Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The "polydrug use" well known at the USA, has sprayed in France and Europe during the last ten years. Harms of polydrug use were pointed out by some specialized centers. The aim of this work is to emphasize the dangers of the abuse of some drug associations. Animal pharmacology, clinical observations and epidemiology are the main research method involved animal in the study of "polydrug use". These methods are often difficult to perform in elderly persons and in pregnant women. It is not easy to extrapolate from animals to man. The pharmacokinetics of drugs often differs from a species to another. Animal models are nevertheless useful for studies dealing with drug interactions, especially with enzyme metabolism. Clinical studies will be dependent on the ethical questions. Some examples are mentioned. Alcohol use develops in many drug addicts, particularly in those on methadone maintenance. The association of cocaine and other amphetamine-type stimulants with morphinics or cannabis is very dangerous. Other associations are quite frequent including various hypnotics or cough suppressants (even nomorphinic). "Polydrug use" generally increase mortality in drug addicts. The medical profession is not well informed on this subject. Further research must be led on the harmful effects of drug associations and on the reasons leading drug addicts to multiplicate drug associations in an almost epidemic way.
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PMID:[Multiple drug addiction]. 147 26

Upper respiratory and pulmonary complications of cocaine addiction have been increasingly reported in recent years, with most of the patients being intravenous addicts, users of freebase, or smokers of "crack." The toxicity of cocaine is complex and is exerted via multiple central and peripheral pathways. Recurrent snorting of cocaine may result in ischemia, necrosis, and infections of the nasal mucosa, sinuses, and adjacent structures. Pulmonary complications of cocaine toxicity include pulmonary edema, pulmonary hemorrhages, pulmonary barotrauma, foreign body granulomas, cocaine related pulmonary infection, obliterative bronchiolitis, asthma, and persistent gas-exchange abnormalities. Respiratory manifestations are nonspecific and include shortness of breath, cough, wheezing, hemoptysis, and chest pains. Severe respiratory difficulties have been reported in neonates of abusing mothers. In the absence of a cocaine-abuse history, it may be difficult to recognize the etiological role of cocaine, especially in the absence of needle tracks pointing to previous intravenous drug abuse and/or negative toxicology.
Recent Dev Alcohol 1992
PMID:Respiratory complications of cocaine abuse. 158 7

Spontaneous regression of a malignant tumor is a rare phenomenon, especially in advanced lung cancer. We reported a case of spontaneous regression of lung cancer with tracheal stenosis due to tumor invasion and multiple skin metastases. A 60-year-old man was admitted to our hospital on September 10, 1985, because of a dry cough. A chest roentgenogram showed a mass shadow in the right upper lung field. Bronchoscopic examination revealed tracheal stenosis due to the tumor mass, and transbronchial aspiration cytology (TBAC) yielded a diagnosis of large cell carcinoma of the lung. In spite of treatment by chemotherapy with cisplatin and vindesin and irradiation, dyspnea deteriorated and multiple skin metastases appeared. After Nd-YAG laser irradiation via a broncho-fiberscope to maintain his airway and ethanol injection into the skin metastases, his dyspnea improved and he was discharged on February 6, 1986. Two months after discharge all skin metastasis had completely disappeared, and the primary lesion also regressed and finally disappeared on chest roentgenogram until August, 1986. The mechanism of regression is unclear, but now he has been free of tumor clinically for four years.
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PMID:[A case of spontaneous regression of lung cancer with skin metastasis]. 164 18

Zipeprol is a non-opioid cough suppressor agent recently abused in Italy. Clinical reports from 30 street abusers show that the drug in high doses has a definite abuse liability and dependence potential. Many of its effects were identical to those induced by opiates, although specific dysperceptive symptoms were commonly reported by patients. Spontaneous withdrawal symptoms were similar to those of opiates. Withdrawal could be also precipitated by naloxone. It is concluded that zipeprol can induce dependence with a mechanism which may be mediated by some types of opioid receptors.
Drug Alcohol Depend 1991 Mar
PMID:Zipeprol is a newly abused antitussive with an opioid spectrum and hallucinogenic effects. 205 60

We investigated whether stimulation of vagal afferent nerve fibers with inhaled capsaicin could induce a nonadrenergic inhibitory reflex in nine mild asthmatic subjects. Changes in total respiratory resistance (Rrs) were measured with a forced oscillation technique. First we induced a rise of 71 +/- 15% in Rrs (P less than 0.001) after leukotriene D4 aerosol. Subsequent inhalation of capsaicin (2 nmol) caused no significant change in mean Rrs of -1.1 +/- 8.2%. After the muscarinic receptor antagonist ipratropium bromide (120 micrograms) was inhaled, leukotriene D4 increased Rrs by 103 +/- 9% (P less than 0.001). Capsaicin subsequently caused bronchodilation in all subjects (Rrs = -22.3 +/- 2.7%, P less than 0.001). Ethanol-saline (diluent) alone caused a nonsignificant fall in Rrs (-9.9 +/- 4.7%) but a deep breath and coughing resulted in bronchodilation (-16.9 +/- 6.1%, P less than 0.05 and -11.6 +/- 2.9%, P less than 0.01, respectively). As observed in normal subjects, capsaicin may initiate an inhibitory reflex, presumably of nonadrenergic origin. This reflex could not be distinguished from that caused by coughing or by deep inhalation. A defect in nonadrenergic mechanisms, at least in mild asthma, seems unlikely.
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PMID:Capsaicin-induced bronchodilation in mild asthmatic subjects: possible role of nonadrenergic inhibitory system. 252 37

