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)

THAM (trometamol; tris-hydroxymethyl aminomethane) is a biologically inert amino alcohol of low toxicity, which buffers carbon dioxide and acids in vitro and in vivo. At 37 degrees C, the pK (the pH at which the weak conjugate acid or base in the solution is 50% ionised) of THAM is 7.8, making it a more effective buffer than bicarbonate in the physiological range of blood pH. THAM is a proton acceptor with a stoichiometric equivalence of titrating 1 proton per molecule. In vivo, THAM supplements the buffering capacity of the blood bicarbonate system, accepting a proton, generating bicarbonate and decreasing the partial pressure of carbon dioxide in arterial blood (paCO2). It rapidly distributes through the extracellular space and slowly penetrates the intracellular space, except for erythrocytes and hepatocytes, and it is excreted by the kidney in its protonated form at a rate that slightly exceeds creatinine clearance. Unlike bicarbonate, which requires an open system for carbon dioxide elimination in order to exert its buffering effect, THAM is effective in a closed or semiclosed system, and maintains its buffering power in the presence of hypothermia. THAM rapidly restores pH and acid-base regulation in acidaemia caused by carbon dioxide retention or metabolic acid accumulation, which have the potential to impair organ function. Tissue irritation and venous thrombosis at the site of administration occurs with THAM base (pH 10.4) administered through a peripheral or umbilical vein: THAM acetate 0.3 mol/L (pH 8.6) is well tolerated, does not cause tissue or venous irritation and is the only formulation available in the US. In large doses, THAM may induce respiratory depression and hypoglycaemia, which will require ventilatory assistance and glucose administration. The initial loading dose of THAM acetate 0.3 mol/L in the treatment of acidaemia may be estimated as follows: THAM (ml of 0.3 mol/L solution) = lean body-weight (kg) x base deficit (mmol/L). The maximum daily dose is 15 mmol/kg for an adult (3.5L of a 0.3 mol/L solution in a 70kg patient). When disturbances result in severe hypercapnic or metabolic acidaemia, which overwhelms the capacity of normal pH homeostatic mechanisms (pH < or = 7.20), the use of THAM within a 'therapeutic window' is an effective therapy. It may restore the pH of the internal milieu, thus permitting the homeostatic mechanisms of acid-base regulation to assume their normal function. In the treatment of respiratory failure, THAM has been used in conjunction with hypothermia and controlled hypercapnia. Other indications are diabetic or renal acidosis, salicylate or barbiturate intoxication, and increased intracranial pressure associated with cerebral trauma. THAM is also used in cardioplegic solutions, during liver transplantation and for chemolysis of renal calculi. THAM administration must follow established guidelines, along with concurrent monitoring of acid-base status (blood gas analysis), ventilation, and plasma electrolytes and glucose.
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PMID:Guidelines for the treatment of acidaemia with THAM. 950 41

Amyotrophic lateral sclerosis (ALS) is a motor neuron disease with evidence of both anterior horn cell and corticospinal tract degeneration. The incidence of ALS is 1 to 2.5 cases per 100,000 population and the disease occurs primarily in adult life. The etiology of sporadic ALS remains unknown, although 5 to 10% of cases are familial. The diagnosis of ALS requires the presence of both upper and lower motor neuron findings and progressive motor dysfunction. Several theories regarding the pathogenesis of ALS have emerged including glutamate excitotoxicity, free radical oxidative stress, neurofilament accumulation, and autoimmunity. Clinical trials involving antiglutamate agents, antioxidants, immunosuppressants, and growth factors have shown no substantial benefit in slowing progression, with death usually occurring 2 to 5 years following the onset of symptoms. The management of ALS patients requires a multidisciplinary team that can provide the numerous medical and physical interventions necessary to treat weakness and fatigue, bulbar dysfunction, spasticity and pain, depression, and respiratory failure.
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PMID:Amyotrophic lateral sclerosis. 956 65

