Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011206 (delirium)
 5,996 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The authors review the literature describing acute symptomatology produced by the gradual or abrupt withdrawal of heterocyclic antidepressants, monoamine oxidase inhibitors (MAOI) and neuroleptics. 2. Withdrawal of heterocyclic antidepressants and antipsychotic agents causes similar symptomatology. Symptoms produced by the discontinuation of these drugs include nausea, emesis, anorexia, diarrhea, rhinorrhea, diaphoresis, myalgias, paresthesias, anxiety, agitation, restlessness, and insomnia. 3. Psychotic relapse is often presaged by anxiety, agitation, restlessness, and insomnia. Prodromal symptoms are distinguished from the effects of neuroleptic withdrawal by a temporal relationship of the latter to reductions in the dosage or discontinuation of antipsychotic agents. 4. Withdrawal of MAOIs can result in severe anxiety, agitation, pressured speech, sleeplessness or drowsiness, hallucinations, delirium, and paranoid psychosis. 5. MAOI withdrawal phenomena resemble the symptoms produced by the discontinuation of chronically administered psychostimulants. 6. The capacity of MAOIs to exert amphetamine-like effects presynaptically and the propensity of somatic treatments for depression to subsensitize presynaptic receptors regulating the release of catecholamines provide a basis for the development of psychotic symptoms upon the withdrawal of MAOI. Evidence for this hypothesis is reviewed.
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PMID:Heterocyclic antidepressant, monoamine oxidase inhibitor and neuroleptic withdrawal phenomena. 196 71

A herd of 15 mature riding horses with a history of anorexia, weight loss, and lethargy was examined. The animals had been fed a 50/50 mixture of commercial sweet feed and corn screenings contaminated with a heavy growth of Fusarium moniliforme. Thirteen of the horses had one or more neurologic signs. The most characteristic signs were profound depression and mild ataxia. Over the 19-day course of the epizootic, the horses had increasing severe neurologic deficits, including unilateral blindness and delirium. Despite the clinical appearance of dehydration, 12 horses had low PCV (16 to 27%), hematocrit (21.2 to 31.0%; determined by automated cell counter), and RBC counts (3.76 to 5.5 x 10(6) RBC/microliters). White blood cell counts were variable (4,900 to 17,000 WBC/microliters). Necropsy findings included diffuse malacia of the white matter of the frontal cortex and severe multifocal perivascular hemorrhage in the white matter of the temporal cortex, basal ganglia, anterior medulla, and pons. One horse had a hepatic lesion consisting of a mixed inflammatory cell infiltrate and bile duct proliferation. The attack rate of this epizootic was 100%. The course of disease was unusually long in some animals. In an experiment, the fusarium-infected corn screenings were fed to horses and did not cause clinical signs or alterations in blood or serum biochemical values.
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PMID:Clinical and epidemiologic features of an epizootic of equine leukoencephalomalacia. 204 19

We describe two patients with methylmalonic aciduria and homocystinuria (Cbl C). The disorder was not diagnosed in patient 1 until 4 1/2 years of age; he had a history of fatigue, anorexia, delirium, and spasticity. Moderate megaloblastic bone marrow changes were observed, and there was hyperreflexia of the lower limbs. His condition improved clinically with hydroxycobalamin therapy. Patient 2 was hospitalized at 6 weeks of age because of lethargy and poor feeding. She was found to have macrocytosis. Despite an initial good clinical response to hydroxycobalamin, she developed a striking pigmentary retinopathy. Methylmalonic aciduria persisted in both patients, and homocystinuria persisted in patient 1 despite therapy. The diagnosis of Cbl C disease has been confirmed in both patients by biochemical studies of cultured fibroblasts, including complementation studies. The differences in age of onset and clinical findings together with the similar biochemical findings in these two patients demonstrate the heterogeneity of phenotypic expression in patients with apparently identical abnormalities of vitamin B12 metabolism.
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PMID:Clinical heterogeneity in cobalamin C variant of combined homocystinuria and methylmalonic aciduria. 395 Aug 20