In seven normal subjects we investigated whether a nonadrenergic bronchodilator nervous system is demonstrable in humans in vivo. After inhalation of leukotriene D4 (LTD4), respiratory resistance (Rrs) increased by 115 +/- 11% (SE). Subsequent inhalation of 2 nmol of capsaicin induced coughing and a fall in Rrs of 22.1 +/- 2% (P less than 0.01). However, inhalation of the diluent of capsaicin, 10% saline-ethanol, decreased Rrs similarly. These bronchodilator responses were not altered by inhaled ipratropium bromide (120 micrograms) and oral propranolol (80 mg). After ipratropium and propranolol, voluntary coughing alone decreased Rrs by 25 +/- 3% (P less than 0.05). We next investigated whether these bronchodilator responses could be blocked by anesthesia of the airways with inhaled lidocaine. After inhalation of lidocaine and LTD4, capsaicin aerosol induced coughing and a transient increase in Rrs of 18 +/- 6% (P less than 0.05) but no bronchodilation. Inhalation of saline-ethanol (n = 4) and a deep inhalation (n = 6) decreased Rrs by 18 +/- 4% (P less than 0.05) and 34 +/- 3% (P less than 0.001), respectively. We conclude that in normal subjects a nonadrenergic, noncholinergic bronchodilator mechanism exists, which can be activated by inhalation of capsaicin and inhibited by local anesthesia.
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PMID:Nonadrenergic bronchodilator mechanisms in normal human subjects in vivo. 296 70

We evaluated in a double-blind study the bronchodilatory properties of 2-decarboxy-2-hydroxymethyl prostaglandin E1 (PGE1-carbinol), described recently as a nonirritant bronchodilator in animals. Fifteen asthmatic patients received by inhalation single doses of 1, 10, and 30 micrograms PGE1-carbinol, 55 micrograms PGE2, and placebo (10% ethanol in normal saline, which was also used as diluent for the PGs). Such pulmonary function tests as forced expiratory volume in 1 second, forced vital capacity, and maximal expiratory flow were monitored during 2 hours following inhalation of each compound. 10 and 30 micrograms PGE1-carbinol produced significant but short-acting bronchodilation, similar to that caused by 55 micrograms PGE2. One-third of the patients reported mild cough and throat irritation during and shortly after inhalation of 30 micrograms PGE1-carbinol or 55 micrograms PGE2. Placebo and 1 microgram PGE1-carbinol produced minimal side effects, but neither agent caused bronchodilation. In an adjunctive, unblinded trial, the same patients received 400 micrograms fenoterol. Fenoterol caused greater bronchodilation 15 and 30 minutes after inhalation than did the PGs in the double-blind study.
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PMID:Bronchodilatory properties of 2-decarboxy-2-hydroxymethyl prostaglandin E1. 385 12

Twenty seven patients, inspected by endoscope, and diagnosed as having the Mallory-Weiss syndrome, have been studied taking into account their age, sex, background, clinic presentation, manifestations, number of lacerations, associated lesions and evolution. Twenty three of them were males and 4 females. The age average was 46.7 years. Only 8 patients had intra-abdominal increased pressure, suffering retching and vomiting 7 of them, while one had a cough access. Out of the 21 patients that we controlled, 9 were chronic alcoholism while 3 had ethanol intoxication previously. Immediate prior ingestion of salicylates had taken place in 6 patients. The clinical presentation of 22 of them was gastrointestinal bleeding, that is, 4.9% of all the upper endoscopies carried out within the bleeding patients. Single laceration was present in 22 cases, double one in 4, and triple in 1. We have frequently found endoscopy lesions associated, the most common one (37%), was hiatal hernia. They all were medically treated except one, who was operated because of gastric perforation was associated. Just one of the Mallory-Weiss syndrome patient died, due to an associated diffused bleeding gastritis.
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PMID:[Mallory-Weiss syndrome. Considerations on 27 cases]. 697 2

The usual presenting features of vitamin A intoxication are pseuotumor cerebri, skeletal pain, desquamative dermatitis, and hepatic inflammation. Our patient was a nine-year-old female who had increasing cough, dyspnea, and abdominal distention for a short time prior to admission. She was said to have been treated with 10,000 units of vitamin A per day for skin rashes. Radiographic studies revealed a very large right sided pleural effusion, ascites, demineralized bones, and retarded skeletal maturation. The diagnosis of hypervitaminosis A was made. More detailed medical history confirmed that the child had, in actuality, received up to 300,000 units/day of vitamin A plus desiccated liver pills and carrot juice for the previous year. Clinical symptoms completely abated following acute medical treatment for ascites and cessation of vitamin A intake. Several months later, a sample of liver, obtained and preserved at the time of exploratory laparotomy, was homogenized and extracted with ethanol/hexane. The retinyl palmitate level was significantly elevated and consistent with vitamin A poisoning.
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PMID:Pleural effusion and ascites: unusual presenting features in a pediatric patient with vitamin A intoxication. 708 15

1 The airway response to inhaled prostaglandin E2 (PGE2) and the effect of oral propranolol on this response was studied in eight normal subjects in a double-blind randomised trial. The airway response was measured as specific airway conductance (sGaw). 2 Inhalation of PGE2 caused retrosternal soreness, coughing and an awareness of mucus production. Despite this, PGE2 caused bronchodilatation and reproducible dose-response curves were obtained, with a maximum increase in sGaw of 53%. 3 Inhalation of the diluent of PGE2, an ethanol/saline mixture, did not cause irritation nor did it alter sGaw. 4 Prior administration of propranolol 80 mg did not alter baseline sGAW, nor the response to PGE2, indicating that the action of PGE2 in vivo is unaffected by bronchial beta-adrenoceptor blockade. 5 This technique should be of value in studying bronchodilator prostaglandins and their interaction with other drugs.
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PMID:Effect of propranolol on the airway response to prostaglandin E2 in normal man. 733 39


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