Pine oil is a common component of household cleaning solutions. We present the case of an elderly woman with dementia who ingested a household cleaning solution that contained pine oil and review the treatment of pine oil ingestion. The patient developed CNS depression and respiratory failure that required intubation and mechanical ventilation. A chest radiograph revealed diffuse alveolar interstitial infiltrates consistent with pneumonitis. The patient improved with supportive care. However, she developed nosocomial pneumonia, sepsis, and multiple organ failure and subsequently died. This case is illustrative of the increased risk for ingestion of toxic household compounds in the growing population of elderly and demented individuals, who are being cared for in the home. Pine oil ingestions are one of the most common accidental ingestions encountered in clinical practice. Clinical features of ingestion include depressed mentation, respiratory failure, and GI dysfunction. The treatment is supportive, and the ingestions are rarely fatal.
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PMID:Pine oil ingestion: a common cause of poisoning. 1059 16

We describe a 4.5-year-old girl in whom post transplantation lymphoproliferative disorder was diagnosed 1 year after liver transplantation. She ran a complicated course with multiple organ involvement: respiratory failure which required mechanical ventilation, renal failure, bone marrow depression and severe protein-losing enteropathy.
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PMID:[EBV-related lymphoproliferative disorder after liver transplantation]. 1095 65

There is nothing more discouraging than for a patient to be given a specific diagnosis, then to be told that there is nothing that can be done. Physicians are equally disheartened to see exponential progress being made in the understanding of the pathophysiology of a complex disorder but few direct benefits resulting for their patients. Over the past 5 years, molecular genetic research has completely revolutionized the way in which the progressive cerebellar ataxias are classified and diagnosed, but it has yet to produce effective gene-based, neuroprotective, or neurorestorative therapies. The treatment of cerebellar ataxia remains primarily a neurorehabilitation challenge, employing physical, occupational, speech, and swallowing therapy; adaptive equipment; driver safety training; and nutritional counseling. Modest additional gains are seen with the use of medications that can improve imbalance, incoordination, or dysarthria (amantadine, buspirone, acetazolamide); cerebellar tremor (clonazepam, propranolol); and cerebellar or central vestibular nystagmus (gabapentin, baclofen, clonazepam). Many of the progressive cerebellar syndromes have associated features involving other neurologic systems (eg, spasticity, dystonia or rigidity, resting or rubral tremor, chorea, motor unit weakness or fatigue, autonomic dysfunction, peripheral or posterior column sensory loss, neuropathic pain or cramping, double vision, vision and hearing loss, dementia, and bowel, bladder, and sexual dysfunction), which can impede the treatment of the ataxic symptoms or can worsen with the use of certain drugs. Treatment of the associated features themselves may in turn worsen the ataxia either directly (as side effects of medication) or indirectly (eg, relaxation of lower limb spasticity that was acting as a stabilizer for an ataxic gait). Secondary complications of progressive ataxia can include deconditioning or immobility, weight loss or gain, skin breakdown, recurrent pulmonary and urinary tract infections, aspiration, occult respiratory failure, and obstructive sleep apnea, all of which can be life threatening. Depression in the patient and family members is common. Although no cures exist for most of the causes of cerebellar ataxia and there are as yet no proven ways to protect neurons from premature cell death or to restore neuronal populations that have been lost, symptomatic treatment can greatly improve the quality of life of these patients and prevent complications that could hasten death. Supportive interventions should always be offered-- education about the disease itself, genetic counseling, individual and family counseling, referral to support groups and advocacy groups, and guidance to online resources. Misinformation, fear, depression, hopelessness, isolation, and financial and interpersonal stress can often cause more harm to the patient and caregiver than the ataxia itself.
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PMID:Cerebellar Ataxia. 1109 49

