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)

Twenty-four patients with bronchial adenoma seen over a 20-year period are reviewed. Follow-up data was available in all patients. They included 19 with carcinoid, 2 with adenoid-cystic carcinoma, and 3 with muco-epidermoid carcinoma. Recurrent pulmonary infection, cough and hemoptysis were the most common clinical manifestations. Surgical resection was performed in all but one patient, who was treated by irradiation; bronchoplastic and conservative resectional procedures were used in 5 patients with carcinoid adenoma. Carcinoid tumors are considered to be very slowly-growing malignant neoplasms that sometimes give rise to metastases to regional lymph nodes. Such metastases were present in only one patient. All patients are alive and well. Adenoid-cystic carcinoma is a more aggressive tumor with a tendency to recur. Much of the difficulty in its treatment is due to its close proximity to the bifurcation of the trachea. One patient was operated upon three times for local recurrences and ultimately died from respiratory failure after the third operation. The other patient received radiation therapy with cobalt and is well, without recurrence, 3 years after the treatment. The 3 muco-epidermoid carcinomas were histologically similar to such tumors of salivary glands but behaved clinically like highly malignant tumors, no patients surviving 8 months after resection. The term bronchial adenoma is a misnomer. The neoplasms grouped under this heading should be called carcinoid adenoma, adenoid-cystic carcinoma, and muco-epidermoid carcinoma and considered as separate entities, since the ultimate course and prognosis is definitely different.
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PMID:[Bronchial adenoma]. 19 6

Palliative therapy for previously irradiated patients with symptomatic recurrent endobronchial malignancy is a difficult problem. We have had the opportunity to treat 20 such patients with high dose rate (50-100 rad/min) endobronchial brachytherapy. Eligible patients had received previous high dose thoracic irradiation (TDF greater than or equal to 90), a performance status of greater than or equal to 50, and symptoms caused by a bronchoscopically defined and implantable lesion. The radiation is produced by a small cobalt-60 source (0.7 Ci) remotely afterloaded by cable control. The source is fed into a 4 mm diameter catheter which is placed with bronchoscopic guidance; it may oscillate if necessary to cover the lesion. A dose of 1,000 rad at 1 cm from the source is delivered. We have performed 22 procedures in 20 patients, four following YAG laser debulking. Most had cough, some with hemoptysis. Eight had dyspnea secondary to obstruction and three had obstructive pneumonitis. In 12, symptoms recurred with a mean time to recurrence of 4.3 months (range 1-9 months). Eighteen patients were followed-up and reexamined via bronchoscope 1-2.5 months following the procedure; two were lost to follow-up. All had at least 50 percent clearance of tumor, and six had complete clearance; most regressions were documented on film or videotape. In six, the palliation was durable. The procedure has been well tolerated with no toxicity. We conclude that palliative endobronchial high dose rate brachytherapy is a useful palliative modality in patients with recurrent endobronchial symptomatic carcinoma.
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PMID:High dose rate intraluminal irradiation in recurrent endobronchial carcinoma. 241 6

Forty-six plate painters, heavily exposed to cobalt blue dye, took part in this cross-sectional study, and 51 top-glaze painters served as the referents. The study comprised a questionnaire, a health examination, a lung function test, and the determination of the blood and urinary cobalt levels. The plate painters were examined twice, at the end of a workfree period and after resuming work. More plate painters complained of irritation from the mucous membranes in the mouth and throat, cough, and expectoration than the referents. The symptoms increased after the plate painters resumed work. The cobalt level of the plate-painting group after six weeks off work was twice as high in the blood and five times higher in the urine than the corresponding values of the reference group. After the plate painters resumed work, the blood and urinary levels increased approximately 4 and 15 times, respectively. Increased airflow resistance was found in the plate group when compared with the referents, and signs of small airway obstruction increased after the plate painters resumed work. The pulse rate was higher among the plate painters, and minor changes in the red blood cell picture were observed. None of these adverse health effects were associated with the cobalt levels in the blood or urine.
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PMID:Health effects due to occupational exposure to cobalt blue dye among plate painters in a porcelain factory in Denmark. 326 37