A patient with multiple enteric fistulae, after months of parenteral hyperalimentation, developed, severe depression accompanied by delirium, dermatitis, pallor, paresthesia, nausea, vomiting, anorexia, and headaches. His symptoms improved after treatment with parenteral biotin. Biotin-deficiency should be suspected in patients on hyperalimentation (without biotin supplementation) who develop similar symptoms.
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PMID:Biotin-responsive depression during hyperalimentation. 640 8

The withdrawal of heterocyclic antidepressants and antipsychotic agents can produce nausea, emesis, anorexia, diarrhoea, rhinorrhoea, diaphoresis, myalgias, paraesthesias, anxiety, agitation, restlessness and insomnia. The withdrawal of monoamine oxidase (MAO) inhibitors may result in severe anxiety, agitation, pressured speech, sleeplessness or drowsiness, hallucinations, cognitive impairment, delirium, suicidality and delusions of persecution. The withdrawal of antipsychotic agents may give rise to symptoms preceding the onset of psychosis. These potential harbingers of relapse include anxiety, agitation, restlessness and insomnia. The withdrawal phenomena reviewed are usually prevented by gradually reducing the total daily dosage of the pertinent drug. Antimuscarinic agents often alleviate the distress produced by the withdrawal of tricyclic antidepressants and antipsychotic agents. MAO inhibitor withdrawal syndromes may constitute medical emergencies. The prevention of the evolution of a MAO inhibitor withdrawal-precipitated syndrome is a high priority.
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PMID:Withdrawal phenomena associated with antidepressant and antipsychotic agents. 791 78

The authors prospectively assessed symptoms induced by the interruption of antidepressants in 16 patients (11 women and 5 men), aged from 33 to 85 years (mean = 52.4 +/- 16.4), treated with antidepressants since at least two weeks. All patients were free of alcohol abuse or dependence disorder and of other dependence to psychoactive substances. None of them presented medical illness. Diagnosis were made by separate evaluations by two authors and confirmed with a semistructered assessment instrument: the Schedule for Affective Disorders and Schizophrenia (Lifetime Version). All patients were submitted to a brutal discontinuation of their antidepressant agent. Patients were assessed twice, before the interruption of the antidepressant, and 72 hours later. Effects of antidepressant interruption were assessed by several means. Modification of anxiety and depression were evaluated using the Montgomery Asberg Depression Rating Scale (MADRS) and the Hamilton Anxiety Scale. Symptoms of withdrawal were assessed with Cassano and al.'s scale SESSH including an evaluation of anxiety, agitation, irritability, anergy, difficulty on concentrating, depersonalization, sleep and appetite disorders, muscle pains, nausea, tremor, sweating, altered taste, hyperosmia, paresthesias, photophobia, motor incoordination, dizziness, hyperacousia pain, delirium. Fourteen of the 16 patients (87.5%) presented modifications of their somatic or psychic state 3 days after the interruption of the antidepressant treatment. Most frequent symptoms were: increase in anxiety (31%), increase in irritability (25%), sleep disorders (19%), decrease of anergia and fatigue (19%). Mean scores of anxiety and depression were not significantly modified by the withdrawal. Following TCAs interruption (7 patients) most frequent symptoms were sleep disorders; increase in anxiety, nausea. Among patients withdrawn from SSRIs (6 patients), most frequent symptoms were increase in anxiety, increase in irritability, headache. Patients also presented a decrease of nausea, and of anorexia.
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PMID:[Prospective evaluation of antidepressant discontinuation]. 969 14

