Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085631 (agitation)
 12,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The reaction of the rats to injection of Dimer-X into the intracranial subarachnoid space or the cerebrum was examined. When 28% iodine Dimer-X was injected into the subarachnoid space, 7 of 10 rats showed agitation, which is the most severe complication, and all died within one hour. All of the reactions were reduced with the lower concentrations of Dimer-X. The rats which were premedicated with Valium and/or Decadron revealed fewer and less severe complications. It is believed that the intracerebral injection method has many disadvantages, the results of its experiment are therefore reported without further elaboration. From the results of the experiment it is concluded as follows: 1) Dimer-X should not be injected into the intracranial subarachnoid space. 2) Dimer-X of low concentration in the subarachnoid space reduces the complications. 3) Complications from the subarachnoid application of Dimer-X can be reduced by premedication with Valium and Decadron.
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PMID:[Dimer-X in the intracranial subarachnoid space--its toxicity (author's transl)]. 108 6

In a double-blind clinical trial comprising 29 depressed patients citalopram, a highly selective 5-HT re-uptake inhibitor and maprotiline, a specific NA re-uptake inhibitor, were compared. Allowing for the small sample and taking into consideration that both groups consisted of severely ill, hospitalized patients, it is notable that half of them appeared to respond to treatment. Comparison of the clinical efficacy of the two drugs showed no significant difference, but the profiles of the side-effects appeared to be different. The patients treated with citalopram showed increased sweating, drowsiness, restlessness and headache. These side-effects were almost entirely reported by the non-responders. The maprotiline patients had anticholinergic symptoms, such as dryness of mouth and constipation, side-effects which were also reported by the responders. No correlation was found between plasma steady-state levels of either drug and clinical outcome. The Dexamethasone Suppression Test (DST) appeared to show some predictive value as regards treatment response. There was a tendency towards better overall treatment results in the non-suppressor group. Determination of post-probenecid 5-HIAA, HVA and MHPG concentrations in lumbar-CSF was made in 22 patients. There was a significant negative correlation between HVA and the severity of depression, as well as a significant negative correlation of MHPG with the Newcastle score. The 5-HIAA concentration was found to be correlated with HVA, but not with MHPG. Rather surprisingly significant negative correlation between 5-HIAA and treatment results with maprotiline was found, but no correlation with MHPG. The lumbar-CSF MHPG and HVA values did not appear to have any predictive value as regards treatment response to citalopram or maprotiline. As expected the serotonin (5-HT) concentration in blood and thrombocytes in patients treated with citalopram showed a highly significant reduction after 2 and 4 weeks of treatment.
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PMID:A double-blind comparative clinical trial of citalopram vs maprotiline in hospitalized depressed patients. 244 51

The vasodilator prostaglandins (PGs), prostacyclin (PGI2) and PGE2, may contribute to the inflammatory response. Because glucocorticosteroids reduce inflammation, possibly through inhibition of arachidonic acid release, we examined the influence of dexamethasone on PG formation in cultures of human endothelial cells. Binding of [3H]dexamethasone by intact cells was competed by unlabeled steroids and was half-maximal at 1.2 X 10(-8) M. A cytosolic fraction complexed with [3H]dexamethasone and migrated on sucrose density gradient centrifugation with a sedimentation coefficient of 8S. 3H-steroid binding was diminished by unlabeled steroid. Histamine, bradykinin, and the ionophore, A23187, stimulated release of PGI2 and PGE2 to as much as 25 times basal release. Dexamethasone (10(-11) to 10(-7) M) reduced PG formation in cells that were stimulated by histamine, bradykinin, calcium ionophore, or mechanical agitation. The inhibitory effect required at least 4 h to develop, was maximal at 24 h, and persisted after the steroid was removed. Hydrocortisone and triamcinolone had similar effects but were less potent than dexamethasone. Testosterone and progesterone did not affect PG generation. Both arachidonic acid and PGH2 augmented formation of PGs but were not inhibited by dexamethasone. Cortisol-21-mesylate, an antagonist of glucocorticoid receptors, blocked the effects of dexamethasone on PG formation, as did treatment of the cells with cycloheximide. We conclude that glucocorticoids inhibit PG production in endothelial cells by interaction with specific steroid receptors. The steroid-mediated inhibitory effect occurs at the level of arachidonic acid release and depends upon protein synthesis.
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PMID:Inhibition of prostaglandin synthesis by glucocorticoids in human endothelial cells. 308 37

