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)

We report 6 patients in whom diffuse alveolar damage (DAD) was found on 1 or more lung biopsy specimens and who experienced recurrent episodes of acute respiratory failure. The patients ranged in age from 43 to 55 years. Two to five episodes of respiratory failure occurred in each over a period of 4 months to 2 years. One patient developed evidence of chronic lung disease; while the others remained well between episodes. Lung biopsies showed the acute stage of DAD in 3, overlapping acute and organizing stages in 3, and the organizing stage in 2. A definite cause was not identifiable in any. However, 4 had been treated with narcotics for chronic pain before the first episode, and 1 received this treatment before the recurrent episode. Three also were receiving psychotropic drugs for anxiety and depression. Five patients had evidence of gastroesophageal reflux disease (GERD) and/or hiatal hernia, 2 of whom underwent Nissen fundoplication in hopes of preventing future recurrences. Although a definite cause of the recurrent DAD was not identified, the findings suggest the possibility of a reaction to narcotics and/or psychotropic drugs in some patients, with a possible additional effect of GERD. A drug history should be carefully elicited in patients with recurrent DAD, and all potentially toxic drugs should be stopped.
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PMID:Diffuse alveolar damage and recurrent respiratory failure: report of 6 cases. 1177 76

A case of the cerebellar form of progressive multifocal leukoencephalopathy (PML) without remarkable immune depression or immune deficiency is reported here. The patient was a 74-year-old-woman who had complications of chronic renal failure and renal anemia for several years. Seven months before her death she had symptoms of general fatigue, gait disturbance and articulation disorder. During her hospitalization period her neurological disorder gradually progressed irreversibly with failure of consciousness and she died of respiratory failure. She did not have remarkable clinical signs of immunodeficiency nor did she receive immunosuppressive therapy. Clinically she had not been diagnosed with PML. At the post-mortem examination different degrees of demyelination were observed in the brain white matter: diffuse and severe in the cerebellum, moderate and coalescent in the brainstem, and light and patchy in the cerebrum. JC virus antigen-positive cells were frequently observed in the demyelinated lesions in the cerebrum and sometimes observed in the brainstem, but were rarely found in the cerebellum. These findings suggest that PML lesions may be present with different degrees of demyelination that are inversely correlated with the number of JC virus-infected cells. This fact should be considered when evaluating the brain biopsies of PML patients.
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PMID:Autopsy case of the cerebellar form of progressive multifocal leukoencephalopathy without immunodeficiency. 1203 Apr 15

Four basic control mechanisms of breathing (brainstem respiratory centre, peripheral and central chemoreceptors, intero- and exteroceptive reflexes and suprapontine influences), as well as their sleep-related disorders are analysed. A decrease in central chemoreceptor sensitivity to CO2 and an increase in upper airway resistance during sleep result in hypoventilation and mild hypoxaemia already in physiological conditions. Compensatory increase in ventilatory effort with synchronous inhibition of pharyngeal dilators during sleep reduces the upper airway lumen manifesting with snoring, upper airway resistance syndrome, and OSA. The resulting hypoxaemia may cause marked cardiovascular, neuro-psychic, endocrine-metabolic and behavioural disorders. The augmented ventilatory effort and hypoxaemia evoke reflex dilation of airways and arousal from sleep, stimulating the sympatho-adrenal system, which provokes autoresuscitation by gasping preventing fatal asphyxia. Failure of this autoresuscitation mechanism seems to cause SIDS. Elimination of voluntary breathing by sleep either in Ondine's curse induced by lesions of respiratory centre, or in congenital central hypoventilation syndrome caused by insufficient central chemoreceptors result in respiratory failure and death. Nocturnal attacks of bronchial and cardiac asthma, lung oedema and other consequences of pulmonary congestion are also discussed. The pathomechanism of extreme daytime sleepiness, chronic fatigue, and disorders of memory, cognitive and other brain functions, are also analysed. Severe cardiovascular consequences of SAS may manifest acutely as angina pectoris, myocardial infarction. dysrhythmias, transient ischaemic attacks and even stroke or sudden cardiac death. OSAS may result also in development of hypertension, central obesity, diabetes mellitus, erectile dysfunction, depression, and various behavioural disorders.
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PMID:[Regulation of respiration and its sleep-related disorders]. 1244 39

