Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A phase I and pharmacokinetic study of recombinant tumor necrosis factor (rH-TNF Asahi) was carried out in 29 patients, who received a total of 72 courses with doses ranging from 1 to 48 X 10(4) units/m2. Drug was given as 1-h i.v. infusions. Acute toxicities, taking the form of fever, chills, tachycardia, hypertension, peripheral cyanosis, nausea and vomiting, headache, chest tightness, low back pain, diarrhea and shortness of breath were seen, but were not dose-limiting or dose-related. Some early rise in SGOT, without any change in serum bilirubin, was noted at the highest doses. Eosinophilia, monocytosis, mild hypocalcemia and an increase in fibrin degradation products were seen in a few patients. The dose-limiting toxicity was hypotension, which occurred after the end of the drug infusion and was seen in all 5 patients treated at the highest dose. There was no mortality or long-term morbidity. There were no responses. Pharmacokinetic studies indicated a rapid plasma clearance and a short plasma half-life, generally less than 0.5 h.
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PMID:Phase I clinical trial of recombinant human tumor necrosis factor. 366 33

Twenty-one subjects exposed to formaldehyde (at levels between 0.12 and 1.6 parts per million [ppm]) in two mobile trailers and the remaining 18 unexposed workers of the same workforce were examined by questionnaire and spirometry. Symptoms of eye and throat irritation and increased headache and fatigue were significantly more common among the exposed group than the comparison group. Irritation of the nose, chest tightness, and shortness of breath were also more common among the exposed. Spirometry revealed no decrease in ventilatory function among the exposed workers. The significant increase in frequency of individuals with symptoms indicated an adverse health effect from exposure to formaldehyde at levels between 0.12 and 1.6 ppm. This may have implications regarding the adequacy of the US permissible exposure limit value and suggests the need for further examination of the health effects of formaldehyde in the nonoccupational environment.
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PMID:Health effects of low-level exposure to formaldehyde. 665 25

To study the clinical and physiologic manifestations of the grain fever syndrome and the potentially pathogenic role of complement activation, 12 subjects (six grain workers and six healthy non-grain workers) underwent inhalation provocations with airborne grain dust. The clinical response was characterized by facial warmth, headache, malaise, myalgias, feverish sensation, chilliness, throat and tracheal burning sensation, chest tightness, dyspnea, cough, and expectoration. Fever developed in four grain workers and two controls. Leukocytosis, ranging between 11,700 and 24,300 leukocytes/mm3 with left shift, developed in five grain workers and five controls. There was no evidence of complement activation by the classical or alternate pathway. None of the subjects had serum precipitins to grain dust. The pulmonary response was characterized by a decrease in FEV1, FVC, MMF, Vmax50, and Vmax75, with significant rise in pulmonary resistance and consistent change in dynamic compliance but without changes in static compliance or diffusing capacity. Hence, grain dust inhalation induced diffuse airways obstruction without detectable parenchymal reaction. The airways response to high concentrations of grain dust inhalation were unrelated to the presence of immediate skin hypersensitivity. Although we cannot exclude the etiopathogenetic role of an immunologic reaction to grain dust, our data do not support the hypothesis that the grain fever syndrome is a precipitin-mediated allergic pneumonitis. More likely, the manifestations of grain fever probably reflect the host reaction to grain dust bacterial endotoxins and/or nonallergic mediator release by grain or grain dust constituents.
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PMID:Grain fever syndrome induced by inhalation of airborne grain dust. 707 83

We tested and proved the safety of recombinant human tumor necrosis factor given intravesically weekly for 11 weeks (dwell time 2 hours) for the treatment of superficial bladder cancer in 8 men and 1 woman 46 to 87 years old (mean age 69 years). Cohorts of 3 patients received 200, 400 and 1,000 micrograms. recombinant human tumor necrosis factor. The maximal tolerated dose was not achieved. There were 9 episodes of urological symptoms, 8 of flu-like symptoms, 4 of headache and 3 of chest tightness. Hematological and gastrointestinal toxicities were minor, and no renal toxicity was encountered. Recombinant human tumor necrosis factor was safe to administer at doses up to 1,000 micrograms. We hope that recombinant human tumor necrosis factor in conjunction with other antitumor agents will lead to a new, effective treatment for superficial bladder cancer.
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PMID:Intravesical recombinant tumor necrosis factor in the treatment of superficial bladder cancer: an Eastern Cooperative Oncology Group study. 777 58

The sick building syndrome (SBS) has been the subject of serious scientific inquiry only in the past 10 years. It is commonly accepted to represent eye, nose, and throat irritation; headaches, lethargy, difficulty concentrating, and sometimes dizziness; nausea, chest tightness; and other symptoms. Evidence suggests that what is called the SBS is at least three separate entities, each of which has at least one cause. This review will summarize the epidemiologic investigations of the SBS and present an overview of etiologic hypotheses.
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PMID:Epidemiology of the sick building syndrome. 807 80

