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)

An outbreak of acute methyl alcohol intoxication occurred in Port Moresby, Papua New Guinea, in March 1977. Twenty-eight young men attended a drinking party and drank methyl alcohol. The amount consumed by each individual ranged from an equivalent of 60--600 ml of pure methanol. Three had prior ethanol ingestion. All 28 became ill 8--36 hours after drinking and were hospitalized. The most commonly observed clinical syndromes were: acute metabolic acidosis, severe visual impairment and acute pancreatitis. Four died within 72 hours after admission to the hospital. All had severe metabolic acidosis and visual impairment and three pancreatitis. Of 24 who recovered, 16 showed no residual complications, six had bi-lateral visual impairment and two had difficulty in speech as well as visual impairment. A three month follow-up examination showed no change in the findings. Coma, seizures and prolonged acidosis were poor prognostic signs. The estimated amount of consumed methanol and the rapidity of the appearance of signs of toxicity following methanol ingestion did not seem to influence the outcome of poisoning. The treatment of acute methyl alcohol intoxication in centres where dialysis is not available is discussed.
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PMID:An outbreak of acute methyl alcohol intoxication. 28 45

An experience with 68 patients with hemorrhagic pancreatitis identified at operation or autopsy is reported. Sixteen of the patients were subjected to operation, and 6 survived after celiotomy and peritoneal irrigation. There were no survivors in the unoperated group. Death when the pancreas is hemorrhagic and due to pancreatitis occurs an average of 10 days after the onset of symptoms or within 7 days of hospitalization. In eight patients who presented in coma, the diagnosis was not established before death. Early recognition of patients with hemorrhagic pancreatitis can be facilitated by the routine use of amylase and methemalbumin determinations and peritoneal lavage. Translocation of large volumes of albumin-rich fluid from the intravascular compartment to the retroperitoneum and pleural and abdominal cavities is in part responsible for many of the signs, symptoms, and complications of hemorrhagic pancreatitis. These include hemoconcentration, hypotension, tachycardia, tachypnea, ascites, abdominal distress, respiratory insufficiency, and renal failure. Adequate initial resuscitation and intensive follow-up are probably the most important elements in the management of patients with hemorrhagic pancreatitis. Careful monitoring of fluid and electrolytes and blood gases is required to avoid shock and renal and pulmonary failure. The need for careful monitoring is emphasized by the number of our patients in whom inadequacies of fluid replacement and ventilation were often not appreciated until the patient was in extremis from shock or respiratory or renal failure. Antibiotics are indicated in patients with biliary tract disease and penetrating ulcer in whom the risk of secondary infection is considerable. Associated diseases that initiated pancreatitis and that in themselves may be life-threatening, such as acute cholecystitis or cholangitis, should be promptly treated by operation. Diagnostic and therapeutic lavage are justified in the treatment of hemorrhagic pancreatitis. Resection of the necrotic pancreas should be considered when the patient fails to improve after lavage and nonoperative resuscitation.
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PMID:Hemorrhagic pancreatitis. 45 56

A 52 year old woman with a history of mild pancreatitis had a palpable mass in the upper abdomen. She died in an unexplained coma. The autopsy revealed an excessive hyperplasia of the exocrine pancreatic tissue resulting in the largest pancreas ever reported (254 gramm). This hyperplasia was accompanied by a chronic pancreatitis. In the central nervous system a Wernick's encephalopathy had developed; severe loss of neurons was stated in the thalamus; extensive degeneration was found in the upper vermis of the cerebellum. The discussion of this case includes the relationship between the diseases of the pancreas and neuropsychiatric and neuropathologic findings. It is assumed that the hyperplasia of the exocrine pancreatic tissue could only be an additional factor in the occurence of post alcoholic complications. This hyperplasia of the exocrine pancreatic tissue is considered to be a hamartom-like formation and it should therefore be distinguished from other pancreatic hyperplasia.
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PMID:[Excessive hyperplasia of the exocrine pancreatic tissue and Wernicke's encephalopathy (author's transl)]. 59 98

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.
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PMID:Magnesium deficiency and cardiac disorders. 80 29

A very rare case of acute pancreatitis with concurrent encephalomalacia and ascites mimicking hepatic coma is described. The possibliity that the pancreatitis was caused by the administration of chlorothiazide in a diabetic patient is suggested as possible etiology. It is emphasized that when a cirrhotic patient develops coma, the possibility of painless,silent pancreatitis with encephalomalacia as well as hepatic coma should be considered in the differential diagnosis.
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PMID:Silent acute pancreatitis with encephalomalacia mimicking hepatic coma. 111 73