Elevated ratings of anxiety and agitation in Dexamethasone Suppression Test (DST) nonsuppressors suggest a role for psychological stress in the generation of the hypothalamic-pituitary-adrenal cortical (HPAC) abnormalities characteristic of depression. We employed the learned helplessness model of depression to test the effectiveness of psychological stress in inducing a resistance of plasma corticosterone levels to dexamethasone suppression. Inescapably shocked rats exhibited corticosterone levels that were significantly more resistant to dexamethasone suppression than were the levels of rats receiving an equivalent amount of escapable shock or no shock. These results confirm the hypothesis that HPAC resistance to dexamethasone suppression is enhanced by the distress associated with the inefficacy of behavioral coping responses. The present findings represent the first analog of the DST in the learned helplessness model of depression. This DST model allows investigations into neurobiological mechanisms underlying the HPAC alterations in depression.
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PMID:Learned helplessness: an experimental model of the DST in rats. 276 3

Most patients with chronic idiopathic thrombocytopenic purpura (TTP) show a good initial response to treatment with corticosteroids. However the disease relapses in more than 90% when steroid dosage is reduced. Recently 100% success was reported for a new therapeutic protocol in 12 patients (ranging in age from 13-60, half of them women) with chronic ITP refractory to corticosteroids or to splenectomy. They were given pulsed therapy with oral dexamethasone, 40 mg/day on 4 consecutive days each month, for 6 months. This treatment protocol was used in an attempt to avoid splenectomy. 5 patients (42%) had a complete response but 7 did not. The median follow-up in those who responded was 7 months (range 6-8). Of the 7 who did not respond, 5 had not completed treatment: 3 because of urgent splenectomy and 2 because of lack of response after 3 courses of therapy accompanied by side-effects. Most patients suffered typical corticosteroid side-effects, principally restlessness, insomnia, and withdrawal effects. These were milder and better tolerated in those treated with Dexacort solution (20 mg ampules) rather than dexamethasone tablets. Despite complete response in only 5 of the 12 patients (42%), we feel that pulsed high-dose dexamethasone is effective and should be tried in TTP refractory to conventional corticosteroid therapy, before resorting to splenectomy.
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PMID:[Pulsed high-dose dexamethasone in resistant immune thrombocytopenic purpura]. 885 71

Dexamethasone was administered orally for 7.5 or 9.5 days to 80 pregnant bitches to terminate unwanted pregnancy at an outpatient clinic. Treatment was initiated at day 30-35 (n = 74) or day 45-50 (n = 6) of confirmed pregnancy using one of two dosages. In 62 bitches, dexamethasone was administered twice a day for 7.5 days increasing from 0.1 to 0.2 mg kg-1 over the first 2 days of administration and decreasing from 0.16 to 0.02 mg kg-1 over the last five administrations. The 18 remaining bitches were given dexamethasone twice a day for 9.5 days, at a dosage of 0.2 mg kg-1 for 7 days and then decreasing from 0.16 to 0.02 mg kg-1 over the last five administrations. Pregnancy was terminated without complication in 75 of the 80 bitches, and uterine contents were absorbed or aborted or both. Pregnancy was not terminated in five bitches treated for 7.5 days beginning at day 30-35 of gestation. In four of them parturition occurred at the normal time; in one, pregnancy was terminated by a second treatment. Pregnancy termination occurred at 7-15 days after the start of treatment. During ultrasonographic imaging of 13 bitches treated with dexamethasone, fetal deaths occurred between 5 and 13 days after the start of treatment. The side effects reported by the owners included polydipsia and polyuria, which were observed in all of the bitches and which disappeared when the treatment was discontinued. Some bitches also experienced vaginal discharge, restlessness, anorexia or emesis. At the first or second cycle after treatment, 20 bitches were mated and had normal pregnancies and normal litters. The results suggest that oral treatment with dexamethasone can be used to terminate pregnancy in bitches, but that in some cases the withdrawal of treatment after 8 days can result in retention of live pups and require a further treatment or the use of another abortifacient.
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PMID:Clinical use of dexamethasone for termination of unwanted pregnancy in dogs. 940 90

Herpes simplex virus type 1 (HSV-1) encephalitis may present with fever and behavioral changes, to the extent of a psychotic state and psychomotor agitation. We developed a clinically relevant experimental model of HSV-1 encephalitis and investigated host brain responses associated with its clinical signs and whether these responses depend on the presence of circulating glucocorticoids. Intracerebral inoculation of HSV-1 in rats induced fever, motor hyperactivity and aggressive behavior. In adrenalectomized rats HSV-1 failed to induce these signs, although mortality rate was identical to sham-operated rats. Hypophysectomy or blocking glucocorticoid receptors also prevented HSV-1-induced fever. Dexamethasone replacement therapy to adrenalectomized rats restored the HSV-1-induced fever and behavioral abnormalities. HSV-1 inoculation produced hyperproduction of prostaglandin E(2) by brain slices. This effect was abolished in adrenalectomized rats and was restored by dexamethasone treatment. In intact rats HSV-1 induced brain interleukin-1beta (IL-1beta) gene expression. Adrenalectomy alone caused brain IL-1beta expression, which did not increase after HSV-1 infection. Similarly, HSV-1 induced IL-1beta expression in astrocyte cultures. Removal of cortisol from the culture medium caused basal IL-1beta mRNA expression which was not increased by infection. In conclusion, fever, motor hyperactivity and aggressive behavior during experimental HSV-1 encephalitis are dependent on brain responses, including prostaglandin E(2) and IL-1beta synthesis. Circulating glucocorticoids play an essential permissive role in the induction of these host brain responses.
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PMID:A novel permissive role for glucocorticoids in induction of febrile and behavioral signs of experimental herpes simplex virus encephalitis. 1173 36

