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 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

On a temporal basis, air has immense capacity for moving a large mass of pollutants. Mammals and birds are exposed to pollutants in air by the inhalation (nose and mouth), cutaneous or ocular routes. Most laboratory studies on air pollutants have been limited to single air pollutants and very little research has been done on the complex mixture of compounds that exist in ambient air. Complex mixtures are further complicated by dynamic chemical reactions that occur after the emissions leave point sources. Exposure parameters are also important in the toxicity of air pollutants. Intermittent exposure of monkeys to ozone increased the adverse pulmonary effects. Superimposing spikes of 0.8 ppm nitrogen dioxide on a baseline of 0.2 ppm, as occurs on a calm winter day, increased the susceptibility of mice to bacteria-induced pneumonia. Sulfur dioxide at concentrations of 5 ppm increased pulmonary resistance by 39%. Sulfuric acid is the predominate acid particle in the atmosphere. Exposure for 1 h to > 200 micrograms sulfuric acid/m3 depressed bronchomucociliary clearance. Concentrations of 100 micrograms/m3 of photochemical products caused headaches and 510 micrograms/m3 produced cough and chest pain. For chemical interactions in dose response, nitrogen dioxide is synergistic with ozone and ammonium sulfate. When all 3 chemicals are used in mixture, the response was 340%. Atmospheric conditions, such as fog, can alter the toxicity of air pollutants. The dose response to a single chemical can be altered by chemical mixtures and pre-existing disease conditions. Understanding these relationships is important for establishing no observable adverse effect levels. Mechanisms for multiple chemical interactions are multifaceted. One chemical may interfere with the metabolism or detoxification of another. Others may interact at cell receptors. To understand the effects of multiple chemical interactions of air pollutants, there is a need for a blend of epidemiological, laboratory and field studies. Studies are expensive. In the rural agricultural settings, the economic and environmental health risks are high. Should field observations and chemical problems be used as "red flags" for action?
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PMID:A review of the toxicology of air pollutants: toxicology of chemical mixtures. 888 47

Patients reporting sensitivity to multiple chemicals at levels usually tolerated by the healthy population were administered standardized questionnaires to evaluate their symptoms and the exposures that aggravated these symptoms. Many patients were referred for medical tests. It is thought that patients with chemical sensitivity have organ abnormalities involving the liver, nervous system (brain, including limbic, peripheral, autonomic), immune system, and porphyrin metabolism, probably reflecting chemical injury to these systems. Laboratory results are not consistent with a psychologic origin of chemical sensitivity. Substantial overlap between chemical sensitivity, fibromyalgia, and chronic fatigue syndrome exists: the latter two conditions often involve chemical sensitivity and may even be the same disorder. Other disorders commonly seen in chemical sensitivity patients include headache (often migraine), chronic fatigue, musculoskeletal aching, chronic respiratory inflammation (rhinitis, sinusitis, laryngitis, asthma), attention deficit, and hyperactivity (affected younger children). Less common disorders include tremor, seizures, and mitral valve prolapse. Patients with these overlapping disorders should be evaluated for chemical sensitivity and excluded from control groups in future research. Agents whose exposures are associated with symptoms and suspected of causing onset of chemical sensitivity with chronic illness include gasoline, kerosene, natural gas, pesticides (especially chlordane and chlorpyrifos), solvents, new carpet and other renovation materials, adhesives/glues, fiberglass, carbonless copy paper, fabric softener, formaldehyde and glutaraldehyde, carpet shampoos (lauryl sulfate) and other cleaning agents, isocyanates, combustion products (poorly vented gas heaters, overheated batteries), and medications (dinitrochlorobenzene for warts, intranasally packed neosynephrine, prolonged antibiotics, and general anesthesia with petrochemicals). Multiple mechanisms of chemical injury that magnify response to exposures in chemically sensitive patients can include neurogenic inflammation (respiratory, gastrointestinal, genitourinary), kindling and time-dependent sensitization (neurologic), impaired porphyrin metabolism (multiple organs), and immune activation.
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PMID:Profile of patients with chemical injury and sensitivity. 916 75

A young patient suffering from schizophrenia had intense headaches and photophobia which were induced by intra-ocular injections of mercury. The clinical diagnosis was established once foreign bodies were visualized on regular X-rays of the patients skull. The mercury intoxication in combination with the secondary irreversible lesions to the eyes necessitated a bilateral enucleation and the use of a chelating treatment with sodium-dimercapto-1-propane sulfate (DMP). Automutilation is a very rare and dramatic complication of schizophrenia. The psychiatric handling and meaning of such dramatic automutilation is discussed in this case report together with a recent review of the toxicologic treatment of mercury intoxication in humans.
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PMID:[Voluntary mercury poisoning: biological consequences and psychiatric significance]. 928 93