The purpose of this study was to determine the prevalence rates of acute and chronic neurologic symptoms among paint workers and the association of such symptoms with the severity of exposure to mixtures of solvents. Two paint manufacturing factories and 25 various kinds of spray painting factories were selected for study. Air concentrations of organic solvents were measured by personal samplers and were analyzed by gas chromatography. A total of 196 workers were given a screening neurological examination and a questionnaire on acute and chronic neurologic symptoms. A detailed personal medical history and a profile on alcohol consumption and medication were also included. The results showed that xylenes and toluene were the major solvents found in almost all the air samples with average contents of 50 and 24% on a weight basis of 73 air samples. We classified workers according to different exposure patterns and different air concentrations of breathing zones: high (8-hr hygienic effect, 0.25-9.86; median, 1.66), short-term high (hygienic effect, 0-3.38; median, 0.12), and low (hygienic effect, 0-0.38; median, 0.12). All workers showed no overt neurological signs such as ataxic gait, poor coordination, or muscle weakness. After excluding those workers who consumed more than 280 g of alcohol per week (n = 8), took antihypertensive medications (n = 4), or were treated with antipsychotic agents (n = 1), we found that the severity of exposure was associated with acute symptoms of headache and chest tightness and chronic symptoms of dizziness, easy fatigability, depressed mood, and palpitation. There was no association between peripheral neurological symptoms and the severity of exposure. Workers in the high exposure group were 2.7 times more likely to develop two or more acute symptoms and 3.3 times more likely to develop three or more chronic symptoms of the central nervous system than the low exposure group. After modeling by multiple logistic regression, we concluded that exposure to a medium level of mixtures of solvents (hygienic effect exceeding 1.66) may produce acute and chronic central neurological symptoms.
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PMID:Acute and chronic neurological symptoms among paint workers exposed to mixtures of organic solvents. 847 64

Two train conductors had chest tightness, painful breathing, muscle cramps, and nausea after fighting a fire in a battery box under a passenger coach. Shortly thereafter, they became anosmic and had excessive fatigue, persistent headaches, sleep disturbances, irritability, unstable moods, and hypertension. Urinary cadmium and nickel levels were elevated. Neurobehavioral testing showed, in comparison to referents, prolonged reaction times, abnormal balance, prolonged blink reflex latency, severely constricted visual fields, and decreased vibration sense. Test scores showed that immediate verbal and visual recall were normal but delayed recall was reduced. Scores on overlearned information were normal. Tests measuring dexterity, coordination, decision making, and peripheral sensation and discrimination revealed abnormalities. Repeat testing 6 and 12 months after exposure showed persistent abnormalities. Cadmium and vinyl chloride are the most plausible causes of the neurotoxicity, but fumes from the fire may have contained other neurotoxic chemicals.
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PMID:Persistent neurotoxicity from a battery fire: is cadmium the culprit? 868 56

Legionella pneumophila is the cause of Legionnaires' disease, and Pontiac fever, an influenza-like condition without pneumonia. We present a case of Pontiac fever after exposure to a hot tub contaminated with L pneumophila. A 37 y/o wf presented to the office with acute onset of sore throat, fever, headache, and myalgia. Patient was hospitalized 3 days later because of worsening shortness of air. Chest x-ray was normal. Patient was treated with 2 days of IV erythromycin and was discharged home on oral erythromycin. Her Legionella IFA was 1:16,384. Two days later, she developed chest tightness, pleuritic chest pain, and increasing shortness of air but did not have any cough or sputum production. She was re-hospitalized with a diagnosis of Pontiac fever and treated with IV erythromycin plus oral rifampin. A repeat chest x-ray remained normal. After a detailed epidemiologic history was obtained, it was noted that she became ill after using a hot tub, which her two children also used and they themselves developed a self limited illness. Water from the hot tub was positive for L pneumophila by DFA, culture, and PCR. Patient improved gradually with therapy and was discharged home. This report emphasizes the importance of a complete epidemiologic history in the diagnosis of respiratory infections. It also demonstrates that aquatic environment can be contaminated with Legionella and serve as a source of infection.
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PMID:Hot tub legionellosis. 885 93

Endotoxins are lipopolysaccharides from the outer cell wall of Gram-negative bacteria. Exposure to endotoxins can take place in industries where organic material is handled, in agriculture, in garbage handling, and sewage treatment. Byssinosis defined as Monday chest tightness and slight dyspnoea in the work place has been related to endotoxin exposure in cotton mills, but studies indicate that similar symptoms may be found in other work places. Other symptoms are: Headache, nausea, gastrointestinal symptoms and influenza-like symptoms. Several studies have shown a decrease in FEV1 following exposure to endotoxins. The relationship between exposure to organic dust, microorganisms, endotoxins and other chemicals in the work place and disease needs further research.
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PMID:[Exposure to endotoxins in the environment. Occurrence and health hazards]. 918 80

A 72-year-old man was exposed to the sarin gas attack in a Tokyo subway on March 20 th, 1995. After exposure, he noticed eye discomfort, chest tightness, headache and weakness of the lower limbs and oropharyngeal muscles. Despite these symptoms, he visited a hot spring on the same day with his family. On March 25 th, his muscle weakness progressed, and a low grade fever appeared. His muscle weakness disappeared 8 days after exposure to sarin, but respiratory failure rapidly developed, necessitating artificial ventilation within four day after hospitalization on March 28th. Chemotherapy with erythromycin, imipenem/cilastatin, and steroid pulse therapy was begu. PCR and culture of sputum collected by bronchofiberscopy were positive for Legionella pneumophila, serogroup I. His respiratory state improved, but subsequent infection with Pseudomonous aeruginosa. Enterobacter cloacae, and Candida tropicalis/glabrata caused his death 71 days after admission. Oropharyngeal muscle weakness caused by sarin-mediated cholinesterase inhibition was strongly suspected as the cause of hot spring water aspiration. Transbronchial lung biopsy revealed organizing pneumonia with fibrosis. Bronchoscopic findings included redness, edema and fragility of all visible areas of the airway, which was thought to be due to bronchitis caused by Legionellosis.
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PMID:[Legionella pneumonia caused by aspiration of hot spring water after sarin exposure]. 965 77


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