Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ethylene glycol (EG) is a toxic chemical found in antifreeze and heat exchangers. Standard therapy for EG intoxication in administration of ethanol (ETOH) to inhibit its metabolism by alcohol dehydrogenase (ADH). Studies indicate 1,3-butylene glycol (BG) binds to ADH more efficiently than EG and is orally less toxic than EG or ETOH. Male rats were divided into 5 groups of 6 animals. Groups received by oral intubation a single dose of EG (32 mmole/kg), BG (39 mmole/kg) initially and every 6 h up to 72 h, ETOH (39 mmole/kg) initially and every 6 h up to 72 h, or EG initially and then either BG or ETOH every 6 h up to 72 h. Administration of ETOH produced hepatotoxicity and pulmonary pathology as indicated by changes in clinical chemistry, urinalysis, and histopathology, while BG did not. Neither ETOH nor BG produced any apparent nephrotoxicity. ETOH produced ataxia, lethargy and central nervous system depression while BG did not. BG produced a higher concentration of urinary EG indicating a better inhibition of ADH metabolism of EG. Ethanol produced a higher EG blood concentration than BG. Ethanol's higher EG blood concentration may be partially attributed to dehydration and a decreased urine output as well as inhibition of ADH metabolism. Ethanol produced mortality in all animals prior to 72 h. The EG/ETOH combination produced mortality more quickly due to additive toxicity of the combination. Lack of any significant toxicity produced by BG and the production of significant toxicities by ETOH indicates that BG is potentially a better antidote than ETOH.
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PMID:The toxicokinetics of 1,3-butylene glycol versus ethanol in the treatment of ethylene glycol poisoning. 162 60

Neurologic disturbances are common following the intensive chemotherapy and radiotherapy of bone marrow transplantation (BMT) conditioning regimens. The somnolence syndrome, which occurs in most children treated for leukemia with prophylactic cranial irradiation, has previously not been reported following BMT. This syndrome consists of transient lethargy, irritability, headaches, low grade fevers, gastrointestinal disturbances and depression. We report the case of a 38-year-old female with acute non-lymphocytic leukemia who developed symptoms typical of the somnolence syndrome 8 weeks following 1320 cGy total body irradiation and cyclophosphamide conditioning. Encephalographic findings were consistent with the syndrome, and no additional infectious or metabolic disorders could be identified. As predicted by the pediatric experience, the symptoms were transient, resolving following steroid and anti-depressant therapy. Among patients undergoing radiation based conditioning regimens, especially those not receiving concurrent steroid therapy, the appearance of post-transplantation somnolence may be an expression of this syndrome.
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PMID:Post-irradiation somnolence syndrome in an adult patient following allogeneic bone marrow transplantation. 162 37

We describe a 55-year-old female who presented with a 1-year history of tiredness, depression and painful stiff joints. The most striking clinical abnormality was bilateral frozen shoulders, local corticosteroid treatment of which provided the first diagnostic clue. She was found to have profound diminution of plasma cortisol secondary to an isolated deficiency of ACTH. There was no obvious cause for this. Steroid replacement eradicated her lethargy within 3 months and evidence of frozen shoulders resolved completely.
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PMID:Isolated ACTH deficiency presenting with bilateral frozen shoulder. 164 65

Acivicin (AT-125) is a glutamine antagonist with dose-limiting, schedule-dependent CNS toxicity and predictable CSF penetration after intravenous administration. Because of these properties, a trial in CNS malignancies was initiated. Thirty-two patients with recurrent or residual malignant astrocytomas were treated with AT-125. The majority of patients had glioblastoma multiforme (24) and had received prior nitrosoureas (21). The median age was 50 years, and Southwest Oncology Group (SWOG) performance status was 2. The major determinant of response was based upon radiologic criteria using computed tomographic (CT) scanning and/or magnetic resonance imaging (MRI) scans. The tumor mass was measured in two perpendicular planes, which yielded the largest cross-sectional area. Standard solid tumor criteria for response were used. All responding patients also had a stable or tapered dose of corticosteroids with stable or improved performance status and neurologic examination. There were four objective responses (12%): one complete remission (3 1/2+ years) and three partial remissions (57, 86, and 322 days). Two patients had improvement in disease that did not meet requirements for a partial remission. Toxicity was mild and primarily consisted of nausea, vomiting, and lethargy. Two patients were removed from study due to neurotoxicity (depression and hallucinations). The strict response criteria used in this trial were not those that have been used in testing other active agents such as carmustine (BCNU). We conclude that AT-125 has objective antitumor activity in malignant astrocytomas and warrants further study.
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PMID:Objective antitumor activity of acivicin in patients with recurrent CNS malignancies: a Southwest Oncology Group trial. 164 69