The main indication for orthotopic liver transplantation (OLTx) in Wilson's disease (WD) is severe hepatic decompensation. Our 15-year-old patient is the second case to date in whom OLTx was performed because of neurologic manifestations resulting from WD. His initial condition involving recurrent headaches, tremor, and athetoid hand movements progressively deteriorated during therapy with D-penicillamine, zinc sulfate, and trientine until he was severely dysarthric, unable to walk, and bedridden. After OLTx, his neurologic condition became almost normal.
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PMID:Cerebral manifestation of Wilson's disease successfully treated with liver transplantation. 974 41

The clinical presentation of malaria is, in most of cases, a malaria attack. It occurs in 90% of imported cases in France within 30 days after return of endemic area. Characteristic malaria paroxism have three stages: chills, high fever (> 39 degrees C) and sweating stage. In this typical form, parasitaemia is easily disclosed. With the increasing spread of chemoresistance P. falciparum strains, many patients experience non specific symptoms before the onset of paroxysm, often complaining of malaise, headaches, myalgias and anorexia. In some cases temperature did not exceed 38 degrees C and physical examination revealed sometimes liver or splenic enlargement. These atypical presentations can masquerade other diseases such as a viral illness. In those patients blood smears were often negative and malaria diagnosis is carried out only by QBC or parasight test. Treatment of malaria attack needs antimalarial drugs effective against chemoresistant P. falciparum strains. Mefloquine of halofantrine can be delivered with the respect of guidelines prescription, given major side effects observed with these drugs (neuropsychiatric disorders with mefloquine and cardiac arrhythmias with halofantrine). Oral quinine sulfate can be used when the above drugs are not allowed.
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PMID:[Simple malaria attack]. 978 Oct 73

Herbal medicinals are being used by an increasing number of patients who typically do not advise their clinicians of concomitant use. Known or potential drug-herb interactions exist and should be screened for. If used beyond 8 weeks, Echinacea could cause hepatotoxicity and therefore should not be used with other known hepatoxic drugs, such as anabolic steroids, amiodarone, methotrexate, and ketoconazole. However, Echinacea lacks the 1,2 saturated necrine ring associated with hepatoxicity of pyrrolizidine alkaloids. Nonsteroidal anti-inflammatory drugs may negate the usefulness of feverfew in the treatment of migraine headaches. Feverfew, garlic, Ginkgo, ginger, and ginseng may alter bleeding time and should not be used concomitantly with warfarin sodium. Additionally, ginseng may cause headache, tremulousness, and manic episodes in patients treated with phenelzine sulfate. Ginseng should also not be used with estrogens or corticosteroids because of possible additive effects. Since the mechanism of action of St John wort is uncertain, concomitant use with monoamine oxidase inhibitors and selective serotonin reuptake inhibitors is ill advised. Valerian should not be used concomitantly with barbiturates because excessive sedation may occur. Kyushin, licorice, plantain, uzara root, hawthorn, and ginseng may interfere with either digoxin pharmacodynamically or with digoxin monitoring. Evening primrose oil and borage should not be used with anticonvulsants because they may lower the seizure threshold. Shankapulshpi, an Ayurvedic preparation, may decrease phenytoin levels as well as diminish drug efficacy. Kava when used with alprazolam has resulted in coma. Immunostimulants (eg, Echinacea and zinc) should not be given with immunosuppressants (eg, corticosteroids and cyclosporine). Tannic acids present in some herbs (eg, St John wort and saw palmetto) may inhibit the absorption of iron. Kelp as a source of iodine may interfere with thyroid replacement therapies. Licorice can offset the pharmacological effect of spironolactone. Numerous herbs (eg, karela and ginseng) may affect blood glucose levels and should not be used in patients with diabetes mellitus.
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PMID:Herbal medicinals: selected clinical considerations focusing on known or potential drug-herb interactions. 1049 30

Exemestane is an irreversible, steroidal, oral aromatase inhibitor under evaluation in postmenopausal women with advanced breast cancer. A phase I study was conducted in 27 postmenopausal patients who were candidates for hormone therapy because they had advanced breast cancer and estrogen receptor-positive or unknown status. Most patients were moderately or heavily pretreated. Cohorts of at least three patients received sequentially escalating daily oral doses of 5-600 mg. The median duration of exemestane treatment was 13 weeks (range: 3-166 weeks). The maximal tolerated dose was not reached because of lack of treatment-related grade 3 or 4 toxicity. The most common adverse events, including those not related to treatment, were mild to moderate headache (44% of patients), dizziness (33%), nausea (33%), hot flushes (30%) and tumor-related pain (30%). There were three complete and four partial responses for an objective response rate of 26% (95% CI: 11.1-46.3%) in the intent-to-treat population; the median duration of response was 74 weeks (95% CI: 48-99 weeks). Exemestane, at the dose of 25 mg, maximally suppressed estradiol, estrone and estrone sulfate serum levels to 13, 5 and 10% of baseline, respectively. Exemestane appears to suppress estrogen, be well tolerated and have antitumor activity in postmenopausal women with advanced breast cancer. A large, safe therapeutic window of up to 600 mg was defined. In view of its safety and estrogen-suppression profiles, the most favorable effects were observed at the 25 mg daily dose.
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PMID:Safety, activity and estrogen inhibition by exemestane in postmenopausal women with advanced breast cancer: a phase I study. 982 25