The role of dexamethasone to reduce delayed emesis following highly emetogenic chemotherapy is proven, but there is less evidence of benefit after mild-moderately emetogenic regimens. Here, we develop and evaluate a Dexamethasone Symptom Questionnaire (DSQ) to assess the side effects of dexamethasone in the week after patients receive moderately emetogenic chemotherapy. The DSQ was first optimised with the aid of a focus group. Sixty patients receiving oral dexamethasone for prophylaxis of delayed emesis after moderately emetogenic chemotherapy for cancer completed and then evaluated the DSQ. Patients reported that the DSQ was clearly worded and addressed items important to them. Patients receiving dexamethasone reported moderate-severe problems with insomnia (45%), indigestion/epigastric discomfort (27%), agitation (27%), increased appetite (19%), weight gain (16%) and acne (15%) in the week following chemotherapy. The side effects of dexamethasone may outweigh its benefits when used with moderately emetogenic chemotherapy. A randomised, double-blind crossover trial is underway to determine the effect of dexamethasone on nausea and vomiting, and the impact of side effects of dexamethasone and of nausea and vomiting on quality of life.
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PMID:Side effects associated with the use of dexamethasone for prophylaxis of delayed emesis after moderately emetogenic chemotherapy. 1655 37

Long-acting neuraxial opioids provide excellent analgesia after surgery, but are associated with higher rates of postoperative nausea and vomiting. Dexamethasone effectively prevents postoperative nausea and vomiting after general anaesthesia, but its value in patients receiving long-acting neuraxial opioids is undetermined. Therefore, the objective of this meta-analysis was to assess the prophylactic anti-emetic efficacy of intravenous (i.v.) dexamethasone in this population. The study methodology followed the PRISMA statement guidelines. The primary outcome was the need for rescue anti-emetics during the first 24 postoperative hours, analysed according to the dose of dexamethasone (low-dose 2.5-5.0 mg; intermediate dose 6.0-10.0 mg), timing of administration (beginning or end of surgery) and route of long-acting opioid administration (intrathecal or epidural). Additionally, the rates of complications (restlessness, infection, hyperglycaemia) were sought. Thirteen trials were identified, representing a total of 1111 patients. When compared with placebo, intravenous dexamethasone reduced the need for rescue anti-emetics (risk ratio (95%CI) 0.44 (0.35-0.56); I2 = 43%; p < 0.00001; quality of GRADE evidence: moderate), without differences between dexamethasone doses (p for sub-group difference = 0.67), timing of administration (p for sub-group difference = 0.32) or route of long-acting opioid (p for sub-group difference = 0.10). No patients developed infection or restlessness among trials that sought these complications. No trial measured blood glucose levels. In conclusion, there is enough evidence to state that intravenous dexamethasone provides effective anti-emetic prophylaxis during the first 24 postoperative hours in patients who receive long-acting neuraxial opioids.
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PMID:Intravenous dexamethasone for prophylaxis of postoperative nausea and vomiting after administration of long-acting neuraxial opioids: a systematic review and meta-analysis. 2922 71

Primary amoebic meningoencephalitis (PAM) is a rare, fulminating, hemorrhagic infection of the brain caused by Naegleria fowleri, a thermophilic, free-living amoeba. A 74-year male presented with sudden severe global headache and fever with features of anomic aphasia. Magnetic resonance imaging (MRI) suggested herpes encephalitis and acyclovir (IV) was started but the patient developed altered sensorium, agitation and progressive weakness of lower limbs with gradual truncal weakness. Repeat MRI showed increase in lesion size and edema with confluent blood areas. Dexamethasone showed significant improvement. Ten days after completion of acyclovir, there was recurrence of altered sensorium with seizures. Repeat MRI showed new lesions appearing. Excisional biopsy of brain confirmed N. fowleri. Amphotericin B and miltefosin was started but patient succumbed to his illness after 10 days. This is a first case of PAM in Nepal, involving elderly immune-competent male without environmental exposure to freshwater, mimicking as herpes encephalitis.
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PMID:Fatal case of amoebic encephalitis masquerading as herpes. 2974 28


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