The calcium antagonists are a heterogeneous class of drugs which block the inward movement of calcium into cells through 'slow channels' from extracellular sites. By inhibiting phase 0 depolarisation in cardiac pacemaker cells and phase 2 plateau in myocardium, and by depressing calcium ion flux in smooth muscle cells of blood vessels, these agents may exert profound effects on the cardiovascular system, particularly in susceptible individuals or in overdose. Sinus node depression, impaired atrioventricular (AV) conduction, depressed myocardial contractility, and peripheral vasodilatation may result. Pharmacokinetic features of calcium antagonists include rapid and complete absorption from the gastrointestinal tract, with extensive first-pass hepatic metabolism yielding generally low bioavailability. The volume of distribution is generally large and protein binding is high. Elimination is almost entirely by the liver. Impaired renal function does not affect pharmacokinetics. Verapamil is the most potent inhibitor of cardiac conduction and contractility, with diltiazem also showing such effects. Nifedipine is the most potent vasodilator, but only occasionally impairs the sinus node or AV conduction. Significant pharmacodynamic effects are common during combination therapy with calcium antagonists, especially verapamil and beta-blockers. Verapamil may significantly elevate serum digoxin concentrations and may exert additive negative effects on chronotropism and dromotropism when this combination is used. Overdoses of calcium entry blockers are becoming more frequent and reflect an extension of the known pharmacodynamic profile of these agents. Typical features include confusion or lethargy, hypotension, sinus node depression and cardiac conduction defects. Onset of symptoms may be delayed if a sustained release preparation is ingested. Management of calcium antagonist overdose includes gut decontamination with lavage and activated charcoal. All symptomatic patients and patients with a history of ingesting a sustained release preparation should be admitted for ECG monitoring. If bradycardia and/or conduction defects contribute to hypotension, atropine or isoprenaline (isoproterenol) may accelerate the ventricular rate. Transvenous pacing may be required. Depressed myocardial contractility usually responds well to calcium chloride or calcium gluconate administration, but further inotropic support may be required. Peripheral vasodilation should be managed with intravenous fluids and a pressor agent such as dopamine or norepinephrine (noradrenaline).
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PMID:Poisoning due to calcium antagonists. Experience with verapamil, diltiazem and nifedipine. 179 22

A 18-year-old boy was admitted to hospital in an unconsciousness state as a result of taking a large dose of several psychotropic drugs simultaneously in an attempt to commit suicide. Blood studies revealed hypoxia (55.7 mmHg) and hypercapnia (59.7 mmHg). Hypoxia (74.3 mmHg) and hypercapnia (46.7 mmHg) were still present on the fourth day after admission, and the patient was becoming lethargic. Reduced vascular markings in the right upper lung field on chest roentgenogram in spite of hypercapnia suggested that the persistent hypoxia was the result of a pulmonary embolism. This diagnosis was supported by a perfusion defect on 99mTc-MAA scintigram and arterial obstruction in right pulmonary angiogram. Hypercapnia is an unusual finding in pulmonary embolism, and in this case was considered due to depression of respiration by psychotropic drugs.
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PMID:[A case of pulmonary embolism following acute respiratory failure with hypercapnia]. 180 86

In order to minimize heat loss cold stress induces peripheral vasoconstriction via the sympathetic nervous system. This effect is most pronounced in the extremities. Vasoconstriction does not appear in the head-neck region--a fact of great importance in emergency situations. In order to compensate for heat loss shivering is an early event, where involuntary muscle contractions increase metabolic rate 2-6 fold. Early tachycardia and elevated blood-pressure, followed by progressive bradycardia and lowered pressure are common cardiovascular effects of hypothermia. Death due to ventricular fibrillation or asystole occurs between 28 degrees-25 degrees C. Cold stress causes an osmolal diuresis with sodium and chloride as the main constituents. The natriuresis is of tubular origin and could be due to impaired autoregulation in the kidney and/or depend on the natriuretic polypeptide. The augmented urine flow decreases blood volume, lowers physical working capacity and increases blood viscosity--all negative events in a hazardous situation. Sudden immersion initiates hyperventilation for 1-2 minutes with an increasing risk of drowning. Thereafter ventilation decreases to rates consistent with metabolic requirements. In severe hypothermia carbon dioxide retention causes respiratory and metabolic acidosis. Hypothermia induces progressive depression of mental functions starting with apathy and bizarre behaviour and ending in lethargy and coma often between 30 degrees-28 degrees C. The paradoxal feeling of heat with undressing in agony could depend on cerebral receptor disturbances.
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PMID:Human physiology under cold exposure. 181 74

A seven-year-old male Border Collie was presented with a history of lethargy, episodic circling, incoordination and polydypsia. Physical examination revealed depression, obesity and bradycardia. A neurological examination indicated the possible presence of a space-occupying lesion in the brain. Results of the clinical investigation revealed hyposthenuria, sinus bradycardia and increased concentration of protein in the cerebrospinal fluid. A computerised axial tomography scan revealed a mass in the region of the hypophysis. The dog was euthanased and a post mortem examination confirmed the presence of a craniopharyngioma.
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PMID:A craniopharyngioma in a seven-year-old dog. 194 90

Rostral and middle cranial fossa tumors affecting the optic chiasm and resulting in acute visual deficits were diagnosed in 7 dogs and 1 cat. Blindness and dilated nonresponsive pupils were the primary signs in all animals. Other concurrent neurologic deficits were either absent or were equivocal. Behavioral changes, including signs of depression and lethargy, were noticed in 1 dog and the cat subsequent to the onset of blindness. Retinal function was assessed as normal by electroretinography in all animals. The histologic necropsy diagnosis was pituitary carcinoma in 1 dog and the cat and paranasal sinus carcinoma with intracranial extension in 1 dog. A cytologic diagnosis of polycentric lymphosarcoma affecting the optic chiasm was diagnosed in 1 dog. In the remaining 4 dogs, results of computed tomographic imaging or endocrine function testing suggested pituitary gland neoplasia. Four dogs were treated with cobalt-60 radiation or chemotherapy. There was partial return of visual function in only 1 of the dogs treated with radiation.
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PMID:Acute blindness associated with intracranial tumors in dogs and cats: eight cases (1984-1989). 195 68

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


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