The simultaneous occurrence of multiple adenomas in the pituitary gland is a rare event. We report the coexistence of three non functioning pituitary microadenomas in a 37-year-old woman, referred to us for oligomenorrhea and headache. Biochemical evaluation revealed prolactin (131 U/liters), follicle-stimulating hormone (4.1 U/liters), luteinizing hormone (3.9 U/liters), 17beta-estradiol (74 pg/mL), free (2.0 pg/mL) and total testosterone (0.5 ng/mL), dehydroepiandrosterone-sulfate (3.5 microg/mL), 17OH-progesterone (0.8 ng/mL), cortisol (13.1 microg/dL), free triiodothyronine (4.8 pmol/L), free thyroxine (18.5 pmol/liters), thyrotropin (1.6 mU/L), and growth hormone (0.2 ng/mL) levels in the normal range, as for as the response to dynamic endocrine tests. MRI showed an enlarged sella turcica, occupied by three distinct hypointense areas that measured less than 5 mm in diameter in the left, medium and right side of the pituitary, respectively. This finding was confirmed 6 months later by a second MRI that revealed also a light increase in microadenomas dimensions. The patient, therefore, underwent neurosurgery by transfenoidal approach. Histologic examination showed no morphologic differences between the specimens obtained from the different microadenomas. Immunohistochemistry evaluation revealed a positive staining for the common alpha-subunit of glycoproteic hormones and negative for the other pituitary hormones tested, while electron microscopy showed cells with a poor secretory apparatus and a variable grade of cell differentiation. In conclusion, we report the fifth case described with multiple pituitary adenomas diagnosed in vivo and the first with three coexisting tumors revealed by MRI before neurosurgery. The occurrence of multiple pituitary tumors emphasizes the role of pituitary and extrahypophiseal factors in the clonal expansion of genetically altered cells.
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PMID:Unusual MRI finding of multiple adenomas in the pituitary gland: a case report and review of the literature. 1023 Nov 91

Preeclampsia is a disease which occurs in Europe in about 6-8%, in the USA in about 7-10% and in Africa in about 18% of all pregnancies. A causal treatment of preeclampsia is, with the exception of delivery, not possible up to now. Since a prematurely delivery of the newborn has to be avoided because of the risks caused by immaturity of lungs, treatment and care of pregnant women having preeclampsia or any other kind of hypertensive diseases is restricted to the following approaches: antihypertensive treatment, volume expansion, and eclampsia prophylaxis with magnesium sulfate. Object of this treatment is to avoid complications on the mother's side caused by the disease and to postpone delivery, as far as possible from the child's side, in order to reduce the consequences of premature birth. During antihypertensive treatment of patients with serious hypertension, i.e. with diastolic blood pressure of 110 x mm Hg and higher, dihydralazine is in clinical use since 40 years, although many patients suffer from side-effects of dihydralazine such as distinctive tachycardia, headaches, fluid retention and nausea. With urapidil a well controllable antihypertensive is available, which prevents the effect of catecholamines at the vascular wall by a postsynaptic alpha-1 receptor blockade. Previous studies related to the application of urapidil in the treatment of hypertension during pregnancy certify the good controllability of urapidil following intravenous application as well as minor side-effects after start of treatment.
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PMID:[Current aspects of antihypertensive therapy in pregnant patients with pre-eclampsia]. 1066 77

More than 2200 subjects were enrolled in the MorphiDex (MS:DM) development program, with a 1:1 (weight:weight) ratio of morphine sulfate (MS) to dextromethorphan hydrobromide (DM). Of the 1400 subjects exposed to MorphiDex, more than 350 subjects were treated for at least 6 months, and over 200 subjects were treated for a year or longer. The clinical population comprised an approximately equal number of men (46.2%) and women (53.8%), ranging in age from 16 to 96 years, and mostly Caucasian (91.8%). The most frequent (54.8%) daily dose of MorphiDex for subjects enrolled in the clinical program was 120 mg or less. Slow DM metabolizers took significantly lower daily doses of MorphiDex than rapid metabolizers without a significant difference in the incidence of adverse events. Plasma bromide concentrations were low and showed a wide margin of safety for both slow and rapid DM metabolizers. There were no clinically significant treatment-related changes in clinical laboratory tests, neurological examinations, or vital signs. The most common adverse events seen in the multiple dose controlled studies were nausea, dizziness, vomiting, somnolence, constipation, confusion, asthenia, headache, and pruritus. With long-term treatment, the prevalence of adverse events was greatest during the first month of MorphiDex exposure and then decreased over time. The incidence of constipation remained fairly constant over time.
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PMID:Long-term safety of MorphiDex. 1068 40


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