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

We describe a patient treated with trazodone, isocarboxazid, and methylphenidate hydrochloride who developed confusion, agitation, poor concentration, rigidity, myoclonus, involuntary movements, orthostatic hypotension, and hyperreflexia. CK was normal, and the syndrome resolved spontaneously over 12 hours. The serotonin syndrome occurs following the use of serotomimetic agents (serotonin reuptake inhibitors, tricyclic and tetracyclic antidepressants, tryptophan, 3,4-methylenedioxy-methamphetamine, dextromethorphan, meperidine, S-adenosylmethionine) alone or in combination with monoamine oxidase inhibitors. It is characterized by various combinations of myoclonus, rigidity, hyperreflexia, shivering, confusion, agitation, restlessness, coma, autonomic instability, low-grade fever, nausea, diarrhea, diaphoresis, flushing, and rarely, rhabdomyolysis and death.
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PMID:Serotonin syndrome. 785 15

There is a new, potentially fatal disorder that is infrequently reported. The apparent rareness may be because of a lack of recognition of the syndrome or its predisposing factors. Fluoxetine (Prozac, Dista Products Co, Division of Eli Lilly Co, Indianapolis, IN), sertraline (Zoloft, Roerig Division, Pfizer Inc, New York, NY), and paroxetine (Paxil, SmithKline Beecham Pharmaceuticals, Philadelphia, PA) belong to a new class of antidepressant medication: the serotonin reuptake-inhibitors (SRIs). The relative safety profile of the SRIs has led to their widespread use. However, a syndrome of excessive serotonergic activity, the "serotonin syndrome" (SS), has recently been recognized. It is characterized by changes in mental status, hypertension, restlessness, myoclonus, hyperreflexia, diaphoresis, shivering, and tremor. A high index of suspicion is required to make the diagnosis in these acutely ill patients. The most common agents implicated in SS are the monoamine oxidase inhibitors in combination with L-tryptophan or fluoxetine. A case of a patient with significant peripheral vascular disease who developed SS while taking paroxetine and an over-the-counter cold medicine is reported. There have been no prior reports of this interaction. Discontinuation of the offending agents, sedation, and supportive care are the mainstays of treatment. The interactions of serotonin with platelets and vascular endothelium are also discussed.
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PMID:The serotonin syndrome associated with paroxetine, an over-the-counter cold remedy, and vascular disease. 766 67

In animals the occurrence of a behavioural syndrome consisting of hyperactivity, stereotyped movements and increase of temperature has been induced by MAOIs, 5-HT precursors (L-tryptophan) and 5-HT reuptake inhibitors. Most of these manifestations were specifically blocked by a pretreatment with an inhibitor of serotonin synthesis. In humans, the association of myoclonus, diarrhea, confusion, hypomania, agitation, hyperreflexia, shivering, incoordination, fever and diaphoresis, when patients are treated with serotoninergic agents, could constitute a "serotonin syndrome". Such cases of serotonin syndrome were reported after treatments with L-tryptophan, MAOIs, serotonin reuptake inhibitors and tricyclics alone or in association. The authors prospectively evaluated all the "serotonin-related" symptoms in 38 depressed inpatients fulfilling DSM III-R criteria of major depression. 16 (42%) out of 38 patients presented at least one symptom of serotonin syndrome. In 14 cases tremor and myoclonus occurred simultaneously and 10 patients presented at the same time tremor, myoclonus, diaphoresis and shivering. Except for two patients, symptoms were transient, lasted less than one week and disappeared with the pursuit of the treatment. Most often, serotonin syndrome thus corresponds to a reaction induced by a combination of serotoninergic agents at high dosages. In very rare cases, a toxic and potentially fatal interaction can occur between MAOIs, tricyclics and selective serotonin reuptake inhibitors at therapeutic dosages. Serotonin syndrome also provides an heuristic model of the putative mode of action of antidepressants. Serotonin-related symptoms are the physical and objective expression of the antidepressant-induced increase in serotonin. The specificity of serotonin-related syndrome also needs to be discussed since most of the symptoms, such as tremor and diaphoresis, are not in all cases related to an increase in serotonin.
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PMID:[The serotonin syndrome: review of the literature and description of an original study]. 852 62

