Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Beta-adrenergic agonists tocolysis is currently the most popular treatment modality in the United States. However, magnesium sulfate is receiving increasing attention as an alternating tocolytic agent in the presence of various clinical situations, such as the treatment of insulin-dependent diabetes. While there is an abundance of information about the maternal and fetal side effects associated with beta-adrenergic tocolysis, little information is available about maternal adverse side effects of magnesium sulfate treatment for preterm labor. Side effects such as pulmonary edema, respiratory depression, hypocalcemia, and hypermagnesemia have been reported in patients receiving this agent for either tocolysis or pre-eclampsia, though their occurrence is quite rare. One of the infrequent complications of beta-adrenergic agonist tocolysis is the occurrence of a paralytic ileus, which to our knowledge has not yet been reported in association with magnesium sulfate tocolysis. This article therefore concerns the development of a paralytic ileus in a patient receiving parenteral magnesium sulfate for tocolysis. The clinical features are described and the possible mechanisms involved discussed.
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PMID:Maternal paralytic ileus as a complication of magnesium sulfate tocolysis. 383 78

A 53-year-old female, who had been severe hypothyroidism for about ten years, was admitted Stanford type A acute aortic dissection. The replacement of ascending aorta with a composite graft and coronary artery bypass grafting were performed immediately. During the post operative period, many complications occurred including delayed awakening from anesthesia, paralytic ileus, colon perforation, hyperbilirubinemia, pulmonary edema, cerebral hemorrhage and bacterial endocarditis. In this case, intravenous administration of steroid and thyroid hormone was effective to keep hormone level in the normal range although enteral administration was ineffective. It was suggested that early active supplement therapy is mandatory to prevent postoperative complications.
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PMID:[A case of acute aortic dissection associated with myxedema]. 808 82

Five children with AML were treated with high-doses of Ara-C (2 g/m2) during consolidation. After 17 cycles the toxicity was evaluated. Granulocytopenia (< 0.5 x 10(9)/l) and thrombocytopenia (< 25 x 10(9)/l) were stated after 15/17 and 13/17 cycles respectively. The nadir of bone marrow suppression appeared between day 10 and 14. In one case treatment related death during severe myelosuppression was noted. In individual cases jaundice with elevated activity of aminotransferases, paralytic ileus and pulmonary oedema were observed. All these adverse reactions were reversible. Other toxicities such as nausea/vomiting, stomatitis, diarrhea, infections and drug related fever were transient. No neurologic toxicity was seen. There is a need for developing a new way of the administration of high-dose Ara-C which could substantially reduce toxicity of the drug.
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PMID:[Preliminary evaluation of adverse effects after administration of arabinoside cytosine (Ara-C) in high doses to children with acute myelogenous leukemia]. 820 12

A 74 year old patient with diabetes mellitus was hospitalized because of nausea, recurrent vomiting and increasing fatigue. Shortly before admittance the patient had diarrhea. He also reported a recent onset of aversion against meat consumption. Clinical investigation revealed a possible right-sided paraumbilical abdominal tumor, normal bowel sounds, a vascular bruit and a normal white blood count with increased band forms. During hospitalisation the general condition of the patient deteriorated rapidly with fever and increasing numbers of immature granulocytes. The patient finally died under the symptoms of a paralytic ileus with hypotonia and hypoglycemia. Autopsy revealed a fist-sized stenosing tumor in the cecum with the histology of a mainly well differentiated, cylindrocellular adenocarcinoma. As immediate cause of death a bilateral paracentral lung embolism with pulmonary edema was found, the latter probably as immediate consequence of preterminal heart failure.
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PMID:[Intestinal paralysis in long-term diabetes mellitus]. 965 91

A case is presented of a fatal drug interaction caused by ingestion of clozapine (Clozaril) and fluoxetine (Prozac). Clozapine is a tricyclic dibenzodiazepine derivative used as an "atypical antipsychotic" in the treatment of severe paranoid schizophrenia. Fluoxetine is a selective serotonin reuptake inhibitor used for the treatment of major depression. Clinical studies have proven that concomitant administration of fluoxetine and clozapine produces increased plasma concentrations of clozapine and enhances clozapine's pharmacological effects due to suspected inhibition of clozapine metabolism by fluoxetine. Blood, gastric, and urine specimens were analyzed for fluoxetine by gas chromatography/mass spectrometry (GC/MS) and for clozapine by gas-liquid chromatography (GLC). Clozapine concentrations were: plasma, 4.9 micrograms/mL; gastric contents, 265 mg; and urine, 51.5 micrograms/mL. Fluoxetine concentrations were: blood, 0.7 microgram/mL; gastric contents, 3.7 mg; and urine 1.6 micrograms/mL. Norfluoxetine concentrations were: blood, 0.6 microgram/mL, and none detected in the gastric contents or urine. Analysis of the biological specimens for other drugs revealed the presence of ethanol (blood, 35 mg/dL; vitreous, 56 mg/dL; and urine 153 mg/dL) and caffeine (present in all specimens). The combination of these drugs produced lethal concentrations of clozapine and high therapeutic to toxic concentrations of fluoxetine. The deceased had pulmonary edema, visceral vascular congestion, paralytic ileus, gastroenteritis and eosinophilia. These conditions are associated with clozapine toxicity. The combined central nervous system, respiratory and cardiovascular depression of these drugs was sufficient to cause death. The death was determined to be a clozapine overdose due to a fatal drug interaction.
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PMID:A fatal drug interaction between clozapine and fluoxetine. 972 31

A thirty-eight year old man took about 180 tablets of Seirogan. He was unconscious and had dyspnea with dark brown urine on admission. He recovered gradually after initial treatment. Seirogan contains a phenolic component. Symptoms and signs of poisoning are unconsciousness, convulsion, digestive tract disorder, pulmonary edema, hepatic failure, renal failure, and miosis. Clinical features include dark brown urine. On day 7, he again showed signs of creosote poisoning: relapse of unconsciousness and dark colored urine. Plasma concentration of phenol determined on the day before the relapse was much higher than that expected from the half-life of blood phenol. It is reported that Creosote poisoning results in a decrease in the intestinal peristalsis, or paralytic ileus. We would like to emphasize that a relapse of Creosote poisoning may occur due to possible delayed absorption of the Seirogan tablets.
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PMID:[Relapse of Creosote poisoning: report of a case taking Seirogan tablets]. 1241 72

Spinal cord injury and especially cervical spinal cord injury implies serious disturbances in autonomic nervous system function. The clinical effects of these disturbances are striking. In the acute phase, the autonomic imbalance and its effect on cardiovascular, respiratory system and temperature regulation may be life threatening. Serious complications such as over-hydration with the risk of pulmonary edema or hyponatremia are seen. The cord-injured person suffers from autonomic nervous system dysfunction also affecting bladder and bowel control, renal and sexual function. Paralytic ileus may cause vomiting and aspiration, which in turn interferes with respiratory function in those with cervical spinal cord injury. The cord-injured person is at risk to develop pressure sores from the moment of the accident. Two to three months post-injury the cord-injured person with a lesion level above the fifth thoracic segment may develop autonomic dysreflexia, characterised by sympathetically mediated vasoconstriction in muscular, skin, renal and presumably gastrointestinal vascular beds induced by an afferent peripheral stimulation below lesion level. The reaction might cause cerebrovascular complications and has effects on metabolism. Some of the autonomic disturbances are transient and a new balance is reached months post-injury, while others persist for life.
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PMID:Autonomic dysfunction in spinal cord injury: clinical presentation of symptoms and signs. 1619 89