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)

We describe the case of a 23-year-old woman with a mild form of systemic lupus erythematosus who presented a febrile illness rapidly followed by general worsening, neurologic involvement, renal failure and coma. While hospitalized in the intensive care unit she also suffered from acute pancreatitis, microangiopathic hemolitic anemia, thrombocytopenia and prolongation of clotting times. Despite aggressive treatment the patient died at day 17 of hospitalization in the intensive care unit. At autopsy necrotico-hemorragic pancreatitis, diffuse pneumonia, peritonitis and cerebral edema were present. Most striking was the presence of invasive aspergillosis, which was detected in all organs examined. In this case thrombotic thrombocytopenic purpura, invasive aspergillosis and multiorgan failure including acute pancreatitis were present. The relationship between the three entities is complex, and it is difficult to establish which of the different events took place first and triggered the others.
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PMID:A fatal case of systemic lupus erythematosus complicated by acute pancreatitis, invasive aspergillosis and features of thrombotic thrombocytopenic purpura. 1276 8

We report the survival of a 15-year-old girl in whom clinical rabies developed one month after she was bitten by a bat. Treatment included induction of coma while a native immune response matured; rabies vaccine was not administered. The patient was treated with ketamine, midazolam, ribavirin, and amantadine. Probable drug-related toxic effects included hemolysis, pancreatitis, acidosis, and hepatotoxicity. Lumbar puncture after eight days showed an increased level of rabies antibody, and sedation was tapered. Paresis and sensory denervation then resolved. The patient was removed from isolation after 31 days and discharged to her home after 76 days. At nearly five months after her initial hospitalization, she was alert and communicative, but with choreoathetosis, dysarthria, and an unsteady gait.
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PMID:Survival after treatment of rabies with induction of coma. 1776 4

The clinical features, complications, and pharmacokinetics of intentional acute valproic acid (VPA) overdoses are described. Alteration in fatty acid metabolism is evaluated and therapy-induced changes are discussed. Central nervous system features were the predominant clinical manifestations (6/6), followed by respiratory failure (5/6) and multiorgan failure (2/6). Mechanical ventilation was required in 5 of 6 patients because of respiratory depression or deep coma. Hemodialysis was applied in 4/6 of the cases due to hyperammonemia, worsening neurologic condition, or organ dysfunction. Cerebral edema and hemorrhagic pancreatitis ensued in 2/6 of the patients and ICU mortality was 2/6. VPA peak levels ranged from 520 to 1700 mg/L with a mean of 1127 mg/L. Ammonia was elevated in all cases with a mean of 550 microg/dL. All patients showed signs of impaired mitochondrial beta-oxidation with increase of medium- and long-chain acylcarnitines in serum. Severe VPA overdose is associated with a high mortality rate requiring early medical interventions. Beside supportive intensive care, hemodialysis can be considered as an adjunctive measure.
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PMID:Acute valproate poisoning: pharmacokinetics, alteration in fatty acid metabolism, and changes during therapy. 1601 83

Citrin, encoded by SLC25A13, is a liver-type mitochondrial aspartate-glutamate carrier (AGC), of which deficiency, in autosomal recessive trait, causes neonatal intrahepatic cholestasis (NICCD) and adult-onset type II citrullinemia (CTLN2). NICCD patients have jaundice, hypoproteinemia, hypoglycemia, galactosemia, growth retardation, fatty liver and multiple aminoacidemia including citrulline, methionine, threonine and tyrosine. Some of the neonates who have experienced NICCD suffer from severe CTLN2 more than 10 years or several decades later. In CTLN2, neuropsychotic symptoms such as disorientation, aberrant behavior, coma and death are observed. Laboratory findings reveal hyperammonemia, citrullinemia, fatty liver and liver-specific decrease in a urea cycle enzyme, argininosuccinate synthetase (ASS). In some cases, hyperlipidemia, pancreatitis and hepatoma are accompanied with CTLN2. Citrin as a liver-type AGC plays a role in supplying aspartate to the cytosol for urea, protein and nucleotide synthesis by exchanging mitochondrial aspartate for cytosolic glutamate and proton, and transporting cytosolic NADH reducing equivalent to mitochondria as a member of malate aspartate shuttle essential for aerobic glycolysis. AGC is also important for gluconeogenesis from lactate. Although it is difficult to explain pathogenesis of the symptoms such as cholestasis in NICCD and liver-specific decrease of ASS protein in CTLN2 from the functions of the AGC, some are understandable by the loss of citrin functions. Many CTLN2 patients have been treated with a low protein and high carbohydrate diet and glycerol at the hyperammonemic coma. We argue that those treatments may result in fatty liver, hyperlipidemia, hyperammonemia and even death due to loss of the citrin functions. Loss of citrin first cause deficiency of aspartate in the cytosol, which results in an increase in cytosolic NADH/NAD(+) ratio and then activation of fatty acid synthesis pathway to compensate the aberrant ratio. This follows inhibition of fatty acid oxidation. The peculiar fondness for food of CTLN2 patients who like protein and dislike carbohydrate and sweets may be related to their metabolic requirements.
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PMID:Metabolic derangements in deficiency of citrin, a liver-type mitochondrial aspartate-glutamate carrier. 1619 99