Diuretics can result in various undesired biochemical changes, such as impotence, skin rashes, nausea, dizziness and lethargy as well as subjective side effects. The side effects are mostly predictable, their effects depending on both the circulatory blood volume and on the transport of water and solute in the renal tubules. Two of the commonest side effects are mild hypovolaemia, when any diuretic is used, and mild hypokalaemia when the non-potassium-sparing diuretics, such as thiazides and frusemide are used. Its occurrence is dose dependent and can be corrected by potassium supplements, but potassium-retaining diuretics, which also correct the often associated fall in serum magnesium, are preferable. Many reports link hypokalaemia with cardiac arrhythmias, but some dispute this association in the absence of the concomitant use of digoxin. Hyponatraemia rarely occurs, but can be life threatening. Calcium excretion is markedly reduced, but unlike other electrolyte disturbances from diuretics, this may be valuable: some suggest diuretics have an anti-osteoporotic action. Diuretics increase glucose and insulin resistance and should be used sparingly in diabetics. They rarely cause a non-ketotic hyperosmolar coma. Urate is raised, but clinical gout is not common. Cholesterol elevation has been reported in some studies, but long-term studies indicate that lipid changes are minor. Other rare side effects are not predictable from their pharmacological actions and these include the occurrence of skin rashes, thrombocytopenia, pancreatitis and interstitial nephritis; and ototoxicity from frusemide.
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PMID:Adverse reactions to diuretics. 148 14

In 27 (78%) of 36 patients with massive hemolysis (defined as a fall in hematocrit of more than 12% within 12 h due to intravascular red cell destruction), hypertriglyceridemia (plasma triglycerides greater than 175 mg/dl) was present or appeared within two days after the hemolytic crisis. Eighteen subjects with triglycerides exceeding 300 mg/dl (peak 516 +/- 39 mg/dl) were further analyzed. The development of hyperlipidemia was independent of the etiology of hemolysis (microangiopathic hemolytic disease 7, toxicemia 3, parainfectious complications 3, autoimmune hemolysis 2, glucose-6-phosphate dehydrogenase deficiency 2). Factors known to increase plasma triglycerides, such as shock, infections, or pancreatitis, were present in only a few cases. Hemolysis-associated complications were activation of intravascular coagulation (16), coma (13), acute renal failure (13), and respiratory insufficiency (5), organ dysfunctions indicating diffuse microvascular injury. Plasma triglycerides fell within a few days if the cause of red cell destruction was eliminated. In 5 of the 8 patients presenting with triglycerides below 175 mg/dl, severe hepatic dysfunction was present. We conclude that hemolysis causes transient hyperlipidemia, either directly by red cell destruction or indirectly by inducing intravascular coagulation, and possibly due to both increased triglyceride synthesis and decreased catabolism.
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PMID:Hyperlipidemia in acute hemolysis. 194 54

Ten patients with the syndrome of non-ketotic hyperosmolar coma are described. The mean age of the patients was 62.3 +/- 17.12 years. One patient was 16 years old. In 9 cases the patients had type II diabetes, one had type I diabetes. In 7 cases the coma was the first sign of diabetes. The factor predisposing in most cases was infection. In the treatment-acting insulin and hypotonic solutions were given. In 2 cases clinical signs of the DIS syndrome were observed manifesting themselves with local changes, including mental disturbances. Heparin was given with good effect. Three patients (30%) died in hospital. The cause of death was serious disease associated with this coma: pancreatitis and myocarditis, purulent bronchopneumonia, myocardial infarction.
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PMID:[Hyperglycemic hyperosmolar nonketotic coma]. 240 21

Groups of mice were given 0 mg, 4 mg, or 2 mg of methylprednisolone acetate (MPA) 7 days prior to, the day of, and 7 days after subcutaneous inoculation with 0 or 2 x 10(5) tachyzoites of Neospora caninum. Clinical signs of disease were seen only in mice given both MPA and N. caninum tachyzoites. Mice given 4 mg MPA and N. caninum tachyzoites developed severe disseminated neosporosis and most died or were killed when comatose 11-13 days postinoculation (PI). Acute pneumonia, polymyositis, encephalitis, hepatitis, and pancreatitis were the main lesions in these mice. Mice given 2 mg MPA and N. caninum developed mild pneumonia and many mice began showing neurological signs 14 days PI. Neurological signs consisted mainly of pronounced head-tilting and associated impairment of movement. Grossly visible 1-2-mm single or multiple, white areas of discoloration were seen in the brains of many of these mice. Encephalitis, ganglioradiculoneuritis, pneumonia, and polymyositis were the main changes seen in these mice. Tissue cysts of N. caninum were only seen in mice given 2 mg MPA and were first seen 21 days PI. Tissue cysts were 16-34 by 13-29 microns and had a 1.5-3.0-microns-thick cyst wall. Tissue cysts were seen only in the brain. Mice given 4 mg MPA and tachyzoites and host cells that had been frozen for 1 wk did not develop clinical signs of infection, indicating that freezing kills tachyzoites and that viruses or other agents were not involved in the genesis of disease seen in mice given MPA and viable tachyzoites.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neospora caninum (Protozoa: apicomplexa) infections in mice. 279 80

Carbon-mineral sorbents successfully combine a high mechanical resistance of the mineral matrix and a high activity of carbons. It is possible to prepare a mineral matrix of the wanted structure and use it as the basis for producing carbon-mineral sorbents. SUMS-1 and SUMS-2 are the sorbents of mild action. In other words, they cause no thrombosis, they do not absorb oxygen and protein from blood, and they have almost no destructive effect on the blood cells. The sorbents are highly effective in adsorbing microorganisms and their toxins. Treatment of patients with different diseases (sepsis, meningitis, bronchial asthma, tuberculosis, pneumonia, thyrotoxicosis, pancreatitis, liver coma, different types of poisoning) with the SUMS-1 and SUMS-2 has given satisfactory results.
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PMID:Physicochemical properties and applications of carbon-mineral sorbents. 345 27


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