Publication rates in Australia, Canada, UK, and US pharmacy schools.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to D F Thompson.
Explore the source record for details and available documents.
Prussian blue is a crystal lattice that exchanges potassium for cesium at the surface of the crystal. When given orally, it binds cesium that is secreted in the gut before it can be reabsorbed. Data suggest that in humans, Prussian blue can reduce cesium's half-life by approximately 43% and reduce total body burdens. Prussian blue is well tolerated at a dosage of 3 g/day with appropriate monitoring of serum potassium levels and observing for signs of constipation. Clinical data on the efficacy of Prussian blue in the management of radiocesium poisoning were evaluated. Articles published in English describing distribution and elimination of cesium in both humans and animals were reviewed, along with articles describing administration of Prussian blue in clinical toxicology.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
OBJECTIVE: To compile and assess the English-language literature on drug-induced nightmares, excluding nightmares secondary to drug withdrawal or drug-associated night terrors. DATA SOURCES: Published articles, letters, case reports, and abstracts in English were identified by MEDLINE (1966-May 1998) searches using the search term nightmares, chemically induced. Additional articles were obtained from bibliographies of retrieved articles. DATA EXTRACTION: All case reports of drug-induced nightmares were evaluated using the Naranjo algorithm for causality. Clinical studies of drugs that reported nightmares as an adverse effect were assessed for frequency of occurrence. DATA SYNTHESIS: Nightmares, defined as nocturnal episodes of intense anxiety and fear associated with a vivid, emotionally charged dream experience, are generally classified as a parasomnia. Possible pharmacologic mechanisms for drug-induced nightmares, such as REM suppression and dopamine receptor stimulation, are reviewed. However, the vast majority of therapeutic agents implicated in causing nightmares have no obvious pharmacologic mechanism. CONCLUSIONS: Assessing causality with an event such as a nightmare is difficult because of the high incidence of nightmares in the healthy population. Using qualitative, quantitative, and possible pharmacologic mechanism criteria, it appears that sedative/hypnotics, beta-blockers, and amphetamines are the therapeutic modalities most frequently associated with nightmares. These drug classes have a plausible pharmacologic mechanism to explain this effect. Dopamine agonists also have evidence of causality, with dopamine receptor stimulation as a possible pharmacologic mechanism.
Fibrin glue is composed of two separate solutions of fibrinogen and thrombin. When mixed together, these two solutions mimic the final stages of the clotting cascade to form a fibrin clot. Because the resulting fibrin patch is a good medium for microbial growth, the addition of antibiotics to one of the components of fibrin glue has been shown to reduce postoperative infections. Seventeen different antibiotics have been investigated in vitro. Of the 17, cefotaxime, mezlocillin, gentamicin, neomycin, and polymixin B, when added to fibrin glue, can decrease the rate of clot formation or the strength of the resultant fibrin clot. Further work is necessary to characterize the effect the addition of antibiotics has on the rate and strength of fibrin clotting and to determine what effect low systemic levels of antibiotics might have on antibiotic resistance patterns.
Pharmacotherapeutic agents are uncommonly associated with hiccups. Corticosteroids and benzodiazepines have been the drug classes mentioned most frequently in the literature as being associated with the development of hiccups. However, by using a strict criterion, there is currently insufficient evidence for any drug to be considered causative in the etiology of hiccups.
Explore the source record for details and available documents.
These data suggest the presence of peripheral opioid receptors that are involved in the clinical perception of pain. This is a radical change in our traditional thinking of opioid pharmacology and pain management. Most clinicians have been taught that opioids work through the central nervous system. These new data depart from this traditionally held view of an exclusively central site of action. Further data, specifically, additional dose-response data with varying amounts of morphine, additional studies in pain syndromes other than knee arthroscopy, and the development and pharmacology of orally active opioid compounds that do not cross the central nervous system, are necessary to confirm and expand the present findings. The possibility of providing opioid pain relief free of central nervous system adverse effects is an exciting prospect. Additional studies of topical opioid preparations also would be of interest.
Numerous studies suggest that opiate antagonists may have antipsychotic properties. A review of the literature describing the use of naloxone to treat schizophrenic patients has shown mixed results. The three studies on naltrexone have found no benefit in controlling auditory hallucinations. We present a synopsis of these studies.