Valproic acid (VPA) is a broad-spectrum antiepileptic drug and is usually well tolerated, but rare serious complications may occur in some patients receiving VPA chronically, including haemorrhagic pancreatitis, bone marrow suppression, VPA-induced hepatotoxicity (VHT) and VPA-induced hyperammonaemic encephalopathy (VHE). Some data suggest that VHT and VHE may be promoted by carnitine deficiency. Acute VPA intoxication also occurs as a consequence of intentional or accidental overdose and its incidence is increasing, because of use of VPA in psychiatric disorders. Although it usually results in mild central nervous system depression, serious toxicity and even fatal cases have been reported. Several studies or isolated clinical observations have suggested the potential value of oral L-carnitine in reversing carnitine deficiency or preventing its development as well as some adverse effects due to VPA. Carnitine supplementation during VPA therapy in high-risk patients is now recommended by some scientific committees and textbooks, especially paediatricians. L-carnitine therapy could also be valuable in those patients who develop VHT or VHE. A few isolated observations also suggest that L-carnitine may be useful in patients with coma or in preventing hepatic dysfunction after acute VPA overdose. However, these issues deserve further investigation in controlled, randomized and probably multicentre trials to evaluate the clinical value and the appropriate dosage of L-carnitine in each of these conditions.
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PMID:Science review: carnitine in the treatment of valproic acid-induced toxicity - what is the evidence? 1627 30

In an effort to better characterize the natural history of pancreatoduodenal injuries, we present a review of clinical experiences in the treatment of combined traumatic pancreatoduodenal injuries, focusing on patients in extremis. Records of patients with abdominal trauma admitted to a level 1 trauma center from 1997 to 2001 were reviewed. Of 240 patients who sustained a pancreatic or duodenal injury, 33 had combined pancreatoduodenal injuries. Eighty-two per cent of the patients (27/33) in this series had penetrating injuries, 72 per cent (24) sustained gunshot wounds (GSW). Thirty-one patients were male, and the mean age was 33 years (range, 7-74). These patients presented with an average Injury Severity Score (ISS) of 22 +/- 12 and an average Glasgow Coma Score of 14 +/- 2. Overall length of stay was 39 +/- 59 days (range, 0-351 days). These 33 patients underwent a total of 57 laparotomies with an average of 1.7 operations per patient (range, 1 to 5 operations). Eighty-four per cent of the patients had an associated gastrointestinal injury and 45 per cent had a major vascular injury. Thirteen of the 33 (39%) patients presented in extremis, all 13 underwent an abbreviated laparotomy. The complication rate was 36 per cent, including fistula, abscess, pancreatitis, and organ dysfunction. There were 6 hospital deaths for a mortality rate of 18 per cent. Pancreatoduodenal injuries are associated with a variety of other serious injuries, which add to the overall complexity of these patients. Abbreviated laparotomy may be helpful when managing combined pancreatoduodenal injuries in patients who are in extremis.
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PMID:Recent trends in the management of combined pancreatoduodenal injuries. 1646 33