A 66-year-old-male patient with a history of depression voluntarily ingested around 400 ml of an insecticide composed of 5% methylparathion, 75% isoparaffin, 8% etoxylated oleic acid, 4% 1,2,4-trimethylbenzene, 6% naphtha, 1% 1,3,5- trimethylbenzene, 0.4% propylbenzene and 0.3% xylene. The patient was conscious and alert at admission. Gastric lavage was performed and activated charcoal administered. There were no clinical symptoms of organophospate ingestion despite reduced concentrations of erythrocyte and plasma cholinesterase. Chest X-ray showed pulmonary infiltrate compatible with bronco-aspiration. The patient evolved to respiratory failure refractory to treatment and died from multiorganic failure 23 days after ingesting the insecticide. The pathological findings included a pulmonary fibrosis in the alveolar spaces which caused enlargement of the intra-alveolar septa. Abundant lipin-laden macrophages were observed within the alveolar spaces. We review the most relevant aspects of cases of fatal lipoid pneumonia and point out that on occasion severe or fatal intoxication is due to the substances accompanying the active ingredients.
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PMID:Fatal lipoid pneumonia due to bronco-aspiration of isoparaffin after ingestion of an organophosphate insecticide. 1280

Respiratory failure occurs due mainly either to lung failure resulting in hypoxaemia or pump failure resulting in alveolar hypoventilation and hypercapnia. Hypercapnic respiratory failure may be the result of mechanical defects, central nervous system depression, imbalance of energy demands and supplies and/or adaptation of central controllers. Hypercapnic respiratory failure may occur either acutely, insidiously or acutely upon chronic carbon dioxide retention. In all these conditions, pathophysiologically, the common denominator is reduced alveolar ventilation for a given carbon dioxide production. Acute hypercapnic respiratory failure is usually caused by defects in the central nervous system, impairment of neuromuscular transmission, mechanical defect of the ribcage and fatigue of the respiratory muscles. The pathophysiological mechanisms responsible for chronic carbon dioxide retention are not yet clear. The most attractive hypothesis for this disorder is the theory of "natural wisdom". Patients facing a load have two options, either to push hard in order to maintain normal arterial carbon dioxide and oxygen tensions at the cost of eventually becoming fatigued and exhausted or to breathe at a lower minute ventilation, avoiding dyspnoea, fatigue and exhaustion but at the expense of reduced alveolar ventilation. Based on most recent work, the favoured hypothesis is that a threshold inspiratory load may exist, which, when exceeded, results in injury to the muscles and, consequently, an adaptive response is elicited to prevent and/or reduce this damage. This consists of cytokine production, which, in turn, modulates the respiratory controllers, either directly through the blood or probably the small afferents or via the hypothalamic-pituitary-adrenal axis. Modulation of the pattern of breathing, however, ultimately results in alveolar hypoventilation and carbon dioxide retention.
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PMID:Respiratory failure. 1462 Nov 12

This paper reports a study undertaken to determine whether differences exist in practice between respiratory physicians, general physicians and intensivists or between individual clinicians in initiating mechanical ventilation in respiratory failure due to chronic obstructive pulmonary disease (COPD), the factors influencing decision-making and their relation to the evidence base. Of 725 questionnaires sent to clinicians, 350 (48%) were completed and analysed. Twenty-five variables were included which clinicians scored 0-3 according to their perceived relevance in the decision. The sum of all the responses was calculated for each clinician: respiratory 15-68, general 12-65, intensivists 16-64. The most important variables in withholding ventilation were lung cancer inoperable due to COPD, and nursing home resident. The least important variables were treated depression and osteoporosis. No significant differences existed in practice between specialties but there were great differences between individuals' practices. Clinicians were influenced by similar factors, but these did not reflect documented poor outcome predictors. Guidelines are needed.
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PMID:Clinical decision-making and mechanical ventilation in patients with respiratory failure due to an exacerbation of COPD. 1470 38

Autopsy is invaluable in identifying the causes of severe depression and very low Apgar score after birth and in assessing contributory conditions. Brain scans are increasingly used in the care of neonates who fail to respond to resuscitation at birth but their interpretation depends on the information gained from sound neuropathological studies. Asphyxia, both acute intrapartum asphyxia and chronic asphyxia, is an important cause of low Apgar scores. The gestational age and the nature of the asphyxial insult both have a profound influence on the ultimate pattern of injury. Asphyxia in the preterm brain tends to damage preferentially the white matter but some white matter damage is also seen in many infants who have an hypoxia-ischaemic insult at term though the predominant site of injury is to the central grey matter. The nature of the cellular damage and reactive change seen at autopsy is described. There is an association between low Apgar scores and intrauterine exposure to infection and maternal pyrexia. Detailed autopsy examination should include the search for infection. The placenta, cord and membranes should be examined in view of the mounting evidence of the association between intrauterine infection of the placenta and fetal membranes and prenatal brain damage. Additionally, the presence of placental thrombosis and infarction should be sought in relation to focal and global injury in the full term infant. Acquired prepartum lesions rarely cause the infant to present with a low Apgar score. The exception to this is severe damage to the brainstem and basal ganglia. Traumatic injury to the brain is now much less common than in previous decades. Subdural haemorrhage occurs more frequently than intraventricular or subarachnoid haemorrhage. Instrumental and assisted deliveries are associated with an increased incidence of subdural haemorrhage though these rarely cause significant long term damage. Careful autopsy, particularly of the neck and paravertebral tissues, spinal cord, brainstem and nerve roots is important where trauma is suspected. Tearing of nerve roots or fibre bundles in the spinal cord is readily demonstrated under the microscope using immunocytochemistry to beta-amyloid precursor protein. Disorders of the spinal cord, peripheral nerve and muscle as well as some metabolic diseases may cause a baby to be both floppy and weak. Metabolic disease, including peroxisomal disorders, non-ketotic hyperglycinaemia, lipid and glycogen storage disorders and mitochondrial diseases may cause profound hypotonia and respiratory failure at birth or shortly afterwards.
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PMID:The value of autopsy in determining the cause of failure to respond to resuscitation at birth. 1525 Nov 49

