Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An unusual case of diabetes secondary to acute pancreatitis in a boy with end-stage renal failure receiving continuous ambulatory peritoneal dialysis (CAPD) is described. A hyperglycaemic, hyperosmolar pre-coma developed, aggravated by associated hypercalcaemia. The glucose content of the dialysis fluid contributed to the hyperglycaemia, which settled as the pancreatitis resolved and lower glucose concentration dialysis fluid was used. Our experience suggests that pancreatic dysfunction should be considered where significant hyperglycaemia occurs during peritoneal dialysis.
 ...
PMID:Non-ketotic hyperosmolar diabetic pre-coma due to pancreatitis in a boy on continuous ambulatory peritoneal dialysis. 354 Jun 93

Following consideration of the nosological role of hyperglycemic states in psychiatry the case report of a fifty-five year-old patient is presented suffering from fatty cell degeneration of the liver and a relapsing pancreatitis due to chronic alcoholism. After a long period of abstinence without previously known diabetes mellitus a sudden ketoacidotic coma developed with maximum serum glucose level of 2020 mg%. Having emerged during coma treatment Wernicke's encephalopathy passed into Korsakoff's syndrome the main features of which remained unchanged for more than one year. In this case thiamine deficiency of different pathogenetical origin is discussed: defective exogeneous availability due to malabsorption; depletion of endogeneous thiamine stores due to enlarged requirements for glucose oxidation during coma therapy; antimetabolic effects to thiamine by nitroimidazole-derivatives administered parenterally.
 ...
PMID:[Diabetic coma and Wernicke-Korsakoff syndrome. On the clinical significance of acquired thiamine deficiency]. 359 52

The treatment is described of 17 patients with presumed viral hepatitis who developed hepatic coma unresponsive to standard conservative measures. Five patients were considered for treatment by exchange transfusion. Four were treated, with transient improvement in two, but all died. Nine patients were considered for treatment by heterologous liver perfusion. Six were treated, with transient improvement in two and complete recovery in one. The last patient remains well 12 months later. Dialysis in four patients had no effect on the coma; the addition of albumin to the dialysate did not increase the extraction of bilirubin. The clinical course in most cases was irregular. Complications were common, the most important being cerebral oedema with medullary coning, bleeding, bacterial infection, hypoglycaemia, and pancreatitis. Heterologous liver perfusion was the most efficient method of removing bilirubin. However, it is not yet clear whether it is more effective than exchange transfusion in the treatment of the patient.
 ...
PMID:Management of hepatic coma complicating viral hepatitis. 530 40

Increased levels of serum amylase were found in 14 out of 34 patients (41%) with coma due to acute liver failure, in 8 out of 55 patients (14%) with hepatic encephalopathy, and in 5 out of 10 patients with a mixed pathogenesis. In 4 patients of the first group (11.7%) and 4 of the second group (7%) pancreatitis was diagnosed at post mortem. The pathogenesis of pancreatitis concomitant with liver failure is unclear. Virus infection and intoxication may do damage to both organs; hemodynamic factors, coagulation defects, and derangements of metabolism may play a role as well.
 ...
PMID:[Concomitant pancreatitis in hepatic coma]. 619 62

Valproic acid, used alone or in combination with other anticonvulsants in 100 children with epilepsy, improved seizure control in all age groups. Mean improvement in seizure control was 82%. Petit mal seizures responded best, but other types of seizures, even with associated mental and physical handicaps, also responded well. A substantial improvement in alertness and behavior often occurred. Leukopenia (27%) and an elevated SGOT value (44%) were frequent but transient. Other side effects included alopecia (1), gastrointestinal distress with vomiting (7), pancreatitis (1), thrombocytopenia (1), edema (2), and coma (2). Three severely retarded children with frequent seizures died while receiving valproic acid, but it is not clear that death was caused by valproic acid. Children must be monitored carefully for potential toxic effects, and drug interactions with other anticonvulsants may cause problems in treatment.
 ...
PMID:Valproic acid therapy in childhood epilepsy. 677 26