Five diamond polishers with interstitial lung disease attributed to cobalt not alloyed to carbides of hard metals are described. The exposure originated from high-speed grinding tools with a polishing surface of microdiamonds cemented in very fine cobalt. Mineralogic analysis of lung tissue, lavage fluid, filtered air, and exhaust dust in the work environment revealed cobalt as the only toxic agent. Complaints consisted of work-related rhinitis, cough, chest tightness, dyspnea, anorexia, and weight loss, and were intensified in the absence of an adequate exhaust ventilation. Three subjects were in a rather subacute stage, as documented by open lung biopsy in 2 of them, and had a severe restrictive defect and markedly decreased diffusing capacity. Two patients presented a more chronic histologic pattern and had a less decreased diffusing capacity. Open lung biopsies showed in these 4 a fibrosing alveolitis, mainly of the centrilobular zones. In the former 2 patients, subacute lesions consisting of a mural mononuclear cell infiltrate, marked intra-alveolar desquamation, and multinucleated giant cells were found, whereas in the latter 2, centrilobular fibrosis with some microcyst formation was also already seen. Multiple multinucleated giant cells were present in the bronchoalveolar lavage fluid. Interruption of the exposure, with or without corticotherapy, caused a rapid regression of the complaints and a partial improvement of lung function.
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PMID:Cobalt lung in diamond polishers. 674 97

A 20-year-old labourer, employed in the metal powder industry, developed increasing shortness of breath and serious urge to cough after 2 1/4 years of exposition to cobalt and tungsten carbide powder. On admission 9 months later pulmonary changes were demonstrated radiographically indicating hard-metal-dust lung. Detailed clinical assessment including transpleural biopsy and lingula resection as well as histochemical investigations and follow-up observations permitted access to the pathogenesis and morphology of the disease. By introduction of steroid treatment, before conclusion of diagnostic steps, limitation of the inflammatory primary reaction was possible inasmuch as loss of pulmonary function could be arrested despite massive, histologically verified, tendency for fibrosis.
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PMID:[Hard metal pulmonary fibrosis]. 711 53

The objectives of the study were to determine whether grinders and brazers of hard metal and stellite blades have more respiratory symptoms and dermatoses than referents and to obtain information on the relation between respiratory symptoms and combined exposure to cobalt and wood dust. Two groups of workers exposed to cobalt (108 workers in the manufacture or maintenance of tools and 116 saw filers in the mechanical wood-processing industry) and two reference groups (106 rolling mill and 103 sawmill workers) were interviewed. The prevalence of ODTS-like symptoms (work-related cough, dyspnoea, or fever or chills) was higher for the saw filers than the sawmill referents. After adjustment for age, time spent in present work, smoking and atopy, saw filers had a higher risk for fever or chills than the other study groups. When the cobalt-exposed and unexposed workers were compared by smoking, differences in the prevalence of ODTS-like symptoms were found only for the non-smokers. The cobalt-exposed workers did not have a higher risk of hand dermatoses or symptoms of metal allergy than the unexposed workers. It seems that combined cobalt and wood dust exposure is associated with ODTS-like symptoms, especially among non-smoking workers.
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PMID:Respiratory symptoms and dermatoses among grinders and brazers of hard metal and stellite blades. 913 16

It is a case report on a 55-year-old non-smoking female, dental technician, with a 36-year history of cobalt exposure. The patient suffered from dyspnea, coughing and decrease in physical load tolerance about 20 years after the first occupational contact with cobalt-containing metal dentures. Skin tests performed with a battery of common allergens (metals: nickel, chrome, cobalt; acrylates; disinfectants; and natural rubber latex) were negative. In the patient, interstitial radiological changes, respiratory insufficiency and decrease in diffusion capacity were observed. While performing a provocation test with 0.05% cobaltous chloride, the patient developed dyspnea with concomitant decrease in 1 second forced expiratory volume (FEV1) and peak respiratory flow (PEF) from the beginning of the 3rd hour after provocation and maximum intensity at the 8th hour. These symptoms persisted until the 24th hour. The authors conclude that occupational exposure of the dental technician to cobalt dust derived from metal dentures may cause chronic airway disease with interstitial inflammation, fibrosis and occupational asthma.
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PMID:[Occupational asthma and interstitial cobalt-induced changes in a dental technician: a case report]. 1292 99

