Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Enprofylline, a xanthine-derivative shown experimentally to lack universal adenosine receptor antagonism, has been examined in patients with partly reversible, chronic, obstructive lung disease. Significant bronchodilation was produced by enprofylline 2 mg/kg, giving a peak plasma concentration of 3.0 +/- 0.6 microgram/ml (mean +/- SD). A dose of 2 + 4 mg/kg dilated the bronchi at least to the same extent as theophylline 9.2 +/- 0.9 mg/kg (plasma level 18.5 +/- 4.7 micrograms/ml). Neither at the low nor at the high dosage (2 +/- 4 mg/kg), giving plasma concentrations of 8.5 +/- 1.4 microgram/ml, did enprofylline produce theophylline-like CNS effects, such as restlessness and tremor, but it did exhibit some of the innocuous side effects expected with xanthine derivatives, such as epigastric discomfort and headache. The comparison with theophylline was limited because different dosage forms had to be used (solution an tablets), which for example, resulted in different absorption rates. Nevertheless, the present findings indicate enprofylline to be potent bronchodilator in patients with obstructive lung disease, suggesting that adenosine-receptor antagonism is not involved in the bronchodilator effects of xanthines.
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PMID:Effects of enprofylline, a xanthine lacking adenosine receptor antagonism, in patients with chronic obstructive lung disease. 628 96

1 Serum theophylline levels were performed in 26 patients with chronic lung disease receiving rapid release theophylline (125 mg 6 hourly) and 28 patients receiving slow release theophylline (250 mg 12 hourly) under steady state conditions. 2 For rapid release theophylline the mean +/- s.d. serum theophylline levels at 0 and 2 h were 41.0 +/- 21.7 and 52.3 +/- 20.9 mumol l-1 respectively and for slow release theophylline at 0, 4 and 6 h 43.7 +/- 25.5, 50.9 +/- 23.0 and 51.7 +/- 26.4 mumol l-1 respectively. 3 Serum theophylline monitoring with slow release theophylline was performed in 70 patients with chronic lung disease. The initial dose was 250 mg administered 12 hourly. 4 The mean +/- s.d. steady state serum theophylline level achieved was 76.0 +/- 18.8 mumol l-1 and the mean +/- s.d. dose to produce this level was 9.4 +/ 2.3 mg kg-1 day-1. There was no correlation between dosage and serum theophylline level. 5 Sixty percent of patients required a dosage change for stabilization (375 to 1000 mg/day). Seventeen patients reported unwanted effects (nausea or tremor), which either settled quickly or resolved with dosage reduction. 6 Serum theophylline levels were obtained at different dosages in 44 patients and 18 patients demonstrated dose-dependent kinetics. 7 An initial dose of 500 mg/day is recommended and dosage increments should not exceed 125 mg/day with monitoring by serum theophylline levels.
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PMID:Serum level monitoring of a new slow release theophylline formulation in patients with chronic lung disease. 743 44

In any febrile patient with an unexplained chest radiographic abnormality who is on medication, the possibility that the observed abnormality is drug-induced must be kept in mind. This is a significant problem in the immunocompromised host receiving chemotherapeutic agents because these agents are almost always associated with a fever, although the fever may not be daily and is usually not associated with sweats or shaking chills. The infiltrate initially can be quite focal and then unilateral, exhibiting diffuse lung disease before becoming bilateral. Thus, in its early stages, it mimics an infectious process. Unfortunately there is no diagnostic test to rule in drug-induced lung disease because it really is a condition of exclusion. Lung biopsy may be required to exclude other causes. It is also important to remember that drugs may be a factor in the immunocompetent patient who is taking medication and has a fever. It is important for the clinician to be aware of which drugs can do this.
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PMID:Drug-induced pulmonary disease. 756 3

The history of the spinal muscular atrophies (SMA) began in the 1890s with Guido Werdnig and Johann Hoffmann. Together, their papers present a rather complete picture of the clinical and pathologic aspects of infantile SMA: onset during the first year of life, occurrence in siblings with normal parents, progressive floppiness and weakness, hand tremor, and death from pneumonia in early childhood. Based on the work of an international collaboration, the following is current nomenclature: SMA type 1 (or I) for onset of symptoms before age 6 months, SMA type 2 (II) for onset between 6 and 18 months, and SMA type 3 (III) for onset after age 18 months. Linkage of autosomal recessive SMA to chromosome 5q11.2-13.3 was reported by Gilliam et al in 1990. A novel gene, whose function remains unknown, called the survival motor neuron gene (SMN) at 5q13, contains deletions in more than 98% of SMA patients. Some patients with atypical forms of SMA have been shown to have mutations in SMN. Because there is no effective therapy for SMA, management consists of preventing or treating the complications of severe weakness, such as restrictive lung disease, poor nutrition, orthopedic deformities, immobility, and psychosocial problems.
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PMID:Spinal muscular atrophy. 956 64

As blood levels of carbon dioxide increase (hypercapnia) in lung disease such as chronic obstructive pulmonary disease (COPD), patients can show signs of delirium, becoming increasingly confused and sleepy. They may also have wrist tremor, muscle twitching, seizures and dilation of conjunctival and superficial facial blood vessels.
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PMID:Use of non-invasive ventilation. 2773 15