Acute respiratory failure is a common complication of drug abuse. It is more likely to develop in the setting of chronic lung disease or debility in those with limited respiratory reserve. Drugs may acutely precipitate respiratory failure by compromising respiratory pump function and/or by causing pulmonary pathology. Polysubstance overdoses are common, and clinicians should anticipate complications related to multiple drugs. Impairment of respiratory pump function may develop from central nervous system (CNS) depression (suppression of the medulla oblongata, stroke or seizures) or respiratory muscle fatigue (increased respiratory workload, metabolic acidosis). Drug-related respiratory pathology may result from parenchymal (aspiration-related events, pulmonary edema, hemorrhage, pneumothorax, infectious and non-infectious pneumonitides), airway (bronchospasm and hemorrhage), or pulmonary vascular insults (endovascular infections, hemorrhage, and vasoconstrictive events). Alcohol, cocaine, amphetamines, opiates, and benzodiazepines are the most commonly abused drugs that may induce events leading to acute respiratory failure. While decontamination and aggressive supportive measures are indicated, specific therapies to correct seizures, metabolic acidosis, pneumothorax, infections, bronchospasm, and agitation should be considered. Drug-related respiratory failure when due to CNS depression alone may portend well, but in patients with drug-related significant pulmonary pathology, a protracted course of illness may be anticipated.
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PMID:Acute respiratory failure from abused substances. 1529 19

Chlorophenoxy herbicides are used widely for the control of broad-leaved weeds. They exhibit a variety of mechanisms of toxicity including dose-dependent cell membrane damage, uncoupling of oxidative phosphorylation and disruption of acetylcoenzyme A metabolism. Following ingestion, vomiting, abdominal pain, diarrhoea and, occasionally, gastrointestinal haemorrhage are early effects. Hypotension, which is common, is due predominantly to intravascular volume loss, although vasodilation and direct myocardial toxicity may also contribute. Coma, hypertonia, hyperreflexia, ataxia, nystagmus, miosis, hallucinations, convulsions, fasciculation and paralysis may then ensue. Hypoventilation is commonly secondary to CNS depression, but respiratory muscle weakness is a factor in the development of respiratory failure in some patients. Myopathic symptoms including limb muscle weakness, loss of tendon reflexes, myotonia and increased creatine kinase activity have been observed. Metabolic acidosis, rhabdomyolysis, renal failure, increased aminotransferase activities, pyrexia and hyperventilation have been reported. Substantial dermal exposure to 2,4-dichlorophenoxy acetic acid (2,4-D) has led occasionally to systemic features including mild gastrointestinal irritation and progressive mixed sensorimotor peripheral neuropathy. Mild, transient gastrointestinal and peripheral neuromuscular symptoms have occurred after occupational inhalation exposure. In addition to supportive care, urine alkalinization with high-flow urine output will enhance herbicide elimination and should be considered in all seriously poisoned patients. Haemodialysis produces similar herbicide clearances to urine alkalinization without the need for urine pH manipulation and the administration of substantial amounts of intravenous fluid in an already compromised patient.
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PMID:Poisoning due to chlorophenoxy herbicides. 1557 61

Spinal muscular atrophy with respiratory distress type 1 (SMARD1) is a fatal autosomal recessive disorder seen in infants. It is characterized by lower motor neuron degeneration, progressive muscle paralysis and respiratory failure, for which no effective treatment exists. The phenotype of neuromuscular degeneration (nmd) mice closely resembles the human SMARD1. The identification of the mutated mouse gene in nmd mice, Ighmbp2, led to the discovery of mutations of the homologous gene in humans with SMARD1. We have studied the nmd mouse model with in vivo electrophysiological techniques and evaluated the efficacy of Mab2256, a monoclonal antibody with agonist effect on the tyrosine kinase receptor C, trkC, on disease progression in nmd mice. Treatment with Mab2256 resulted in a significant but transient improvement of muscle strength in nmd mice, as well as normalization of the neuromuscular depression during high-frequency nerve stimulation. These results suggest the potential of using monoclonal agonist antibodies for neurotrophin receptors in lower motor neuron diseases such as SMARD1.
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PMID:Treatment with trkC agonist antibodies delays disease progression in neuromuscular degeneration (nmd) mice. 1588 78


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