The internal motion of lysozyme was described by the steady-state and time-resolved fluorescence anisotropy of its tryptophan residues. The fluorescence of mutant lysozymes W62Y- and W108Y-lysozyme, in which Trp62 or Trp108 of hen egg white lysozyme was replaced with a tyrosine residue, could be respectively assigned to Trp108 or Trp62 at the longer wavelength region of the total fluorescence spectrum. The segmental motion of Trp62 as shown by its fluorescence anisotropy decay was described with two components originating from the fluctuational rotation of an indole moiety about the Calpha-Cbeta bond and rotational wobble of the peptide segment adjacent to Trp62. Although Trp62 showed a high degree of motional freedom, its motion was significantly suppressed by the interaction of the mutant protein with a trimer of N-acetyl-D-glucosamine. By contrast, the segmental motion of Trp108 is hindered by the local cage structure at temperatures below 30 degreesC, but Relief from restricted motion occurred on the formation of ligand complex or by thermal agitation. Because of overlaps of the fluorescence spectrum, it is difficult to assign the segmental motion of Trp28 or Trp111, the other two tryptophan residues in lysozyme. However, a careful analysis of the fluorescence anisotropy decay of W62Y- and W108Y-lysozyme showed that the fluctuation of the hydrophobic matrix box was greater than that expected from lysozyme's crystal structure, although it was suppressed by the binding of the ligand to the active site of lysozyme.
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PMID:Internal motion of lysozyme studied by time-resolved fluorescence depolarization of tryptophan residues. 954 45

There is some evidence that the neurotransmitter serotonin (5-hydroxytryptamine; 5-HT) may be involved in the pathogenesis of seasonal affective disorder (SAD). Short-term tryptophan (TRP) depletion was carried out in 18 drug-free remitted patients who met DSM-IV criteria for SAD. Behavioral effects were measured with the Hamilton Depression Rating Scale (HDRS) both 24 h before and 24 h after TRP depletion. Some of the patients showed behavioral responses such as lowered mood, feelings of guilt, loss of interest, agitation, loss of energy, fatigue, social withdrawal, increased appetite, and carbohydrate craving. It was the aim of our study to investigate whether the genotypes of the serotonin transporter gene were associated with symptoms of transient depressive relapse after TRP depletion. In addition, we matched the SAD patients with healthy control subjects to see if alleles and genotypes of the serotonin transporter gene were associated with SAD. High molecular weight DNA was isolated from peripheral blood leukocytes using standard methods. For the 5-HTT receptor gene, a 17-bp repetitive element of intron 2 was genotyped (variable number tandem repeat, VNTR). Alterations in HDRS scores after TRP depletion showed no significant association with alleles or genotypes of the 5-HTT gene, although heterozygotes showed a trend toward increased HDRS scores. The serotonin transporter is known to play a critical role in the termination of serotonergic neurotransmission by sodium-dependent uptake of 5-HT into the presynaptic neuron. The present study in a small group of SAD patients was unable to demonstrate that the 5-HTT gene plays a role in the pathogenesis of SAD or in short-term depressive relapse after TRP depletion.
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PMID:Behavioral effects of tryptophan depletion in seasonal affective disorder associated with the serotonin transporter gene? 1033 77

Twenty-eight high trait hostility male volunteers played a "cooperative" computer game 4.5 hours after an amino acid drink enhanced with, or depleted of, tryptophan. Each trial involved steering a tank through minefields following directions from an unknown "partner." Failure was experienced when the tank hit a mine or when time ran out. Subjects' moods, verbal aggression, attributions of blame, vocal acoustics, and blood pressure were assessed. Differences between tryptophan groups were not significant for primary measures of anger and verbal aggression. However, depleted subjects reported greater increases in feelings of restlessness and incompetence, were less successful in avoiding mines and showed greater increases in blood pressure during the game. Subjects in both groups sent more negative ratings when they lost the game by virtue of hitting a mine rather than losing by running out of time. However, ratings of the depleted group were less influenced by the reason for losing the game. Also, vocal acoustics showed a group X reason-for-losing interaction in the high-frequency band. Tryptophan-depleted subjects with high scores on Behavioral-Activation-System-Drive were most likely to send negative ratings and those scoring high on Buss-Durkee Hostility Inventory Assault and Guilt to report increased anger after the game.
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PMID:Tryptophan enhancement/depletion and reactions to failure on a cooperative computer game. 1063 81

We describe a patient treated with SSRI and Ldopa, who developed agitation, rigidity, hyperreflexia, restlessness, autonomic instability, fever and finally death. CSF examination, MRI of the brain, laboratory investigations, except for serum CK, glycemia and WBC, were normal. His condition was thought to result from an central serotonin activity. The serotonin syndrome occurs following the use of serotomimetic agents (serotonin reuptake inhibitors, tricyclic and tetracyclic antidepressants, tryptophan alone or in combination with monoamine oxidase inhibitors).
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PMID:Serotonin syndrome: a reported case. 1254 41