Six patients with severe and complicated falciparum malaria (6.7 +/- 2.7 WHO criteria) were admitted to our Intensive Care Unit. All patients acquired the disease while travelling in tropical Africa without appropriate chemoprophylaxis. The clinical manifestations included hyperpyrexia (all patients), chills (4), sweating (2), asthenia (3), anorexia (2), headache (1), arthralgias (1), vomiting (4), diarrhoea or abdominal discomfort (3), jaundice (2) and disturbances of consciousness (4). All patients had anemia, thrombocytopenia, hyponatremia, hypoproteinemia, hypoalbuminemia, hypocalcemia and acute renal failure, in one case associated with anuria. A low grade parasitemia was observed in two patients and a high grade parasitemia (20%-58% of erythrocytes) in four. Exchange transfusion was performed only in high parasitemic patients and all of them survived. All patients were treated with quinine, a sulfonamide and pyrimethamine. Additionally, five patients received oxytetracycline, doxycycline or clindamycin. Three patients required hemodyalisis. Five patients had delirium, coma or seizures. All patients had at least one sign of hepatic impairment: liver enlargement, jaundice or increased bilirubin or aminotransferase levels. Two patients had spleen enlargement. Laboratory findings suggested disseminated intravascular coagulation in four patients. Four patients developed pulmonary changes and three of them required mechanical ventilation. A Swan-Ganz catheter was placed in four patients. In three of them (two with pulmonary edema) the pulmonary capillary wedge pressure was initially increased, which suggested a cardiogenic or hypervolemia mechanism, but soon returned to normal level. One patient with low grade parasitemia died because of adult respiratory distress syndrome after 18 days. In our series, the degree of parasitemia was not related to the severity of the disease.
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PMID:[Severe and complicated malaria. Report of six cases]. 977 80

Cytokines have a major role in promoting the growth and spread of cancers. Elevated levels of several cytokines have been described in cancer patients. Evidence from animal and human studies suggests that cytokines may contribute to a wide range of symptoms in advanced cancer, including: asthenia, pain, drowsiness, cognitive failure, agitated delirium, autonomic dysfunction, anorexia, cachexia, fever and metabolic abnormalities. Considerable effort is being directed at finding anticytokine treatments, raising the possibility of new options for symptoms that are currently difficult to control.
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PMID:Cytokines and advanced cancer. 1101 40

Managing the symptoms of advanced disease at the end of life is one of the most challenging aspects of medicine for most clinicians. Traditional textbooks provide limited resources for treating patients at this stoichiometric point in their disease. This article provides an overview in the treatment of common symptoms at the end of life, such as anxiety, anorexia and cachexia, constipation, delirium, dyspnea, fatigue and asthenia, nausea and vomiting, malignant intestinal obstruction, and terminal restlessness. By addressing these symptoms, the physician can play a key role in the patient's achievement of a peaceful, symptom-free, and dignified death in the setting of their choice.
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PMID:Symptom management in hospice and palliative care. 1150 77

Physical symptoms other than pain often contribute to suffering near the end of life. In addition to pain, the most common symptoms in the terminal stages of an illness such as cancer or acquired immunodeficiency syndrome are fatigue, anorexia, cachexia, nausea, vomiting, constipation, delirium and dyspnea. Management involves a diagnostic evaluation for the cause of each symptom when possible, treatment of the identified cause when reasonable, and concomitant treatment of the symptom using nonpharmacologic and adjunctive pharmacologic measures. Part I of this two-part article discusses fatigue, anorexia, cachexia, nausea and vomiting. Fatigue is the most common symptom at the end of life, but little is known about its pathophysiology and specific treatment. Education of the patient and family is the foundation of treatment with the possible use of adjunctive psychostimulants. Anorexia and cachexia caused by wasting syndromes are best managed with patient and family education, as well as a possible trial of appetite stimulants such as megestrol or dexamethasone. For appropriate pharmacologic treatment, it is helpful to identify the pathophysiologic origin of nausea in each patient.
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PMID:Management of common symptoms in terminally ill patients: Part I. Fatigue, anorexia, cachexia, nausea and vomiting. 1156 72


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