Bleeding in the tracheobronchial tree in intubated patients on an intensive care unit is a potentially life-threatening incident. The antecedent state of disease and frequent respiratory failure require immediate and effective therapeutic measures to avoid further respiratory and cardiocirculatory depression. We present our bronchoscopic management of endobronchial bleeding. Cardiorespiratory function must be maintained by modification of the mechanical ventilation and drug therapy owing to the patient's condition. Seven consecutive patients with acute endobronchial bleeding were treated with fiberoptic bronchoscopy and instillation of cold epinephrine-saline solution (1:10,000-100,000) during the period of July 1997 to December 1997. Control of bleeding was achieved after 1 to 20 (mean +/- SEM: 5.86 +/- 0.93) bronchoscopic interventions during a period of 0.5 hours to 10 days. One control bronchoscopy was performed additionally in every patient. Cardiocirculatory instability was observed in five patients. Six patients survived; one patient died of uncontrolled bleeding caused by severe pulmonary aspergillosis. Fiberoptic endobronchial epinephrine instillation is an effective therapy for life-threatening hemoptysis in critically ill patients. Widespread use of flexible bronchoscopy makes this procedure immediately applicable in critical situations. Intubated and mechanically ventilated patients with life-threatening hemoptysis especially benefit from this rapidly feasible procedure.
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PMID:Fiberoptic bronchoscopy of intubated patients with life-threatening hemoptysis. 1121 48

This article focuses on factors related to decreased food intake of infants and children, but does not address anorexia or bulimia nervosa. The nature of feeding problems may be behavioral, organic, or a mixture of both. Behavioral problems that affect intake have their roots in 1) parental or cultural expectations for food intake and body habit, 2) parental anxiety about weight gain in a vulnerable child or insecurity about parental skills, 3) power struggles between parent and child that manifest in eating habits, 4) conditions that may have enhanced the gag reflex, such as prolonged orotracheal intubation or a nasogastric tube, 5) failure to establish links between hunger, food intake, and satiety in infants who had not been fed orally for a relatively prolonged period of time at a critical age, and 6) anxiety or depression. Organic causes that lead to decreased food intake include swallowing problems (neurologic or conditioned hypersensitive gag, structural anomalies of the oropharynx, dyscoordinated swallow, painful swallow, and obstructed swallow ), respiratory distress, excessive fatigability (heart failure, respiratory failure), and lack of appetite (many chronic systemic illnesses). At particular risk for feeding problems are infants of premature birth, children with craniofacial anomalies, those with certain genetic syndromes, and those with neurologic involvement. An evaluation by specialists is recommended for children with obvious behavioral problems but for whom the usual recommendations have failed and for those in whom symptoms cannot be explained solely by behavioral issues or in whom organic causes are suspected. The evaluation preferably should be performed by a team specialized in pediatric feeding disorders or otherwise by an occupational therapist or speech pathologist with expertise in the area of feeding.
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PMID:Feeding Problems in Infants and Children. 1156 Jul 92

Effective use of sedative-hypnotic and analgesic agents is an integral part of providing patient comfort and safety. Of the numerous drugs administered, benzodiazepines, propofol, and narcotics are the most popular. Even these proven, time-tested sedative-hypnotics and analgesics are not perfect, however, and modern intensive care demands a more ideal product. The development of dexmedetomidine, an alpha2-agonist, is an attempt to improve sedative/analgesic use and provide a drug that possesses the characteristics outlined in Table 1. It stimulates alpha2-adrenergic receptors in the locus ceruleus to provide sedation and in the spinal cord to enhance analgesia. It also causes sympatholysis via central and peripheral mechanisms. Dexmedetomidine binds alpha2-receptors eight times more avidly than clonidine and is shorter acting. It was initially evaluated as an anesthetic, but was associated with excessive bradycardia and hypertension, followed by hypotension. In late 1999, dexmedetomidine was approved for adult ICU use for less than 24 hours as a sedative infusion. It currently lacks approval in Europe. Most of the clinical experience with dexmedetomidine has been with surgical patients undergoing cardiac and vascular procedures. Careful patient selection and proper drug infusion are needed to avoid excessive deleterious hemodynamic results. Slower bolus loading over 20 minutes results in minimally decreased heart rate and blood pressure. Continuous infusion maintains unique sedation (patients appear to be asleep, but are readily roused), analgesic sparing effect, and minimal depression of respiratory drive. More experience with dexmedetomidine infusion in medical ICU patients and patients with complex end-organ dysfunction such as respiratory failure or systemic inflammatory response syndrome is needed before conclusions can be drawn about the drug's potential for wider application and its long-term (> 24 h) safety and effectiveness.
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PMID:Dexmedetomidine. 1157 17