Even in the twenty-first century, welding is still a common and a highly skilled occupation. The hazardous agents associated with welding processes are acetylene, carbon monoxide, oxides of nitrogen, ozone, phosgene, tungsten, arsenic, beryllium, cadmium, chromium, cobalt, copper, iron, lead, manganese, nickel, silver, tin, and zinc. All welding processes involve the potential hazards for inhalation exposures that may lead to acute or chronic respiratory diseases. According to literature described earlier it has been suggested that welding fumes cause the lung function impairment, obstructive and restrictive lung disease, cough, dyspnea, rhinitis, asthma, pneumonitis, pneumoconiosis, carcinoma of the lungs. In addition, welding workers suffer from eye irritation, photokeratitis, cataract, skin irritation, erythema, pterygium, non-melanocytic skin cancer, malignant melanoma, reduced sperm count, motility and infertility. Most of the studies have been attempted previously to evaluate the effects of welding fumes. However, no collectively effort illuminating the general effects of welding fumes on different organs or systems or both in human has not been published. Therefore, the aim of this review is to gather the potential toxic effects of welding fumes documented by individual efforts and provide informations to community on hazards of welding.
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PMID:Health hazards of welding fumes. 1464 49

Chronic toxic dust bronchitis in workers exposed to wolfram and cobalt has been progressing in the course of many-year exposure to hazardous occupational factors. Its prevalence among the main-occupation workers is 2.2-fold higher versus workers of the control group who have never contacted the metal aerosols. The disease onset is slow and gradual in an overwhelming majority of cases and has the below clinical-and-functional peculiarities: 1) predominance of dyspnea over cough in the early bronchitis stage; 2) an early and often development of the concurrent asthmatic component; 3) subjective symptoms are far ahead of objective examination findings in the early disease stage; 4) obstructive changes in the distal sections of the air-conducting system (maximum-air-velocity volume75), if detected in latent bronchitis, can be a basis for an early disease diagnosis; 5) as well as lower key hemodynamic parameters and development of the hypokinetic blood circulation type, whereas, compensatory hyperfunctioning of the myocardium and the hyperkinetic blood circulation type are found in patients with occupational dust bronchitis working in other productions.
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PMID:[Specific clinical course of occupational toxic dust bronchitis in workers exposed to wolfram and cobalt]. 1510 76

The case of a forty-six year old, male patient with asthma caused by exposure to dust containing chrome is presented. When the patient was nineteen years old, he started working as a stonemason in a factory. He cut and ground stone with a stone-cutter to make statues and tombstones. Three years after staring to work, contact dermatitis was observed on his arms and hands. Within six years of work, he suffered from chronic coughing. After eight years, he experienced bronchial asthma attacks with wheezing and dyspnea. He had been exposed to dust for eight years before developing asthma. The symptoms increased gradually. He fell into severe asthma attacks causing unconsciousness and dyspnea. Several common therapies were not effective. The characteristics of his clinical course and occupational history suggested that the asthma must be caused by exposure to dust containing metal generated in the factory. Skin Patch Tests (SPT) were performed for cobalt, copper, iron, chrome, tin, and manganese salt. The result of the SPT indicated a strong positive result for potassium dichromate and positive for chromium sulfate, but did not show any indications in the control or for other metallic salt. Fluorescent X-ray analysis detected that chrome was present in the powder dust under the stone-cutter machine. However, the fluorescent X-ray analysis did not detect chrome in the stone materials. It was suggested that chrome must be contained in the metal dust generated from the steel cutter used to cut off and grind the stone. The metal component in the used cutter edge and the unused cutter edge were analyzed with electro-probe microanalyzer (EPMA). The result revealed that chrome was contained in the used, dull cutter edge and not in the new sharp cutter edge. Thus, the patient had been exposed to the dust containing chrome generated from part of the stainless steel of cutter. He had sensitized to chrome and this had caused the occupational chrome-asthma.
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PMID:[A case of chrome asthma induced by exposure to the stone cutter dust]. 1718 17


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