Strategic lesions of the thalamus interfere with cognitive functions and produce complex neuropsychological symptoms. Bilateral, simultaneous thalamic hemorrhages are unusual causes of thalamic dementia. We present clinical, neuropsychological and structural neuroimaging data of a 12-month follow-up period of a patient with bilateral thalamic hemorrhages. After the operation of pancreatitis acuta hemorrhagico-necroticans, the patient developed coma. Computed tomography (CT) and magnetic resonance (MR) of the brain showed medially situated bithalamic hematomas. During the follow-up period, patient's level of consciousness has improved. Moderate dementia (MMSE 20/30) was found with severe temporal and spatial disorientation. Neuropsychological tests showed that attention and concentration were prominently impaired; there were severe verbal and less prominent, visual memory deficits, with anterograde and retrograde amnesia, accompanied by confabulations. Loss of cognitive flexibility and dysexecutive syndrome were also demonstrated. Dynamic apraxia, visual organization and visual construction deficit and impairment of categorial and phonemic fluency were noted. Language was only moderately impaired (anomia). A year later, neuropsychological profile was similar with moderate improvement of retrograde amnesia, whereas anterograde deficits persisted. Neuropsychological syndrome in our patient with bilateral thalamic hemorrhages was characteristic for subcortico-cortical cognitive deficit and was caused by disruption of the cortico-thalamic circuitry.
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PMID:Neuropsychological deficits after bithalamic hemorrhages. 1739 6

Pancreatitis, pulmonary embolism, and diabetic acidosis and coma see the greatest improvements in mortality rates. Structure, process, and evaluation cited as the keys to achieving high quality. Available process measures from national organizations seem to contribute to lower mortality rates.
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PMID:Top hospitals record a 71% lower mortality rate. 1801 91

The hyperosmolar hyperglycemic nonketotic state (HHNS) is an acute metabolic complication occurring characteristically in elderly type-2 diabetic patients. It may account for 10 up to 47% of cases of severe hyperglycemia with or without ketoacidosis. Many factors associated with advanced age may explain the predilection of both elderly subjects in general and older diabetics in particular to develop hyperosmolar coma, including reduced glomerular filtration rate and elevated renal threshold for glucose (which fail to correct hyperglycemia by osmotic diuresis), lack of thirst appropriate to the state of hydratation and some iatrogenic factors. In HHNS the age of the patients is the best known prognostic indicator. The increased mortality rate in the elderly diabetics depends on the severity of precipitating acute diseases (gastrointestinal hemorrhage, cardiovascular accident, pneumonia, pancreatitis, etc.), but the frequent compromises of the hemodynamic state and renal function of aged subjects substantially contributes. However, the role of erroneous management is not negligible and difficulties may be encountered in conciliating correction of metabolic disorder with treatment of precipitating illness. Insulin, water and electrolytes are the most important therapeutical tools for the treatment of hyperglycemic emergencies. In HHNS, the aggressive fluid replacement with isotonic or hypotonic NaCl solutions have first priority. Such a type of strategy is difficult to perform in patients suffering from cerebral stroke (which needs of anti-edema therapy) or congestive heart failure (necessitating to avoid fluid excess). According to the literary data, in our experience these two precipitating factors are frequent causes of death. We outline the validity of prefixed protocols of management; on the other hand, we think that the pathophysiological understanding of HHNS in the single patient is essential to decide the proper corrections and to permit a successful outcome. The primary way aiming at diminishing mortality by HHNS is its prevention; it is fundamental to warrant an appropriate fluid intake and to utilize with caution some drugs (thiazides, steroids, phenytoin, etc.) in aged diabetics, especially when nephropathic or unable, or living in nursing homes.
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PMID:Diabetic non ketotic hyperosmolar state: a special care in aged patients. 1865 40

This case report describes a case of acute necrotic-hemorrhagic pancreatitis complicated by Wernicke's encephalopathy (WE) and stresses the importance of a correct dietetic regimen. A 39-year-old Chinese male patient with negative remote pathological anamnesis was hospitalized in the Medical Department with a diagnosis of gallstones. The clinical course was complicated with the onset of acute pancreatitis. Enteral fasting was imposed with intravenous feeding without vitamin supplementation. The progressive worsening of the clinical, radiodiagnostic and laboratory profile combined with deterioration in the state of consciousness promoted, on the 36th day exploratory laparotomy revealed necrotic-hemorrhagic pancreatitis. The patient was, therefore, admitted to the Intensive Care Unit in a deep coma. The recent medical history, neurological examination, and encephalic computed tomography suggested a revealing diagnosis of WE combined with pancreatic encephalopathy.
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PMID:Wernicke's encephalopathy and pancreatic encephalopathy after necrotic-hemorrhagic pancreatitis. A case report. 1918 37


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