1,1-Dichloroethane (DCE) is a solvent that is often found as a contaminant of drinking water and a pollutant at hazardous waste sites. Information on its short- and long-term toxicity is so limited that the U.S. EPA and ATSDR have not established oral reference doses or minimal risk levels for the volatile organic chemical (VOC). The acute oral LD(50) in male Sprague-Dawley (S-D) rats was estimated in the present study to be 8.2 g/kg of body weight (bw). Deaths appeared to be due to CNS depression and respiratory failure. In an acute/subacute experiment, male S-D rats were given 0, 1, 2, 4, or 8 g DCE/kg in corn oil by gavage for 1, 5, or 10 consecutive days. The animals were housed in metabolism cages for collection of urine and sacrificed for blood and tissue sampling 24 h after their last dose. There were decreases in body weight gain and relative liver weight at all dosage levels, as well as increased renal nonprotein sulfhydryl levels at 2 and 4 g/kg after 5 and 10 days. Elevated serum enzyme levels, histopathological changes, and abnormal urinalyses were not manifest. For the subchronic study, adult male S-D rats were gavaged with 0.5, 1, 2, or 4 g DCE/kg 5 times weekly for up to 13 weeks. Animals receiving 4 g/kg exhibited pronounced CNS depression, with more than one-half dying by week 11. The 2-g/kg rats exhibited moderate CNS depression. One 2-g/kg rat died during week 6. There were very few manifestations of organ damage in animals that succumbed or in survivors at any dosage level. Decreases in bw gain and transient increases in enzymuria were noted at 2 and 4 g/kg. Serum enzyme levels and blood urea nitrogen were not elevated, nor were glycosuria or proteinuria present. Chemically induced histological changes were not seen in the liver, kidney, lung, brain, adrenal, spleen, stomach, epididymis, or testis. Hepatic microsomal cytochrome P450 experiments revealed that single, high oral doses of DCE did not alter total P450 levels, but did induce CYP2E1 levels and activity and inhibit CYP1A1 activity. These effects were reversible and regressed with repeated DCE exposure. There was no apparent progression of organ damage during the 13-week subchronic study, nor appearance of adverse effects not seen in the short-term exposures. One g/kg orally (po) was found to be the acute, subacute, and subchronic LOAEL for DCE, under the conditions of this investigation. In each instance, 0.5 g/kg was the NOAEL.
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PMID:Acute, subacute, and subchronic oral toxicity studies of 1,1-dichloroethane in rats: application to risk evaluation. 1160 9

We present a 1 7-year-old female with acute extra-pyramidal parkinsonism complicating a suicidal attempt with the organophosphate insecticide chlorpyrifos, who was initially suspected to have developed severe depression or psychosis. On admission she was stupurous, with diarrhoea and massive salivation lapsing into respiratory failure and coma. Following atropine and toxogonin treatment along with mechanical ventilation she developed overt extrapyramidal parkinsonism and encephalopathy, characterized by impaired sensorium and agitation, mask facies along with a muffled voice and swallowing impairment, a resting tremor with cogwheel rigidity switching to bradykinetic choreoathetotic movements. Once a parkinsonian syndrome was diagnosed, she was given amantadine therapy with complete recovery. The patient is presently maintained on amantadine therapy; there was mild worsening of her extrapyramidal signs following unplanned discontinuation of this medication, and on follow-up assessments after 9 months she is virtually asymptomatic. A parkinsonian extrapyramidal syndrome, complicating organophosphate intoxication, should therefore also be taken into account in any patient with organophosphate poisoning, presenting with marked behavioural alterations, rigidity or akinetic mutism, and beneficial response to amantadine.
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PMID:Extra-pyramidal parkinsonism complicating organophosphate insecticide poisoning. 1176 85


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