The authors report a case of severe hypertriglyceridemia (148.5 mmol/l) in a 27-year-old woman admitted for coma of unknown origin. Initial investigations revealed ketoacidosis, pancreatitis and noncardiogenic pulmonary edema. The diabetes was unknown. Ketoacidosis was rapidly controlled. The hypertriglyceridemia was corrected by one course of plasma exchange (4,400 ml) during which the patient returned to consciousness. The patient recovered without any sequelae. Only 2 similar cases, treated by plasma exchange, have been reported in the literature until now.
 ...
PMID:Treatment by plasma exchange of a patient with hyperlipidemia and diabetic ketoacidosis with lesional pulmonary edema and acute pancreatitis. 681 94

Adamantinoma of the tibia is a rare bone lesion, in which it is impossible to predict the biological behaviour. A case of extremely late local recurrence and lung metastasis is presented. Additionally, the patient developed pneumothorax on the right side months before intrapulmonary metastasis could be detected by X ray. Finally 1 week before her death the young woman suffered from paraneoplastic severe hypercalcemia leading to hypercalcemic coma and pancreatitis.
 ...
PMID:An unusual case of adamantinoma of long bones. 716 13

Hyperamylasemia of pancreatic origin has been noted in patients with severe head injury without abdominal trauma or evidence of pancreatitis. Thirty-eight patients with intracranial bleeding of various types were evaluated for elevated pancreatic amylase and lipase enzymes without associated pancreatitis. Twenty-five patients had elevated serum lipase; 17 of 25 also had elevated amylase without pancreatitis. Most lipase elevations occurred earlier than those of amylase. Six clinical variables--mannitol, ceftriaxone, nimodipine, steroids, Glasgow Coma Score, and total parenteral and enteral hyperalimentation--were evaluated to determine relationship to the enzyme elevations. A significant relationship exists between patients not treated with steroids and elevated lipase and amylase enzyme activities. Multivariate analysis revealed a significant interaction between lipase elevation and decreasing Glasgow Coma Score, indicative of increasing severity of intracranial bleeding. Proposed causes of enzyme elevations in intracranial bleeding include vagal stimulation, altered modulation of the central control of pancreatic enzyme release, and release of cholecystokinin from the brain. Physician awareness of the association of intracranial bleeding with the elevation of amylase and lipase without pancreatitis can save the patient needless cost and manipulation.
 ...
PMID:Significance of elevated pancreatic enzymes in intracranial bleeding. 752 51

Painful acute pancreatitis masking pancreatic carcinoma and painless acute pancreatitis with shock or coma as leading symptoms have been described before. We report a first case of almost-painless pancreatitis mimicking pancreatic carcinoma with spontaneous normalization of symptoms and biochemical as well as imaging procedure findings.
 ...
PMID:Painless acute pancreatitis mimicking pancreatic carcinoma. 779 99

Since our last report on valproate (VPA)-related hepatotoxicity in 1988, 8 other children have died of VPA-associated liver failure in Germany and Switzerland. We compared the clinical course of these children with that of 6 children with a reversible outcome of severe hepatotoxicity related to VPA. Thirty-five percent of patients with fatal liver failure were normally developed, 23.5% were receiving VPA monotherapy, and 35.3% were aged < or = 2 years. The initial clinical symptoms of VPA-related hepatotoxicity were nausea, vomiting, apathy or coma, and increasing seizures in more than 50% of patients, in combination with febrile infections at onset of symptoms. As compared with the series of German patients reported in 1988, one third of the fatalities occurred after the first 6 months of therapy as compared with 6% in the 1988 series. Clinical symptoms and laboratory findings were the same in patients with reversible and with fatal outcome. Early or immediate withdrawal of VPA after the first signs of VPA-associated hepatotoxicity may be responsible for the increased number of children who recovered after VPA-related severe liver failure. The pathogenesis of liver failure during VPA treatment remains unknown; metabolic defects and cofactors such as polypharmacy or infections have become increasingly likely to contribute by depleting intracellular CoA. Worldwide, 132 patients have died of VPA-associated liver failure and/or pancreatitis. Because a group at risk for fatalities with VPA cannot be defined precisely, patients treated with VPA and their families must be made well aware of the clinical symptoms of hepatotoxicity such as apathy, vomiting, or increased seizure frequency, especially in the presence of febrile infections. Laboratory tests and clinical controls during the first 6 months of therapy should not be neglected.
 ...
PMID:Severe hepatotoxicity during valproate therapy: an update and report of eight new fatalities. 792 43


<< Previous 1 2 3 4 5 Next >>