OBJECTIVE: To evaluate recent data that suggest that total iron binding capacity (TIBC) is not a reliable laboratory parameter in assessing acute iron overdose. DATA SOURCES: A MEDLINE search of the literature with a fan search of relevant articles. STUDY SELECTION AND DATA EXTRACTION: Laboratory, human, and animal studies on the measurement and relevance of TIBC in acute iron poisoning were reviewed. These data were analyzed in light of the current guidelines for use of TIBC in assessing iron poisoning. DATA SYNTHESIS: There are significant data to suggest that the sensitivity of TIBC in acute iron poisoning is unacceptable. This lack of sensitivity is also reflected in the poor positive predictive value of TIBC. The specificity and negative predictive value are higher but not without error. One survey of 500 laboratories reported a coefficient of variation for TIBC of 16 percent (95 percent confidence interval), suggesting unacceptable accuracy. CONCLUSIONS: These data suggest that TIBC may not be a reliable laboratory parameter in assessing acute iron poisoning. Studies are needed to develop a reliable analytical procedure for TIBC and to correlate TIBC with clinical outcomes in acute iron poisonings.
OBJECTIVE: To review doxorubicin-induced cardiotoxicity and to evaluate the use of dexrazoxane in its prevention. DATA SOURCES: All animal and human reports involving doxorubicin-induced cardiac adverse effects were searched using MEDLINE combined with a fan search of relevant papers. DATA EXTRACTION: Animal, in vitro cellular, and human data are thoroughly reviewed with particular emphasis on doxorubicin-induced cardiotoxicity, including clinical manifestations, risk factors, and mechanisms of toxicity. The role of dexrazoxane in the prevention of doxorubicin-induced cardiotoxicity is reviewed, including mechanism of effect, animal data, and human trials. DATA SYNTHESIS: Anthracyclines are associated with a cumulative, dose-dependent, irreversible cardiomyopathy that can lead to congestive heart failure and death. The incidence of cardiotoxicity rises sharply at a total lifetime dose of more than 550 mg/m2. Through its semiquinone metabolite, doxorubicin appears to generate superoxide anion and superhydroxide free radicals with iron as a cofactor. Because of poor myocardial concentrations of superoxide dismutase, catalase, and glutathione peroxidase, these free radicals cause extensive lipid peroxidation and mitochondrial destruction. CONCLUSIONS: Dexrazoxane is hydrolyzed to its active form intracellularly and binds iron to prevent the formation of superhydroxide radicals, thus preventing mitochondrial destruction. The effect of dexrazoxane on the prevention of doxorubicin-induced cardiotoxicity is impressive in both animal and human studies. Further research is needed to clearly demonstrate the effect dexrazoxane has on the antitumor effects of combination chemotherapy while defining optimal dosing strategies to minimize myelosuppression and maximize cardioprotection.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Thrombocytosis is generally defined as platelet counts greater than 400,000/mm3. Thrombocytosis can be either primary or secondary. Adrenalin was one of the first drugs noticed to cause platelet elevations, probably due to demargination of platelets in the pulmonary vasculature. Vinca alkaloids have the most convincing data to show that they can induce thrombocytosis through their thrombocyte-stimulating properties. Miconazole has been implicated in causing thrombocytosis and has a documented case validated by drug rechallenge. Iron, predictably, can cause a transient thrombocytosis. The beta-lactam antibiotic data are very difficult to interpret due to the possibility of an acute-phase reaction in an infected patient being the cause of the thrombocytosis.
Drug-induced parotitis is a relatively uncommon adverse drug reaction. Most of the data on drug-induced parotitis consist of isolated case reports with few attempts at rechallenge to confirm the aetiology. Phenylbutazone and oxyphenbutazone have a significant number of reports suggesting that these drugs may be implicated in causing parotitis. Antipsychotics, particularly thioridazine, have been associated with parotitis. Most of these reports relate the anticholinergic oral drying as a predisposing factor in the development of a parotid gland infection. There is inadequate literature on the histamine (H2) receptor blockers, interferon-alpha, doxycycline, trimipramine, nifedipine, methyldopa, nitrofurantoin, nicardipine, isoproterenol or ritodrine to link them as aetiological agents in the development of parotitis.
OBJECTIVE: To review the evidence that antenatal phenobarbital can reduce the incidence or severity of periventricular-intraventricular hemorrhage (PIVH) in low-birthweight neonates. DATA SOURCES: MEDLINE searches were conducted with fan searches of all papers. STUDY SELECTION: Emphasis was placed on human data supplemented by relevant animal data. DATA SYNTHESIS: The barbiturates have been used to reduce hypoxic-ischemic cerebral events. Giving phenobarbital to high-risk pregnant women allows the drug to be in therapeutic concentrations during the critical period when PIVH occurs in low-birthweight infants. Current data suggest that antenatal phenobarbital can decrease the severity of PIVH; fewer data are available stating that it can decrease the incidence of PIVH. CONCLUSIONS: Evidence supports the hypothesis that antenatal phenobarbital is effective in decreasing the severity of PIVH in low-birthweight neonates. Further data are necessary regarding the incidence of low Apgar scores and respiratory depression in neonates given antenatal phenobarbital.
Explore the source record for details and available documents.