A strain of genetically modified Saccharomyces cerevisiae (S. cerevisiae) W303 181 was used to improve glucose-6-phosphate dehydrogenase (G6PDH) production in aerobic culture. Fed-batch cultures were carried out in a 5 L fermentor at variable values of the parameter K, namely, 0.2, 0.3, 0.5, 0.7, and 0.8 h(-)(1). The highest G6PDH production (1164 U/L) and specific activity (517 U/g(cell)) were obtained using the following conditions: glucose, 5.0 g/L; adenine, 8 microg/mL; histidine, 8 microg/mL; tryptophan, 8 microg/mL; temperature, 30 degrees C; inoculum, 1.28 g/L; pH, 5.7; agitation, 400 rpm; aeration, 2.2 vvm; and K, 0.2 h(-)(1). The exponential feeding pattern increased cell density (2.14 g/L), enzyme productivity (149.27), and biomass yield (0.18 g(glu)/g(cell)( )(mass)). The level of G6PDH in the genetically modified S. cerevisiae was approximately 4.1-fold higher than that found in a commercial strain.
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PMID:Effect of flow rate pattern on glucose-6-phosphate dehydrogenase synthesis in fed-batch culture of recombinant Saccharomyces cerevisiae. 1267 66

23% of all septic patients develop septic encephalopathy which is associated with an increased mortality rate. Symptoms such as agitation, confusion and disorientation ranging from stupor to coma often develop in early sepsis. Severe hypotension is significantly associated with the development of septic encephalopathy. Several other factors which may play a role are also discussed: effects of inflammatory mediators on the brain, inadequate cerebral perfusion pressure, blood-brain barrier derangements, disturbances of the cerebral microcirculation, cerebral ischemia e.g. due to hypocapnia,metabolic changes, altered amino acid levels, transmitter imbalances, liver insufficiency, multiple organ failure and infections of the CNS, respectively. Compared to patients with an isolated infection,patients in septic shock have increased levels of aromatic amino acids such as phenylalanine and tryptophan in the plasma and brain as well as decreased levels of branched chain amino acids. Patients who died had higher levels of aromatic amino acids than the survivors. The correlation between aromatic amino acids and the APACHE II score was significant. The tryptophan metabolite quinolinic acid which can be synthesized in activated macrophages could act as an excitatory transmitter on the N-methyl-D-aspartate (NMDA) -receptor. Observations from experimental models indicate that activated NMDA receptors activate the neuronal isoform of the NO-synthase and other calcium dependent enzymes. This releases free radicals which may damage the DNA and activate the nuclear enzyme Poly-ADP-ribose-synthetase (PARS), resulting in energy depletion and cell death. Sepsis is the main cause of metabolic encephalopathies in critically ill patients. The differential diagnoses include hepatic, renal,hypoxic-ischemic or cardiovascular encephalopathies as well as encephalopathies,metabolic disorders and organ dysfunctions of other origin. Therapeutic interventions are numerous,however, so far only investigated in few controlled studies. The primary therapeutic goal is to maintain an adequate perfusion pressure and to prevent hypoxia and hypocapnia. Although the infusion of branched chain amino acids is controversial, experimental investigations demonstrated improvements improvements in an animal model with septic encephalopathy. Further investigations with respect to glutamate receptor antagonists, new radical scavengers, NO- and PARS-inhibitors may show whether these substances are suitable for the prophylaxis or early therapy of septic encephalopathy.
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PMID:[Septic encephalopathy. Diagnosis und therapy]. 1275 14

Toennies, G. (Institute for Cancer Research, Philadelphia, Pa.), L. Iszard, N. B. Rogers, and G. D. Shockman. Cell multiplication studied with an electronic particle counter. J. Bacteriol. 82:857-866. 1961.-Suitable conditions are described for the application of the Counter electronic particle counter to the study of bacterial number and particle size distribution in growing cultures. When Streptococcus faecalis and Escherichia coli were each grown in a different medium, exponential growth was accompanied by a continuous decrease in average particle size. The average apparent particle volume of S. faecalis decreased by about 50% in five generations. Microscopic studies of S. faecalis indicated that this was due to a decrease in the average chain length of the cultures. The following observations concerning average particle size during exponential growth of S. faecalis in a synthetic medium were made: (i) A decreased concentration of tryptophan, serine, or proline resulted in a significant decrease in average particle size. Similar changes in numerous other nutrients produced no or only minor changes. (ii) The addition of a cytoplasmic extract prepared from exponentially growing cells resulted in changes similar to those resulting from the partial withdrawal from the medium of certain nutrients. (iii) The effect of the cytoplasmic extract could be counteracted by the addition of tryptophan. (iv) A limited survey, including the effects of the rate of exponential growth, mechanical agitation, the presence of indoleacetic acid, indole, kinetin, lysozyme, or ascorbate, disclosed no additional factor which significantly influenced the particle size distribution.
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PMID:Cell multiplication studied with an electronic particle counter. 1392 27


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