Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixteen patients with intracerebral tumors received intraarterial cisplatin, teniposide, and BCNU combined with intravenous cisplatin, teniposide, and cytosine arabinoside. Oral glycerol and intravenous mannitol were given along with the intravenous chemotherapy in an attempt to increase drug delivery to tumor by augmenting tumor blood flow. Thirteen additional patients were treated with the same regimen, but received all the chemotherapy intravenously. Of the 16 patients receiving intraarterial chemotherapy (median survival, 14 weeks), none responded, 5 (31%) were stable for > 8 weeks, 8 (50%) failed, and 3 (19%) were unevaluable due to early death. Of the 13 patients receiving all their treatment intravenously (median survival, 13 weeks), 3 (23%) responded, 1 (8%) was stable, 7 (54%) failed, and 2 (15%) were unevaluable due to early death. In the patients receiving intraarterial chemotherapy, toxicity included ipsilateral retinal toxicity (2 patients), ocular pain or headache (10), periorbital swelling and flushing (6), increased brain edema with focal neurological deficits and drowsiness (5), and catheter-related carotid artery thrombosis followed by fatal herniation (1). Myelosuppression was worse in patients who received all their treatment intravenously than in those receiving intraarterial chemotherapy (p < 0.05). Neutropenic sepsis developed in 4 patients on the intraarterial arm (1 fatal) and in 5 patients on the intravenous arm (2 fatal). Other toxic effects were similar whether or not patients received intraarterial treatment or only intravenous treatment. Overall, toxicity of this regimen was excessive, and response rates were lower than would have been expected with single agent therapy.
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PMID:Feasibility study of intraarterial vs intravenous cisplatin, BCNU, and teniposide combined with systemic cisplatin, teniposide, cytosine arabinoside, glycerol and mannitol in the treatment of primary and metastatic brain tumors. 812 May 74

In response to a question on how to avoid the rare, inadvertent intravascular or ip injection of hypertonic saline solution during therapeutic abortion, 3 consultants replied. According to Reid and Frigoletto, to avoid intravascular or ip infusion, place a small indwelling polyethylene catheter in the amniotic sac rather than a metal needle. This virtually precludes the possibility of inadvertent iv injection. When and if necessary, correct catheter placement may be confirmed by the use of fluoroscopy and amniography prior to the injection of hypertonic saline solution. The chemical imbalances associated with this accident are those encountered in severe hypernatremia with resultant brain edema and hemorrhagic softening. Bizarre paresthesia, pyrexia, altered consciousness, and, eventually, convulsions preceded the fatal cases. Peritoneal dialysis may be life saving in the event of ip injection. Naturiuretics, appropriate parenteral fluid administration, and possibly exchange transfusion might be indicated for intravascular accidents. In Goodlin's hospital there have been no cases of acute hypernatremia in the last 500 therapeutic abortions done with hypertonic saline solution. This is believed to be related to 2 changes in technique: 1) not losing the amniotic space by removing only as much amniotic fluid as can easily be obtained and 2) using a simple gravity infusion technique for the instillation of the hypertonic saline solution. During infusion it is essential that the patient be alert, for the first symptoms of intravascular injection are a slight pain, burning, or a feeling of warmth in the pelvis. If these minor symptoms are ignored and the procedure is continued, a sensation of flushing occurs throughout the body with tingling in the scalp and ringing in the ears followed finally by seizures, apnea, or coma or both. Late symptoms are those of hemolytic anemia and renal failure. From experience, serum sodium levels during these events are as high as 185 mEq/1. Along with occurrence of acute hypernatremia the contents of the amniotic cavity are sometimes extruded extraovularly through the fallopian tube into the peritoneal cavity when labor begins. Cases with serum sodium levels of 170 mEq/1 some 6-7 hours after saline instillation were observed, but by contrast these patients' only symptoms were extreme thirst and peritoneal discomfort (Lancet 1: 305, 1968). The treatment of hypernatremia is to force fluids either by mouth or iv. Since most commercial 5% dextrose in water solutions are actually 4.5% (regulations permit a 10% error), such hypotonic fluids are useful for treating hypernatremia.
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PMID:Hypernatremia from intravascular saline infusion during therapeutic abortion. 1230 84

The aim in this study was to investigate whether our experimental model for stroke therapy, flushing the ischemic territory with saline prior to reperfusion, could ameliorate disruption of microvascular integrity by reducing matrix metalloproteinase (MMP) expression during reperfusion. Stroke in Sprague Dawley rats (n = 42) was induced by a 2-h right middle cerebral artery (MCA) occlusion using a novel intraluminal hollow filament. Prior to reperfusion, 24 of the ischemic rats received 6ml isotonic saline at 37 degrees C infused into the ischemic area through the filament. Brain edema was determined by comparing the percentage difference in brain volume between the right and left (contralateral to stroke site) hemispheres, while the expressions of MMP-2 and -9 mRNA were analyzed by real-time reverse transcriptase-polymerase chain reaction (real-time RT-PCR). A significant (p < 0.01) brain edema, determined by an increased brain volume of 19 +/- 4%, and overexpression of the mRNA encoding MMPs, determined by increased relative mRNA level ratio, were found in ischemic rats. The brain damage, in terms of brain edema (4 +/- 1%) and overexpression of MMPs, was significantly (p < 0.05) ameliorated as a result of saline flushing into the ischemic territory prior to reperfusion. This study has enhanced our understanding of the causal mechanisms by which the neuroprotective effect of ischemic area "flushing" can be achieved.
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PMID:Reduced brain edema and matrix metalloproteinase (MMP) expression by pre-reperfusion infusion into ischemic territory in rat. 1553 Oct 84

Corticorelin is a synthetic analog of the naturally occurring human peptide corticotropin-releasing factor (CRF). Several studies have indicated the ability of CRF to reduce the brain edema caused by brain tumors. Peritumoral brain edema (PBE), caused by an intracerebral tumor, manifests several features of vasogenic edema, which is a type of edema characterized by disruption of the blood-brain barrier. Traditionally, PBE has been treated using corticosteroids, primarily dexamethasone. Introduced more than four decades ago, dexamethasone revolutionized the treatment of PBE, but the side effects and withdrawal symptoms associated with corticosteroids propelled the investigation of other drugs. Clinical trials with the synthetic human CRF (hCRF) corticorelin (Xerecept, NEU-3002; Celtic Pharmaceutical Holdings) have indicated that this drug has a distinct advantage over classical corticosteroids in the treatment of PBE. Fewer and/or milder side effects have been reported for corticorelin compared with dexamethasone, although at higher doses of corticorelin several side effects, including hypotension and transient flushing, have been reported. Nevertheless, corticorelin was reasonably well tolerated in patients and healthy volunteers, and may be a good candidate for reducing PBE and associated neural damage, as well as improving neurological symptoms.
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PMID:Corticorelin, a synthetic human corticotropin-releasing factor analog, for the treatment of peritumoral brain edema. 2115 69