illness, and it persisted until his death 20 days later. Hyponatremia or rapid correction of hyponatremia never occurred. These observations suggest that osmotic stress and oligodendrocyte topography rather than rapid correction of hyponatremia may be the key to the development of central pontine myelinolysis (osmotic myelinolysis).
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PMID:Osmotic stress, osmotic myelinolysis, and oligodendrocyte topography. 258 51

Diabetic lipemia with and without acute pancreatitis in chronic alcoholism. A report of 4 cases. Diabetic lipemia was observed in 4 chronic alcoholic men after ingestion of high doses of alcohol and/or sugar-rich beverages, including one patient who was treated for insulin-dependent diabetes. None had a previous history of serum lipid disturbances. All had marked hyperglycemia, hyperosmolality and hypertriglyceridemia (mean: 60.8 mmol/l), 2 of undetermined type and 2 of type IV with eruptive xanthomas. Factitious hyponatremia was present in 3 cases, but true serum sodium was normal (138 mmol/l) or elevated (154, 156, 182 mmol/l) after correction. Three patients developed acute pancreatitis ascribed to high serum triglyceride levels and/or to alcohol ingestion. Serum and urine amylase activity was inhibited by hypertriglyceridemia. The diagnosis of pancreatitis was assessed twice by echography and computed tomographic scan, and once by tomographic scan and an elevation of the amylase on creatinine clearance ratio. It is likely that hypertriglyceridemia predisposed these patients to develop pancreatitis, alcoholism being a precipitating factor. We suggest that the diagnosis of acute pancreatitis should be systematically considered in any case of diabetic lipemia without true hyponatremia.
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PMID:[Diabetic hyperlipemia with or without acute pancreatitis in patients with chronic alcoholism. A study of 4 cases]. 274 Jun 61